Klima-, Energi- og Forsyningsudvalget 2020-21
L 42 Bilag 1
Offentligt
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Advokat Christian F. Jensen (L)
Øverødvej 5, 2. sal
2840 Holte
Tlf. 29 82 70 04
[email protected]
RESPONSUM
om
hvorvidt det vil være i strid med menneske- og miljøretlige regler
at etablere 5G-systemet i Danmark
ENDELIG UDGAVE
Rachel Santini, leder af forskernetværket ”Dansk Institut for Folkesundhed”, Rådet for
Helbredssikker Telekommunikation, EHS-foreningen og Oplysningsforbundet May Day har bedt mig
udarbejde et responsum om ovennævnte problemstilling.
Responsummet baseres på retsreglerne i Den Europæiske Menneskerettighedskonvention, FN's
børnekonvention, EU's habitatdirektiv, fuglebeskyttelsesdirektiv og forsigtighedsprincip, samt Bern-
og Bonn-konventionerne om beskyttelse af dyr og planter.
Besvarelsen er opdelt i et pkt. 1, som vedrører faktum (om 5G-systemet samt forskning i
skadevirkninger ved radiofrekvent elektromagnetisk stråling), og et pkt. 2, der sammenholder
faktum med ovennævnte retsregler. Pkt. 3 indeholder en overordnet konklusion.
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Indholdsfortegnelse
1. Faktum.
1.1. Hvad er 5G?
1.2. Forskningen.
1.2.1. Fokus i nærværende responsum.
1.2.2. Mennesker: Helbredsmæssige skader og risici.
1.2.2.1. DNA-skader.
1.2.2.1.1. Delkonklusion.
1.2.2.2. Kræft.
1.2.2.2.1. Klassificering.
1.2.2.2.2. Øvrigt.
1.2.2.3. Andre helbredsskader på mennesker.
1.2.2.4. Særligt vedr. børn og kræft eller andre helbredsskader.
1.2.2.5. Delkonklusion.
1.2.3. Dyr.
1.2.3.1. Fugle.
1.2.3.1.1. Delkonklusion.
1.2.3.2. Andre dyr.
1.2.3.2.1. Delkonklusion.
1.2.4. Yderligere om leveområder samt planter.
1.2.4.1. Delkonklusion.
1.3. Overordnet delkonklusion.
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2. Jus.
2.1 De i Danmark anvendte grænser for eksponering for radiofrekvent elektromagnetisk stråling
2.2. Retsbeskyttelsen af mennesker (menneskerettigheder).
2.2.1. Den Europæiske Menneskerettighedskonvention (EMRK).
2.2.1.1. Art. 2 – retten til livet og statens positive forpligtelser.
2.2.1.1.1. Delkonklusion.
2.2.1.2. Art. 8 – retten til respekt for privat- og familieliv.
2.2.1.2.1. Delkonklusion.
2.2.2. FN's børnekonvention.
2.2.2.1. Delkonklusion.
2.3. Miljøretlige regler.
2.3.1. Forsigtighedsprincippet i EU-retten.
2.3.2. Fuglebeskyttelsesdirektivet.
2.3.2.1. Delkonklusion.
2.3.3. Habitat-direktivet
2.3.3.1. Delkonklusion.
2.4. Bern-konventionen
2.4.1. Delkonklusion.
2.5. Bonn-konventionen
2.5.1. Delkonklusion.
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3. Konklusion og afsluttende bemærkninger.
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1. Faktum.
1.1. Hvad er 5G?
”5G” er en samlebetegnelse for den næste (femte) generation af kommunikationssystem til
mobiltelefoner og internetbrug. Det har ikke nogen lovbaseret definition og er tilsyneladende
hverken fuldstændigt fastlagt eller standardiseret.
Den tilgængelige information om det påtænkte system kommer primært til udtryk via de
tiltænkte opgaver og formål, som 5G skal varetage, jf. f.eks. Europa-Kommissionens ”Working
document” af 14. september 2016, pkt. 3, og teleindustriens 5G-manifest
1
af 7. juli 2016.
5G-systemet er bl.a. beskrevet således i den videnskabelige litteratur, jf. Neufeld og Kuster
(2018), p. 705:
”THE FIFTH generation of wireless communication technology (5G) promises to facilitate
transmission at data rates up to a factor of 100 times higher than 4G. For that purpose, higher
frequencies (including millimeter-wave bands), broadband modulation schemes, and thus
faster signals with steeper rise and fall times will be employed, potentially in combination with
pulsed operation for time domain multiple access. 5G is designed as a ubiquitous
communication system spanning applications such as high-bandwidth mobile data and
telephony, real-time machine-to-machine communication (e.g., autonomous mobility), and the
Internet of Things (IoT).”
Det er bl.a. ikke endnu fastlagt, hvilke frekvensbånd 5G-systemet ville benytte, og det fremgår
af følgende tabel, at de frekvenser, der bl.a. overvejes, er de samme, som hidtil har været
udnyttet til tidligere generationer
2
:
Det hedder i et svar af 1. april 2019 fra Energi-, Forsynings- og Klimaministeren til folketingets
udvalg om samme om systemets påtænkte implementering i Danmark bl.a.:
”De grænseværdier, der bliver anvendt i Danmark, har baggrund i anbefalinger fra EU, der er
baseret på værdier fastlagt af den Internationale Kommission for Ikke-ioniserende Stråling
1
http://ec.europa.eu/newsroom/dae/document.cfm?action=display&doc_id=16579
2
Tabellen er anvendt i Europa-Parlamentets rapport af april 2019 om ”5G Deployment – State of play in Europe,
USA and Asia”, s. 10.
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(ICNIRP).
Teleselskaberne skal sikre overholdelse af grænseværdierne, som er 2 W/kg, hvor folk
opholder sig og færdes. Disse grænseværdier er teknologineutrale og det betyder, at
grænseværdierne gælder, uanset hvilken teknologi der er tale om fx 2G, 3G, 4G eller 5G.
Teleselskaberne har oplyst, at de forventer, at antallet af antennepositioner vil blive forøget
med 15-25 % frem mod 2025 som følge af udrulningen af 5G. Det er teleselskabernes
forventning, at den samlede elektromagnetiske eksponering (stråling) vil blive øget med 10-20
% i forhold til i dag.
Teleselskaberne forventer, at eksponeringen fra mobilnettene fortsat vil ligge langt under
grænseværdierne, også når 5G-nettene er fuldt udbyggede.
5G-nettet vil være baseret på højere frekvenser end de øvrige teknologier, og mobilsignalerne
vil derfor række kortere. Det betyder, at der vil være behov for at lave et mere fintmasket net
med flere basestationer (small cells). Disse basestationer vil sende med en lavere effekt end fx
de antenner, som sender på 2G, 3G og 4G. Strålingen vil derfor også være tilsvarende
mindre.”
3
1.2. Forskningen.
I hvert fald siden 1966 har der været videnskabelig forskning, som dokumenterede
helbredsmæssige skadevirkninger ved elektromagnetiske felter.
4
Det er denne forskning, som skal sammenholdes med det påtænkte 5G-systems kendte
karakteristika, jf. pkt. 1.1. ovenfor, og de ”grænseværdier” (maksima for udledning af en
bestemt form for miljøpåvirkning), der p.t. anvendes i EU og Danmark, jf. pkt. 2.1. nedenfor.
Det har ikke været praktisk muligt at gennemgå det fulde tilgængelige videnskabelige
materiale, som underbygger de ovenfor beskrevne skadevirkninger på menneskers og dyrs
helbred ved eksponering for radiofrekvent elektromagnetisk stråling, da dette materiale tæller
flere tusinder artikler.
Det gennemgåede materiale er dels fremfundet af undertegnede selv, dels fremsendt af
bestiller, herunder efter anmodning fra undertegnede.
1.2.1. Fokus i nærværende responsum.
Opmærksomheden er centreret omkring de resultater, der positivt dokumenterer enten
egentlige skadevirkninger eller risici herfor på mennesker, dyr og planter.
I det omfang sådanne dokumenterbare forskningsresultater foreligger, er disse i sagens natur
af langt større betydning end undersøgelser, der ikke har været i stand til at identificere en
skadevirkning eller risiko herfor, al den stund sidstnævnte gruppering ikke i sig selv udelukker,
at der rent faktisk er skadevirkninger eller risici.
Er det én gang lødigt videnskabeligt bevist, at der er enten skadevirkning eller risiko for skade,
er det ikke relevant, om der ti andre gange er gennemført lødige forsøg, som ikke kunne
påvise en sådan skadevirkning eller risiko. Det er blot op til videnskaben at afklare, hvorfor de
ti øvrige lødige forsøg ikke påviste det, der nu foreligger videnskabeligt bevist, for på denne
3 Se i øvrigt pkt. 2.1 nedenfor om de i Danmark anvendte grænseværdier.
4 Jf. Pall 2018 p. 9, der henviser til Marha K. 1966, artiklen:
”Biological effects of high-frequency electromagnetic
fields (translation)”.
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måde bedre at kunne forstå, hvorfor og hvordan skaderne opstår eller kan opstå.
5
Dette kan muligvis illustreres med undersøgelse af bestanden af svaner: Konstateres det ved
én undersøgelse, at der findes sorte svaner, er det ikke relevant, at der ved ti andre
undersøgelser ikke er fundet nogen svaner, der var sorte. Det er nu engang påvist, at den
sorte svane eksisterer, og det kan muligvis være nyttigt at afklare, hvorfor de ti andre
undersøgelser ikke konstaterede det samme.
6
Det ville være misvisende, om man forsøgte sig med en ”statistisk gennemsnitsbetragtning”,
og på den måde f.eks. konkluderede, at der kun er 1/11 sandsynlighed for, at den sorte svane
rent faktisk findes, fordi dette kun er bevist ved én undersøgelse, mens ti andre ikke fandt
noget bevis herfor.
1.2.2. Mennesker: Helbredsmæssige skader og risici.
1.2.2.1. DNA-skader.
I 2015 foretoges en videnskabelig gennemgang af de dengang mere end 100 tilgængelige
peer-reviewed studier, som vedrørte undersøgelsen af såkaldt ”oxidative effekter” af
lavintensitets-radiofrekvent stråling (herefter forkortet: RFR).
Undersøgelsen (Yakymenko et al 2015
7
) viste bl.a., at det var plausibelt, at EHS-lignende
8
tilstande i hvert fald til dels forårsages af eksponering over for lav-intensitets RFR (p. 195), og
at eksponeringen kunne medføre kræft (p. 196), begge fremkaldt af ”oxidativt stress”. Det
konstateredes således, at 93% af undersøgelser viste at strålingen medførte dannelsen af
reaktive oxidative forbindelser og oxidativt stress i alle undersøgte levende organismer fra
celler, planter, insekter, forsøgsdyr til mennesker (sædceller), jf. ibid. p. 186.
Yakymenko et al 2015, p. 186:
”All above mentioned studies dealt with the effects of low-intensity RFR. This means that the
intensity of radiation was far below observable thermal effects in biological tissues, and far
below safety limits of the International Commissions on Non-Ionizing Radiation Protection
(ICNIRP) (ICNIRP, 1998).”
9
Ibid., p. 187:
”Low-intensity RFR is referred to as radiation with intensities which do not induce significant
thermal effects in biological tissues. Accordingly, any intensity of RFR under the ICNIRP limits
can be referred to as low-intensity. In this paper we will analyze only the effects of low-
intensity RFR.”
Ibid., p. 196 (konklusion):
”...a broad biological potential of ROS and other free radicals, including both their mutagenic
effects and their signaling regulatory potential, makes RFR a potentially hazardous factor for
5 Se i samme retning Philips et al (2009),
”Electromagnetic fields and DNA damage.”,
offentliggjort i det
videnskabelige tidsskrift ”Pathophysiology” nr. 16 (2009), pp. 79–88, pp. 84 – 85. P. 85 anføres:
”Each study to
investigate RFR-induced DNA damage must be evaluated on its own merits, and then studies that both show effects
and do not show effects must be carefully evaluated to define the relationship of experimental variables to
experimental outcomes and to assess the value of experimental methodologies to detect and measure these outcomes
(see Section 2).”
6 Eksemplet er bl.a. anvendt af videnskabsfilosoffen Karl Popper.
7 Offentliggjort i det videnskabelige tidsskrift ”Electromagnetic Biology and Medicine”, nr. 35 2016, pp. 186 – 202.
8 EHS står for Elektro Hyper Sensitivitet, og er en fysisk lidelse, hvorefter personen får en række symptomer af
ophold i nærheden af udstyr, der afgiver elektromagnetisk stråling. Kaldes ofte ”el-overfølsomhed”.
9 Disse grænseværdier omtales nærmere i pkt. 2.1 nedenfor.
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human health. We suggest minimizing the intensity and time of RFR exposures, and taking a
precautionary approach towards wireless technologies in everyday human life.”
----
Det amerikansk baserede, forskerdrevne ”BioInitiative 2012 - A Rationale for Biologically-based
Exposure Standard for Low-Intensity Electromagnetic Radiation” har d. 15. november 2017
offentliggjort en gennemgang af 200 da foreliggende undersøgelser af radiofrekvent
elektromagnetisk strålings påvirkning af frie radikaler (”free
radicals”),
som fremkalder såkaldt
”oxidativt stress”, jf. omtalen af Yakymenko (2015) ovenfor.
Gennemgangen viste, at der i 180 af de 200 undersøgelser (90 %) var konstateret statistisk
signifikante effekter, medens der i de sidste 20 (10 %) ikke var reporteret nogen statistisk
signifikant effekt.
----
Martin Pall 2018
10
konstaterede maj 2018, at der på det tidspunkt eksisterede minimum 21
videnskabelige undersøgelser (siden 1971), som dokumenterede DNA-skader ved
radiofrekvent elektromagnetisk stråling, og at disse førte til kromosomskader og andre
mutationer.
Endvidere konstaterede han, at der var minimum 19 studier (siden
dokumenterede, at denne stråling fremkaldte frie radikaler og oxidativt stress
11
.
----
REFLEX-studiet (2004) blev gennemført af 12 forskningsinstitutioner på vegne af EU med et
budget på 3 mio. euro. Blandt resultaterne var, at der ved en stråleabsorptionsrate (herefter
forkortet ”SAR”) på 1,3 W/kg (dvs. under de af ICNIRP anbefalede grænseværdier på 2,0 W/kg
for krop og hoved, jf. pkt. 2.1. nedenfor) skete en betydelig forøgelse af DNA-skader (p. 109):
”RF-EMF exposure at a SAR of 1.0 W/kg and below had no effect on Comet formation in HL-60
cells (expressed as Olive Tail Moment OTM) as compared to control and sham-exposed cells.
On the other hand RF-EMF at SAR of 1.3 W/kg and above caused a significant increase in DNA
strand breaks. The maximum of this effect was observed at SAR 1.3 W/kg (OTM = 2.20 ±
0.16) and 1.6 W/kg (2.24 ± 0.10).”
Endvidere var denne strålingsstyrke den, som producerede den største effekt på DNA (p. 119,
gentaget p. 222):
”...were applied following RF-field exposure of HL-60 cells at that exposure condition with the
most significant effect on DNA integrity (1800 MHz, continuous wave, 1.3 W/kg, 24h).”
Ibid., p. 223, afsnit 5.2.1., laboratoriedeltager 2, konklusion 9:
”Within the investigated SAR energy ranges RF-EMF under the in-vitro conditions used are
genotoxic in HL-60 cells without affecting cell-cycle distribution cell proliferation or cell
progression.”
Ibid., konklusion 10:
”The partial-body SAR for any 10-gram tissue like for example the head as exposed region to
10 PhD, prof.emeritus i biokemi og Basic Medical Sciences, Martin L. Pall -
”5G: Great risk for EU, U.S. and
International Health! Compelling Evidence for Eight Distinct Types of Great Harm Caused by Electromagnetic
Field (EMF) Exposures and the Mechanism that Causes Them”,
pp. 6 – 8.
11 Ibid., pp. 11 – 12.
6
1981),
som
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mobile phone electromagnetic fields should not exceed 2 W/kg according to the Radio-
Radiation Protection Guidelines. Notably, our findings on genotoxic effects of RF-fields in HL-60
cells have been shown for SAR levels below these acceptable partial-body SAR levels.”
Ibid., p. 223, afsnit 5.2.2., laboratoriedeltager 3:
”Our results imply a genotoxic action of RF-EMFs below proposed radiation safety levels.”
Det blev dog tillige samlet set konkluderet (p. 226), at eftersom der ”alene” var tale om
laboriatorieforsøg, var REFLEX-studiet ikke i sig selv nok til at konkludere, at de (fortsat)
gældende grænseværdier medførte fare for menneskers helbred, men at forsøget gjorde en
sådan konklusion mere nærliggende. Endvidere konkluderedes, at:
”Furthermore, there exists no justification anymore to claim, that we are not aware of any
pathophysiological mechanisms which could be the basis for the development of functional
disturbances and any kind of chronic diseases in animal and man.”
----
Udover REFLEX-studiet har der ifølge i øvrigt tilgængelige oplysninger været udført mere end
40 studier, som viser DNA-skader ved eksponering for radiofrekvent elektromagnetisk
stråling
12
.
Disse omfatter bl.a.:
Burlaka et al (2013),
”Overproduction of free radical species in embryonal cells exposed to low
intensity radiofrequency radiation.”
13
,
p. 223:
”In conclusion,the exposure of developing quail
14
embryos in ovo to extremely low intensity
RF-EMR of GSM 900MHz during at least one hundred and fifty-eight hours discontinuously
leads to the significantly increased rates of superoxide and nitrogen oxide generation in
embryo cells. This was accompanied by a significantly increased level of lipid peroxidation,a
depression of key antioxidant enzymes activity,and significantly,2–3-fold,increased level of
oxidative damage of DNA in embryo cells.”
----
Blank og Goodman (2011),
”DNA is a fractal antenna in electromagnetic fields.”
15
, p. 411:
“Since DNA can interact with EMF over a wide range of frequencies, and does not appear to be
limited to an optimal frequency, it has the functional properties of a fractal antenna.
…
From the above analysis of the effect of EMF on the stress response, DNA strand breaks and
cancer epidemiology, the fractal property of DNA is apparent in the ELF and RF ranges.
…
Electron transfer is a plausible mechanism for EMF interactions with DNA at higher frequencies
where higher energies are involved. The damage due to DNA strand breaks that occur at
12 Dokumentationsliste vedhæftes responsummet som
bilag 1.
13 Offentliggjort i det videnskabelige tidsskrift ”International Journal of Radiation Biology” vol. 87, no. 4, 2011, pp.
409-15.
14 Det er almindeligt at anvende dyr til at evaluere helbredsrisici for mennesker, og at anvende sådanne undersøgelser
som basis for retningslinjer og grænseværdier, jf. f.eks. Engels et al (2014),
”Anthropogenic electromagnetic noise
disrupts magnetic compass orientation in a migratory bird”
(Nature 2014, vol. 509), p. 354:”...animal
studies are
commonly used to evaluate human health risks and have contributed to guidelines for human exposures...”
Det
foreligger oplyst, at Miljøstyrelsen i skriftligt svar af 20. februar 2019 har oplyst tilsvarende og henvist til European
Chemicals Agency med linket
https://echa.europa.eu/da/information-on-chemicals/biocidal-active-substances
15 Offentliggjort i det videnskabelige tidsskrift ”Experimental Oncology”, vol. 35, no. 3, pp. 219 – 225.
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higher frequencies, including ionising radiation, is generally attributed to oxidation, another
chemical name for electron transfer. Because of the greater energy at higher frequencies,
reactive oxygen species, such as peroxides, contribute to the DNA damage. However, DNA
strand breaks occur over a wide range of frequencies, and do not demonstrate frequency
optima related to molecular reaction kinetics.”
(understreget her)
Det hedder videre om de p.t. anvendte grænseværdier for menneskers eksponering over for
radiofrekvent elektromagnetisk stråling (jf. pkt. 2.1 nedenfor) p. 413:
”...The existing 100 mT ELF exposure limit set by ICNIRP (International Commission for Non-
Ionizing Radiation Protection) is many times higher than the 0.4 mT where a doubling of
childhood leukemia risk is widely acknowledged. It has also been pointed out that the specific
absorption rate (SAR), the widely used thermal standard for EMF safety, does not relate at all
to the biological thresholds of the stress response in the ELF and RF ranges, and that the
threshold for the same biological process differs by many orders of magnitude in the two
ranges (Blank and Goodman 2004).”
----
Philips et al (2009),
”Electromagnetic fields and DNA damage.”
16
, p. 85:
”RFR exposure does indeed appear to affect DNA damage and repair, and the total body of
available data contains clues as to conditions producing effects and methodologies to detect
them.
…
The lack of a causal or proven mechanism(s) to explain RFR-induced effects on DNA damage
and repair does not decrease the credibility of studies in the scientific literature that report
effects of RFR exposure, because there are several plausible mechanisms of action that can
account for the observed effects. The relationship between cigarette smoking and lung cancer
was accepted long before a mechanism was established. ...”
----
Panagopoulos (2019),
”Comparing DNA damage induced by mobile telephony and other types
of
man-made electromagnetic fields”
17
, p. 53 (resumé):
”The number of studies showing adverse effects on living organisms induced by different types
of man-made Electromagnetic Fields (EMFs) has increased tremendously. Hundreds of peer
reviewed published studies show a variety of effects, the most important being DNA damage
which is linked to cancer, neurodegenerative diseases, reproductive declines etc. Those studies
that are far more effective in showing effects employ real-life Mobile Telephony (MT)
exposures emitted by commercially available mobile phones....”
(understreget her)
Undersøgelsen konstaterer videre, at andre egenskaber end udelukkende signalstyrken er
væsentlige årsager til skadevirkningerne, jf. ibid.:
”...The crucial parameter for the intense bioactivity seems to be the extreme variability of the
polarized MT signals, mainly due to the large unpredictable intensity changes.”
Tilsvarende fra konklusionen, ibid. p. 60:
”The importance of exposure variability shown in the present study implies the need to define
EMF-exposures not only by frequency components and average intensity values, but by
reporting maximum and minimum intensity as well, frequency variations, pulsing or
16 Offentliggjort i det videnskabelige tidsskrift ”Pathophysiology” nr. 16 (2009), pp. 79–88.
17 Offentliggjort i det videnskabelige tidsskrift
”Mutation Research-Reviews in Mutation Research”
nr. 781, 2019, pp.
53–62.
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continuous wave, modulation, and - of course - polarization.”
Ibid., p. 59 – 60 (konklusion):
”It comes that variability in the EMF exposure is an extremely important factor in order for the
specific type of polarized EMF to be able to induce biological/health effects.
…
The extreme and unpredictable variability of the real-life MT signals that apparently seems to
be the reason for the corresponding intense bioactivity, does not concern only the 2nd
generation (GSM) MT signals tested in our experiments and in the present review, but all
existing types of digital MT signals (2nd, 3rd, 4th generation), and all types of modern digital
microwave telecommunication signals/EMFs (DECT phones, Wi-Fi routers, etc.), since they all
operate under the same principles combining RF carrier signals with ELF pulsing and
modulation of similar frequency bands, emitting variable information each moment which in
turn makes the emission variable in intensity, frequency, waveform etc. In fact, with every
new generation of telecommunication devices (e.g. 3rd, 4th, 5th generation mobile phones or
base antennas) the amount of information transmitted each moment (speech, text, images,
video, internet, etc.) is increased, resulting in higher variability and complexity of the signals
with the living cells/ organisms even more unable to adapt. The result of the recent study that
found a real 3rd generation (UMTS) MT EMF to be more bioactive than real 2nd generation
(GSM) MT EMF emitted by the same device
[36] is in
line with this fact.”
(understreget her)
Studiet D'Silva et al (2017)
18
, omtalt som reference [36] i ovennævnte undersøgelse, rummer
følgende beskrivelse af sine resultater og konklusion, jf. det tilhørende resumé:
”Results: In our study, the exposure of developing chick embryos to 2G and 3G cell phone
radiations caused structural changes in liver in the form of dilated sinusoidal spaces with
haemorrhage, increased vacuolations in cytoplasm, increased nuclear diameter and
karyorrhexis and significantly increased DNA damage.
Conclusion:
The chronic exposure of chick embryo liver to RFR emitted from 2G and 3G cell
phone resulted in various structural changes and DNA damage. The changes were more
pronounced in 3G experimental group. Based on these findings it is necessary to create
awareness among public about the possible ill effects of RFR exposure from cell phone.”
Om den anvendte metode er bl.a. oplyst følgende, ibid. p. 6:
”A popular brand cell phone hand set and a service provider were used for network connection
for both 2G and 3G exposure. For exposure activation, the cell phone was rung from another
cell phone for duration of three minutes each, every half an hour, with the first exposure given
at 12th hour of incubation (4.30 am-4.30 pm). The total exposure for a 12 hour period was 75
minutes followed by 12 hour of exposure-free period. This was repeated daily up to 12 th day
of incubation.”
Studiet refererede endvidere, at:
”Non-thermal stress is more deleterious than thermal stress and is known to cause oxidative
stress [5], production of free radicals [6], structural changes in plasma membrane [7],
changes in ionic transport [8] and also increased DNA damage [9].”
1.2.2.1.1. Delkonklusion.
Der foreligger klar videnskabelig dokumentation for, at radiofrekvent elektromagnetisk stråling,
også under de i Danmark anvendte grænseværdier, jf. pkt. 2.1 nedenfor, forårsager DNA-
skader på både mennesker og dyr.
18 Offentliggjort i det videnskabelige tidsskrift
”Journal
of Clinical and Diagnostic Research”,
2017 Jul, Vol-
11(7), pp. 5 – 9.
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Panagopoulos (2019) dokumenterer, at det ikke alene er strålestyrken, der har betydning for
den
forventelige
skadevirkning.
Derudover
dokumenteres,
at
fundene
pga.
teknologifællesskabet mellem generationerne også vil være gældende for 5G.
1.2.2.2. Kræft.
1.2.2.2.1. Klassificering.
IARC (International Agency for Research on Cancer) er WHOs agentur for kræftforskning.
Agenturet har i 2011 klassificeret elektromagnetisk stråling som ”muligvis kræftfremkaldende
for mennesker”.
19
En senere videnskabelig undersøgelse offentliggjort november 2018 konkluderede, at der i
henhold til IARCs kriterier er grundlag for at klassificere elektromagnetisk stråling som
”kræftfremkaldende for mennesker”
20
, hvilken var begrundet således, med henvisning til
gennemgang af en række undersøgelser foretaget forud herfor:
Miller et al november 2018
21
, p. 674:
”...Analysis of a subset of cases (58% of all cases) based on operator-recorded information
showed significant brain cancer risks for children with a significant trend of increase in risk
with increasing years of use. Based on children's memory of both ipsilateral and contralateral
use there were significant increased risk of brain cancer along with a marginal increase of risk
with an increasing number of calls...”
Ibid., p. 675:
”Carlberg and Hardell (2013) also reported that persons diagnosed with a glioblastoma
multiforme (GBM) exposed to RFR
22
emanating from WTDs
23
had a significantly shorter survival
period than those without such exposures.”
Ibid., p. 676:
”Coureau et al. (2014) reported on a French national study of mobile phone use and brain
tumors (glioma and meningioma) between 2004 and 2006.
…
There was a marginal increase in risk with increasing hours of use (p
trend
=0.07). A small
number of urban users showed a significant 8-fold increased risk for brain tumors excluding
temporal or frontal lobes (OR
24
8.2. 1.37–49.07). The authors commented: 'Finally, we
observed increased OR for urban use for gliomas, a result inconsistent with the hypothesis of a
higher RF power output during calls in rural areas, documented by some Swedish study.
However, our results are consistent with a recent international study showing no difference
between rural and urban exposition in most countries except in Sweden, and a Hardell study
when considering gliomas separately.'”
Ibid., p. 676:
”Momoli et al. (2017) undertook a re-analysis of the Canadian data from the 13-country case-
control Interphone Study (2001–2004).
19
20
21
22
23
24
Jf. IARC monograph vol. 102 (2013), p. 419, pkt. 6.3.
En såkaldt ”klasse 1-klassifikation” i IARC's system.
Offentliggjort i det videnskabelige tidsskrift ”Environmental Research”, 2018 nr. 167, pp. 673 – 683.
Radiofrequency radiation, jf. ibid. p. 673.
Wireless Transmitter Devices, jf. ibid. p. 673.
Odds ratio, jf. ibid. p. 674.
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…
For glioma, when comparing those in the highest quartile of use (> 558 lifetime hours) to
those who were not regular users, the odds ratio was 2.0 (95% confidence interval: 1.2, 3.4).
After adjustment for selection and recall biases, the odds ratio was 2.2 (95% limits: 1.3, 4.1),
thus allaying concerns that bias could explain the positive findings in the Interphone study.”
Ibid., p. 676:
”Akhavan-Sigari et al. (2014) reported that patients with glioblastoma multiforme who had
used cellphones≤3 h per day had better survival than those with cellphone use of ≥3 h per
day.
…
This study shows that genetic changes, compatible with carcinogenic effects, result from
higher exposure to RFR.”
25
Ibid., p. 676:
”Carlberg and Hardell (2015) performed a pooled analysis from 1997 to 2003 and 2007–2009
of the risk of meningioma from cell and cordless phone use. In total, 1625 meningioma cases
and 3530 controls were analyzed. Overall no association with use of mobile or cordless phones
was found. However, they reported an increased risk among heavy users of both mobile and
cordless phones from various wireless phone types (wireless combines all phone types) (Table
11). The risk increased significantly per 100 h of use from four wireless phones categories.”
Ibid., p. 677:
”Hardell et al. (2013a) pooled acoustic neuroma results from casecontrol studies conducted in
1997–2003 and 2007–2009, including 316 participating cases and 3530 controls. ... There is
some evidence of a dose-response relationship is evident with mobile and cordless phones
associated with ORs of 4.5 and 6.5 respectively for 20 or more years of use. There were
similar results per cumulative hours of use (Table 12).”
Ibid., p. 677:
”Moon et al. (2014), in a matched case-control study from Korea examining 119 cases of
vestibular schwannoma and 238 controls attending for routine examinations in the same
institution found no difference between cases and controls in the duration, time of use or
cumulative use of mobile phones. However, in a case-case analysis they found that vestibular
Schwannoma tumor volume was greater in those with higher use compared to lower use of
mobile phones and in those with regular compared to non-regular use (Table 13).”
Ibid., p. 678:
”Zada et al. (2012) examined data from three major U.S. cancer registries: Los Angeles
County, California Cancer Registry, and the National Cancer Institute's Surveillance,
Epidemiology and End Result for 12 U.S. states (SEER 12) from 1992. The APC for GBM (grade
IV glioma) and Glioma was reported by brain region. Table 17 shows APC changes by cancer
registry for GBM and for glioma located in three anatomical regions of the brain, showing
significant increases compatible with increasing use of mobile phones.
Consistent with the study above, Cardis et al. (2011) reported that the combined percentage
of the total radiation absorbed by the frontal lobe (19%), the temporal lobe (50%) and the
cerebellum (18%) was 81% at 900 MHz and was 86% at 1800 MHz (frontal lobe 14%,
temporal lobe 50%, cerebellum 13%).”
Ibid., p. 679:
25 Patienterne i studiet (63 voksne, heraf 38 M 25 K) blev opereret for kræftsvulster år 2008 – 2011, jf. Akhavan-Sigari
et al 2014, p. 117.
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”7. Case series
West et al. (2013) reported multiple
26
primary breast cancers in young women who had
regularly placed a cellphone in their bras (Table 20). Tumors were reported to have occurred
subcutaneously directly under the antennas of the phones. Subsequently, a number of other
such cases have come to light with unusually located breast tumors relative to reported cell
phone storage in the bra.
Peleg (2012) discussed a cancer cluster among young workers at an Israeli Antenna Range
Facility. It was believed that significant RFR exposures took place as a result of workplace
conditions. Five of about 30 workers were diagnosed with cancer. This was regarded as
significantly greater than the expectation. Peleg et al. (2018) extended this analysis to 47
patients with cancer previously exposed to whole-body prolonged RFR, mainly from
communication equipment and radar. They found that the percentage frequency of haemo-
lymphatic (HL) cancers in the case series was very high, at 40% with only 23% expected for
the series age and gender profile, 95% confidence interval: 26–56%, p < 0.01; 19 out of the
47 patients had HL cancers.
Stein et al. (2011) studied 56 cancers among 49 military personnel (47 male, 7 females)
exposed to intense prolonged RFR between 1992 and 2011. Based on exposure information
reconstructed from reported histories, it was assumed that significant RFR exposures took
place as a result of workplace conditions. The average duration of exposure was 13 years; the
average age at diagnoses was 43. There appeared to be an excess of both haemolymphatic
and testicular cancers.”
Ibid., p. 680 (diskussion af resultater):
”Nevertheless
27
, recent case-control studies from Sweden and France corroborate findings of
earlier studies in providing support for making a causal connection between cell phone use and
brain cancer, as well as acoustic neuroma, also called Vestibular Schwannoma. Hardell and
Carlberg (2013) concluded that the Bradford Hill criteria for causality have now been ful filled.
It is notable that three recent meta-analyses all confirm significant increased risk of glioma
after 10 or more years of use of cell phones (Bortkiewicz et al., 2017; Prasad et al., 2017;
Yang et al., 2017). The Aydin et al. (2011) data that relied on billing records along with
children's recall of their uses of phones approaches and in some instances met conventional
tests of statistical significance and indicated that four years or more of heavy cell phone
radiation causes glioma in children. This finding is consistent with that of Hardell and Carlberg
(2015) who showed that those who began using cell phones and/or cordless phones regularly
as children had between 4 and 8-fold increased risk of glioma as adults.”
Ibid., p. 680 (diskussion af resultater):
”Potential cancer sites and other outcomes for consideration in new studies include... Other
sites than brain and acoustic neuroma could potentially increase in incidence when untested
whole-body exposure occurs, this may be the case with several evolving technologies....other
possible sources of exposures that have not been evaluated include areas close to cellular base
station antennas, the yet-to-be introduced 5 G communication systems, and rapidly evolving
occupational exposure and novel systems for Wi-Fi (Peleg, 2009).”
Ibid., p. 681 (diskussion af resultater):
”There are indications particularly from the Ramazzini animal studies that other environmental
exposures might make people more susceptible to a combination of exposures (Falcioni et al.,
2018). This combinatorial issue been noted in studies of occupational exposure to chemicals,
metals and electromagnetic fields (Navas-Acien et al., 2002). Separately, no effects were
26 Der var tale om 4 patienter i alderen 21, 21, 33 og 39, jf. ibid. tabel 20.
27 Citatet er i artiklen efterstillet en gennemgang af sædvanlige forbehold i forbindelse med anvendelse af de
forskellige, gængse forskningsmetoder, som ligeledes har været anvendt i de i artiklen omhandlede studier.
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observed but when combined with EMF strong results were found. In the Ramazzini studies
finding a synergistic interaction between RFR and ionizing radiation, RFR served as a promoter
while in the NTP animal studies RFR served as a direct carcinogen and genotoxic agent
(National Toxicology Program, a, b, 2018.).”
Ibid., p. 681 (diskussion af resultater):
”Individual hypersensitivity to electric and radiofrequency fields (EHS) is a relatively newly
reported phenomenon in the west, although cases of radiation sickness have been found in the
former Soviet literature from the 1960s and 1970s. Case studies and individual reports
together identify a population which would benefit from RFR exposure reduction (Davis et al.,
2017). Because of serious methodological difficulties in operationalizing the concept and a lack
of investment in research, definitive epidemiological studies of EHS have not yet been
conducted.”
Ibid., p. 681 (diskussion af resultater):
”However, non-cancer outcomes such as sperm damage, hearing loss and loss of visual acuity
are likely to be more commonly linked to mobile phone use.”
Ibid., p. 681 (konklusioner):
”The Epidemiological studies reported since the 2011 IARC Working Group meeting are
adequate to consider RFR as a probable human carcinogen (Group 2 A). However, they must
be supplemented with the recently reported animal data as performed at the Ramazzini
Institute and the US National Toxicology Program as well as by mechanistic studies. These
experimental findings together with the epidemiology reviewed here are sufficient in our
opinion, to upgrade the IARC categorization of RFR to Group 1, carcinogenic to humans.
…
In light of the evolving science concerning mobile phone and screen time exposures and the
longer-term risk of cancer established by both epidemiological and toxicological studies,
current evidence is strong enough to go from precaution concerning possible risk to prevention
of known risks.
…
The precautionary principle should be applied now and suitable warning messages provided to
adults and critically to children and their parents.
…
experimental evaluations and modeling are essential before distributing newer systems (e.g. 5
G) for which no safety data have been obtained. The absence of systematic testing of such
technologies should not be confused with proof of safety.
…
In the meantime, the evidence amassed thus far from epidemiology strengthens the case for
instituting the precautionary principle with respect to exposures to RFR, especially to young
children and men and women that wish to reproduce. … Where studies have been carried out
on human sperm quantity and quality there are increasing indications of serious human health
impacts. To ignore those findings and subject humans to unevaluated novel RFR frequencies
places current and future generations at risk.”
(understreget her)
1.2.2.2.2. Øvrigt.
En lang række øvrige videnskabelige studier bekræfter, at udsættelse for radiofrekvent
elektromagnetisk stråling (også under de p.t. i Danmark anvendte grænseværdier, jf. pkt. 2.1
nedenfor) kan være kræftfremkaldende. En række af dem er:
Blank og Goodman (2011),
”DNA is a fractal antenna in electromagnetic fields.”
28
, p. 411:
28 Offentliggjort i det videnskabelige tidsskrift ”Experimental Oncology”, vol. 35, no. 3, pp. 219 – 225.
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“Regarding the connection between EMF and the incidence of cancer, the different EMF energy
levels in the non-ionising and ionising ranges all involve interaction with and activation of DNA
and induction of protein synthesis. The ability of EMF to cause DNA strand breaks and damage
to proteins in the non-ionising range is similar to the destructive effects on DNA of the much
more energetic X-rays and gamma rays in the ionising ranges, where it is generally
acknowledged that the cancers are due to DNA damage. The recent epidemiology studies in
the non-ionising range link EMF-caused changes in DNA with cancer. Additional support comes
from the study showing that the absence of DNA repair genes is associated with a greater
incidence of leukemia from exposure to low frequency EMF (Yang et al. 2008).”
(understreget
her)
----
Lerchl et al (2015),
”Tumor promotion by exposure to radiofrequency electromagnetic fields
below exposure limits for humans”,
p. 585 (resumé):
”...Since many of the tumor-promoting effects in our study were seen at low to moderate
exposure levels (0.04 and 0.4 W/kg SAR), thus well below exposure limits for the users of
mobile phones, further studies are warranted to investigate the underlying mechanisms. Our
findings may help to understand the repeatedly reported increased incidences of brain tumors
in heavy users of mobile phones.”
----
Yakymenko et al 2015, jf. pkt. 1.2.1. ovenfor, viste bl.a., at lav-intensitets RFR kunne medføre
kræft (p. 196).
----
Prasad et al (2017),
”Mobile phone use and risk of brain tumours: a systematic review of
association between study quality, source of funding, and research outcomes.”
29
, p. 808
(konklusion):
”In our review of the literature and meta-analysis of case–control studies, we found evidence
linking mobile phone use and risk of brain tumours especially in long-term users (>10 years).
We also found a significantly positive correlation between study quality and outcome in the
form of risk of brain tumour associated with use of mobile phones. Higher quality studies show
a statistically significant association between mobile phone use and risk of brain tumour. Even
the source of funding was found to affect the quality of results produced by the studies.”
Der er tale om et systematisk, videnskabeligt review af den foreliggende forskning, som altså
fandt klar basis for at kæde brugen af mobiltelefoner sammen med kræftsvulster i hjernen.
Endvidere fandt det pågældende review, at de studier, der havde den bedste videnskabelige
kvalitet, var de samme, som dem, der fandt den pågældende sammenhæng, og at
finansieringskilden også havde spillet en rolle i studiernes kvalitet.
----
Det amerikanske National Institute of Health udgav november 2018 rapporten
”TOXICOLOGY
AND CARCINOGENESIS STUDIES IN Hsd:SPRAGUE DAWLEY SD RATS EXPOSED TO WHOLE-
BODY RADIO FREQUENCY RADIATION AT A FREQUENCY (900 MHz) AND MODULATIONS (GSM
AND CDMA) USED BY CELL PHONES”,
hvoraf fremgår p. 125 - 126 (konklusioner):
”GSM-Modulated
RFR
29 Offentliggjort i det videnskabelige tidsskrift ”Neurological Sciences”, 2017, vol. 38, pp. 797 – 810.
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Under the conditions of this 2-year whole-body exposure study, there was clear evidence of
carcinogenic activity*
30
of GSM-modulated cell phone RFR at 900 MHz in male Hsd:Sprague
Dawley SD rats based on the incidences of malignant schwannoma of the heart. The
incidences of malignant glioma of the brain and benign, malignant, or complex
pheochromocytoma (combined) of the adrenal medulla were also related to RFR exposure. The
incidences of benign or malignant granular cell tumors of the brain, adenoma or carcinoma
(combined) of the prostate gland, adenoma of the pars distalis of the pituitary gland, and
pancreatic islet cell adenoma or carcinoma (com-bined) may have been related to RFR
exposure. There was equivocal evidence of carcinogenic activity of GSM-modulated cell phone
RFR at 900 MHz in female Hsd:Sprague Dawley SD rats based on the incidences of
schwannomas of the heart.
…
CDMA-Modulated RFR
Under the conditions of this 2-year whole-body exposure study, there was clear evidence of
carcinogenic activity of CDMA-modulated cell phone RFR at 900 MHz in male Hsd:Sprague
Dawley SD rats based on the incidences of malignant schwannoma of the heart. The inci-
dences of malignant glioma of the brain were also related to RFR exposure. The incidences of
adenoma of the pars distalis of the pituitary gland and adenoma or carcinoma (combined) of
the liver may have been related to RFR exposure. There was equivocal evidence of
carcinogenic activity of CDMA-modulated cell phone RFR at 900 MHz in female Hsd:Sprague
Dawley SD rats based on the incidences of malignant schwannoma of the heart, malignant
glioma of the brain, and benign, malignant, or complex pheochromocytoma (combined) of the
adrenal medulla. Increases in nonneoplastic lesions of the heart, brain, and prostate gland in
male rats, and of the brain in female rats occurred with exposures to CDMA-modulated RFR at
900 Mhz.”
(understreget her)
Om den umiddelbare overførbarhed af disse resultater på mennesker hedder det, ibid. p. 125:
”The malignant schwannomas of the heart observed in male rats in the current studies and the
malignant gliomas observed in the brain of male rats, arise from the same cell type as the
acoustic neuromas (vestibular schwannomas) observed in humans, though in a different
location. This lends credence to the possible association of these tumors with cellular phone
use. The cellular origin of malignant gliomas in the rat brain is unclear, but they do arise from
glial cells (support cells in the brain), as do human glioblastomas, so it is possible that such an
association exists for these tumors as well. However, the interpretation of these findings with
respect to specific risks to humans from cellular telephone use is beyond the scope of the
current studies. Further efforts to characterize the molecular basis by which RFR elicits its
effects in rats, and a more complete assessment of the exposure conditions in the current
studies in relation to exposures to humans from cellular telephone technologies should provide
con-text to aid understanding of the implications of the current findings to human health.”
(understreget her)
Falcioni et al. (2018),
”Report of final results regarding brain and heart tumors in Sprague-
Dawley rats exposed from prenatal life until natural death to mobile phone radiofrequency field
representative of a 1.8 GHz GSM base station environmental emission”
31
, p. 496 (resumé):
”The RI
32
findings on far field exposure
33
to RFR are consistent with and reinforce the results of
30 Asterisken refererer til undersøgelsens p. 16, hvor de forskellige bevisstandarder er nærmere defineret. ”Clear
evidence” er defineret som:
”...studies that are interpreted as showing a dose-related (i) increase of malignant
neoplasms, (ii) increase of a combination of malignant and benign neoplasms, or (iii) marked increase of benign
neoplasms if there is an indication from this or other studies of the ability of such tumors to progress to
malignancy.”
31 Offentliggjort i det videnskabelige tidsskrift ”Environmental Research”, 2018, vol. 165, pp. 496 – 503.
32 RI står for ”Ramazzini Institute”, som var det forskningsinstitut, hvor undersøgelsen blev foretaget.
33 Far field exposure indebærer i dette tilfælde, at undersøgelsen genskabte forholdene for bestråling med en 1.8 GHz
mobilmast, jf. ibid. p. 497, pkt. 2.1.
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the NTP study
34
on near field exposure, as both reported an increase in the incidence of tumors
of the brain and heart in RFR-exposed Sprague-Dawley rats. These tumors are of the same
histotype of those observed in some epidemiological studies on cell phone users. These
experimental studies provide sufficient evidence to call for the reevaluation of IARC
conclusions regarding the carcinogenic potential of RFR in humans.”
(understreget her)
Uddybende er konstateret, jf. ibid. p. 501:
”...The statistically significant increase in the incidence of heart Schwannomas observed in
male rats in the late part of their life, both in the RI and NTP studies, are consistent with the
epidemiological findings, where the highest increase in risk of vestibular Schwannoma among
humans exposed to RFR was observed in men over 50 years of age with the highest
cumulative exposure (Hardell et al., 2013, 2003).”
Forsøget blev gennemført således, at de eksponerede dyr blev udsat for en stråleabsorption på
estimeret 0,001 til 0,3 W/kg (jf. p. 499), hvilket er betydeligt lavere end den anvendte
grænseværdi i Danmark på 2 W/kg, jf. pkt. 2.1 nedenfor.
De statistisk signifikante resultater fremkom i den gruppe af rotter, som var blevet udsat for en
feltstyrke på 50 V/m. Dette er under grænseværdien på 58,34 V/m, som anvendes i Danmark
for en frekvens på 1,8 GHz, jf. pkt. 2.1 nedenfor.
----
Martin Pall 2018
35
konstaterede maj 2018, at der på det tidspunkt eksisterede minimum 35
videnskabelige undersøgelser (siden 1978), som dokumenterede, at radiofrekvent
elektromagnetisk stråling var kræftfremkaldende.
----
Panagopoulos (2019), jf. pkt. 1.2.1. ovenfor, henviste ligeledes til ”hundreder af peer
reviewed-artikler”, som viste en række effekter fra elektromagnetiske felter, inkl. kræft (p. 53).
----
Sundhedsministeren har i sin besvarelse af 12. april 2019 af spørgsmål 693 i Folketingets
Sundheds- og Ældreudvalg fremlagt en opgørelse fra Sundhedsdatastyrelsens cancerregister,
som viser en klar stigning i registrerede tilfælde af kræft i form af glioblastom inden for de
sidste 20 år.
Stigningen er særligt markant fra 2005 til 2006 i aldersgruppen >30 år, og viser
gennemsnitligt set en fordobling af tilfældene i denne aldersgruppe i perioden 2006 til 2017,
set i forhold til den forudgående periode 1995 til 2006.
Samlet ses en stigning på op mod 80 % i forekomsten i de senere år 2015 – 2017,
sammenlignet med det generelle niveau før 2006.
34 ”NTP-studiet” er det umiddelbart ovenfor omtalte fra det amerikanske National Health Institute.
35 PhD, prof.emeritus i biokemi og Basic Medical Sciences, Martin L. Pall -
”5G: Great risk for EU, U.S. and
International Health! Compelling Evidence for Eight Distinct Types of Great Harm Caused by Electromagnetic
Field (EMF) Exposures and the Mechanism that Causes Them”,
pp. 15 – 16.
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Den samme fordoblingstendens er dokumenteret i England, jf. Philips et al (2018),
”Brain
Tumours: Rise in Glioblastoma Multiforme Incidence in England 1995–2015 Suggests an
Adverse Environmental or Lifestyle Factor”
36
, hvoraf fremgår følgende (p. 1, resumé):
”Results. We report a sustained and highly statistically significant ASR
37
rise in
glioblastomamultiforme (GBM) across all ages.The ASR for GBM more than doubled from 2.4
to 5.0, with annual case numbers rising from 983 to 2531. Overall, this rise is mostly hidden in
the overall data by a reduced incidence of lower-grade tumours.
Conclusions.
The rise is of
importance for clinical resources and brain tumour aetiology. The rise cannot be fully
accounted for by promotion of lower–grade tumours, random chance or improvement in
diagnostic techniques as it affects specific areas of the brain and only one type of brain
tumour. Despite the large variation in case numbers by age, the percentage rise is similar
across the age groups, which suggests widespread environmental or lifestyle factors may be
responsible.”
(understreget her)
I Holland er dokumenteret en stigning på 20 % over en 21-årig periode fra 1989 til 2010, jf.
Vincent et al (2014),
”Changing incidence and improved survival of gliomas”
38
, p. 2311:
”The incidence rate of glioma increased from 4.9 per 100,000 inhabitants in 1989 to 5.9 in
2010...”
36 Offentliggjort i det videnskabelige tidsskrift ”Journal of Environmental and Public Health” 2018, art.ID 7910754.
37 Forkortelse for ”Age Standardised Rate”.
38 Offentliggjort i det videnskabelige tidsskrift ”European Journal of Cancer”, 2014, vol. 50, pp. 2309 – 2318.
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1.2.2.3. Andre helbredsskader på mennesker.
Neufeld og Kuster (2018) har i artiklen
”SYSTEMATIC DERIVATION OF SAFETY LIMITS FOR
TIME-VARYING 5G RADIOFREQUENCY EXPOSURE BASED ON ANALYTICAL MODELS AND
THERMAL DOSE”
konstateret, at selv ved korte eksponeringer over for stråling svarende til den
planlagte 5G-stråling med højere frekvenser og/eller ændret modulation, m.v., jf. pkt. 1.1.
ovenfor, vil der kunne ske vævsskader på mennesker, jf. p. 705, 706 og 711:
”Extreme broadband wireless devices operating above 10 GHz may transmit data in bursts of a
few milliseconds to seconds. …these bursts may lead to short temperature spikes in the skin of
exposed people. … To stay consistent with the current safety guidelines, safety factors of 10
for occupational exposure and 50 for the general public were applied. … The results also show
that the peak-to-average ratio of 1,000 tolerated by the International Council on Non-Ionizing
Radiation Protection guidelines may lead to permanent tissue damage after even short
exposures, highlighting the importance of revisiting existing exposure guidelines.
…
THE FIFTH generation of wireless communication technology (5G) promises to facilitate
transmission at data rates up to a factor of 100 times higher than 4G. For that purpose, higher
frequencies (including millimeter-wave bands), broadband modulation schemes, and thus
faster signals with steeper rise and fall times will be employed, potentially in combination with
pulsed operation for time domain multiple access. 5G is designed as a ubiquitous
communication system spanning applications such as high-bandwidth mobile data and
telephony, real-time machine-to-machine communication (e.g., autonomous mobility), and the
Internet of Things (IoT). Exposure to radiofrequency (RF) radiation from wireless devices to
large radar installations and medical equipment can result in increases in body core
temperature or cause localized temperature rises, with the potential for adverse health effects.
The thresholds for frequencies above 10 MHz set in current exposure guidelines (ICNIRP 1998;
IEEE 2005, 2010) are intended to limit tissue heating.
…
However, short pulses can lead to important temperature oscillations, which may be further
exacerbated at high frequencies (>10 GHz, fundamental to 5G), where the shallow penetration
depth leads to intense surface heating and a steep, rapid rise in temperature...
…
The recommendations in the ICNIRP guidelines limit the power density during short pulses to
1,000 times the limit for the time-averaged incident power density. The IEEE standard limits
the radiant exposure (energy absorption per unit area) during any 100 ms to one-fifth of the
total radiant exposure for the whole averaging time. The physical or biological rationales for
these limits, however, are not provided.
…
Laakso et al. (2017) … The authors conclude that the current guidelines do not adequately
prevent excessive heating from pulsed exposure, as peak temperatures can easily exceed the
mean temperature by more than a factor of 3 and suggest that radiant exposure limits be
introduced.
Morimoto et al. (2017) … They conclude that the thermal time constants can be as short as 30
s for narrow-beam exposures and that short pulses can carry enough energy to cause injuries;
…
Another conclusion of this study is that the current ICNIRP (1998) and IEEE (2005, 2010)
guidelines urgently need to be revised, as the duty cycle of 1,000 currently tolerated can
produce unacceptable temperature increases that may result in permanent tissue damage. ...”
(understreget her)
----
Cindy Russell (2018),
”5 G wireless telecommunications expansion: Public health and
environmental implications”,
p. 485:
”There are no long term exposure guidelines, nor are there guidelines for low level, non-
thermal or biological effects considered in the International Commission on Non-Ionizing
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Radiation Protection (ICNIRP) standards which are the basis for standards used worldwide...”
Videre ibid., p. 491:
”Although 5G technology may have many unimagined uses and benefits, it is also increasingly
clear that significant negative consequences to human health and ecosystems could occur if it
is widely adopted. Current radiofrequency radiation wavelengths we are exposed to appear to
act as a toxin to biological systems. A moratorium on the deployment of 5G is warranted,
along with development of independent health and environmental advisory boards that include
independent scientists who research biological effects and exposure levels of radiofrequency
radiation.
…
Public health regulations need to be updated to match appropriate independent science with
the adoption of biologically based exposure standards prior to further deployment of 4G or 5G
technology.”
----
Martin Pall 2018
39
konstaterede maj 2018, at der kunne påvises følgende yderligere
skadevirkninger ved radiofrekvent elektromagnetisk stråling på mennesker:
nedsat fertilitet og kønsdrift, øgede spontane aborter, m.v. (18 studier siden 1971),
neurologiske/neorupsykiatriske effekter (25 studier siden 1966),
apoptose/celledød (13 studier siden 1971),
hormonelle effekter (12 studier siden 1971), og
forøget niveau af calciumioner intracellulært, hvilket forårsager en række sygdomme
(15 studier siden 1988).
Pall anførte, ibid. p. 1 – 2:
”Each of these effects is produced via the main mechanism of action of microwave/lower
frequency EMFs, activation of voltage-gated calcium channels (VGCCs) (Chapter 2). Each of
them is produced via what are called downstream effects of VGCC activation. It follows from
this that we have a good understanding not only that these effects occur, but also how they
can occur. The extraordinary sensitivity of the VGCC voltage sensor to the forces of the EMFs
tells us that the current safety guidelines allow us to be exposed to EMF levels that are
something like 7.2 milion times too high. That sensitivity is predicted by the physics.
Therefore, the physics and the biology are each pointing to the same mechanism of action of
non-thermal EMFs. The different effects produced are obviously very deep concerns. They
become much deeper and become existential threats when one considers that several of these
effects are both cumulative and eventually irreversible.
…
Obviously 4G and 5G will make the situation much worse.”
(understreget her)
1.2.2.4. Særligt vedr. børn og kræft eller andre helbredsskader.
Der findes en række undersøgelser, hvoraf visse tillige er omtalt ovenfor, som specifikt omtaler
skadevirkninger og risici for kræft eller andre helbredsskader for børn, hvoraf fremhæves:
Divan et al (2012),
”Cell phone use and behavioural problems in young children”
40
, p. 524
(resumé):
39 PhD, prof.emeritus i biokemi og Basic Medical Sciences, Martin L. Pall -
”5G: Great risk for EU, U.S. and
International Health! Compelling Evidence for Eight Distinct Types of Great Harm Caused by Electromagnetic
Field (EMF) Exposures and the Mechanism that Causes Them”,
pp. 8 - 15.
40 Offentliggjort i det videnskabelige tidsskrift ”Journal of Epidemiology and Community Health”, 2012, vol. 66, nr. 6,
pp. 524 – 529.
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”The findings of the previous publication were replicated in this separate group of participants
demonstrating that cell phone use was associated with behavioural problems at age 7 years in
children, and this association was not limited to early users of the technology. Although
weaker in the new dataset, even with further control for an extended set of potential
confounders, the associations remained.”
Denne undersøgelse, som var en gentagelse af en tidligere undersøgelse foretaget af samme
forskere, bekræftede, at der var en sammenhæng imellem adfærdsproblemer hos børn i 7-
årsalderen og brug af mobiltelefoner hos moderen før fødslen samt børnenes egen brug efter
fødslen, uden at det på baggrund af undersøgelsen med sikkerhed kunne lægges til grund, at
der var en årsagsforbindelse, jf. p. 529. Undersøgelsen bekræftede således en mulig risiko.
----
Birks et al (2017),
”Maternal cell phone use during pregnancy and child behavioral problems
in five birth cohorts”
41
, p. 1 (resumé, manuskriptudgave):
”Overall, 38.8% of mothers, mostly from the Danish cohort, reported no cell phone use during
pregnancy and these mothers were less likely to have a child with overall behavioral,
hyperactivity/inattention or emotional problems. Evidence for a trend of increasing risk of child
behavioral problems through the maternal cell phone use categories was observed for
hyperactivity/inattention problems (OR for problems in the clinical range: 1.11, 95%CI 1.01,
1.22; 1.28, 95%CI 1.12, 1.48, among children of medium and high users, respectively). This
association was fairly consistent across cohorts and between cohorts with retrospectively and
prospectively collected cell phone use data.”
(understreget her)
Ibid., p. 13 (konklusion, manuskriptudgave):
”Maternal cell phone use during pregnancy may be associated with an increased risk of
behavioral problems, particularly hyperactivity/inattention problems, in the offspring. This is
the largest study to date to evaluate these associations and to show mostly consistent results
across cohorts with retrospectively and prospectively assessed maternal cell phone use. Still,
the interpretation of these results is unclear and should take into consideration that
uncontrolled confounding by social factors or maternal hyperactivity may influence both
maternal cell phone use and child behavioral problems.”
Der er således tale om et forbeholdende, men konsistent, resultat, som bekræfter, at der kan
være en øget risiko for helbredsproblemer for børn ved mødres brug af mobiltelefon under
graviditeten.
----
Sudan et al (2018),
”Maternal cell phone use during pregnancy and child cognition at age 5
years in 3 birth cohorts”
42
, p. 155 (resumé):
”We observed patterns of lower mean cognition scores among children in relation to high
frequency maternal prenatal cell phone use. The causal nature and mechanism of this
relationship remain unknown.”
----
Der foreligger en række relaterede forsøg på dyrefostre, bl.a.:
41 Offentliggjort i det videnskabelige tidsskrift ”Environment International”, 2017, vol. 104, pp. 122 – 131.
42 Offentliggjort i det videnskabelige tidsskrift ”Environment International”, 2018, vol. 120, pp. 155 – 162.
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Jing et al (2012),
”The influence of microwave radiation from cellular phone on fetal rat brain”,
p. 64:
”In order to protect human’s health from the microwave damage, the relevant radiation limits
have been given by many countries. The current limited guidelines for microwave from cellular
phone in U.S. and Europe are 1.6 W/kg and 2.0 W/kg, respectively. New lower limits should
also be used for children and/or pregnant women.
Due to the proximity of cellular phone antenna to the user’s ear and head, the brain is
inevitably exposed to EMFs with a relatively high specific absorption ratio (SAR), so the
potentially danger from EMFs has been a concern of more and more people, especially by
pregnant women.
…
As a whole, the results obtained in the present study indicate that exposure to EMFs of cellular
phone (SAR 0.9 W/kg) could induce modifications in the fetal rat brain, not only oxidative
stress system but also neurotransmitters. Because of the widespread use of cellular phones,
further investigations with complementary techniques will be necessary to understand the
mechanism of relation between EMFs of cellular phone and physiological implications.”
Det bemærkes, at stråleabsorptionsraten ligger under den p.t. anvendte grænseværdi i
Danmark, på 2 W/kg, jf. pkt. 2.1 nedenfor.
Megha et al (2015),
”Low intensity microwave radiation induced oxidative stress, inflammatory
response and DNA damage in rat brain”
43
, p. 164 (konklusion):
”In conclusion, prolonged exposure to low intensity microwave radiation at frequencies 900,
1800 and 2450 MHz leads to oxidative stress and inflammatory imbalances which
subsequently leads to DNA damage in brain. These findings suggest that microwave radiation
induced oxidative stress and inflammatory imbalances may be the causative factors involved in
causing DNA strand breaks in brain cells.”
Aldad et al (2012),
”Fetal Radiofrequency Radiation Exposure From 800-1900 Mhz-Rated
Cellular Telephones Affects Neurodevelopment and Behavior in Mice”
44
, p. 2 og 6:
”Overall, the mice exposed in-utero to radiation were hyperactive, had decreased memory,
and decreased anxiety.
…
Our findings indicated significant electrophysiological and behavioral changes in mice exposed
in-utero to radiation. The significant trend between the groups treated for 0, 9, 15, and 24
hours/day demonstrates that the effects are directly proportional to usage time, and suggests
that safety limits, particularly for pregnant women, can be established. Though it is difficult to
translate these findings to human risks and vulnerability, we identify a novel potential
contribution to the increased prevalence in hyperactive children, one that is easily prevented.
However, it is important to note that hyperactivity and anxiety are closely related and may
confound one another.
...
In summary, we demonstrate that fetal radiofrequency radiation exposure led to
neurobehavioral disorders in mice. We anticipate these findings will improve our understanding
of the etiology of neurobehavioral disorders. The rise in behavioral disorders in developed
countries may be, at least in part, due to a contribution from fetal cellular telephone radiation
exposure. Further testing is warranted in humans and non-human primates to determine if the
risks are similar and to establish safe exposure limits during pregnancy.”
43 Offentliggjort i det videnskabelige tidsskrift ”NeuroToxicology” 2015, vol. 51, pp. 158 – 165.
44 Offentliggjort i det videnskabelige tidsskrift ”Nature Scientific Reports” 2, art.no. 312, 2012. Der er i 2013 udstedt
en korrektion til artiklen, som ikke ændrer konklusionerne, der har art.nr.. 1320.
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----
Buchner og Eger (2011),
”Changes of Clinically Important Neurotransmitters under the
Influence of Modulated RF Fields—A Long-term Study under Real-life Conditions”
45
, p. 1
(oversat fra tysk):
”Since the 1960s, occupational studies on workers with continuous microwave radiation
exposures (radar, manufacturing, communications) in the Soviet Union have shown that RF
radiation exposures below current limits represent a considerable risk potential. A com-
prehensive overview is given in the review of 878 scientific studies by Prof. Hecht, which he
conducted on behalf of the German Federal Institute of Telecommunications (contract no.
4231/630402) (2, 3).
As early as the 1980s, US research projects also demonstrated in long-term studies that rats
raised under sterile conditions and exposed to "low-level" RF radiation showed signs of stress
by increased incidences of endocrine tumors...”
Endvidere p. 9 (summary of results):
”...dopamine levels decrease substantially after the exposure begins. Even after one and a half
years, the initial levels are not restored. Six months after the activation of the transmitter, PEA
levels decrease continuously over the entire exposure period. Only in the exposure group
above 100 μW/m2 is this effect observed immediately. All findings were observed well below
current exposure limits (14).”
46
Tillige p. 12 (epidemiological evidence):
”As part of the German Mobile Telecommunication Research Programme, approximately 3000
children and adolescents were studied in Bavaria for their individual cell phone radiation
exposure levels in relation to health problems. Among the various data sets, the data set
regarding behavioral problems showed a significant increased risk for both adolescents (OR:
3.7, 95%-CI: 1.6-8.4) and also children (OR: 2.9, 95%-CI: 1.4-5.9) in the highest exposure
group (56). For the first time, the "Rimbach Study" provides a model of explanation in
biochemical terms. ”
----
Sudan et al (2012),
”Prenatal and Postnatal Cell Phone Exposures and Headaches in Children.”
47
, p. 1 (resumé, manuskriptudgave):
“In this study, cell phone exposures were associated with headaches in children, but the
associations may not be causal given the potential for uncontrolled confounding and
misclassification in observational studies such as this. However, given the widespread use of
cell phones, if a causal effect exists it would have great public health impact.”
----
Byun et al (2013),
”Mobile Phone Use, Blood Lead Levels, and Attention Deficit Hyperactivity
Symptoms in Children: A Longitudinal Study”
48
, p. 1:
”The results suggest that simultaneous exposure to lead and RF from mobile phone use was
associated with increased ADHD symptom risk, although possible reverse causality could not
be ruled out.”
45 Oprindeligt offentliggjort på tysk i det videnskabelige tidsskrift ”Umwelt-Medizin-Gesellschaft”, 2011, vol. 24, nr.
1, pp. 44 – 57.
46 (14) er forskernes henvisning til ICNIRP-grænseværdierne, jf. pkt. 2.1. nedenfor.
47 Offentliggjort i det videnskabelige tidsskrift ”The Open Pediatric Medicine Journal” 2012, nr. 6, pp. 46 – 52.
48 Offentligt i det videnskabelige onlineskrift ”PLOS One” d. 21. marts 2013.
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----
Herbert og Sage (2013),
”Autism and EMF? Plausibility of a pathophysiological link part II ”,
p.
211 (resumé):
”Autism spectrum conditions (ASCs) are defined behaviorally, but they also involve
multileveled disturbances of underlying biology that find striking parallels in the physiological
impacts of electromagnetic frequency and radiofrequency radiation exposures (EMF/RFR).
…
Brain oxidative stress and inflammation as well as measures consistent with blood–brain
barrier and brain perfusion compromise have been documented. Part II of this paper
documents how behaviors in ASCs may emerge from alterations of electrophysiological
oscillatory synchronization, how EMF/RFR could contribute to these by detuning the organism,
and policy implications of these vulnerabilities. It details evidence for mitochondrial
dysfunction, immune system dysregulation, neuroinflammation and brain blood flow
alterations, altered electrophysiology, disruption of electromagnetic signaling, synchrony, and
sensory processing, detuning of the brain and organism, with autistic behaviors as emergent
properties emanating from this pathophysiology.
…
All of these phenomena also occur with EMF/RFR exposure that can add to system overload
(‘allostatic load’) in ASCs by increasing risk, and can worsen challenging biological problems
and symptoms; conversely, reducing exposure might ameliorate symptoms of ASCs by
reducing obstruction of physiological repair.
…
With dramatic increases in reported ASCs that are coincident in time with the deployment of
wireless technologies, we need aggressive investigation of potential ASC—EMF/RFR links. The
evidence is sufficient to warrant new public exposure standards benchmarked to low-intensity
(non-thermal) exposure levels now known to be biologically disruptive, and strong, interim
precautionary practices are advocated.”
(understreget her)
----
Wiart et al (2008)
49
konstaterede, baseret på modeller af hoveder, at børns hoveder
absorberede omkring 2 gange så meget stråling som voksne, jf. p. 3693:
”...The comparisons have also shown that the maximum SAR in 1 g of peripheral brain tissues
of child models aged between 8 and 15 is comparable to the maximum SAR in 1 g of
peripheral brain tissues of adult models while it is about two times higher for child models
aged between 5 and 8. This is certainly due to the smaller thicknesses of pinna, skin and skull.
… The results obtained in this study need to be confirmed since they have been derived from
data sets of limited size. Nevertheless these results are comparable to those obtained in other
studies involving several phantoms (Beard et al 2006, Kainz et al 2005). ...”
----
Hardell et al (2011),
”Pooled analysis of case-control studies on malignant brain tumours and
the use of mobile and cordless phones including living and deceased subjects”
50
,
p. 1465
(resumé) fandt:
”...an increased risk was found for glioma and use of mobile or cordless phone. The risk
increased with latency time and cumulative use in hours and was highest in subjects with first
use before the age of 20.”
----
49 Offentligt i det videnskabelige tidsskrift ”Physics in Medicine & Biology” 2008, vol. 53, nr. 13, pp. 3681 – 3695.
50 Offentligt i det videnskabelige tidsskrift ”International Journal of Oncology” 2011, vol. 38, nr. 5, pp. 1465 – 1474.
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Fra Miller et al november 2018, p. 676 – 677:
”In a population-based case-control study of children Li et al. (2012) included 939 leukemia
and 394 brain neoplasm
51
cases newly diagnosed between 2003 and 2007, aged 15 years or
less.
…
They reported that a higher than median averaged APD
52
was significantly associated with an
increased Adjusted Odds Ratio (AOR) for all neoplasms (1.13; 1.01–1.28), and for leukemia
(1.23; 0.99–1.52), but not for all brain neoplasms (1.14, 0.83–1.55). They did not specifically
analyze data on gliomas.”
Ibid., p. 681 (konklusioner):
”The precautionary principle should be applied now and suitable warning messages provided to
adults and critically to children and their parents. Until technology has been devised that
substantially lowers exposures, special efforts should be advanced to ensure that the
exposures of children are limited to those deemed essential. Children should be encouraged to
text to reduce their exposure to RFR, while every attempt should be made to reduce exposure
to RFR in schools, as well as homes.”
1.2.2.5. Delkonklusion.
Det fremgår klart og videnskabeligt veldokumenteret, at eksponering for radiofrekvent
elektromagnetisk stråling (også under de p.t. i Danmark anvendte grænseværdier, jf. pkt. 2.1
nedenfor) kan være kræftfremkaldende, og i så henseende udgør en helbredsfare for
mennesker, der kan udvikle sig livstruende.
Dertil kommer den af Pall 2018 opsummerede videnskabelige dokumentation for en række
andre skader, inkl. nedsat fertilitet, spontane aborter, neurologiske/neuropsykiatriske effekter,
m.v.
Endvidere må det lægges til grund, at børn er særligt sårbare, og adskillige undersøgelser
peger på en mulig forbindelse mellem eksponering for radiofrekvent elektromagnetisk stråling
og adfærdsvanskeligheder, autisme, forståelsesevner, m.v.
51
Neoplasmer er abnormale væv, som kan udvikle sig til svulster og i værste fald ondartede kræftsvulster.
52 Står for ”Average Power Density”, jf. ibid. p. 677.
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1.2.3. Dyr.
Overordnet kan om dyr henvises til f.eks. Alfonso Balmoris gennemgang af den videnskabelige
litteratur i
”Electromagnetic pollution from phone masts. Effects on wildlife”
53
, p. ,
konklusionerne (der vedrører både fugle, pattedyr og insekter):
”This literature review shows that pulsed telephony microwave radiation can produce effects
especially on nervous, cardiovascular, immune and reproductive systems
[111]:
- Damage to the nervous system by altering electroencephalogram, changes in neural
response or changes of the blood–brain barrier.
- Disruption of circadian rhythms (sleep–wake) by interfering with the pineal gland and
hormonal imbalances.
- Changes in heart rate and blood pressure.
- Impairment of health and immunity towards pathogens, weakness, exhaustion, deterioration
of plumage and growth problems.
- Problems in building the nest or impaired fertility, number of eggs, embryonic development,
hatching percentage and survival of chickens.
- Genetic and developmental problems: problems of locomotion, partial albinism and
melanism or promotion of tumors.
In the light of current knowledge there is enough evidence of serious effects from this
technology to wildlife. For this reason precautionary measures should be developed, alongside
environmental impact assessments prior to installation, and a ban on installation of phone
masts in protected natural areas and in places where endangered species are present. Surveys
should take place to objectively assess the severity of effects.”
1.2.3.1. Fugle.
Der findes en større mængde videnskabelige undersøgelser, som dokumenterer direkte
skadevirkning eller risiko herfor på fugle (og følgelig også deres levesteder, hvis f.eks. en mast
er placeret tilstrækkeligt nært).
I det følgende gennemgås en række heraf, med fokus på dokumentation for skadevirkninger
eller risici:
Balmori (2005),
”Possible Effects of Electromagnetic Fields from Phone Masts on a Population
of White Stork (Ciconia ciconia)”
54
,
p. 109 og 113 – 114:
”Monitoring of a white stork population in Valladolid (Spain) in the vicinity of Cellular Phone
Base Stations was carried out, with the objective of detecting possible effects.
…
Birds are especially sensitive to the magnetic fields [48]. The white stork (Ciconia ciconia)
build their nests on pinnacles and other very high places with high electromagnetic
contamination (exposed to the microwaves). Also, they usually live inside the urban
environment, where the electromagnetic contamination is higher, and remain in the nest a lot
of the time, for this reason the decrease on the brood can be a good biological indicator to
detect the effects of these radiations. The results indicate a difference in total productivity but
not in partial productivity between the near nests and those far from the antennae. This
indicate the existence of nests without chicks, or the death of young in their first stages in the
nests near cellsites (40% of nest without young, compared to 3.3% in nests further 300 m).
…
The faithfulness of the white stork to nest sites can increase the effects of the microwaves.
53 Offentligt i det videnskabelige tidsskrift
”Pathophysiology”,
2009, vol. 16.
54 Offentligt i det videnskabelige tidsskrift ”Electromagnetic
Biology and Medicine”,
2005, vol. 24, pp. 109 – 119.
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…
Other studies find a decrease of fertility, increase of deaths after the birth in rats and
dystrophic changes in their reproductive organs [16]. A recent study shows a statistically
significant high mortality rate of chicken embryos subjected to the radiation from a cellphone,
compared to the control group [43]. ...”
Den hvide stork er optaget på fuglebeskyttelsesdirektivets ”bilag I” og hører således til de
arter, for hvilke der skal træffes ”særlige beskyttelsesforanstaltninger”, jf. pkt. 2.3.2. nedenfor.
Balmori og Hallberg (2007),
”The Urban Decline of the House Sparrow (Passer domesticus): A
Possible Link with Electromagnetic Radiation”
55
, p. 141 (resumé):
”During recent decades, there has been a marked decline of the house sparrow (Passer
domesticus) population in the United Kingdom and in several western European countries. The
aims of this study were to determine whether the population is also declining in Spain and to
evaluate the hypothesis that electromagnetic radiation (microwaves) from phone antennae is
correlated with the decline in the sparrow population.
Between October 2002 and May 2006, point transect sampling was performed at 30 points
during 40 visits to Valladolid, Spain. At each point, we carried out counts of sparrows and
measured the mean electric field strength (radiofrequencies and microwaves: 1MHz–3GHz
range). Significant declines (P
=
0.0037) were observed in the mean bird density over time, and
significantly low bird density was observed in areas with high electric field strength. The
logarithmic regression of the mean bird density vs. field strength groups (considering field
strength in 0.1V/m increments) was R
= −0 87
P
= 0 0001.
The results of this article support the hypothesis that electromagnetic signals are associated
with the observed decline in the sparrow population. We conclude that electromagnetic
pollution may be responsible, either by itself or in combination with other factors, for the
observed decline of the species in European cities during recent years. The appearently strong
dependence between bird density and field strength according to this work could be used for a
more controlled study to test the hypothesis”
Uddybende i forhold til de
konstateredes p. 145 – 146:
fortsat
anvendte
grænseværdier,
jf.
pkt.
2.1.
nedenfor,
”According to this calculation, no sparrows would be expected to be found in an area with field
strength >4V/m. ... In monitored Area 14, Plaza de la Libertad, a picocell was installed at the
beginning of January 2005 and removed at the end of March 2005. Between January and
March 2005, the mean field strength was greater than 3V/m, and the number of sparrows
decreased drastically (generally, the number of sparrows increases towards a midwinter peak).
In April 2005, after the picocell was removed, the sparrows became abundant again.”
Disse elektriske feltstyrker (V/m) ligger under de af ICNIRP anbefalede og i Danmark anvendte
grænseværdier, jf. pkt. 2.1. nedenfor.
Cucurachi et al (2012)
56
,
”A review of the ecological effects of radiofrequency electromagnetic
fields (RF-EMF)”,
p. 122:
”Balmori (2005) monitored the variation of a population of white storks (Ciconia ciconia) in the
vicinity of a GSM base station i.e. 900–1800 MHz with 217 Hz modulation) in search of
possible effects from the exposure. Total productivity within 200 m was on average 46% less
than that found at a distance greater than 300 m from the emitting station. An analogous
significant difference was found in the breeding success: in 40% more of the cases no new-
born chicks were found in the nest.
…
55 Offentligt i det videnskabelige tidsskrift ”Electromagnetic
Biology and Medicine”,
2007, vol. 26, pp. 141 – 151.
56 Offentligt i det videnskabelige tidsskrift ”Environment International”, 2013, vol. 51, pp. 116-140.
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Amongst the more recent laboratory studies, evidence of an effect of RF-EMF on mortality and
development of embryos was in all cases found at both high and low dosages. In all the five
field studies found a significant effect of RF-EMF on breeding density, reproduction or species
composition. Field observations give a closer representation of real-life exposure, thus RF-EMF,
especially in the 900 MHz GSM band could be a certain factor influencing the ecology of birds.”
Burlaka et al (2013), p. 223:
”In conclusion, the exposure of developing quail embryos in ovo to extremely low intensity RF-
EMR of GSM 900MHz during at least one hundred and fifty-eight hours discontinuously leads to
the significantly increased rates of superoxide and nitrogen oxide generation in embryo cells.
This was accompanied by a significantly increased level of lipid peroxidation, a depression of
key antioxidant enzymes activity,and significantly, 2–3-fold, increased level of oxidative
damage of DNA in embryo cells.”
(understreget her)
Alfonso Balmori (2015),
”Anthropogenic radiofrequency electromagnetic fields as an emerging
threat to wildlife orientation”
57
, p. 59:
Low-voltage electricity current-generated electromagnetic field can produce a significantly
negative effect on the breeding success of birds (Ciconia ciconia) nesting directly on electricity
lines (Vaitkuvienė and Dagys, 2014) and these same results have been found in nests exposed
to radiofrequency radiation near phone masts (Balmori, 2005).”
Yakymenko et al (2015), p. 194:
”We could ascertain the signaling effects of moderate levels of free radicals from our
experiments in quail embryos irradiated with the commercial cell phone. Thus, we were able to
show that the prolonged exposures of embryos in ovo led to robust repression of their
development (Tsybulin et al., 2013), which was concomitant with significant overproduction of
superoxide radical and NO radical, increased rates of lipid peroxidation and oxidative damage
of DNA (Burlaka et al., 2013; Tsybulin et al., 2012).”
(understreget her)
Shende et al (2015),
”Electromagnetic Radiations: A Possible Impact on Population of
House Sparrow (Passer Domesticus)”
58
, p. 45:
”By monthly monitoring in urban and rural area, it is found that the population of house
sparrow is declining in the urban area, where cell phone towers are more as compared to the
rural area in every season.”
----
Et særligt fokusområde i den videnskabelige litteratur udgøres af undersøgelser af
radiofrekvent elektromagnetisk strålings virkning på fugles biologisk determinerede muligheder
for at orientere sig.
Fugle er – ligesom en række andre dyr, jf. pkt. 1.2.3.2. nedenfor – født med, hvad der kan
beskrives som en art indbygget, magnetisk baseret kompas, som indebærer, at de kan finde
vej under deres migration.
Der kan bl.a. henvises til Alfonso Balmori (2015),
”Anthropogenic radiofrequency
electromagnetic fields as an emerging threat to wildlife orientation”
59
, p. 58 – 59:
”Radio frequency
fields in the MHz range disrupt birds' orientation interfering directly with the
primary processes of magnetoreception and therefore disable the avian compass as long as
57 Offentligt i det videnskabelige tidsskrift ”Science of the Total Environment” 2015, pp. 58 – 60.
58 Offentligt i det videnskabelige tidsskrift ”Engineering International”, 2015, vol. 3, nr. 1, pp. 45 – 52.
59 Offentligt i det videnskabelige tidsskrift ”Science of the Total Environment” 2015, pp. 58 – 60.
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they are present (Wiltschko et al., 2014). Ritz et al. (2004 & 2009) reported the sensitivity for
orientation of European robins (Erithacus rubecula) to radiofrequency magnetic fields. The
orientation of migratory birds is disrupted when very weak high-frequency fields (broadband
field of 0.1–10 MHz of 85 nT or a 1.315 MHz field of 480 nT) are added to the static
geomagnetic field of 46.000 nT (Thalau et al., 2006). It was convincingly demonstrated that
robins are unable to use their magnetic compass in the presence of urban electromagnetic
radiofrequency noise in the frequency range of 2 kHz –5 MHz (Engels et al., 2014). Therefore,
electrosmog scrambles birds' magnetic sense and this finding could inform policies written to
protect the habitats of endangered species.(understreget
her)
Balmori (2005),
”Possible Effects of Electromagnetic Fields from Phone Masts on a Population
of White Stork (Ciconia ciconia)”
60
,
p. 115:
”... The perception to the terrestrial magnetic field can be altered by the electromagnetic
radiation from the antennae. The reports of carrier pigeons losing direction in the vicinity of
cellsites are numerous, and more investigation is necessary. ...”
Det EU-baserede forskningsprojekt EKLIPSE udgav v/ Malkemper et al i 2018 en rapport med
titlen
”The
impacts of artificial Electromagnetic Radiation on wildlife (flora and fauna). Current
knowledge overview: a background document to the web conference”,
hvoraf bl.a. fremgår s.
15:
”...It
is established that the magnetic compass of migratory birds can be disrupted by the
weak RF background in larger cities (nT-intensities) but it is currently unclear which exact
frequencies are most effective.
...”
Ang. denne effekt henvises endvidere til Engels et al (2014),
”Anthropogenic electromagnetic
noise disrupts magnetic compass orientation in a migratory bird”
61
, p. 353 (resumé):
”...Here we show that migratory birds are unable to use their magnetic compass in the
presence of urban electromagnetic noise. When European robins, Erithacus rubecula, were
exposed to the background electromagnetic noise present in unscreened wooden huts at the
University of Oldenburg campus, they could not orient using their magnetic compass. Their
magnetic orientation capabilities reappeared in electrically grounded, aluminium-screened
huts, which attenuated electromagnetic noise in the frequency range from 50
 
kHz to 5
 
MHz by
approximately two orders of magnitude. When the grounding was removed or when broadband
electromagnetic noise was deliberately generated inside the screened and grounded huts, the
birds again lost their magnetic orientation capabilities. The disruptive effect of radiofrequency
electromagnetic fields is not confined to a narrow frequency band and birds tested far from
sources of electromagnetic noise required no screening to orient with their magnetic compass.
These fully double-blinded tests document a reproducible effect of anthropogenic
electromagnetic noise on the behaviour of an intact vertebrate.”
(understreget her)
1.2.3.1.1. Delkonklusion.
Ligesom tilfældet er i forhold til helbredsskader og risici herfor på mennesker, forekommer det
særdeles videnskabeligt veldokumenteret, at radiofrekvent elektromagnetisk stråling, også den
som holder sig inden for de af myndighederne fastlagte grænseværdier, henholdsvis er og kan
være helbredsskadeligt for fugle og (in extenso) deres levesteder.
Dertil kommer det særlige forhold ved fugle i forhold til mennesker, at deres evner til at
orientere sig til dels er baseret på interaktion med jordens naturligt forekommende
magnetfelter. Radiofrekvent elektromagnetisk strålings virkning på fugles biologisk
determinerede muligheder for at orientere sig kan være ødelæggende for bevarelsen af arten,
60 Offentligt i det videnskabelige tidsskrift ”Electromagnetic
Biology and Medicine”,
2005, vol. 24, pp. 109 – 119.
61 Offentligt i det videnskabelige tidsskrift ”Nature” 2014, nr. 509, pp. 353 – 356.
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herunder i de dertil særligt udpegede beskyttede yngleområder. Særligt vedr. dette emne skal
dog fremhæves, at dette for indeværende ikke synes at vedrøre 5G-frekvenser, m.v., men det
kunne være tilfældet. Studier herom dokumenterer p.t. så vidt ses kun, at fugles biologisk
determinerede orienteringssans påvirkes negativt af radiofrekvent elektromagnetisk stråling.
1.2.3.2. Andre dyr.
For så vidt angår insekter kan bl.a. henvises til Alfonso Balmori (2015),
”Anthropogenic
radiofrequency electromagnetic fields as an emerging threat to wildlife orientation”
62
, p. 59:
”As with birds, radio frequency magnetic fields disrupt magnetoreception in insects. The
geomagnetic field reception in American cockroach is sensitive to weak radio frequency field
causing a disruptive effect (Vacha et al., 2009), so these authors suggest that electromagnetic
smog will have to be taken more seriously in animal magnetoreception experiments. In an
experimentally-generated electromagnetic field of about 1 V/m with a realistic (and even
lower) power intensity similar to those surrounding communication masts, the results and
observations suggest that GSM (Global System for Mobile communications) 900 MHz radiation
might have a severe impact on the nerve cells of exposed ants, especially affecting the visual
and olfactory memory, causing the loss of their ability to use visual cues and suggesting that
electromagnetic radiation may have an impact on the orientation behaviour and navigation of
animals that use magnetic fields to find their way (Cammaerts et al., 2012, 2014). Honeybees
are sensitive to pulsed electromagnetic fields generated by mobile phones and observable
changes in the bee behaviour could be one explanation for the loss of colonies (Favre, 2011).
Magnetoreception system in Monarch butterfly orientation (Guerra et al., 2014) may be also
suffering interference with anthropogenic radio frequency magnetic fields and this, together
with other factors (Brower et al., 2012), may be a cause of their population decline.”
(understreget her)
Tilsvarende i Cucurachi et al (2012)
63
, p. 116:
”Information was collected from 113 studies from original peer-reviewed publications or from
relevant existing reviews… The majority of the studies were conducted in a laboratory setting
on birds (embryos or eggs), small rodents and plants. In 65% of the studies, ecological effects
of RF-EMF (50% of the animal studies and about 75% of the plant studies) were found both at
high as well as at low dosages. ...”
Ibid., p. 122 – 123:
”It has been demonstrated that insects can sense magnetic fields as a means for navigation
and orientation (Abraçado et al., 2005; Kirschvink et al., 2001; Liedvogel and Mouritsen,
2010; Wajnberg et al., 2010; Winklhofer, 2010). Magneto-reception has been associated with
the use of ferromagnetic iron oxide particles embedded in tissue or through pairs of molecules
with unpaired electrons (known as radical pairs) that are associated with a light sensitive
photoreceptor (Ritz et al., 2002; Knight, 2009; Vácha et al. 2009). The exposure to RF-EMF
might disrupt this magneto-reception mechanism, which could in turn affect the survival of
insects. The most commonly studied species are the honey bee (A. mellifera) and the fruit fly
(Drosophila melanogaster).”
Og p. 129:
”The studies analysing the effects of RF-EMF on fruit flies found in all cases a significant effect.
Results of one study show an increased reproductive success after exposure. The remaining
studies, which were conducted by the same research institute in Greece, found in all cases a
significant depression of growth and reproduction at both 900 and 1800 MHz. Two studies on
62 Offentligt i det videnskabelige tidsskrift ”Science of the Total Environment” 2015, pp. 58 – 60.
63 Offentligt i det videnskabelige tidsskrift ”Environment International”, 2013, vol. 51, pp. 116-140.
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the American cockroach and a species of ant analysed the effects of exposure to RF-EMF on
the magneto-reception and orientation of the insects. The behaviour of target systems was
disrupted by the exposure to RF-EMF.”
Samt p. 136 (konklusioner):
”...The effects of RF-EMF on different biological groups were investigated. With reference to
the groups under investigations in the selected studies (i.e. birds, honeybees, mammals,
plants, Drosophila and others) there is ecologically relevant evidence that the RF-EMF caused
an effect in about 50% of the animal studies and about 90% of the plant studies. ...”
----
Kumar et al (2011),
”Exposure to cell phone radiations produces biochemical changes in
worker honey bees”
64
, (resumé, resultater og diskussion):
”The present study was carried out to find the effect of cell phone radiations on various
biomolecules in the adult workers of Apis mellifera L. The results of the treated adults were
analyzed and compared with the control. Radiation from the cell phone influences honey bees’
behavior and physiology. There was reduced motor activity of the worker bees on the comb
initially, followed by en masse migration and movement toward “talk mode” cell phone. The
initial quiet period was characterized by rise in concentration of biomolecules including
proteins, carbohydrates and lipids, perhaps due to stimulation of body mechanism to fight the
stressful condition created by the radiations.
At later stages of exposure, there was a slight decline in the concentration of biomolecules
probably because the body had adapted to the stimulus.
…
Very little work has been done on biochemical, metabolic and physiological influences of cell
phone radiations pertaining to health risk in man.[8] Therefore, the present investigations on
the influence of cell phone radiations on some biochemical and physiological aspects of
honeybee biology were undertaken. That the behavior of honeybee is altered to some extent
by high or low energy fields or electromagnetic radiations has been known for quite some
time.[9]
During the present investigation, it was observed that there was an increase in concentration
of total carbohydrates in the bees exposed to cell phone radiation for 10 min as compared to
unexposed or control bees. Increasing the exposure time to 20 min resulted in further increase
in the concentration, while an exposure of 40 min had a reverse effect and there was a decline
in carbohydrate concentration, though it was still higher as compared to control. Hemolymph
glycogen and glucose content also showed the same trend, i.e., there was increase in content
up to 20 min exposure after which there was a slight decline in the concentration which
remained more than the control. Sharma[10] had also reported increase in glycogen and
glucose levels in the exposed pupa of A. mellifera.
Lipids are the major energy reserves of insects. Certain lipid classes are structure components
of membranes while others are raw materials for a variety of hormones and pheromones.
Estimation of total lipids and cholesterol during the present study showed that the trend was
similar to that of carbohydrates. After an initial increase in concentration at the 10 and 20 min
exposure period, a decline was observed in the concentration of total lipids and cholesterol at
40 min exposure.
It was interesting to note that during the present study as the exposure time increased, it
appeared that the bees having assessed the source of the disturbance decided to move and a
large scale movement of the workers toward the talk-mode (not toward the listening mobile)
was observed. Also, the bees became slightly aggressive and started beating their wings in
agitation. This mobility of the bees could be responsible for increase utilization of energy
sources and consequent decrease in concentration of carbohydrates and lipids in the 40 min
exposed sample.”
(understreget her)
64 Offentligt i det videnskabelige tidsskrift ”Toxicology International”, 2011, vol. 18, nr. 1, pp. 70 – 72.
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----
Margaritis et al (2014),
”Drosophila oogenesis as a bio-marker responding to EMF sources”
65
,
p. 165 (resumé):
”A total of 280 different experiments were performed using newly emerged flies exposed for
short time daily for 3–7 d to various EMF sources including: GSM 900/1800 MHz mobile phone,
1880–1900 MHz DECT wireless base, DECT wireless handset, mobile phone-DECT handset
combination, 2.44 GHz wireless network (Wi-Fi), 2.44 GHz blue tooth, 92.8 MHz FM generator,
27.15 MHz baby monitor, 900 MHz CW RF generator and microwave oven’s 2.44 GHz RF and
magnetic field components.
…
All EMF sources used created statistically significant effects regarding fecundity and cell death-
apoptosis induction, even at very low intensity levels (0.3 V/m blue tooth radiation), well
below ICNIRP’s guidelines, suggesting that Drosophila oogenesis system is suitable to be used
as a biomarker for exploring potential EMF bioactivity. Also, there is no linear cumulative effect
when increasing the duration of exposure or using one EMF source after the other (i.e. mobile
phone and DECT handset) at the specific conditions used. ...”
Studiet blev udført på bananfluer, og det blev på baggrund af fundene anbefalet, at dette
insekt fremover anvendes som biologisk markør ved undersøgelser af effekter af radiofrekvent
elektromagnetisk stråling.
Som det fremgår, opstod der celledød endog ved meget lave intensiteter af stråling, helt ned til
0,3 V/m fra Blue Tooth-produkter.
Undersøgelsen viser, at udstyr som ligger inden for de af ICNIRP anbefalede grænseværdier
(f.eks. 61 V/m for udstyr på med et frekvensområde på 2 – 300 GHz), jf. også pkt. 2.1
nedenfor, må forventes at være stærkt skadeligt for insekter.
Visse insekter er omfattet af EU's habitatdirektivbeskyttelse, jf. pkt. 2.3.3. nedenfor.
Dertil kommer, at fugle, der lever af insekter, ligeledes vil få ødelagt deres levesteder. For
indholdet EU's fuglebeskyttelsesdirektiv henvises til pkt. 2.3.2. nedenfor.
----
Cammaerts og Johansson (2014),
”Ants can be used as bio-indicators to reveal biological
effects of electromagnetic waves from some wireless apparatus”
66
, p. 286, pkt. 3:
”All radiating sources tested in this study on the ants demonstrated clear and statistically
significant effects. It was already known that a mobile phone in standby mode affects living
organisms (e.g. see Cammaerts et al.,2011; Favre, 2011; Panagopoulos et al., 2004; Sharma
and Kumar, 2010). In this study, we showed that a common mobile phone has an effect while
in standby mode and even in off-condition. Of course, when activated, the effect of a mobile
phone is stronger. Without its battery, such a phone has no longer an effect. Our ants
demonstrated that a modern smartphone and even more so a DECT phone do affect living
organisms. Furthermore, the electromagnetic waves generated by a WiFi router impact our
ants and such an effect increases during the course of the exposure time. Persons working in
rooms provided with wireless equipment should note this result. A modern personal computer
also generates electromagnetic waves. This is due to the PC WiFi function, which is
automatically activated. Based on these results, we advice users to deactivate the WiFi
function of their PC as long as they do not use it. This can also be deduced from the study
65 Offentligt i det videnskabelige tidsskrift ”Electromagnetic Biology and Medicine”, 2014, vol 33, nr. 3, pp. 165 –
189.
66 Offentligt i det videnskabelige tidsskrift ”Electromagnetic Biology and Medicine”, 2014, vol 33, nr. 4, pp. 282 –
288.
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related
in
http://bigbrouser.blog.lemonde.fr/2011/12/01/microonde-le-wi-fi-tueur-de-
spermatozoı¨des/.”
(understreget her)
----
Særligt for så vidt angår bestøvere skal henvises til Lázaro et al (2016),
”Electromagnetic
radiation of mobile telecommunication antennas affects the abundance and composition of wild
pollinators”
67
, p. 322 (konklusion):
”Electromagnetic radiation from telecommunication antennas affected the abundance and
composition of wild pollinators in natural habitats....Pollinators and their host plants constitute
pollination networks. Although the architecture of these mutualistic networks can increase the
capacity of pollinator populations to persist under harsh conditions, once a tipping point in
human-induced environmental
change is reached, pollinator populations may collapse
simultaneously (Lever et al. 2014). Therefore, these changes in the composition of pollinator
communities associated with electromagnetic smog may have important ecological and
economic impacts on the pollination service that could significantly
affect the maintenance of
wild plant diversity, crop production and human welfare.”
Studiet viser således en sammenhæng mellem stråling fra mobilmaster og antallet af
(flyvende) insekter.
Sammensætningen af bestøvere må anses for et vigtigt økologisk element og vigtig økonomisk
parameter for produktion af afgrøder, menneskets velfærd samt for biodiversiteten generelt.
----
Vilic et al (2017),
”Effects of short-term exposure to mobile phone radiofrequency (900 MHz)
on the oxidative response and genotoxicity in honey bee larvae”
68
, p. 430 (resumé):
”Exposure of different animal species to radiofrequency electromagnetic fields (RF-EMF) could
cause various biological effects such as oxidative stress, genotoxic effects and dysfunction of
the immune system. However, there are a lack of results on oxidative stress response and
genotoxicity in the honey bee (Apis mellifera) after exposure to RF-EMF. This study was
performed to investigate the effects of exposure to RF-EMF on the activity of catalase,
superoxide dismutase, glutathione S-transferase, lipid peroxidation level and DNA damage in
honey bee larvae. Honey bee larvae were exposed to RF-EMF at 900 Mhz and field levels of 10,
23, 41 and 120 V m−1 for 2 h. At a field level of 23 V m−1 the effect of 80% AM 1 kHz
sinusoidal and 217 Hz modulation was investigated as well. Catalase activity and the lipid
peroxidation level decreased significantly in the honey bee larvae exposed to the unmodulated
field at 10 V m−1 compared to the control. Superoxide dismutase and glutathione S-
transferase activity in the honey bee larvae exposed to unmodulated fields were not
statistically different compared to the control. DNA damage increased significantly in honey
bee larvae exposed to modulated (80% AM 1 kHz sinus) field at 23 V m −1 compared to the
control and all other exposure groups. These results suggest that RF-EMF effects in honey bee
larvae appeared only after exposure to a certain EMF conditions. The increase of the field level
did not cause a linear dose-response in any of the measured parameters. Modulated RF-EMF
produced more negative effects than the corresponding unmodulated field. Although honey
bees in nature would not be exposed to such high field levels as used in our experiments, our
results show the need for further intensive research in all stages of honey bee development.”
(understreget her)
Ibid., p. 437 (konklusion):
”In conclusion, the results of our study showed that effects of RF-EMF at 900 MHz in honey
67 Offentligt i det videnskabelige tidsskrift ”Journal of Insect Conservation”, 2016, vol. 20, nr. 2, pp. 315 – 324.
68 Offentligt i det videnskabelige tidsskrift ”Journal of Apicultural Research”, 2017, vol. 56, nr. 4, pp. 430 – 438.
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bee larvae appeared only after exposure to the certain EMF conditions. RF-EMF modulated at 1
kHz showed an increase of DNA damage, while unmodulated RF-EMF produced alteration in
catalase activity and lipid peroxidation at the lowest field level of 10 V m −1. Evidently, the
increase of the field level did not cause a linear dose-response relationship in any of the
measured parameters. Although honey bees in nature would not be exposed to such high field
levels as used in our experiments, our results show the need for further intensive research in
all stages of honey bee development, as well as the intensive research on the possible
existence of a “window” effect under natural conditions during the annual cycling of bees.”
----
Thielens et al (2018),
”Exposure
of Insects to Radio-Frequency Electromagnetic Fields from 2
to 120 GHz”,
p. 9 (konklusion, manuskriptudgave):
”The
insects show a maximum in absorbed radio frequency power at wavelengths that are
comparable to their body size. They show a general increase in absorbed radio-frequency
power above 6 GHz (until the frequencies where the wavelengths are comparable to their body
size), which indicates that if the used power densities do not decrease, but shift (partly) to
higher frequencies, the absorption in the studied insects will increase as well. A shift of 10% of
the incident power density to frequencies above 6 GHz would lead to an increase in absorbed
power between 3–370%. This could lead to changes in insect behaviour, physiology, and
morphology over time due to an increase in body temperatures, from dielectric heating. The
studied insects that are smaller than 1 cm show a peak in absorption at frequencies (above 6
GHz), which are currently not often used for telecommunication, but are planned to be used in
the next generation of wireless telecommunication systems. At frequencies above the peak
frequency (smaller wavelengths) the absorbed power decreases slightly.”
Som det fremgår af de sidste, understregne linjer, vedrører denne undersøgelse tillige de
højere frekvenser over 6 GHz, som vil blive taget i anvendelse ved 5G.
----
Studier ang. effekt af radiofrekvent elektromagnetisk strålingpå flagermus
69
er gennemført i
bl.a. Nicholls og Racey (2009),
”The
Aversive Effect of Electromagnetic Radiation on Foraging
Bats—A Possible Means of Discouraging Bats from Approaching Wind Turbines”,
hvori der bl.a.
findes som følger, jf. p. 1 (resumé):
”Large
numbers of bats are killed by collisions with wind turbines and there is at present no
accepted method of reducing or preventing this mortality. Following our demonstration that
bat activity is reduced in the vicinity of large air traffic control and weather radars, we tested
the hypothesis that an electromagnetic signal from a small portable radar can act as a
deterrent to foraging bats. From June to September 2007 bat activity was compared at 20
foraging sites in northeast Scotland during experimental trials (radar switched on) and control
trials (no radar signal). Starting 45 minutes after sunset, bat activity was recorded for a period
of 30 minutes during each trial and the order of trials were alternated between nights. From
July to September 2008 aerial insects at 16 of these sites were sampled using two miniature
light-suction traps.
At each site one of the traps was exposed to a radar signal and the other
functioned as a control. Bat activity and foraging effort per unit time were significantly reduced
during experimental trials when the radar antenna was fixed to produce a unidirectional signal
therefore maximising exposure of foraging bats to the radar beam. However, although bat
activity was significantly reduced during such trials, the radar had no significant effect
on the
abundance of insects captured by the traps.”
(understreget her)
Tilsvarende i Balmori (2009),
“Electromagnetic pollution from phone masts. Effects on
69 15 arter af flagermus er omfattet af habitatdirektivets bestemmelser om særlige beskyttelsesforanstaltninger, jf. pkt.
2.3.3. nedenfor.
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wildlife”
70
, p. 4:
“Electromagnetic
radiation can exert an aversive behavioral response in bats. Bat activity is
significantly reduced in habitats exposed to an electromagnetic field strength greater than 2
V/m
[73].
During a study in a free-tailed bat colony (Tadarida teniotis) the number of bats
decreased when several phone masts were placed 80m from the colony
[74].”
Ang. padder kan bl.a. henvises til Alfonso Balmori (2010),
”Mobile
Phone Mast Effects on
Common Frog (Rana temporaria) Tadpoles: The City Turned into a Laboratory”
71
, p. 35:
”...Most
prevailing hypotheses suggest that a field acts to directionally guide the growth and
migration of some embryonic cells (Hotary and Robinson, 1992).
Strong magnetic fields (1.74–16.7T) disrupt cell division of exposed frog eggs (Xenopus laevis)
(Denegre et al., 1998). Valles (2002) proposed a model to explain their influence.
Several studies on effects of electromagnetic fields on amphibians have been conducted in
laboratories. When amphibian eggs and embryos of Ambystoma maculatum and Rana
sylvatica were exposed to high magnetic fields (6.3 103 G), a brief treatment of early
embryos produced several types of abnormalities, incuding microcephaly, retarded (abnormal)
growth, edema, and scoliosis (Levengood, 1969).
Adult newts (Notophthalmus viridescens) exposed to a pulsed electromagnetic field (1 T and
0.15 V/m, approx.) for the first 30 days post forelimbs were amputated and produced more
abnormalities in their skeletal patterns than the native limbs or the normal regenerates.
Twelve percent exhibited unique abnormalities not observed in either the native or regenerate
limb population. These forelimbs demonstrated one or more of the following gross defects:
acheiria (lack of carpus and digits), aphalangia, or oligodactylia (loss of digits) as well as
carpal bone and long bone (radius and ulna) abnormalities (Landesman and Douglas, 1990).
Exposed frog tadpoles (Rana temporaria) developed under electromagnetic field (50Hz,
260A/m) show an increase in mortality. Exposed tadpoles developed more slowly and less
synchronously than control tadpoles and remained at the early stages for longer. Tadpoles
developed allergies and EMF caused changes in their blood counts (Grefner et al., 1998).
These results are consistent with the observations of this work.
Deformities and disappearance of amphibians and other organisms is part of the global
biodiversity crisis (Blaustein and Johnson, 2003). Some authors consider that the
electromagnetic pollution is destroying nature (Warnke, 2007; Firstenberg, 1997).
Balmori (2006) proposed that electromagnetic pollution (in the microwave and radiofrequency
range) along with other environmental factors is a possible cause for decline and deformations
of some wild amphibian populations exposed. The results of this experiment conducted in a
real situation in the city of Valladolid (Spain) indicate that the tadpoles that live near such
facilities, exposed to relatively low levels of environmental electromagnetic fields (1.8–3.5V/m)
may suffer adverse effects (low coordination of movements, asynchronous growth, and high
mortality), and this may be a cause (together with other environmental factors) of decline of
amphibian populations.”
(understreget her)
Studiet er således udført på, hvad der måske er Danmarks mest almindelige frø, butsnudet frø.
Dyret er optaget på bilag II til EU's habitatdirektiv, og er således omfattet af særlige
beskyttelsesforanstaltninger, jf. pkt. 2.3.3. nedenfor.
Undersøgelsen påpeger, udover indikation for mutationer og en lang række sundhedsskader på
padder, at den elektromagnetiske forurening fra selv relativt svage elektromagnetiske felter,
miljøet udsættes for, er en mulig årsag (sammen med andre miljømæssige faktorer) til tabet af
krybdyrspopulationer.
På mus kan bl.a. henvises til følgende, udover de i øvrigt i responsummet omtalte artikler:
Magras og Xenos (1997),
”RF
Radiation–Induced Changes in the Prenatal Development of
70 Offentligt i det videnskabelige tidsskrift ”Pathopsyiology”, 2009,
71 Offentligt i det videnskabelige tidsskrift ”Electromagnetic Biology and Medicine”, 2010, vol. 29, pp. 31 – 35.
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Mice”,
p. 455:
”The
possible effects of radiofrequency (RF) radiation on prenatal development has been
investigated in mice. This study consisted of RF level measurements and in vivo experiments
at several places around an ‘‘antenna park.’’ At these locations RF power densities between
168 nW/cm2 and 1053 nW/cm2 were measured. Twelve pairs of mice, divided in two groups,
were placed in locations of different power densities and were repeatedly mated five times.
One hundred eighteen newborns were collected. They were measured, weighed, and examined
macro- and microscopically. A progressive decrease in the number of newborns per dam was
observed, which ended in irreversible infertility. The prenatal development of the newborns,
however, evaluated by the crown-rump length, the body weight, and the number of the
lumbar, sacral, and coccygeal vertebrae, was improved.”
(understreget her)
Mekanismen for den observerede sterilitet hos musene er forklaret således i Shahin et al
(2017),
”Mobile
phone (1800 MHz) radiation impairs female reproduction in mice, Mus
musculus, through stress induced inhibition of ovarian anduterine activity”,
p. 41 (resumé):
”Present
study investigated the long-term effects of mobile phone (1800 MHz) radiation in
stand-by, dialing and receiving modes on the female reproductive function (ovarian and
uterine histo-architecture, andsteroidogenesis) and stress responses (oxidative and nitrosative
stress). We observed that mobile phone radiation induces significant elevation in ROS, NO,
lipid peroxidation, total carbonyl content and serumcorticosterone coupled with significant
decrease in antioxidant enzymes in hypothalamus, ovary anduterus of mice. Compared to
control group, exposed mice exhibited reduced number of developing and mature follicles as
well as corpus lutea. Significantly decreased serum levels of pituitary gonadotrophins(LH,
FSH), sex steroids (E2 and P4) and expression of SF-1, StAR, P-450scc, 3 -HSD, 17 -HSD,
cytochrome P-450 aromatase, ER- and ER- were observed in all the exposed groups of mice,
compared to control. These findings suggest that mobile phone radiation induces oxidative and
nitrosative stress, which affects the reproductive performance of female mice.”
(understreget
her)
Videre hedder det ibid., p. 57:
”...Mobile phone radiation may result in ovarian and uterine dysfunction by increasing ROS and
RNS production and disturbing antioxidant status. Oxidative and nitrosative stress created at
the hypothalamus and peripheral level (ovary and uterus) as a consequence of long-term
mobile phone exposure may severely reduce both steroidogenesis and folliculogenesis in the
ovary as well as the structural and functional status of the uterus. These results led us to
conclude that chronic exposure to long-term mobile phone radiation may severely affect the
ovarian and uterine activity of female mice and thus may lead to infertility. ...”
1.2.3.2.1. Delkonklusion.
Det forekommer videnskabeligt veldokumenteret, at radiofrekvent elektromagnetisk stråling,
også den som holder sig inden for de af myndighederne fastlagte grænseværdier, henholdsvis
er og kan være helbredsskadeligt for insekter.
Dertil kommer det særlige forhold, at også insekternes evne til at orientere sig til dels er
baseret på interaktion med naturligt forekommende felter i f.eks. de blomster, som skal
bestøves. Virkningen af radiofrekvent elektromagnetisk stråling på insekters biologisk
determinerede muligheder for at orientere sig kan være ødelæggende for bevarelsen af arten.
Dertil kommer, at insekters forsvinden fra et område kan have afgørende betydning for
insektædende fugles muligheder for at overleve som arter.
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1.2.4. Yderligere om leveområder samt planter.
En del af den i pkt. 1.2.3. ovenfor omtalte forskning omhandler leveområder (habitatområder),
idet den angår undersøgelser af strålings påvirkning af dyr i de områder, hvor de har deres
reder, jagtområder, osv., eller belyser, hvad effekten er i også disse områder.
Dertil kan føjes videnskabelige undersøgelser foretaget af radiofrekvent elektromagnetisk
stråling på planter, herunder træer:
Magone (1996),
”The effect of electromagnetic radiation from the Skrunda Radio Location
Station on Spirodela polyrhiza (L.) Schleiden cultures”
72
, p. 75 (resumé):
”The effect of electromagnetic radiation from the Skrunda Radio Location Station was studied
on the vegetative growth and morphology of the duckweed Spirodela polyrhiza (L.) Schleiden
plant in the next generation. The impact of plant development stage and length of the
exposure period were examined. The effect of short-term (5-day) exposures of Spirodela
cultures depended on the stage of development at the time of exposure. Generally, the
vegetative reproduction rate was accelerated in the first 20 days after the end of exposure.
Exposure of plants just beginning formation lowered the vegetative growth rate. Eighty-eight-
hour exposure caused the appearance of some abnormal individuals after 30 days of growth.
At 55 days, various morphological and developmental abnormalities appeared in 6–10
daughter plants from 10 exposed mother plants, compared with 0.1 plants per 10 in the
control condition. Plants developed completely to daughter fronds under exposure from the
electromagnetic field had a shorter life-span (67 days compared to 87 days in the control) and
fewer subsequent daughters (total eight compared to 10 in the control group).”
(understreget
her)
Undersøgelsen vedrørte andemad.
----
Katie Haggerty (2010),
”Adverse Influence of Radio Frequency Background on Trembling
Aspen Seedlings: Preliminary Observations”
73
, p. :
”The results of this preliminary experiment indicate that the RF background may be adversely
affecting leaf and shoot growth and inhibiting fall production of anthocyanins associated with
leaf senescence in trembling aspen seedlings. These effects suggest that exposure to the RF
background may be an underlying factor in the recent rapid decline of aspen populations.
Further studies are underway to test this hypothesis in a more rigorous way.”
Undersøgelsen vedrørte poppeltræer.
----
Waldman et al (2016),
”Radiofrequency radiation injures trees around mobile phone base
stations”,
p. 554 – 555 (resumé):
”...detailed long-term (2006–2015) field monitoring study was performed in the cities of
Bamberg and Hallstadt (Germany). During monitoring, observations and photographic
recordings of unusual or unexplainable tree damage were taken, alongside the measurement
of electromagnetic radiation. In 2015 measurements of RF-EMF (Radiofrequency
Electromagnetic Fields) were carried out. A polygon spanning both cities was chosen as the
study site, where 144 measurements of the radiofrequency of electromagnetic fields were
taken at a height of 1.5 m in streets and parks at different locations.
72
Offentligt i det videnskabelige tidsskrift ”Science of The Total Environment”, 1996, vol. 180, nr. 1, pp. 75 – 80.
73 Offentligt i det videnskabelige tidsskrift ”International Journal of Forestry Research” 2010, Article ID 836278.
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...
The measurements of all trees revealed significant differences between the damaged side
facing a phone mast and the opposite side, as well as differences between the exposed side of
damaged trees and all other groups of trees in both sides. Thus, we found that side differences
in measured values of power flux density corresponded to side differences in damage. The 30
selected trees in low radiation areas (no visual contact to any phonemast and power flux
density under 50 μW/m2) showed no damage. Statistical analysis demonstrated that
electromagnetic radiation from mobile phone masts is harmful for trees. These results are
consistent with the fact that damage afflicted on trees by mobile phone towers usually start on
one side, extending to the whole tree over time.”
(understreget her)
----
Malka Halgamuge (2017),
”Review: Weak radiofrequency radiation exposure from mobile
phone radiation on plants”
74
, p. 213 (resumé):
”Subject and methods: In this study, we performed an analysis of the data extracted from the
45 peer-reviewed scientific publications (1996–2016) describing 169 experimental
observations to detect the physiological and morphological changes in plants due to the non-
thermal RF-EMF effects from mobile phone radiation. Twenty-nine different species of plants
were considered in this work. Results: Our analysis demonstrates that the data from a
substantial amount of the studies on RF-EMFs from mobile phones show physiological and/or
morphological effects (89.9%, p < 0.001). Additionally, our analysis of the results from these
reported studies demonstrates that the maize, roselle, pea, fenugreek, duckweeds, tomato,
onions and mungbean plants seem to be very sensitive to RF-EMFs. Our findings also suggest
that plants seem to be more responsive to certain frequencies, especially the frequencies
between (i) 800 and 1500 MHz ( p < 0.0001), (ii) 1500 and 2400 MHz (p < 0.0001) and (iii)
3500
75
and 8000 MHz (p = 0.0161).”
(understreget her)
1.2.4.1. Delkonklusion.
Det forekommer videnskabeligt veldokumenteret, at radiofrekvent elektromagnetisk stråling,
også den som holder sig inden for de af myndighederne fastlagte grænseværdier, henholdsvis
er og kan være skadelig for planter.
Dertil kommer, at planters forsvinden fra et område kan have afgørende betydning for fugles
og insekters muligheder for at overleve som arter.
74 Offentligt i det videnskabelige tidsskrift ”ELECTROMAGNETIC BIOLOGY AND MEDICINE”, 2017, vol. 36, nr.
2, pp. 213 – 235.
75 3,5 GHz er blandt de frekvenser, der ifølge Energistyrelsens handlingsplan af februar 2019 for 5G er afsat til dette
system, jf.
https://ens.dk/sites/ens.dk/files/Tele/5g-handlingsplan_for_danmark.pdf,
s. 10.
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1.3. Overordnet delkonklusion.
Det ovenfor gennemgåede forskningsmateriale dokumenterer efter min opfattelse en klar og
bastant underbygget årsagssammenhæng imellem udsættelse af mennesker og dyr for
radiofrekvent elektromagnetisk stråling på den ene side og en række skadevirkninger samt
mulige skadevirkninger på begge grupper, herunder livstruende.
Der foreligger tillige en velunderbygget årsagssammenhæng for så vidt angår skader på
planter.
Dette gør sig også gældende under de p.t. fastsatte grænseværdier, jf. også pkt. 2.1. nedenfor.
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2. Jus.
2.1. De i Danmark anvendte
elektromagnetisk stråling.
grænseværdier
for
eksponering
for
radiofrekvent
Sundhedsstyrelsen anvender grænseværdier som anbefalet i 1998
76
(gentaget i 2009
77
) af
organisationen ICNIRP (International Commission on Non-Ionizing Radiation Protection). Tillige
opereres med en SAR-grænseværdi på 2 W/kg for producenter af trådløst udstyr. Disse
grænseværdier vil ligeledes blive anvendt i forhold til 5G
78
. En særlig grænseværdi for
fuldkropsbestråling er på gennemsnitligt 0,08 W/kg.
Grænseværdierne er baseret på termisk opvarmning o.l. kortsigtede og umiddelbare effekter,
medens en række af de i pkt. 1.2 ovennævnte forskningsresultater dokumenterer, at
radiofrekvent elektromagnetisk stråling er skadeligt uden termisk opvarmning
79
, medens andre
sandsynliggør dette. Det hedder i ICNIRPs retningslinjer, p. 496:
”BASIS
FOR LIMITING EXPOSURE
These guidelines for limiting exposure have been developed following a thorough review of all
published scientific literature. The criteria applied in the course of the review were designed to
evaluate the credibility of the various reported findings (Repacholi and Stolwijk 1991;
Repacholi and Cardis 1997); only established effects were used as the basis for the proposed
exposure restrictions. Induction of cancer from long-term EMF exposure was not considered to
be established, and so these guidelines are based on short-term, immediate health effects
such as stimulation of peripheral nerves and muscles, shocks and burns caused by touching
conducting objects, and elevated tissue temperatures resulting from absorption of energy
during exposure to EMF. In the case of potential long-term effects of exposure, such as an
increased risk of cancer, ICNIRP concluded that available data are insufficient to provide a
basis for setting exposure restrictions, although epidemiological research has provided
suggestive, but unconvincing, evidence of an association between possible carcinogenic effects
and exposure at levels of 50/60 Hz magnetic flux densities substantially lower than those
recommended in these guidelines.
...”
(understreget her)
Sundhedsstyrelsen anfører nærmere om 5G på sin hjemmeside bl.a.:
”...Helt overordnet er det Sundhedsstyrelsens vurdering, at der ikke er grund til at være
bekymret for, at der skulle være en sundhedsrisiko forbundet med 5G. Målinger viser, at den
samlede stråling fra mobiltelefoner, wifi og andet apparatur, som i dag udsender ikke-
ioniserende stråling, er svag, og ligger langt under grænseværdierne for, hvad der er
sundhedsskadeligt. Baseret på den tilgængelige viden har vi ingen grund til at tro, at 5G vil
ændre på det.
I lovgivningen om radioudstyr er der fastsat regler om, at radioudstyr skal være konstrueret,
så det sikrer menneskers sundhed. Det betyder, at antenner mv. til 5G skal følge de samme
fælleseuropæiske grænseværdier som alt andet nuværende udstyr til telekommunikation. ...”
Ved sammenholdelsen mellem den i pkt. 1.2. ovenfor omtalte forskning og de af
Sundhedsstyrelsen anvendte grænseværdier er beregningerne i følgende skema lagt til
grund
80
:
76 ”ICNIRP guidelines for limiting exposure to time-varying electric, magnetic and electromagnetic fields (up to 300
Ghz)”, offentliggjort i det videnskabelige tidsskrift ”Health Physics” (1998) nr. 74, pp. 494 – 522.
77 ”ICNIRP statement on the 'guidelines for limiting exposure to time-varying electric, magnetic and electromagnetic
fields (up to 300 Ghz)'”, offentliggjort i det videnskabelige tidsskrift ”Health Physics” (2009) nr. 97, p. 257 – 258.
78 Jf. Energi-, Forsynings- og Klimaministerens svar af 1. april 2019 på spørgsmål 226 i samme folketingsudvalg samt
Sundhedsstyrelsens hjemmeside: https://www.sst.dk/da/straalebeskyttelse/mobiltelefoni,-traadloese-netvaerk-med-
mere/5g
79 Se f.eks. Philips et al (2009), p. 83, med referencer til to studier.
80
Kilden er Rådet for Helbredssikker Telekommunikation.
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En række af de i pkt. 1.2 – 1.4 ovennævnte forskningsresultater dokumenterer, at stråling
under de pågældende grænseværdier kan være helbredsskadelig for mennesker og/eller dyr,
bl.a.:
Balmori og Hallberg 2007, p. 145 – 146.
Blank og Goodman 2011, p. 413.
Jing et al 2012, p. 64.
REFLEX-studiet p. 109 og 223.
Yakymenko et al 2015, p. 186.
Lerchl et al 2015, p. 585.
Falcioni et al. 2018, p. 499.
Russell 2018, p. 485.
Neufeld og Kuster 2018, p. 711.
Dertil kommer, at en række studier er udført med kommercielt tilgængelige produkter inkl.
følgende fra pkt. 1.2 – 1.4 ovenfor:
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D'Silva et al 2017, p. 6.
Panagopoulos 2019, p. 55 (v.sp., nederst).
----
Pr. 1. september 2018 havde 244 forskere fra over 40 lande, som tilsammen havde
offentliggjort over 2.000 forskningsartikler om elektromagnetiske felter, underskrevet en appel
til FN og WHO, hvori de opfordrede til, at der etableres en bedre beskyttelse af menneskers
(og dyrs) helbred i forhold til brugen af elektromagnetiske installationer såsom 5G.
81
Disse 244
forskere har i appellens afsnit med overskriften
”Inadequate non-ionizing EMF international
guidelines”
anført som deres opfattelse, at:
”The various agencies setting safety standards have failed to impose sufficient guidelines to
protect the general public, particularly children who are more vulnerable to the effects of EMF.
...
It is our opinion that, because the ICNIRP guidelines do not cover long-term exposure and
low-intensity effects, they are insufficient to protect public health. ”
De 244 forskeres
”...opfattelse...”
er spejlet i den i pkt. 1.2 ovenfor nævnte videnskabelige
litteratur.
----
Pall 2018 konkluderede i sin gennemgang bl.a. følgende om ICNIRPs grænseværdier:
”Each of these reviews, typically cite from 5 to over 100 primary literature citations, each
showing that non-thermal EMF exposures produce the effect under which they are listed. It
follows from this, that there are not only 11 or more reviews documenting each of these
effects, but there is also a massive primary literature documenting these effects as well. It
follows from this that the ICNIRP, FCC and International Safety Guidelines, which are entirely
based only on thermal effects are inadequate and there have been petitions and other
statements of international groups of scientists expressing great concern about this. It follows
that the ICNIRP, FCC and International safety guidelines are completely unscientific and
cannot be relied upon to protect our safety.”
(understreget her)
----
Europarådet har i resolution 1815 af 2011, pkt. 8.1.2. anbefalet medlemsstaterne følgende:
”8.1.2. reconsider the scientific basis for the present standards on exposure to electromagnetic
fields set by the International Commission on Non-Ionising Radiation Protection, which have
serious limitations, and apply ALARA
82
principles, covering both thermal effects and the
athermic or biological effects of electromagnetic emissions or radiation;”
81 Jf. https://emfscientist.org/index.php/emf-scientist-appeal
82 Står for ”As Low As Reasonably Achievable”.
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2.2. Retsbeskyttelsen af mennesker (menneskerettigheder).
2.2.1. Den Europæiske Menneskerettighedskonvention (EMRK).
Konventionen blev inkorporeret direkte i dansk ret ved lov nr. 285 af 1992 og er således en del
af ”almindelig” national ret, som kan påberåbes direkte for de danske domstole.
Dertil kommer, at den ifølge Højesterets praksis anvendes på den måde, at andre
lovbestemmelser ”fortolkes i lyset af” konventionen og den dertilhørende praksis.
----
Det er et generelt fortolkningsprincip ved anvendelsen af bestemmelserne i konventionen, at
de skal fortolkes således, at rettighederne indeholdt heri er praktisk anvendelige og effektive,
jf. f.eks. Storkammerdom af 27. september 1995 i sagen McCann m.fl. mod Storbritannien,
præmis 146:
”146. The Court’s approach to the interpretation of Article 2 (art. 2) must be guided by the
fact that the object and purpose of the Convention as an instrument for the protection of
individual human beings requires that its provisions be interpreted and applied so as to make
its safeguards practical and effective (see, inter alia, the Soering v. the United Kingdom
judgment of 7 July 1989, Series A no. 161, p. 34, para. 87, and the Loizidou v. Turkey
(Preliminary Objections) judgment of 23 March 1995, Series A no. 310, p. 27, para. 72).”
2.2.1.1. Art. 2 – retten til livet og statens positive forpligtelser.
EMRK art. 2 lyder:
”Artikel
2.
Ethvert menneskes ret til livet skal beskyttes ved lov. Ingen må forsætligt berøves
livet undtagen ved fuldbyrdelse af en dødsdom, afsagt af en domstol i tilfælde, hvor der ved
lov er fastsat dødsstraf for den pågældende forbrydelse.
Stk. 2. Berøvelse af livet betragtes ikke som sket i modstrid med denne artikel, når den er en
følge af magtanvendelse, der ikke gå ud over det absolut nødvendige:
a) for at forsvare nogen mod ulovlig vold;
b) for at iværksætte en lovlig anholdelse eller forhindre flugt
fra lovlig frihedsberøvelse;
c) for lovligt at undertrykke optøjer eller opstand.”
Det er således alene stk. 1, 1. pkt. samt 2. pkt., 1. led, der har betydning for den retlige
problemstilling i nærværende responsum.
Den Europæiske Menneskerettighedsdomstol (EMD) har i sin praksis fortolket bestemmelsen
således, at den rummer en række materielle, positive forpligtelser (dvs.: handlepligter), bl.a.
under visse betingelser at hindre, at mennesker dør som følge af forurening, der har været
tilladt eller ikke hindret af staten.
Forpligtelserne i henhold til art. 2 skal – henset til vigtigheden af den rettighed, den skal
beskytte – fortolkes strengt, jf. f.eks. Storkammerdom af 27. september 1995 i sagen McCann
m.fl. mod Storbritannien, præmis 147:
”147. It must also be borne in mind that, as a provision (art. 2) which not only safeguards the
right to life but sets out the circumstances when the deprivation of life may be justified, Article
2 (art. 2) ranks as one of the most fundamental provisions in the Convention - indeed one
which, in peacetime, admits of no derogation under Article 15 (art. 15). Together with Article 3
(art. 15+3) of the Convention, it also enshrines one of the basic values of the democratic
societies making up the Council of Europe (see the above-mentioned Soering judgment, p. 34,
para. 88). As such, its provisions must be strictly construed.”
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I relation til nærværende responsums emne bør
Storkammerdom af 30. november 2004, fremhæves
83
.
sagen
Öneryildiz
mod
Tyrkiet,
Sagen drejede sig om en dødelig eksplosion på en losseplads, der kostede i alt 39 mennesker
livet, inkl. flere af klagerens nære familiemedlemmer.
Det blev bl.a. statueret, at staten har en positiv forpligtelse til at opstille retlige og
administrative rammer, som er designet til at medføre et effektivt værn imod livsfare.
Præmis 89 – 90 (med yderligere praksishenvisninger):
”(a)
General principles applicable in the present case(i)
Principles relating to the
prevention of infringements of the right to life as a result of dangerous activities: the
substantive aspect of Article 2 of the Convention
89. The positive obligation to take all appropriate steps to safeguard life for the purposes of
Article 2 (see paragraph 71 above) entails above all a primary duty on the State to put in
place a legislative and administrative framework designed to provide effective deterrence
against threats to the right to life (see, for example, mutatis mutandis, Osman, cited above, p.
3159, § 115; Paul and Audrey Edwards, cited above, § 54; İlhan v. Turkey [GC], no.
22277/93, § 91, ECHR 2000-VII; Kılıç v. Turkey, no. 22492/93, § 62, ECHR 2000-III; and
Mahmut Kaya v. Turkey, no. 22535/93, § 85, ECHR 2000-III).
90. This obligation indisputably applies in the particular context of dangerous activities,
where, in addition, special emphasis must be placed on regulations geared to the special
features of the activity in question, particularly with regard to the level of the potential risk to
human lives. They must govern the licensing, setting up, operation, security and supervision of
the activity and must make it compulsory for all those concerned to take practical measures to
ensure the effective protection of citizens whose lives might be endangered by the inherent
risks.
Among these preventive measures, particular emphasis should be placed on the public’s
right to information, as established in the case-law of the Convention institutions. The Grand
Chamber agrees with the Chamber (see paragraph 84 of the Chamber judgment) that this
right, which has already been recognised under Article 8 (see Guerra and Others, cited above,
p. 228, § 60), may also, in principle, be relied on for the protection of the right to life,
particularly as this interpretation is supported by current developments in European standards
(see paragraph 62 above).
In any event, the relevant regulations must also provide for appropriate procedures, taking
into account the technical aspects of the activity in question, for identifying shortcomings in
the processes concerned and any errors committed by those responsible at different levels.”
(understreget her)
Der skal således være effektive hindringer imod trusler over for retten til livet, inkl. farlige
aktiviteter, såsom den i sagen omhandlede drift af losseplads.
Når der er tale om farlige aktiviteter, skal der lægges særligt vægt på regler, som er egnede til
de særlige forhold, som den pågældende aktivitet frembyder, og da især under hensyntagen til
den potentielle fare for menneskeliv.
Det er således ikke et krav i art. 2s forstand, at der kan påvises en sikker skadevirkning, som
kan være eller med sikkerhed er livstruende. Det er tilstrækkeligt, for at den pågældende
adfærd falder ind under beskyttelsen af retten til livet, at der kan påvises en risiko for fare for
menneskeliv.
Staten skal pålægge aktørerne, og herunder således dem, der måtte ønske at opføre den
relevante infrastruktur, at der foretages praktiske foranstaltninger, som effektivt beskytter
imod de fareelementer, som kan koste mennesker livet.
83 Der kan tillige henvises til f.eks. Kolyadenko m.fl. mod Rusland, præmis 157 – 161.
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Henset til det foreliggende forskningsmateriale, jf. pkt. 1.2. ovenfor, er det min vurdering, at
staten klart ikke på nuværende tidspunkt har efterkommet sine forpligtelser til at opstille
relevante grænseværdier, endsige forbyde aktiviteter, som indebærer en klart dokumenteret
risiko for fare for menneskeliv.
----
Art. 2 finder ikke kun anvendelse, hvor der er tale om en pludselig hændelse, som resulterer i
dødsfald. Udsættelse for forurening over en længere periode er også omfattet.
EMD bringer bestemmelsen i anvendelse, uanset om klager er afgået ved døden eller ”blot” er i
alvorlig livsfare.
84
Det er ikke afgørende, om det er en offentlig eller privat forurener.
Hvor det må lægges til grund, at det er denne forurening, der har medført dødsfaldet eller
livsfaren, og hvor staten ikke har handlet over for en kendt fare (f.eks. fordi forureningen ikke
har været i strid med gældende, national ret, herunder grænseværdier), vil det som
udgangspunkt udgøre en krænkelse af retten til livet, jf. i det hele f.eks. dom af 24. juli 2014 i
sagen Brincat m.fl. mod Malta, præmis 79 – 81 og 83 (med yderligere praksishenvisninger):
”79. The Court reiterates that Article 2 does not solely concern deaths resulting from the use
of unjustified force by agents of the State but also, in the first sentence of its first paragraph,
lays down a positive obligation on States to take appropriate steps to safeguard the lives of
those within their jurisdiction (see, for example, L.C.B. v. the United Kingdom, 9 June 1998, §
36, Reports 1998-III, and Paul and Audrey Edwards, cited above, § 54).
80. This obligation is construed as applying in the context of any activity, whether public or
not, in which the right to life may be at stake, and a fortiori in the case of industrial activities
which by their very nature are dangerous, such as the operation of waste-collection sites (see
Öneryıldız v. Turkey [GC], no. 48939/99, §71, ECHR 2004-XII) or nuclear testing (see L.C.B.
cited above, § 36) or cases concerning toxic emissions from a fertiliser factory (see Guerra and
Others v. Italy, 19 February 1998, §§ 60 and 62, Reports 1998-I, although in this case the
Court found that it was not necessary to examine the issue under Article 2, it having been
examined under Article 8).
81. The Court considers that the same obligations may apply in cases, such as the present
one, dealing with exposure to asbestos at a workplace which was run by a public corporation
owned and controlled by the Government.
82. The Court reiterates that it has applied Article 2 both where an individual has died (see, for
example, Öneryıldız, cited above) and where there was a serious risk of an ensuing death,
even if the applicant was alive at the time of the application. Examples include cases where
the physical integrity of an applicant was threatened by the action of a third party (see Osman
v. the United Kingdom, 28 October 1998, §§ 115-122, Reports 1998-VIII) or as a result of a
natural catastrophe which left no doubt as to the existence of a threat to the applicants’
physical integrity (see Budayeva and Others v. Russia, nos. 15339/02, 21166/02, 20058/02,
11673/02 and 15343/02, § 146, ECHR 2008 (extracts)). More particularly, the Court has
repeatedly examined complaints under Article 2 from persons suffering from serious illnesses.
Such cases include G.N. and Others v. Italy (no. 43134/05, 1 December 2009) in which the
applicants suffered from the potentially life-threatening disease hepatitis C; L.C.B. v. the
United Kingdom (cited above), where the applicant suffered from leukaemia diminishing her
chances of survival, Hristozov and Others v. Bulgaria, nos. 47039/11 and 358/12, ECHR 2012
84 Udover Brincat m.fl. mod Malta kan f.eks. henvises til Vilnes m.fl. mod Norge, præmis 219:
”...the applicant was
found to be the victim of conduct which by its very nature had put his life at risk, even though he survived. The
Court found there that Article 2 was applicable and sees no reason for arriving at a different conclusion in the
present case.”
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(extracts), concerning applicants suffering from different types of terminal cancer; Karchen
and Others v. France ((dec.), no. 5722/04, 4 March 2008) and Oyal v. Turkey (no. 4864/05,
23 March 2010), in which the applicants had been infected with the HIV virus, which
endangered their life; Nitecki v. Poland ((dec.), no. 65653/01, 21 March 2002), in which the
applicant suffered from amyotrophic lateral sclerosis; Gheorghe v. Romania ((dec.), no.
19215/04, 22 September 2005), in which the applicant suffered from haemophilia; and De
Santis and Olanda v. Italy ((dec.), 35887/11, 9 July 2013) in which the applicant – who was
severely disabled – suffered a cerebral haemorrhage as a consequence of an infection acquired
in hospital.
83. The medical certification indicated that Mr Attard’s death was likely to be a result of
asbestos exposure; malignant mesothelioma is known to be a rare cancer associated with
asbestos exposure. The Court observes that it has not been contested or denied that Mr Attard
worked at Malta Drydocks for more than a decade (1959-1974), during which time he was
repeatedly exposed to asbestos. Neither has it been shown that Mr Attard could have been
contaminated elsewhere or that he was affected by other factors that could have led to the
disease. In these circumstances, and given that Mr Attard has died as a result of his cancer,
the Court considers that Article 2 is applicable to the complaint brought by the applicants in
application no. 62338/11 relating to the death of the said Mr Attard.”
(understreget her)
2.2.1.1.1. Delkonklusion.
Set på baggrund af de i pkt. 1.2 ovenfor gennemgåede forskningsresultater er der efter min
vurdering ikke nogen rimelig tvivl om, at 5G-systemet udgør en industriel aktivitet, som er
farlig for mennesker.
Så længe de nuværende grænseværdier (som meddelt af Sundhedsstyrelsen, jf. pkt. 2.1
ovenfor) anvendes, må livstruende helbredstilstande forårsaget af radiofrekvent
elektromagnetisk stråling ved iværksættelse af 5G-systemet ganske klart forventes, hvilket vil
være i strid med den danske stats positive forpligtelser efter EMRK art. 2.
Da det må lægges til grund, at risikoen er velkendt af den danske stat, er det endvidere
oplagt, at der i relation til 5G-systemet
85
vil skulle indtræde ansvar efter EMRK art. 2, senest
når de livstruende helbredstilstande viser sig.
2.2.1.2. Art. 8 – retten til respekt for privat- og familieliv.
EMRK art. 8 lyder:
”Artikel
8.
Enhver har ret til respekt for sit privatliv og familieliv, sit hjem og sin
korrespondance.
Stk. 2. Ingen offentlig myndighed må gøre indgreb i udøvelsen af denne ret, medmindre det
sker i overensstemmelse med loven og er nødvendigt i et demokratisk samfund af hensyn til
den nationale sikkerhed, den offentlige tryghed eller landets økonomiske velfærd, for at
forebygge uro eller forbrydelse, for at beskytte sundheden eller sædeligheden eller for at
beskytte andres rettigheder og friheder.”
Alvorlig miljøforurening kan påvirke individers velbefindende og forhindre dem i at udøve deres
privat- og familieliv. En sådan tilstand vil udgøre et indgreb i borgernes rettigheder efter EMRK
art. 8, jf. f.eks. Guerra m.fl. v. Italien, Storkammerdom af 19. februar 1998
86
.
85 Det falder udenfor området for nærværende responsum at fremkomme med tilsvarende vurderinger ang. 2G, 3G og
4G, m.v.
86 Fordi Storkammeret fandt en krænkelse af art. 8, var det ikke nødvendigt at vurdere en klage over krænkelse af
retten til livet, jf. EMRK art. 2, p.g.a. de samme kræftdødsfald.
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Præmis 60:
”60. The Court reiterates that severe environmental pollution may affect individuals’ well-being
and prevent them from enjoying their homes in such a way as to affect their private and
family life adversely (see, mutatis mutandis, the Lόpez Ostra judgment cited above, p. 54, §
51). In the instant case the applicants waited, right up until the production of fertilisers ceased
in 1994, for essential information that would have enabled them to assess the risks they and
their families might run if they continued to live at Manfredonia, a town particularly exposed to
danger in the event of an accident at the factory.
The Court holds, therefore, that the respondent State did not fulfil its obligation to secure the
applicants’ right to respect for their private and family life, in breach of Article 8 of the
Convention.
There has consequently been a violation of that provision.”
De positive forpligtelser i så henseende overlapper i vidt omfang de ovenfor nævnte efter art.
2, jf. f.eks. dom af 20. marts 2008 i sagen Budayeva m.fl. mod Rusland, præmis 133 og dom
af 28. februar 2012 i sagen Kolyadenko m.fl. mod Rusland, præmis 216.
Retten til beskyttelse af privat- og familielivet kan bringes i anvendelse, hvor en
sygdomstilstand ikke har udviklet sig livsfarligt og heller ikke nødvendigvis gør det. I denne
sammenhæng anvendes bestemmelsen af EMD som en slags ”mindre i det mere” i forhold til
art. 2, jf. ovenfor.
Dette blev f.eks. fremgangsmåden for alle klager undtagen én i dom af 24. juli 2014 i sagen
Brincat m.fl. mod Malta, præmis 85:
”85. However, in the context of dangerous activities, the scope of the positive obligations
under Article 2 of the Convention largely overlaps with that of those under Article 8 (see
Öneryıldız, cited above, §§ 90 and 160). The latter provision has allowed complaints of this
nature to be examined where the circumstances were not such as to engage Article 2, but
clearly affected a person’s family and private life under Article 8 (see Lόpez Ostra v. Spain, 9
December 1994, Series A no. 303-C and Guerra and Others, cited above). The Court therefore
considers it appropriate to examine the complaints in respect of the remaining applicants
under Article 8, which is applicable in the present case (see also Roche v. the United Kingdom
[GC], no. 32555/96, §§ 155-156, ECHR 2005-X).”
Der skal foreligge en sygdomstilstand, som har en sådan karakter, at den vil udgøre et indgreb
i vedkommendes privat- eller familieliv. Sygdomme som nødvendiggør f.eks. langvarige eller
hyppige hospitalsindlæggelser, varige og indgribende funktionsnedsættelser (herunder lidelser
såsom EHS, der indebærer overfølsomhed over for udstyr, der afgiver elektromagnetisk
stråling, evt. også i meget små doser), markant nedsat fertilitet eller spontane aborter, m.v.,
kunne være egnede eksempler.
Hvor en begivenhed eller tilstand indtræffer, som gør indgreb i retten til privat- eller
familielivet, vil EMD kunne forventes at påse, om f.eks. de tekniske forudsætninger var til
stede for, at begivenheden eller tilstanden ikke indtraf, og om dette burde have været forudset
af staten.
Finder EMD, at dette er tilfældet, vil det som udgangspunkt udgøre en krænkelse af statens
positive forpligtelser efter art. 8. Der kan fra praksis henvises til dom af 28. februar 2012 i
sagen Kolyadenko m.fl. mod Rusland, præmis 215 – 216 (sagen drejede sig om brud på et
vandreservoir, som medførte livsfare og skader på menneskers hjem):
”215. The Court further notes that the Government seem to have argued, with reference to
the findings of the domestic courts in the applicants’ civil cases, that the alleged infringements
of their rights under Article 8 and Article 1 of Protocol No. 1 were the result of a natural
disaster, in the form of exceptionally heavy rain, which could not have been foreseen, and
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could therefore not be imputed to the State. The Court cannot accept this argument. It
reiterates in this connection that, being sensitive to the subsidiary nature of its role and
cautious about taking on the role of a first-instance tribunal of fact, the Court nevertheless is
not bound by the findings of domestic courts and may depart from them where this is
rendered unavoidable by the circumstances of a particular case (see, for example, Matyar v.
Turkey, no. 23423/94, § 108, 21 February 2002). In the present case, the Court has
established in paragraphs 162-165 above that the flooding of 7 August 2001 occurred after the
urgent large-scale evacuation of water from the Pionerskoye reservoir, the likelihood and
potential consequences of which the authorities should have foreseen. The Court has
furthermore established that the main reason for the flood, as confirmed by the expert
reports, was the poor state of repair of the Pionerskaya river channel because of the
authorities’ manifest failure to take measures to keep it clear and in particular to make sure its
throughput capacity was adequate in the event of the release of water from the Pionerskoye
reservoir. The Court has concluded that this failure as well as the authorities’ failure to apply
town planning restrictions corresponding to the technical requirements of the exploitation of
the reservoir put the lives of those living near it at risk (see paragraphs 168-180 and 185
above).
216. The Court has no doubt that the causal link established between the negligence
attributable to the State and the endangering of the lives of those living in the vicinity of the
Pionerskoye reservoir also applies to the damage caused to the applicants’ homes and
property by the flood. Similarly, the resulting infringement amounts not to “interference” but
to the breach of a positive obligation, since the State officials and authorities failed to do
everything in their power to protect the applicants’ rights secured by Article 8 of the
Convention and Article 1 of Protocol No. 1 (see Öneryıldız, cited above, § 135). Indeed, the
positive obligation under Article 8 and Article 1 of Protocol No. 1 required the national
authorities to take the same practical measures as those expected of them in the context of
their positive obligation under Article 2 of the Convention (see, mutatis mutandis, Öneryıldız,
cited above, § 136). Since it is clear that no such measures were taken, the Court concludes
that the Russian authorities failed in their positive obligation to protect the applicants’ homes
and property.
217. There has, accordingly, been a violation of Article 8 of the Convention and Article 1 of
Protocol No. 1 to the Convention in the present case.”
EMD foretog ikke en udtrykkelig proportionalitetsafvejning i den pågældende sag, hvilket synes
at være konsekvensen af, at staten intet havde foretaget sig, uanset den burde have forudset
den skadegørende hændelse og kunne have handlet til afværgelse heraf.
2.2.1.2.1. Delkonklusion.
Der gælder i det væsentlige de samme positive forpligtelser efter art. 8 som art. 2 m.h.t.
beskyttelse af mennesker over for forurening, jf. pkt. 2.2.1.1.1. Allerede derfor må
iværksættelsen af 5G-netværket, ved brug af de nugældende grænseværdier, klart forventes at
medføre sådanne forstyrrelser af borgeres privat- og familieliv p.g.a. sygdomme, at der tillige
vil ske en krænkelse af disse menneskers rettigheder i henhold til art. 8.
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2.2.2. FN's børnekonvention.
Konventionen af 20. december 1989 om barnets rettigheder blev ratificeret ved kgl. resolution
af 5. juli 1991. Den er ikke inkorporeret i dansk ret, og gældende ret skal så vidt muligt
fortolkes i overensstemmelse med de forpligtelser, Danmark har valgt at påtage sig ved
ratifikationen (Dette gælder, så længe det ikke er nødvendigt direkte at tilsidesætte en
lovbestemmelse i national ret.)
Art. 24, stk. 1 og 2, litra (c), i konventionen lyder:
”1. Deltagerstaterne anerkender barnets ret til at nyde den højest opnåelige sundhedstilstand,
adgang til at få sygdomsbehandling og genoprettelse af helbredet. Deltagende stater skal
stræbe mod at sikre, at intet barn fratages sin ret til adgang til at opnå sådan behandling og
pleje.
2.
Deltagerstaterne skal arbejde for fuld gennemførelse af denne ret og især tage passende
forholdsregler for:
...
(c) at bekæmpe sygdom og underernæring, herunder inden for rammerne af den
primære sundhedspleje, blandt andet ved anvendelse af let tilgængelig teknologi og
gennem ydelse af tilstrækkelig og nærende mad og rent drikkevand under hensyntagen
til de farer og risici, der er knyttet til forurening af miljøet;
...”
Statens egentlige forpligtelse går ud på, at den skal ”stræbe mod at sikre” sådan behandling
og pleje, og at ”arbejde for fuld gennemførelse” af barnets ret til den højest opnåelige
sundhedstilstand.
Den højest opnåelige sundhedstilstand kan ikke indebære, at staten tillader børn (som tilhører
en særligt sårbar gruppe også i denne henseende) at blive udsat for stråling af
helbredsskadelig karakter eller styrke.
Der foreligger videnskabelig dokumentation for, at en etablering af 5G-systemet, der vil
indebære udsættelse for dels kraftigere og dels mere farlig
87
radiofrekvent elektromagnetisk
stråling end de allerede etablerede 2G-, 3G- og 4G-systemer (som ifølge den foreliggende
dokumentation i sig selv er skadegørende eller indebærer en risiko herfor), i sin nuværende
form, jf. pkt. 1.1. ovenfor, klart forventeligt vil være direkte helbredsskadelig og indebære
risiko for skader, og som sådan i strid med Danmarks forpligtelser efter art. 24 i FN's
børnekonvention.
FN's børnekomité, som også træffer afgørelse i konkrete klagesager, har udstedt en ”general
comment” nr. 15 i 2013, som er retningslinjer for, hvorledes komitéen fortolker konventionens
art. 24.
Det fremgår pkt. III.A, om artiklens normative indhold, at:
”The notion of “the highest attainable standard of health” takes into account both the child’s
biological, social, cultural and economic preconditions and the State’s available resources,
supplemented by resources made available by other sources, including nongovernmental
organizations, the international community and the private sector.
Children’s right to health contains a set of freedoms and entitlements. ... The entitlements
include access to a range of facilities, goods, services and conditions that provide equality of
opportunity for every child to enjoy the highest attainable standard of health.”
(understreget
87 Dele af den stråling, der ifølge det foreliggende vil blive udsendt fra 5G-systemet, vil have en mindre styrke, men vil
pga. de øvrige karakteristika ikke desto mindre være farligere end den nuværende fra 2G-, 3G- og 4G-systemerne.
Se Kuster et al (2018) i pkt. 1.2.2.1.3. ovenfor.
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her)
Teleselskaberne har i forvejen stillet effektive kommunikationsmidler til rådighed, som ikke
indebærer en implementering 5G-systemet.
Yderligere om stk. 2, litra (c), ang. forurening af miljøet har komitéen anført følgende, jf. ibid.,
s. 6 – 7:
”States should take measures to address the dangers and risks that local environmental
pollution poses to children’s health in all settings. ... States should regulate and monitor the
environmental impact of business activities that may compromise children’s right to health,...”
(understreget her)
Formuleringen
”may
compromise”
indikerer
kraftigt,
at komitéen anvender
et
forsigtighedsprincip, og at konstateringen af en risiko er tilstrækkelig til at staten skal regulere
og monitorere sådanne aktiviteter.
Ud fra en formålsfortolkning må dette indebære, at hensynet til børns helbred (der i sig selv
må antages at veje særdeles tungt, særligt over for økonomiske interesser) skal føre til, at
staten forbyder former for forurening, som kan skade børns helbred. Dette vil i henhold til den
foreliggende videnskabelige dokumentation indebære, at børnekonventionen er til hinder for
iværksættelse af 5G-systemet, hvis systemet blot skal overholde de af ICNIRP anbefalede
grænseværdier.
----
Der foreligger kun én afgørelse fra FN's børnekomité, der vedrører art. 24 (kommunikésagsnr.
35/2017). Sagen, der ikke er indholdsmæssigt beskrevet på komitéens hjemmeside, ses ikke
ud fra de sparsomme beskrivelser (flygtningebarn) at have relevans for nærværende
responsums emne.
Der er ikke taget stilling til spørgsmålet i national, dansk ret.
Der er således ikke en autoritativ retskilde, som kan bekræfte ovenstående fortolkning.
2.2.2.1. Delkonklusion.
Ud fra en fortolkning af FN's børnekonventions ordlyd og formål, sammenholdt med den
foreliggende videnskabelige dokumentation for såvel skadevirkninger som skaderisici, er det
min vurdering, at en aktivering af 5G-systemet, som det foreligger beskrevet, jf. pkt. 1.1.
ovenfor, vil være i strid med den danske stats forpligtelser efter konventionens art. 24.
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2.3. Miljøretlige regler.
2.3.1. Forsigtighedsprincippet i EU-retten.
Det EU-retlige forsigtighedsprincip er i dag at finde i Traktaten om den Europæiske Unions
Funktionsmåde (TFEU) art. 191, stk. 2:
”Unionens politik på miljøområdet tager sigte på et højt beskyttelsesniveau under hensyntagen
til de forskelligartede forhold, der gør sig gældende i de forskellige områder i Unionen. Den
bygger på forsigtighedsprincippet og princippet om forebyggende indsats, ...”
I
henhold
til
Europa-Kommissionens
meddelelse
af
20.
februar
2000
om
forsigtighedsprincippet, s. 9 – 10, kan det anvendes,
”...hvor de videnskabelige data er
utilstrækkelige, foreløbige eller usikre, og den indledende objektive videnskabelige
undersøgelse tyder på, at der er rimelig grund til bekymring for, at mulige farlige følger for
miljø samt menneskers, dyrs og planters sundhed ikke stemmer overens med det valgte
beskyttelsesniveau.”
For så vidt angår nærværende responsums emneområde, vil princippet klart være relevant at
bringe i anvendelse, hvis det måtte lægges til grund, at der ikke foreligger tilstrækkelig
videnskabelig sikkerhed for at konkludere, at radiofrekvent elektromagnetisk stråling inden for
de p.t. anvendte grænseværdier, jf. pkt. 2.1. ovenfor, vil være helbredsskadeligt for (in casu)
fugle, dyr og planter omfattet af de i det følgende behandlede miljøretlige direktiver.
2.3.2. Fuglebeskyttelsesdirektivet.
EU-direktivet ”om beskyttelse af vilde fugle”, kodificeret udgave af 30. november 2009,
indeholder en række forpligtelser for EU-lande til at ”træffe alle nødvendige foranstaltninger” til
”beskyttelse” (herunder bevarelse) af fugle, deres æg, reder og levesteder, jf. art. 1.
De for nærværende responsums problemstilling relevante bestemmelser i direktivet er på det
foreliggende grundlag følgende (understregninger indsat her), hvortil der er indsat løbende
kommentarer:
Art. 1:
”1. Dette direktiv vedrører beskyttelse af alle de fuglearter, som i vild tilstand har deres
naturlige ophold på medlemsstaternes område i Europa, hvor traktaten finder anvendelse. Det
omhandler bevarelse, forvaltning og regulering af de pågældende arter og fastsætter regler for
udnyttelse af de nævnte arter.
2. Dette direktiv gælder for fugle samt for deres æg, reder og levesteder.”
Dette vil sige, at direktivbeskyttelsen omfatter enhver vild fugleart og deres levesteder.
Art. 2:
”Medlemsstaterne træffer alle nødvendige foranstaltninger til at opretholde eller tilpasse
bestanden af samtlige de i artikel 1 omhandlede arter på et niveau, som især imødekommer
økologiske, videnskabelige og kulturelle krav og samtidig tilgodeser økonomiske og rekreative
hensyn.”
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Art. 3, stk. 1:
”Medlemsstaterne træffer ud fra de i artikel 2 omhandlede hensyn alle nødvendige
foranstaltninger for at beskytte, opretholde eller genskabe tilstrækkeligt forskelligartede og
vidtstrakte levesteder for alle de i artikel 1 omhandlede fuglearter.”
De i pkt. 1.2.3.1. ovenfor i øvrigt citerede undersøgelser kan i princippet være relevante på
samtlige fugle omfattet af direktivet.
Henvisningen til art. 2 giver medlemsstaterne en vis skønsmæssig beføjelse til, hvorledes
hensynene i art. 3 skal varetages, uanset det er klart udtrykt i art. 2, at de økonomiske hensyn
ikke må være de mest tungtvejende.
Det mest sandsynlige baseret på den i pkt. 1.2.3.1. ovenfor gennemgåede forskning er, at en
indførelse af 5G-systemet i områder, hvor fuglene har deres levesteder, vil udgøre en
overtrædelse af denne bestemmelse.
Art. 4, stk. 1 og 4:
”1. For arter, som er anført i bilag I, træffes der særlige beskyttelsesforanstaltninger med
hensyn til deres levesteder for at sikre, at de kan overleve og formere sig i deres
udbredelsesområde.
I denne forbindelse tages der hensyn til:
a)
b)
…
4. Medlemsstaterne træffer egnede foranstaltninger med henblik på i de i stk. 1 og 2 nævnte
beskyttede områder at undgå forurening eller forringelse af levestederne samt forstyrrelse af
fuglene, i det omfang en sådan forurening, forringelse eller forstyrrelse har væsentlig
betydning for formålet med denne artikel. Medlemsstaterne bestræber sig på at undgå
forurening eller forringelse af levesteder også uden for disse beskyttede områder.”
Der er tale om en vidtfavnende beskyttelse, som bl.a. omfatter den hvide stork, der var
genstand for den videnskabelige undersøgelse, der er refereret til ovenfor pkt. 1.2.3.1.
(Balmori 2005). Undersøgelsen påviste bl.a., at der var forskelle i mængden af afkom, og at
der var en sammenhæng med nærheden til telemaster, og at nogle reder således var helt uden
afkom. Undersøgelsens resultater var endvidere underbygget af eksperimentelle studier på
fugleæg.
De i pkt. 1.2.3.1. ovenfor i øvrigt citerede undersøgelser kan i princippet være relevante på
samtlige fugle omfattet af bilag I.
Da undersøgelserne samtidig udgør en bastant, videnskabelig dokumentation for, at
radiofrekvent elektromagnetisk stråling både kan reducere afkommet, mutere det og påføre
skader på levende fugle (og muligvis herunder hindre deres navigationsevne), er det min
vurdering, at der ved indførelsen af den påtænkte 5G-system sker en overtrædelse af
Danmarks forpligtelser i henhold til fuglebeskyttelsesdirektivets art. 4, stk. 1, idet det ikke
”sikres”, at de beskyttede fugle kan overleve og formere sig.
Danmark vil ligeledes heller ikke have truffet egnede foranstaltninger til at undgå forurening
eller forringelse af fuglenes levesteder eller forstyrrelse af fuglene, uanset dette vil have
væsentlig betydning for formålet med art. 4.
arter, der trues af udslettelse
arter, der er følsomme over for bestemte ændringer af deres levesteder
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Der vil heller ikke være sket nogen bestræbelse på at undgå forurening eller forringelse af
levesteder for disse fugle også uden for de beskyttede områder, jf. stk. 4, in fine.
Væsentlig nedbringelse af bestanden af dyr, som insektædende fugle skal kunne leve af, jf. pkt.
1.2.3.2. ovenfor, må ligeledes forventes at have den betydning, at fuglenes levesteder
forstyrres i en sådan grad, at det vil have væsentlig betydning for deres
overlevelsesmuligheder.
Art. 5, stk. 1, litra a), b) og d):
”Med forbehold af artikel 7 og 9 træffer medlemsstaterne de nødvendige foranstaltninger til at
indføre en generel ordning til beskyttelse af alle de i artikel 1 omhandlede fuglearter, herunder
især forbud mod:
a)
b)
...
d)
forsætligt at forstyrre fuglene navnlig i yngletiden, i det omfang, en sådan forstyrrelse
har væsentlig betydning for formålet med dette direktiv
forsætligt at dræbe eller indfange dem, uanset hvilken metode der anvendes
forsætligt at ødelægge eller beskadige deres reder og æg samt fjerne deres reder
...”
Artikel 7, der drejer sig om jagt, og artikel 9, der indeholder en række
undtagelsesbestemmelser uden betydning for etablering af 5G-netværk, er ikke relevante i
nærværende sammenhæng.
Artiklen forpligter medlemsstaterne til at etablere generelle beskyttelsesordninger til
beskyttelse af de i artikel 1 omhandlede fugle, og det er særligt fremhævet, at der skal være
forbud imod bl.a. forsætligt drab på fugle, uanset hvilken metode, der anvendes, og forsætligt
at ødelægge eller beskadige reder og æg.
Uanset det ikke er formålet med opstillingen af f.eks. 5G-telemaster at dræbe fugle eller at
ødelægge deres reder og æg, er dette en klar og forudsigelig effekt, hvis de opstilles i tilpas
nærhed af fuglenes levesteder.
Art. 8, stk. 1:
”For så vidt angår jagt på, fangst af eller drab på fugle i overensstemmelse med dette direktiv
forbyder medlemsstaterne anvendelse af alle midler, indretninger eller metoder til
massefangst eller -drab eller ikke-selektiv fangst eller drab, som kan medføre, at en art
forsvinder lokalt; de forbyder herunder navnlig anvendelse af de i bilag IV, litra a), nævnte
midler, indretninger og metoder.”
Art. 8 omhandler alene drab, der i forvejen foretages i overensstemmelse med direktivet.
Det bemærkelsesværdige ved formuleringen er, at forbuddet omfatter ikke-selektiv drab, som
kan medføre, at en art forsvinder lokalt. Dvs. at bestemmelsen er risikobaseret, således at den
blotte fare for, at indretningen eller metoden kan medføre, at en art forsvinder lokalt, er
tilstrækkelig til, at den pågældende indretning eller metode skal forbydes. Der fremgår ikke en
sådan direkte udtrykt risikobaseret beskyttelse af de i øvrigt ovenfor citerede artikler. I stedet
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anvendes udtryk såsom ”beskyttelse”, ”alle nødvendige foranstaltninger”, ”sikre, at de kan
overleve”, o.l. Disse anderledes formuleringer lægger i større eller mindre grad op til, at der i
disse andre bestemmelser ligeledes skal indfortolkes såvel en risikobaseret beskyttelse som
anvendelse af forsigtighedsprincippet. Formuleringen af art. 8, der oven i købet vedrører arter
omfattet af den lavere rangerende beskyttelse i direktivets ”bilag II”, underbygger en sådan
fortolkning af de øvrige bestemmelser, hvilket endvidere vil være i god overensstemmelse med
direktivets beskyttelsesformål.
2.3.2.1. Delkonklusion.
Det er på baggrund af den i pkt. 1.2 ovenfor refererede forskning min vurdering, at hvis 5G-
systemet aktiveres, så vil det medføre eller kunne medføre væsentlig skade på de beskyttede
vildfugle, der har deres levesteder tilstrækkeligt tæt på f.eks. en relevant telemast.
Denne virkning vil blive forstærket af, at disse installationer påviseligt også har betydelig
skadevirkning på de dyr, som insektædende fugle skal leve af, jf. pkt. 1.2.3.2. ovenfor.
Det må følgelig også være min vurdering, at aktiveringen heraf vil udgøre en overtrædelse af
Danmarks forpligtelser efter fuglebeskyttelsesdirektivets art. 4 og 5, samt formentlig art. 3.
Hvis det lagdes til grund, at der fortsat består en videnskabelig usikkerhed, bør anvendelsen af
forsigtighedsprincippet føre til samme delkonklusioner.
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2.3.3. Habitat-direktivet
EU-direktivet ”om bevaring af naturtyper samt vilde dyr og planter” af 21. maj 1992
indeholder en række forpligtelser for EU-lande til at ”sikre” opretholdelse af gunstig
bevaringsstatus for de af direktivet omfattede naturtyper og levesteder for beskyttede arter, og
at ”sikre sig” ikke at skade de beskyttede lokaliteters integritet eller at ”forstyrre” arterne på
en måde, som har betydelige konsekvenser for direktivets formål.
Det er således ikke alle dyr og planter, der er omfattet af beskyttelsen. Imidlertid kan den i
pkt. 1.3. ovenfor omtalte forskning ikke tages til indtægt for, at den alene finder anvendelse på
de specifikke undersøgte arter. Dette gør sig særligt gældende, al den stund mange af dem
vedrører forstyrrelse af almene mekanismer, ligesom det i flere tilfælde er udtrykkeligt anført,
at de undersøgte arter (f.eks. bananfluer) vil udgøre ”gode indikatorer”.
De for nærværende responsums problemstilling relevante bestemmelser i direktivet er på det
foreliggende grundlag følgende (understregninger indsat her), hvortil der er indsat løbende
kommentarer:
Art. 2:
”1. Formålet med dette direktiv er at bidrage til at sikre den biologiske diversitet ved at bevare
naturtyperne samt de vilde dyr og planter inden for det af medlemsstaternes område i Europa,
hvor Traktaten finder anvendelse.
2. De foranstaltninger, der træffes efter dette direktiv, tager sigte på at opretholde eller
genoprette en gunstig bevaringsstatus for naturtyper samt vilde dyre- og plantearter af
fællesskabsbetydning.
3. De foranstaltninger, der træffes efter dette direktiv, tager hensyn til de økonomiske, sociale
og kulturelle behov og til regionale og lokale særpræg.”
Art. 3, stk. 1:
”Der oprettes et sammenhængende europæisk økologisk net af særlige bevaringsområder
under betegnelsen Natura 2000. Dette net, der består af lokaliteter, der omfatter de
naturtyper, der er nævnt i bilag I, og levesteder for de arter, der er nævnt i bilag II, skal sikre
opretholdelse eller i givet fald genopretning af en gunstig bevaringsstatus for de pågældende
naturtyper og levestederne for de pågældende arter i deres naturlige udbredelsesområde.
Natura 2000-nettet omfatter ligeledes de særligt beskyttede områder, som medlemsstaterne
har udlagt i medfør af direktiv 79/409/EØF.”
I henhold til denne bestemmelse skal staterne ”sikre” opretholdelse/genopretning af en gunstig
bevaringsstatus for levestederne for de af bilag II omfattede arter. Dette gælder bl.a. den
hvide stork og de flagermus, som det fremgår af afsnit 1.2.3.1. og 1.2.3.2. ovenfor.
Når der henses til den videnskabelige dokumentation for skadevirkningerne, forekommer dette
ikke at være muligt.
Dertil kommer, at en evt. (tilstrækkeligt videnskabeligt funderet) usikkerhed vil skulle afklares.
Art. 6, stk. 2 til 4:
”2. Medlemsstaterne træffer passende foranstaltninger for at undgå forringelse af naturtyperne
og levestederne for arterne i de særlige bevaringsområder samt forstyrrelser af de arter, for
hvilke områderne er udpeget, for så vidt disse forstyrrelser har betydelige konsekvenser for
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dette direktivs målsætninger.
3. Alle planer eller projekter, der ikke er direkte forbundet med eller nødvendige for
lokalitetens forvaltning, men som i sig selv eller i forbindelse med andre planer og projekter
kan påvirke en sådan lokalitet væsentligt, vurderes med hensyn til deres virkninger på
lokaliteten under hensyn til bevaringsmålsætningerne for denne. På baggrund af
konklusionerne af vurderingen af virkningerne på lokaliteten, og med forbehold af stk. 4, giver
de kompetente nationale myndigheder først deres tilslutning til en plan eller et projekt, når de
har sikret sig, at den/det ikke skader lokalitetens integritet, og når de - hvis det anses for
nødvendigt - har hørt offentligheden.
4. Hvis en plan eller et projekt, på trods af at virkningerne på lokaliteten vurderes negativt,
alligevel skal gennemføres af bydende nødvendige hensyn til væsentlige samfundsinteresser,
herunder af social eller økonomisk art, fordi der ikke findes nogen alternativ løsning, træffer
medlemsstaten alle nødvendige kompensationsforanstaltninger for at sikre, at den globale
sammenhæng i Natura 2000 beskyttes. Medlemsstaten underretter Kommissionen om, hvilke
kompensationsforanstaltninger der træffes.
Hvis der er tale om en lokalitet med en prioriteret naturtype og/eller en prioriteret art, kan der
alene henvises til hensynet til menneskers sundhed og den offentlige sikkerhed eller
væsentlige gavnlige virkninger på miljøet, eller, efter udtalelse fra Kommissionen, andre
bydende nødvendige hensyn til væsentlige samfundsinteresser.”
Særligt ad stk. 3:
Forpligtelsen går ud på, at myndighederne skal sikre sig, at et projekt m.v. (f.eks. indførelse af
5G-systemet ved opførelse af nye telemaster eller opsættelse af 5G-sendere på eksisterende
telemaster) ikke skader lokalitetens integritet.
Når der henses til den videnskabelige dokumentation for skadevirkningerne, forekommer dette
ikke at være muligt.
Dertil kommer, at en evt. (tilstrækkeligt videnskabeligt funderet) usikkerhed vil skulle afklares.
Særligt ad stk. 4:
I og med at Sundhedsstyrelsen ikke anerkender henholdsvis skadevirkninger og -risici som
gennemgået ovenfor, er der heller ikke grundlag for at antage, at staten har truffet ”alle
nødvendige kompensationsforanstaltninger”, jf. stk. 4, hvis det må lægges til grund, at
forskningen i pkt. 1.2 ovenfor er retvisende.
For så vidt angår lokaliteter med en prioriteret naturtype og/eller prioriteret art, finder ingen af
de særlige undtagelser anvendelse. Etablering af et 5G-netværk har således ikke nogen
væsentlig gavnlig virkning for menneskers sundhed, den offentlige sikkerhed eller miljøet,
herunder når der sammenlignes med andre teknologiske muligheder. For så vidt angår
hensynet til menneskers sundhed, er det tværtimod klart, at det vil have en skadelig virkning.
Der foreligger heller ikke nogen udtalelse fra Kommissionen desangående.
Art. 7:
”Forpligtelserne i artikel 6, stk. 2, 3 og 4, i nærværende direktiv træder i stedet for
forpligtelserne i artikel 4, stk. 4, første punktum, i direktiv 79/409/EØF, for så vidt angår de
områder, der er udlagt som særligt beskyttede efter artikel 4, stk. 1, eller tilsvarende
anerkendt efter artikel 4, stk. 2, deri, fra datoen for nærværende direktivs iværksættelse eller
fra den dato, hvor en medlemsstat har udlagt eller anerkendt områderne efter direktiv
79/409/EØF, hvis denne dato er senere.”
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Direktiv 79/409/EØF er det ovenfor omtalte fuglebeskyttelsesdirektiv (nu: kodificeret ved
direktiv
2009/147/EF).
Det
nye
fuglebeskyttelsesdirektiv
er
også
omfattet
af
henvisningsbestemmelsen i habitatdirektivets art. 7, jf. fuglebeskyttelsesdirektivets art. 18,
stk. 2.
Art. 12, stk. 1, 3 og 4:
”1. Medlemsstaterne træffer de nødvendige foranstaltninger til at indføre en streng
beskyttelsesordning i det naturlige udbredelsesområde for de dyrearter, der er nævnt i bilag
IV, litra a), med forbud mod:
a) alle former for forsætlig indfangning eller drab af enheder af disse arter i naturen
b) forsætlig forstyrrelse af disse arter, i særdeleshed i perioder, hvor dyrene yngler, udviser
yngelpleje, overvintrer eller vandrer
c) forsætlig ødelæggelse eller indsamling af æg i naturen
d) beskadigelse eller ødelæggelse af yngle- eller rasteområder.
...
3. Forbuddene i stk. 1, litra a) og b), samt stk. 2 gælder for alle livsstadier hos de dyr, der er
omfattet af denne artikel.
4. Medlemsstaterne indfører en ordning med tilsyn med uforsætlig indfangning eller drab af de
dyrearter, der er nævnt i bilag IV, litra a). På grundlag af de indhentede oplysninger
gennemfører
medlemsstaterne
de
yderligere
undersøgelser
eller
træffer
de
bevaringsforanstaltninger, der er nødvendige for at sikre, at uforsætlig indfangning eller drab
ikke får en væsentlig negativ virkning for de pågældende dyrearter.”
Uanset det ikke er formålet med opstillingen af f.eks. 5G-telemaster at dræbe dyr eller at
ødelægge deres reder og æg, er dette en klar og forudsigelig effekt af, hvis de opstilles i tilpas
nærhed af de beskyttede dyrs levesteder.
Beskyttelsen i habitatdirektivet gælder udtrykkeligt for alle livsstadier hos de omfattede dyr,
hvor det i fuglebeskyttelsesdirektivet er anført, at beskyttelsen gælder fugle, deres reder og
æg. Der er næppe tilsigtet nogen forskellig anvendelse af bestemmelserne, henset til, at et
”hul” i beskyttelsen af de pågældende arter ville kunne gøre reglerne ineffektive.
Art. 13, stk. 1, litra a) og stk. 2:
”1. Medlemsstaterne træffer de nødvendige foranstaltninger for at indføre en streng
beskyttelsesordning for de plantearter, der er nævnt i bilag IV, litra b), med forbud mod:
a) forsætlig plukning, indsamling, afskæring, oprivning med rod eller ødelæggelse af disse
vildtvoksende planter i naturen
¨...
2. Forbuddene i stk. 1, litra a) og b), gælder for alle livsstadier for de planter, der er omfattet
af denne artikel.”
Art. 15:
”Ved indfangning eller drab af de vilde dyrearter, som er nævnt i bilag V, litra a), og ved
anvendelse efter artikel 16 af fravigelser i forbindelse med indsamling, indfangning eller drab
af de arter, der er nævnt i bilag IV, litra a), forbyder medlemsstaterne anvendelse af alle ikke-
selektive midler, der lokalt kan medføre, at bestande af en art forsvinder eller udsættes for
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alvorlige forstyrrelser, navnlig
a) anvendelse af de indfangnings- og drabsmetoder, der er nævnt i bilag VI b)
...”
I bilag VI (rettelig er der tale om bilag VI a), ikke b)) er bl.a. nævnt
”...elektriske og
elektroniske apparater, som kan dræbe eller lamme...”
Det er ikke afklaret, om der i denne
definition kan inkluderes apparater såsom telemaster, antenner, m.v., som over en længere
eller meget lang periode kan gøre dødelig skade på de af direktivet omfattede dyr. Det kan
ikke udelukkes, uanset der med selve formuleringen formentlig er ment apparater, som mere
umiddelbart kan dræbe eller lamme. Med anvendelsen af udtrykket ”navnlig” i selve art. 15
anføres imidlertid, at de i bilag VI a) nævnte midler ikke er udtømmende, og at forbuddet
omfatter ethvert middel, som lokalt vil kunne medføre, at en artsbestand forsvinder eller
forstyrres alvorligt.
Det forekommer således oplagt, at påtænkte 5G-installationer er i strid med selve art. 15,
uanset de evt. også kan henføres til de specifikke apparater i bilag VI a).
Art. 16, stk. 1, litra c):
”1. Hvis der ikke findes nogen anden brugbar løsning, og fravigelsen ikke hindrer opretholdelse
af den pågældende bestands bevaringsstatus i dens naturlige udbredelsesområde, kan
medlemsstaterne fravige bestemmelserne i artikel 12, 13, 14 og 15, litra a) og b):
...
c) af hensyn til den offentlige sundhed og sikkerhed eller af andre bydende nødvendige hensyn
til væsentlige samfundsinteresser, herunder af social og økonomisk art, og hensyn til
væsentlige gavnlige virkninger på miljøet
...”
Der findes andre, brugbare løsninger.
Dertil kommer, at det på baggrund af det i pkt. 1.2 behandlede forskningsmateriale må være
min vurdering, at en fravigelse af beskyttelsen med stor sandsynlighed over tid vil kunne
hindre opretholdelse af bestandene.
2.3.3.1. Delkonklusion.
Det er på baggrund af den i pkt. 1.2 ovenfor refererede forskning min vurdering, at hvis 5G-
systemet aktiveres, så vil det medføre eller kunne medføre væsentlig skade på de beskyttede
dyre- og plantearter, der har deres levesteder tilstrækkeligt tæt på f.eks. en telemast.
Denne virkning vil blive forstærket af, at disse installationer påviseligt også har betydelig
skadevirkning på insektædere, jf. pkt. 1.2.3.2. ovenfor.
Det må følgelig også være min vurdering, at aktiveringen heraf vil udgøre en overtrædelse af
Danmarks forpligtelser efter habitatdirektivets art. 6, stk. 2 – 4.
Hvis det lagdes til grund, at der fortsat består en videnskabelig usikkerhed, bør anvendelsen af
forsigtighedsprincippet føre til samme delkonklusioner.
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2.4. Bern-konventionen
Konvention af 19. september 1979 ”om beskyttelse af Europas vilde dyr og planter samt
naturlige levesteder” (herefter:
”Bern-konventionen”)
blev ratificeret af Danmark i henhold til
kongelig resolution af 5. juli 1982. Den er ikke inkorporeret i dansk ret, og gældende ret skal
så vidt muligt fortolkes i overensstemmelse med de forpligtelser, Danmark har valgt at påtage
sig ved ratifikationen (Dette gælder, så længe det ikke er nødvendigt direkte at tilsidesætte en
lovbestemmelse i national ret.)
Konventionen indeholder bl.a. en række bestemmelser, hvormed de kontraherende stater har
forpligtet sig til at
”...sikre...”
beskyttelsen af en række vilde dyr og planter, således at
bestanden opretholdes, samtidig med at der ”tages hensyn til de økonomiske behov”, alt jf.
art. 2.
De for nærværende responsums problemstilling relevante bestemmelser i konventionen er på
det foreliggende grundlag følgende (understregninger indsat her), hvortil der er indsat løbende
kommentarer:
Art. 2:
”De kontraherende parter skal træffe de nødvendige foranstaltninger for at opretholde
bestanden af vilde dyr og planter på, eller at tilpasse den til, et niveau, som svarer til de
særlige økologiske, videnskabelige og kulturelle behov, idet der samtidig tages hensyn til de
økonomiske og rekreative behov og behov hos underarter, geografiske racer eller former, som
trues lokalt.”
Art. 3, stk. 2:
”Hver kontraherende part forpligter sig til i sin planlægnings- og egnsudviklingspolitik og i sine
foranstaltninger mod forurening at tage hensyn til beskyttelsen af vilde dyr og planter.”
Art. 4, stk. 1 til 3:
”1. Hver kontraherende part skal træffe passende og nødvendige lovgivningsmæssige og
administrative foranstaltninger for at sikre beskyttelsen af levesteder for vilde dyre- og
plantearter, navnlig de i liste I og II anførte, og beskyttelsen af truede naturlige levesteder.
2. De kontraherende parter skal i deres planlægnings- og egnsudviklingspolitik tage hensyn til
beskyttelsesbehovene i de områder, som skal beskyttes i henhold til stk. 1, således at man
undgår eller så vidt muligt begrænser en hvilken som helst forringelse af sådanne områder.
3. De kontraherende parter forpligter sig til at tage særligt hensyn til beskyttelsen af områder,
som er af betydning for de migrerende arter, der er anført i liste II og III, og som har en
passende beliggenhed i forhold til migrationsruter som overvintringsområder, rastepladser,
fourageringspladser, yngleområder eller fældningsområder.”
Art. 5, 1. pkt.:
”Hver kontraherende part skal træffe passende og nødvendige lovgivningsmæssige og
administrative foranstaltninger for at sikre en særlig beskyttelse af de vilde plantearter, som
er anført i liste I. ...”
Art. 6:
”Hver kontraherende part skal træffe passende og nødvendige lovgivningsmæssige og
administrative foranstaltninger for at sikre en særlig beskyttelse af de vilde dyrearter, som er
anført i liste II. Navnlig skal der i forbindelse med disse arter være forbud mod følgende:
-a.- alle former for forsætlig indfangning og fangenskabshold samt forsætlig ihjelslagning,
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-b. forsætlig skade på eller ødelæggelse af yngle- og rastepladser,
-c.- forsætlig forstyrrelse af vilde dyr, i særdeleshed i perioder, når de yngler, udviser
ynglepleje og overvintrer, for så vidt som forstyrrelsen måtte være væsentlig i forbindelse
med denne konventions målsætninger,
…”
Art. 7, stk. 1 og 2:
”Hver kontraherende part skal træffe passende og nødvendige lovgivningsmæssige og
administrative foranstaltninger for at sikre beskyttelse af de vilde dyrearter, som er anført i
liste III.
Enhver udnyttelse af de vilde dyrearter, som er anført i liste III, skal under hensyntagen til
bestemmelserne i artikel 2 reguleres med henblik på at forebygge, at bestandene bliver truet.”
Til art. 4 til 7:
Den forudsatte ”sikring” af beskyttelsen af de i liste I og II anførte arter er efter min vurdering
på baggrund af den i pkt. 1.2. ovenfor gennemgåede forskning sammenholdt med de p.t.
værende grænseværdier ikke mulig ved indførelsen af det påtænkte 5G-system.
Dette er særligt tydeligt for så vidt angår forpligtelsen i art. 4, stk. 2, til at undgå eller så vidt
muligt begrænse en hvilken som helst forringelse af sådanne områder.
Art. 8:
”I forbindelse med indfangning eller ihjelslagning af de vilde dyrearter, som er anført i liste III,
og i tilfælde af benyttelsen af undtagelser i medfør af artikel 9 på de arter, som er anført i liste
II, skal de kontraherende parter forbyde anvendelsen af ikke-selektive fangst- og
drabsmetoder og af alle midler, som vil kunne medføre, at bestande af en art forsvinder i et
lokalt område eller forstyrres alvorligt, samt navnlig anvendelsen af de midler, som er
opregnet i liste IV.”
Bestemmelsen er formuleret som risikobaseret, således at forbuddet gælder den blotte
mulighed for, at den ikke-selektive drabsmetode eller middel vil kunne medføre bestandenes
forsvinden. (Det er således særligt oplagt at bringe forsigtighedsprincippet i anvendelse, hvis
det lægges til grund, at der fortsat foreligger videnskabelig uklarhed.)
Endvidere indeholder art. 8 en reference til en
”Liste IV”
med angivelse af forbudte midler og
metoder til ihjelslagning, m.v., af vilde dyr omfattet af konventionens
”Liste III”
(jf. art. 7
ovenfor). Listen omfatter bl.a. et forbud imod at anvende
”Elektriske apparater, som kan
dræbe eller lamme”
i forhold til både pattedyr og fugle. Det er ikke afklaret, om der i denne
definition kan inkluderes apparater såsom telemaster, antenner, m.v., som over en længere
eller meget lang periode kan gøre dødelig skade på de i liste III omfattede dyr. Det kan ikke
udelukkes, uanset der med selve formuleringen formentlig er ment apparater, som mere
umiddelbart kan dræbe eller lamme. Med anvendelsen af udtrykket ”navnlig” i selve art. 8
anføres imidlertid, at de i liste IV nævnte midler og metoder ikke er udtømmende, og at
forbuddet omfatter ethvert middel, som vil kunne medføre at en artsbestand forsvinder eller
forstyrres alvorligt i det lokale område.
Art. 9, stk. 1:
”Hver kontraherende part kan gøre undtagelser fra bestemmelserne i artiklerne 4, 5, 6 og 7,
og fra forbudet mod anvendelse af de midler, der er nævnt i artikel 8, hvis der ikke findes
andre tilfredsstillende løsninger, og hvis undtagelsen ikke er til skade for den berørte bestands
overlevelse:
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- for at beskytte dyr og planter,
- for at forhindre alvorlig skade på afgrøder, besætning, skove, fiskeri, vand og andre former
for ejendom,
- af hensyn til den offentlige sundhed og sikkerhed, sikkerheden for luftfarten eller andre
offentlige interesser, der måtte gå forud,
...”
Der findes andre tilfredsstillende løsninger.
Dertil kommer, at det på baggrund af det i pkt. 1.2 behandlede forskningsmateriale må være
min vurdering, at en fravigelse af beskyttelsen med stor sandsynlighed vil være til skade for
bestandenes overlevelse.
2.4.1. Delkonklusion.
Den forudsatte ”sikring” af beskyttelsen af de i liste I og II anførte arter er efter min vurdering
på baggrund af den i pkt. 1.2. ovenfor gennemgåede forskning sammenholdt med de p.t.
værende grænseværdier ikke mulig ved indførelsen af det påtænkte 5G-system.
Det forekommer sandsynligt, at beskyttelsen efter art. 8 af ”liste III-arter” ligeledes ikke vil
blive respekteret ved etableringen af 5G-systemet sammenholdt med de p.t. værende
grænseværdier.
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2.5. Bonn-konventionen
Konvention af 23. juni 1979 ”om beskyttelse af migrerende arter af vilde dyr” (herefter:”Bonn-
konventionen”)
blev ratificeret af Danmark i henhold til kongelig resolution af 5. juli 1982,
samme dato som Bern-konventionen ovenfor. Den er ikke inkorporeret i dansk ret, og
gældende ret skal så vidt muligt fortolkes i overensstemmelse med de forpligtelser,
Danmark har valgt at påtage sig ved ratifikationen (Dette gælder, så længe det ikke er
nødvendigt direkte at tilsidesætte en lovbestemmelse i national ret.)
Konventionen indeholder bl.a. en række bestemmelser, hvormed de kontraherende stater har
forpligtet sig til ”i passende omfang” at ”tage skridt til” at bevare truede, migrerende dyrearter,
samt deres bosteder, jf. art. 2, stk. 1.
De for nærværende responsums problemstilling relevante bestemmelser i konventionen er på
det foreliggende grundlag følgende (understregninger indsat her), hvortil der er indsat løbende
kommentarer:
Art. 2, stk. 1 og 2:
”1. The Parties acknowledge the importance of migratory species being conserved and of
Range States agreeing to take action to this end whenever possible and appropriate, paying
special attention to migratory species the conservation status of which is unfavourable, and
taking individually or in co-operation appropriate and necessary steps to conserve such species
and their habitat.
2. The Parties acknowledge the need to take action to avoid any migratory species becoming
endangered.”
(understreget her)
Den forudsatte beskyttelse af migrerende arter er efter min vurdering på baggrund af den i
pkt. 1.2. ovenfor gennemgåede forskning sammenholdt med de p.t. værende grænseværdier
ikke mulig ved indførelsen af det påtænkte 5G-system.
Dertil kommer, at fastholdelsen af de nuværende grænseværdier efter min vurdering vil
udelukke, at Danmark kan anses for at have taget ”de nødvendige skridt” til opretholdelse af
de migrerende arter.
Art. 3, stk. 4:
”Parties that are Range States of a migratory species listed in Appendix I shall endeavour:
a) to conserve and, where feasible and appropriate, restore those habitats of the species which
are of importance in removing the species from danger of extinction;
b) to prevent, remove, compensate for or minimize, as appropriate, the adverse effects of
activities or obstacles that seriously impede or prevent the migration of the species; and
c) to the extent feasible and appropriate, to prevent, reduce or control factors that are
endangering or are likely to further endanger the species, including strictly controlling the
introduction of, or controlling or eliminating, already introduced exotic species.”
Formuleringen
”to the extent … appropriate”
(i passende omfang), som begrænser forpligtelsen
i henhold til litra c, er ikke at finde i litra a og b.
Den forudsatte beskyttelse af migrerende arter er efter min vurdering på baggrund af den i
pkt. 1.2. ovenfor gennemgåede forskning sammenholdt med de p.t. værende grænseværdier
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ikke mulig ved indførelsen af det påtænkte 5G-system.
2.5.1. Delkonklusion.
Den forudsatte beskyttelse af migrerende arter er efter min vurdering på baggrund af den i
pkt. 1.2. ovenfor gennemgåede forskning sammenholdt med de p.t. værende grænseværdier
ikke mulig ved indførelsen af det påtænkte 5G-system.
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3. Konklusion og afsluttende bemærkninger.
Det konkluderes i nærværende responsum, at etablering og aktivering af et 5G-netværk,
således som det p.t. foreligger beskrevet, vil være i strid med gældende menneskeretlige og
miljøretlige regler i EMRK, FN's børnekonvention, EU-regler og Bern- og Bonn-konventionerne.
Årsagen hertil er den meget betydelige, videnskabelige dokumentation, der foreligger for, at
radiofrekvent elektromagnetisk stråling er helbredsskadelig og farlig for mennesker (og særligt
for børn), dyr og planter.
Dette gælder også, når strålingen holder sig inden for de retningslinjer, som anbefales af
ICNIRP, og som anvendes af Danmark og bredt i EU.
De nøjagtige helbredsmæssige skadevirkninger af 5G-systemet er ikke kendte, idet der ikke er
tale om et eksakt defineret system, men det er på baggrund af den foreliggende forskning i
radiofrekvent elektromagnetisk strålings påvirkninger af f.eks. menneskers og dyrs krop,
herunder ved fremkaldelsen af DNA-skader og oxidativt stress, stærkt usandsynligt, at det ikke
skulle medføre tilsvarende skadevirkninger som de hidtidige systemer, særligt al den stund det
er baseret på samme grundlæggende stråling.
Den danske stat tjener betydelige beløb på at tillade oprettelse og drift af
kommunikationssystemerne, bl.a. ved beskatning af overskud og auktioner over de
frekvensbånd, som teleselskaber benytter til at opbygge den kommunikationsinfrastruktur, der
kan indbringe selskaberne selv milliarder.
Alfonso Balmori er én blandt mange forskere, der har udtalt sig på følgende måde om den
iboende interessekonflikt i dette strukturelle problem, jf. Balmori 2005 p. 116:
”Controversy is frequent when the scientists recognize serious effects on health and on the
environment that cause high economic losses.”
Holte, d. 4. maj 2019
Christian F. Jensen
advokat (L)
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Agarwal A. et al. 2009, Effects of radiofrequency electromagnetic waves (RF-
EMW) from cellular phones on human ejaculated semen: an in vitro pilot study
https://www.sciencedirect.com/science/article/pii/S0015028208033566
"Result(s) Samples exposed to RF-EMW showed a significant decrease in sperm motility and
viability, increase in ROS level, and decrease in ROS-TAC score. Levels of TAC [Total Antioxidant
Capacity] and DNA damage showed no significant differences from the unexposed group."
Aitken R.J. et al. 2005, Impact of radio frequency electromagnetic radiation on
DNA integrity in the male germline.
"In this study, mice were exposed to 900 MHz RFEMR at a specific absorption rate of
approximately 90 mW/kg inside a waveguide for 7 days at 12 h per day. Following exposure, DNA
damage to caudal epididymal spermatozoa was assessed by quantitative PCR (QPCR) as well as
alkaline and pulsed-field gel electrophoresis... This study suggests that while RFEMR does not have
a dramatic impact on male germ cell development, a significant genotoxic effect on epididymal
spermatozoa is evident and deserves further investigation."
Fulltext & PDF:
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2605.2005.00531.x
Avendaño C. et al. 2011, Use of laptop computers connected to internet through
Wi-Fi decreases human sperm motility and increases sperm DNA fragmentation
exposure of human spermatozoa to a wireless internet-connected laptop decreased motility and
induced DNA fragmentation by a nonthermal effect.
Fulltext & PDF:
https://www.fertstert.org/article/S0015-0282(11)02678-1/fulltext
Behari J. et al. 2006, Single strand DNA breaks in rat brain cells exposed to
microwave radiation
This study shows that the chronic exposure to these radiations (2.45 and 16.5 GHz, SAR 1.0 and
2.01 W/kg, respectively) cause statistically significant (p < 0.001) increase in DNA single strand
breaks in brain cells of rat.
https://www.sciencedirect.com/science/article/pii/S0027510705005361
Belyaev I.Y. et al. 2009, Microwaves from UMTS/GSM mobile phones induce
long‐lasting inhibition of 53BP1/γ‐H2AX DNA repair foci in human
lymphocytes
"All data were pooled and highly significant inhibitory effects on formation of DNA repair foci were
found as analyzed immediately after 1 h exposure to UMTS, 915 MHz and heat shock...The most
striking observation was that these MW-
induced inhibitory effects continued up to 3 days following 1 h exposure to MWs... These effects
depended on carrier frequency and type of signal and suggested misbalance between DNA damage
and DNA repair"
https://onlinelibrary.wiley.com/doi/abs/10.1002/bem.20445
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Blank M. et al. 2011, DNA is a fractal antenna in electromagnetic fields
Since DNA can interact with EMF over a wide range of frequencies, and does not appear to be
limited to an optimal frequency, it has the functional properties of a fractal antenna....From the
above analysis of the effect of EMF on the stress response, DNA strand breaks and cancer
epidemiology, the fractal property of DNA is apparent in the ELF and RF ranges.
https://www.tandfonline.com/doi/full/10.3109/09553002.2011.538130
Burlaka A. et al. 2013, Overproduction of free radical species in embryonal cells
exposed to low intensity radiofrequency radiation
CONCLUSION: Exposure of developing quail embryos to extremely low intensity RF-EMR of
GSM 900 MHz during at least one hundred and fifty-eight hours leads to a significant
overproduction of free radicals/reactive oxygen species and oxidative damage of DNA in embryo
cells. These oxidative changes may lead to pathologies up to oncogenic transformation of cells.
Fulltext & PDF:
http://exp-oncology.com.ua/article/6079
Busljeta I. et al. 2004, Erythropoietic changes in rats after 2.45 GJz nonthermal
irradiation.
"Adult male Wistar rats (N=40) were exposed to 2.45 GHz continuous RF/MW fields for 2 hours
daily, 7 days a week, at 5-10 mW/cm2... In the applied experimental condition, RF/MW radiation
might cause disturbance in red cell maturation and proliferation, and induce micronucleus
formation in erythropoietic cells."
https://www.ncbi.nlm.nih.gov/pubmed/15729835
Cam ST et al. 2011, Single-strand DNA breaks in human hair root cells exposed
to mobile phone radiation
Conclusions: A short-term exposure (15 and 30 min) to RFR (900-MHz) from a mobile phone
caused a significant increase in DNA single-strand breaks in human hair root cells located around
the ear which is used for the phone calls.
https://www.tandfonline.com/doi/full/10.3109/09553002.2012.666005
Campisi A. et al. 2010, Reactive oxygen species levels and DNA fragmentation on
astrocytes in primary culture after acute exposure to low intensity microwave
electromagnetic field
Our data demonstrate, for the first time, that even acute exposure to low intensity EMF induces
ROS production and DNA fragmentation in astrocytes in primary cultures, which also represent the
principal target of modulated EMF. Our findings also suggest the hypothesis that the effects could
be due to hyperstimulation of the glutamate receptors, which play a crucial role in acute and
chronic brain damage. Furthermore, the results show the importance of the amplitude modulation
in the interaction between EMF and neocortical astrocytes.
https://www.sciencedirect.com/science/article/abs/pii/S030439401000176X
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d'Ambrosio G et al. 2002, Cytogenetic damage in human lymphocytes following
GMSK phase modulated microwave exposure
Human peripheral blood cultures were exposed to 1.748 GHz, either continuous wave (CW) or
phase only modulated wave (GMSK), for 15 min. The maximum specific absorption rate
(approximately 5 W/kg) was higher than that occurring in the head of mobile phone users; however,
no changes were found in cell proliferation kinetics after exposure to either CW or GMSK fields. As
far as genotoxicity is concerned, the micronucleus frequency result was not affected by CW
exposure; however, a statistically significant micronucleus effect was found following exposure to
phase modulated field. These results would suggest a genotoxic power of the phase modulation per
se.
https://www.ncbi.nlm.nih.gov/pubmed/11793401
De Luliis G.N. et al. 2009, Mobile Phone Radiation Induces Reactive Oxygen
Species Production and DNA Damage in Human Spermatozoa In Vitro
"Principal Findings: Purified human spermatozoa were exposed to radio-frequency
electromagnetic radiation (RF-EMR) tuned to 1.8 GHz and covering a range of specific absorption
rates (SAR) from 0.4 W/kg to 27.5 W/kg. In step with increasing SAR, motility and vitality were
significantly reduced after RF-EMR exposure, while the mitochondrial generation of reactive
oxygen species and DNA fragmentation were significantly elevated (P<0.001). Furthermore, we
also observed highly significant relationships between SAR, the oxidative DNA damage bio-marker,
8-OH-dG, and DNA fragmentation after RF-EMR exposure."
"Conclusions: RF-EMR in both the power density and frequency range of mobile phones enhances
mitochondrial reactive oxygen species generation by human spermatozoa, decreasing the motility
and vitality of these cells while stimulating DNAbase adduct formation and, ultimately DNA
fragmentation. These findings have clear implications for the safety of extensive mobile phone use
by males of reproductive age, potentially affecting both their fertility and the health and wellbeing
of their offspring."
Fulltext & PDF:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714176/
Diem E. et al. 2005, Non-thermal DNA breakage by mobile-phone radiation
(1800 MHz) in human fibroblasts and in transformed GFSH-R17 rat granulosa
cells in vitro.
"Abstract: Cultured human diploid fibroblasts and cultured rat granulosa cells were exposed to
intermittent and continuous radiofrequency electromagnetic fields (RF-EMF) used in mobile
phones, with different specific absorption rates (SAR) and different mobile-phone modulations.
DNA strand breaks were determined by means of the alkaline and neutral comet assay. RF-EMF
exposure (1800 MHz; SAR 1.2 or 2 W/kg; different modulations; during 4, 16 and 24h; intermittent
5 min on/10 min off or continuous wave) induced DNA single- and double-strand breaks. Effects
occurred after 16 h exposure in both cell types and after different mobile-phone modulations. The
intermittent exposure showed a stronger effect in the comet assay than continuous exposure.
Therefore we conclude that the induced DNA damage cannot be based on thermal effects."
https://www.sciencedirect.com/science/article/abs/pii/S1383571805000896
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D'Silva M.H. et al. 2017, Effect of Radiofrequency Radiation Emitted from 2G
and 3G Cell Phone on Developing Liver of Chick Embryo – A Comparative
Study
Conclusion: The chronic exposure of chick embryo liver to RFR emitted from 2G and 3G cell phone
resulted in various structural changes and DNA damage. The changes were more pronounced in 3G
experimental group. Based on these findings it is necessary to create awareness among public
about the possible ill effects of RFR exposure from cell phone.
Fulltext og PDF:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583901/
Fucić A. et al. 1992, X-rays, microwaves and vinyl chloride monomer: their
clastogenic and aneugenic activity, using the micronucleus assay on human
lymphocytes.
"In our study we chose the micronucleus assay with a new mathematical approach to separate
clastogenic from aneugenic activity of three well-known mutagens (vinyl chloride monomer, X-rays
and microwaves) on the genome of human somatic cells... Microwaves possess some mutagenic
characteristics typical of chemical mutagens."
https://www.sciencedirect.com/science/article/pii/0165799292901333
Gajski G. et al. 2009, Radioprotective effects of honeybee venom (Apis mellifera)
against 915-MHz microwave radiation-induced DNA damage in wistar rat
lymphocytes: in vitro study.
The aim of this study is to investigate the radioprotective effect of bee venom against DNA damage
induced by 915-MHz microwave radiation (specific absorption rate of 0.6 W/kg) in Wistar rats...
Bee venom is demonstrated to have a radioprotective effect against basal and oxidative DNA
damage. Furthermore, bee venom is not genotoxic and does not produce oxidative damage in the
low concentrations used in this study.
https://journals.sagepub.com/doi/full/10.1177/1091581809335051
Gandhi G. et al. 2005, Cytogenetic Damage in Mobile Phone Users: Preliminary
Data.
"The aim of the present study hence was to detect any cytogenetic damage in mobile phone users by
analysing short term peripheral lymphocytes cultures for chromosomal aberrations and the buccal
mucosal cells for micronuclei (aneugenicity and clastogenicity). The results revealed increased
number of micronucleated buccal cells and cytological abnormalities in cultured lymphocytes
indicating the genotoxic response from mobile phone use."
https://www.tandfonline.com/doi/abs/10.1080/09723757.2005.11885936
PDF:
http://www.krepublishers.com/02-Journals/IJHG/IJHG-05-0-000-000-2005-Web/IJHG-05-4-
225-288-2005-Abst-PDF/IJHG-05-4-259-265-2005-210-Gandhi-G/IJHG-05-4-259-265-2005-210-
Gandhi-G.pdf
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Gandhi G. et al. 2015, A cross-sectional case control study on genetic damage in
individuals residing in the vicinity of a mobile phone base station.
Genetic damage parameters of DNA migration length, damage frequency (DF) and damage index
were significantly (p = 0.000) elevated in the sample group compared to respective values in
healthy controls.
https://www.tandfonline.com/doi/abs/10.3109/15368378.2014.933349
Garaj-Vrhovac V et al. 1992, The correlation between the frequency of
micronuclei and specific chromosome aberrations in human lymphocytes
exposed to microwave radiation in vitro.
Human whole-blood samples were exposed to continuous microwave radiation, frequency 7.7 GHz,
power density 0.5, 10 and 30 mW/cm2 for 10, 30 and 60 min. A correlation between specific
chromosomal aberrations and the incidence of micronuclei after in vitro exposure was observed. In
all experimental conditions, the frequency of all types of chromosomal aberrations was significantly
higher than in the control samples... The results of the study indicate that microwave radiation
causes changes in the genome of somatic human cells and that the applied tests are equally sensitive
for the detection of the genotoxicity of microwaves.
https://www.sciencedirect.com/science/article/pii/0165799292900064
Gorpinchenko I. et al. 2014, The influence of direct mobile phone radiation on
sperm quality.
CONCLUSIONS: A correlation exists between mobile phone radiation exposure, DNA-
fragmentation level and decreased sperm motility.
Fulltext & PDF:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074720/
Güler G et al. 2012, The effect of radiofrequency radiation on DNA and lipid
damage in female and male infant rabbits.
CONCLUSION: Consequently, it can be concluded that GSM-like RF radiation may induce
biochemical changes by increasing free radical attacks to structural biomolecules in the rabbit as
an experimental animal model.
https://www.tandfonline.com/doi/full/10.3109/09553002.2012.646349
Gursatej A.G. 2005, Genetic damage in mobile phone users: some preliminary
findings.
"In the present study, DNA and chromosomal damage investigations were carried out on the
peripheral blood lymphocytes of individuals using mobile phones, being exposed to MW frequency
ranging from 800 to 2000 MHz.... CONCLUSIONS: These results highlight a correlation between
mobile phone use (exposure to RFR) and genetic damage and require interim public health actions
in the wake of widespread use of mobile telephony."
https://tspace.library.utoronto.ca/handle/1807/5943
PDF:
https://tspace.library.utoronto.ca/bitstream/1807/5943/1/hg05022.pdf
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Karaca E. et al. 2011, The genotoxic effect of radiofrequency waves on mouse
brain
Brain cell cultures of the mice were exposed to 10.715 GHz with specific absorbtion rate (SAR)
0.725 W/kG signals for 6 h in 3 days at 25°C to check for the changes in the micronucleus (MNi)
assay and in the expression of 11 proapoptotic and antiapoptotic genes. It was found that MNi rate
increased 11-fold and STAT3 expression decreased 7-fold in the cell cultures which were exposed to
RF. Cell phones which spread RF may damage DNA and change gene expression in brain cells.
https://link.springer.com/article/10.1007%2Fs11060-011-0644-z
Kesari K.K. et al. 2013, Effect of 3G cell phone exposure with computer
controlled 2-D stepper motor on non-thermal activation of the hsp27/p38MAPK
stress pathway in rat brain.
Result shows that microwave radiation emitted from 3G mobile phone significantly induced DNA
strand breaks in brain.
https://link.springer.com/article/10.1007%2Fs12013-013-9715-4
Kumar S. et al. 2014, Effect of electromagnetic irradiation produced by 3G
mobile phone on male rat reproductive system in a simulated scenario.
"Significant decrease in sperm count, increase in the lipid peroxidation damage in sperm cells,
reduction in seminiferous tubules and testicular weight and DNA damage were observed following
exposure to EMF in male albino rats. The results suggest that mobile phone exposure adversely
affects male fertility."
http://nopr.niscair.res.in/bitstream/123456789/29335/1/IJEB%2052%289%29%20890-897.pdf
Liu C. et al. 2013, Mobile phone radiation induces mode-dependent DNA
damage in a mouse spermatocyte-derived cell line: a protective role of
melatonin.
RESULTS:The levels of DNA damage were significantly increased following exposure to Mobile
Phone Radiation(MPR) in the listen, dialed and dialing modes. Moreover, there were
significantly higher increases in the dialed and dialing modes than in the listen mode.
Interestingly, these results were consistent with the radiation intensities of these modes. However,
the DNA damage effects of MPR in the dialing mode were efficiently attenuated by melatonin
pretreatment.
Link:https://www.ncbi.nlm.nih.gov/pubmed/23952262
Lu Y. et al. 2012, Reactive Oxygen Species Formation and Apoptosis in Human
Peripheral Blood Mononuclear Cell Induced by 900 MHz Mobile Phone
Radiation
Abstract: We demonstrate that reactive oxygen species (ROS) plays an important role in the process
of apoptosis in human peripheral blood mononuclear cell (PBMC) which is induced by the
radiation of 900 MHz radiofrequency electromagnetic field (RFEMF) at a specific absorption rate
(SAR) of ~0.4 W/kg when the exposure lasts longer than two hours. The apoptosis is induced
through the mitochondrial pathway and mediated by activating ROS and caspase-3, and decreasing
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the mitochondrial potential. The activation of ROS is triggered by the conformation disturbance of
lipids, protein, and DNA induced by the exposure of GSM RFEMF. Although human PBMC was
found to have a self-protection mechanism of releasing carotenoid in response to oxidative stress to
lessen the further increase of ROS, the imbalance between the antioxidant defenses and ROS
formation still results in an increase of cell death with the exposure time and can cause about 37%
human PBMC death in eight hours.
Fulltext & PDF:
https://www.hindawi.com/journals/omcl/2012/740280/
Markova E. et al. 2010, Microwaves from Mobile Phones Inhibit 53BP1 Focus
Formation in Human Stem Cells More Strongly Than in Differentiated Cells:
Possible Mechanistic Link to Cancer Risk
"We studied whether microwaves from mobile telephones of the Global System for Mobile
Communication (GSM) and the Universal Global Telecommunications System (UMTS) induce
DSBs or affect DSB repair in stem cells... Microwaves from mobile phones inhibited formation of
53BP1 foci in human primary fibroblasts and mesenchymal stem cells. These data parallel our
previous findings for human lymphocytes. Importantly, the same GSM carrier frequency (915 MHz)
and UMTS frequency band (1947.4 MHz) were effective for all cell types. Exposure at 905 MHz did
not inhibit 53BP1 foci in differentiated cells, either fibroblasts or lymphocytes, whereas some
effects were seen in stem cells at 905 MHz. Contrary to fibroblasts, stem cells did not adapt to
chronic exposure during 2 weeks."
Fulltext & PDF:
https://ehp.niehs.nih.gov/doi/abs/10.1289/ehp.0900781
Megha K. et al. 2015, Low intensity microwave radiation induced oxidative
stress, inflammatory response and DNA damage in rat brain.
In conclusion, the present study suggests that low intensity microwave radiation induces oxidative
stress, inflammatory response and DNA damage in brain by exerting a frequency dependent effect.
The study also indicates that increased oxidative stress and inflammatory response might be the
factors involved in DNA damage following low intensity microwave exposure.
https://www.sciencedirect.com/science/article/pii/S0161813X15300097
Panagopoulos D.J. 2007, Cell death induced by GSM 900-MHz and DCS 1800-
MHz mobile telephony radiation.
Results (uddrag): The data reveal that both GSM 900 and DCS 1800 mobile telephony radiations
strongly induce cell death (DNA fragmentation) in ovarian egg chambers of the exposed groups,
(63.01% in 900, 45.08% in 900A and 39.43% in 1800), while in the SE [Sham Exposed] and C
[Control] groups the corresponding percentage of cell death was only 7.78% and 7.75%,
respectively.
https://www.sciencedirect.com/science/article/abs/pii/S1383571806003202
Pandey N. et al. 2016 Radiofrequency radiation (900 MHz)-induced DNA
damage and cell cycle arrest in testicular germ cells in swiss albino mice
"Result: Swiss albino mice were exposed to RFR (900 MHz) for 4 h and 8 h duration per day for 35
days. One group of animals was terminated after the exposure period, while others were kept for an
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additional 35 days post-exposure. RFR exposure caused depolarization of mitochondrial
membranes resulting in destabilized cellular redox homeostasis. Statistically significant increases
in the damage index in germ cells and sperm head defects were noted in RFR-exposed animals."
https://journals.sagepub.com/doi/abs/10.1177/0748233716671206
Phillips JL et al. 2009, Electromagnetic fields and DNA damage
This review describes the comet assay and its utility to qualitatively and quantitatively assess DNA
damage, reviews studies that have investigated DNA strand breaks and other changes in DNA
structure, and then discusses important lessons learned from our work in this area.
Dette er jo kun
et review. det er ikke en artikel der repræsenterer et studie hvor sammenhængen er påvist. MEN
DEN ERVIGTIG fordi den giver en oversigt over hvilke faktorer der er afgørende for om der findes
genotoxiske effekter eller ej i videnskabelige forsøg. (feks celletype og strålingens pulsering)
Fulltext & PDF:
https://www.pathophysiologyjournal.com/article/S0928-4680(09)00014-5/fulltext
Salford L et al. 2003, Nerve cell damage in mammalian brain after exposure to
microwaves from GSM mobile phones
Three groups each of eight rats were exposed for 2 hr to Global System for Mobile Communications
(GSM) mobile phone electromagnetic fields of different strengths [0.24. 2.4, and 24 W/m
2
]. We
found highly significant (p< 0.002) evidence for neuronal damage in the cortex, hippocampus, and
basalganglia in the brains of exposed rats.
Fulltext & PDF:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241519/
Schwarz C. 2008, Radiofrequency electromagnetic fields (UMTS, 1,950 MHz)
induce genotoxic effects in vitro in human fibroblasts but not in lymphocytes.
CONCLUSION: UMTS [3G] exposure may cause genetic alterations in some but not in all
human cells in vitro.
https://link.springer.com/article/10.1007%2Fs00420-008-0305-5
Semra T.C. et al. 2012, Single-strand DNA breaks in human hair root cells
exposed to mobile phone radiation
Conclusions: A short-term exposure (15 and 30 min) to RFR (900-MHz) from a mobile phone
caused a significant increase in DNA single-strand breaks in human hair root cells located around
the ear which is used for the phone calls.
https://www.tandfonline.com/doi/abs/10.3109/09553002.2012.666005
Tice R.R. et al. 2002, Genotoxicity of radiofrequency signals. I. Investigation of
DNA damage and micronuclei induction in cultured human blood cells.
This research demonstrates that, under extended exposure conditions, RF signals at an average
SAR of at least 5.0 W/kg are capable of inducing chromosomal damage in human lymphocytes.
https://onlinelibrary.wiley.com/doi/abs/10.1002/bem.104
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Trosic I et al. 2011, Effect of electromagnetic radiofrequency radiation on the
rats' brain, liver and kidney cells measured by comet assay
The results of this study suggest that, under the experimental conditions applied, repeated 915 MHz
irradiation could be a cause of DNA breaks in renal and liver cells, but not affect the cell genome at
the higher extent compared to the basal damage.
https://www.researchgate.net/publication/
221683991_Effect_of_Electromagnetic_Radiofrequency_Radiation_on_the_Rats'_Brain_Liver_and
_Kidney_Cells_Measured_by_Comet_Assay
Verschaeve L. 2009, Genetic damage in subjects exposed to radiofrequency
radiation
A majority of these studies do show that RF-exposed individuals have increased frequencies of
genetic damage (e.g., chromosomal aberrations) in their lymphocytes or exfoliated buccal cells.
https://www.sciencedirect.com/science/article/pii/S1383574208001415
Xu S. et al. 2010, Exposure to 1800 MHz radiofrequency radiation induces
oxidative damage to mitochondrial DNA in primary cultured neurons.
In this study, we exposed primary cultured cortical neurons to pulsed RF electromagnetic fields at a
frequency of 1800 MHz modulated by 217 Hz at an average special absorption rate (SAR) of 2
W/kg. At 24 h after exposure, we found that RF radiation induced a significant increase in the levels
of 8-hydroxyguanine (8-OHdG), a common biomarker of DNA oxidative damage, in the
mitochondria of neurons. Concomitant with this finding, the copy number of mtDNA and the levels
of mitochondrial RNA (mtRNA) transcripts showed an obvious reduction after RF exposure. Each
of these mtDNA disturbances could be reversed by pretreatment with melatonin, which is known to
be an efficient antioxidant in the brain. Together, these results suggested that 1800 MHz RF
radiation could cause oxidative damage to mtDNA in primary cultured neurons. Oxidative damage
to mtDNA may account for the neurotoxicity of RF radiation in the brain.
https://www.sciencedirect.com/science/article/pii/S0006899309022999
Yakymenko I. et al, 2010, Risks of carcinogenesis from electromagnetic radiation
of mobile telephony devices.
Among reproducible biological effects of low-intensive MWs are reactive oxygen species
overproduction, heat shock proteins expression, DNA damages, apoptosis. The lack of generally
accepted mechanism of biological effects of low-intensive non-ionizing radiation doesn't permit to
disregard the obvious epidemiological and experimental data of its biological activity.
Fulltext &
PDF:
https://www.researchgate.net/publication/45538585_Risks_of_carcinogenesis_from_electrom
agnetic_radiation_of_mobile_telephony_devices
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Zalata A. et al. 2015 , In vitro effect of cell phone radiation on motility, DNA
fragmentation and clusterin gene expression in human sperm.
CONCLUSION: Cell phone emissions have a negative impact on exposed sperm motility index,
sperm acrosin activity, sperm DNA fragmentation and seminal CLU gene expression, especially
in OAT* cases.
* = tilfælde hvor koncentration af sædceller er lav.
Fulltext & PDF:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410031/
Zothansiama et al. 2017, Impact of radiofrequency radiation on DNA damage
and antioxidants in peripheral blood lymphocytes of humans residing in the
vicinity of mobile phone base stations
Testpersoner bosat indenfor 80m radius af mobilmast havde signifikant flere mikronuklei (blod
markør for DNA-skader) og nedsat anti-oxidant status end i personer bosat udenfor 300m radius.
https://www.tandfonline.com/doi/abs/10.1080/15368378.2017.1350584
Zotti-Martelli L. et al. 2005, Individual responsiveness to induction of
micronuclei in human lymphocytes after exposure in vitro to 1800-MHz
microwave radiation.
The results show that microwaves are able to induce MN [micronuclei] in short-time exposures to
medium power density fields. Our data analysis highlights a wide inter-individual variability in the
response, which was confirmed to be a characteristic reproducible trait by means of the second
experiment.
https://www.sciencedirect.com/science/article/abs/pii/S138357180500032X
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MyU-EOP-MBC
Nº Expediente: 18011666
Sr. D.
ANGEL CRUZ BAYÓN GOZALO
PRESIDENTE ASOC. VALLISOLETANA AFECTADOS
POR ANTENAS TELEC. AVAATE
CALLE ANDRÉS DE LA ORDEN Nº S/Nº
47003 VALLADOLID
EL DEFENSOR DEL PUEBLO
REGISTRO
SALIDA
21/08/2019 - 19080322
Estimado Sr.:
En relación con la queja arriba indicada, se le comunica que se ha recibido un
informe elaborado por la Dirección General de Telecomunicaciones, dependiente de la
Secretaría de Estado para el Avance Digital, que puede resumirse como sigue:
I.
El Plan Nacional 5G, publicado por el anterior Ministerio de Energía, Turismo y
Agenda Digital en diciembre de 2017, pretende contribuir a la consecución de los
objetivos marcados a nivel europeo en el Plan de Acción de 5G para Europa aprobado
por las instituciones comunitarias en abril de 2016 como estrategia para mejorar la
competitividad europea en el desarrollo de esta tecnología emergente, en el que se
incluye diversos objetivos para los Estados Miembros, entre ellos, la aprobación de
planes de trabajo nacionales.
El Plan se enmarca en un contexto internacional en el que los principales países
europeos (Alemania, Francia, Reino Unido, etc.) y de otras regiones del mundo (USA,
Japón, Corea, etc.) están aprobando sus estrategias para el desarrollo del 5G, y España
no podía quedarse atrás.
No obstante, el Plan Nacional 5G no es una norma que establezca preceptos
jurídicos relacionados con los despliegues 5G, que deban ser objeto de una evaluación
específica y previa a su aprobación y publicación, ni un documento vinculante que
genere efectos frente a terceros. El Plan es únicamente un documento de carácter
general y de referencia que define y trata de impulsar una estrategia de una política
pública, en el que se identifican los tipos de medidas, de carácter estratégico, que se
considera se deben a llevar a cabo para que España no quede retrasada en el desarrollo
de esta nueva tecnología, y pueda perder las oportunidades que proporcionará en el
futuro. Los aspectos ambientales deben ser analizados cuando se proceda al despliegue
real de las infraestructuras que sirvan de soporte para la tecnología 5G.
II.
Así, el Plan Nacional 5G no se ha sometido a evaluación ambiental estratégica.
Se trata de un plan que contiene los principios programáticos y relaciona las líneas
estratégicas que se considera deben ser ejecutadas para lograr el impulso de esta
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www.defensordelpueblo.es
[email protected]
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“nueva tecnología disruptiva” a nivel social y económico. Es un documento estratégico
que identifica las líneas directrices y distintas políticas públicas que deberían ser
tenidas en cuenta para situar a nuestro país en una situación de liderazgo en la
adopción y consolidación de la tecnología 5G. No es un norma ni un documento
vinculante que genere efectos frente a terceros, como ser un plan general de
ordenación urbana, que sea directamente aplicable y ejecutable, y que, en
consecuencia, deba haber efectuado un evaluación medioambiental. Por tanto, el Plan
Nacional 5G, atendiendo a su naturaleza y finalidad, “no
ha sido sometido a evaluación
de impacto ambiental”
(sic).
Otra cuestión es el despliegue en concreto de las infraestructuras de red, en
particular, de las estaciones base, en que se plasmará finalmente los recursos
necesarios para poder utilizar la tecnología 5G a través la prestación de una serie de
servicios a instituciones, empresas y ciudadanos.
En tal sentido, el artículo 34.6 de la Ley 9/2014, de 9 de mayo, General de
Telecomunicaciones, establece:
“
6. Para la instalación de las estaciones o infraestructuras radioeléctricas utilizadas para la
prestación de servicios de comunicaciones electrónicas disponibles para el público a las que se
refiere la disposición adicional tercera de la Ley 12/2012, de 26 de diciembre, de medidas
urgentes de liberalización del comercio y de determinados servicios, no podrá exigirse la
obtención de licencia previa de instalaciones, de funcionamiento o de actividad, ni otras de clase
similar o análogas, en los términos indicados en la citada ley.
Para la instalación de redes públicas de comunicaciones electrónicas o de estaciones
radioeléctricas en dominio privado distintas de las señaladas en el párrafo anterior, no podrá
exigirse por parte de las administraciones públicas competentes la obtención de licencia o
autorización previa de instalaciones, de funcionamiento o de actividad, o de carácter
medioambiental, ni otras licencias o aprobaciones de clase similar o análogas que sujeten a previa
autorización dicha instalación, en el caso de que el operador haya presentado a la administración
pública competente para el otorgamiento de la licencia o autorización un plan de despliegue o
instalación de red de comunicaciones electrónicas, en el que se contemplen dichas
infraestructuras o estaciones, y siempre que el citado plan haya sido aprobado por dicha
administración.
(…)
Las licencias o autorizaciones previas que, de acuerdo con los párrafos anteriores, no puedan ser
exigidas, serán sustituidas por declaraciones responsables, de conformidad con lo establecido en
el artículo 71 bis de la Ley 30/1992, de 26 de noviembre, de Régimen Jurídico de las
administraciones públicas y del Procedimiento Administrativo Común, relativas al cumplimiento
de las previsiones legales establecidas en la normativa vigente. En todo caso, el declarante deberá
estar en posesión del justificante de pago del tributo correspondiente cuando sea preceptivo.
(…)
La presentación de la declaración responsable, con el consiguiente efecto de habilitación a partir
de ese momento para ejecutar la instalación, no prejuzgará en modo alguno la situación y efectivo
acomodo de las condiciones de la infraestructura o estación radioeléctrica a la normativa
aplicable, ni limitará el ejercicio de las potestades administrativas de comprobación, inspección,
2 de 17
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Tel.: (+34) – 91 432 79 00 Fax: (+34) – 91 308 11 58
www.defensordelpueblo.es
[email protected]
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sanción, y, en general, de control que a la administración en cualquier orden, estatal, autonómico
o local, le estén atribuidas por el ordenamiento sectorial aplicable en cada caso
”.
En todo caso, el inicio de la implantación de la tecnología 5G a corto y medio
plazo se va a efectuar a través de la infraestructuras y estaciones bases actualmente
desplegadas, que suelen estar utilizando la tecnología 4G en las mencionadas bandas de
frecuencia que son objeto de uso a nivel masivo por diferentes servicios radioeléctricos
comerciales (700 MHz, 800 MHz, 900 MHz, 1,8 GHz, 2,1 GHz, 2,6 GHz, 3,5 GHz),
estaciones base que ya previamente han sido autorizadas tanto en lo relativo a su
proyecto técnico como en su puesta en servicio.
Así, cabe traer a colación nuevamente la Ley General de Telecomunicaciones,
cuyo artículo 34.7 prevé expresamente el supuesto de una renovación puramente
tecnológica de una estación base previamente instalada, no sujetándola a un riguroso
control administrativo en diferentes ámbitos de actuación, incluido el medioambiental:
“7. En el caso de que sobre una infraestructura de red pública de comunicaciones electrónicas,
fija o móvil, incluidas las estaciones radioeléctricas de comunicaciones electrónicas, ya esté
ubicada en dominio público o privado, se realicen actuaciones de innovación tecnológica o
adaptación técnica que supongan la incorporación de nuevo equipamiento o la realización de
emisiones radioeléctricas en nuevas bandas de frecuencias o con otras tecnologías, sin variar los
elementos de obra civil y mástil, no se requerirá ningún tipo de concesión, autorización o licencia
nueva o modificación de la existente o declaración responsable o comunicación previa a las
administraciones públicas competentes por razones de ordenación del territorio, urbanismo o
medioambientales”
.
Así se concluye que el Plan Nacional 5G, atendiendo a su naturaleza y finalidad,
no ha sido sometido a evaluación de impacto ambiental ni se solicitó su evaluación.
III.
El Plan Nacional 5G de España prevé la realización de proyectos piloto para
probar las nuevas funcionalidades que ofrecerá la tecnología 5G. En particular, se han
convocado 2 proyectos piloto por la entidad pública Red.es, que han sido adjudicados
por dicha entidad mediante Resolución del 30 de abril de 2019.
Una parte de estas pruebas se desarrollan introduciendo nuevas funcionalidades
en estaciones 4G ya existentes y en servicio. Cuando se requiere la instalación y
operación durante un tiempo de una nueva estación, para la instalación y uso de la
misma es aplicable la regulación del uso del dominio público radioeléctrico, que
garantiza un control exhaustivo en la instalación y uso en el tiempo de todo centro
emisor o estación base radioeléctrica.
IV.
Los límites de las emisiones radioeléctricas no dependen de la tecnología
utilizada en la comunicación (2G, 3G, 4G o 5G) sino de las características específicas de
cada banda de frecuencias. Las bandas de frecuencias que se van a utilizar para la
tecnología 5G, en un primer estadio o posterior, van a ser las que ya están siendo
utilizadas masivamente por diferentes servicios radioeléctricos comerciales (700 MHz,
800 MHz, 900 MHz, 1,8 GHz, 2,1 GHz, 2,6 GHz, 3,5 GHz) con el único añadido de la
3 de 17
Paseo de Eduardo Dato, 31 – 28010 Madrid
Tel.: (+34) – 91 432 79 00 Fax: (+34) – 91 308 11 58
www.defensordelpueblo.es
[email protected]
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banda de 26 GHz. Esta última banda no ha sido aún adjudicada para el uso de 5G en
España para servicios comerciales masivos.
Los organismos internacionales de normalización ya están trabajando en una
norma técnica que cubra el cálculo y el procedimiento de medida de emisiones en las
bandas milimétricas, como es esta de 26 GHz. En concreto, la Comisión Electrotécnica
Internacional (IEC) está desarrollando la norma IEC 62232 (Determination
of RF field
strength, power density and SAR in the vicinity of radiocommunication base stations for
the purpose of evaluating human exposure),
en avanzado estado de elaboración, que
permitirá la evaluación de los niveles de emisión en estas bandas milimétricas.
Asimismo, la Comisión Internacional sobre la Protección contra la Radiación No
Ionizante (International Commission on Non-Ionizing Radiation Protection, ICNIRP), está
estudiando y revisando las directrices científicas por ella. Estas directrices derivadas de
los estudios de la exposición a campos electromagnéticos sirvieron de base para
Recomendación 1999/519/CE del Consejo de Sanidad de la Unión Europea, de 12 de
julio de 1999, relativa a la exposición del público en general a campos
electromagnéticos desde 0 Hz a 300 GHz. Este es el marco europeo que garantiza el
nivel de protección de la población en la exposición a los campos electromagnéticos
procedentes de productos y aparatos eléctricos o electrónicos.
La ICNIRP publicará, en caso de que lo considere necesario, una actualización de
las directrices científicas. Y en el caso de que se produzca esta revisión, se espera que
consecuentemente sea revisada la Recomendación 1999/519/CE del Consejo de Sanidad
de la Unión Europea, así como el Real Decreto 1066/2001 por el que se aprueba el
Reglamento que establece condiciones de protección del dominio público
radioeléctrico, restricciones a las emisiones radioeléctricas y medidas de protección
sanitaria frente a emisiones radioeléctricas. Este decreto incorpora los criterios de
protección sanitaria establecidos en la Recomendación, y su anexo II establece los
límites de exposición, en el que se incluyen los límites máximos de emisión para las
bandas de frecuencias usadas por las comunicaciones móviles, que son las que utilizará
también la tecnología 5G. Así, este Real Decreto establece que el Ministerio de Sanidad
y Consumo adaptará al progreso científico el mencionado anexo II, teniendo en cuenta
el principio de precaución y las evaluaciones realizadas por las organizaciones
nacionales e internacionales competentes.
Las directrices científicas de la ICNIRP son los estándares internacionales que
tienen el respaldo de la Organización Mundial de la Salud (OMS). La OMS recomienda
una estricta adhesión a los estándares internacionales citados con anterioridad, que han
sido desarrollados para proteger tanto a los usuarios de telefonía móvil, como a las
personas que trabajan cerca o viven alrededor de estaciones base de telefonía móvil, y
a la gente que no hace uso de este tipo de comunicación. La OMS también recomienda
que no se impongan límites arbitrarios, desautorizando o desconfiando de la regulación
existente, pues esta se basa en el conocimiento científico.
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V.
El Reglamento sobre el uso del dominio público radioeléctrico, aprobado por
el Real Decreto 123/2017, prevé mecanismos de seguimiento de los niveles de
exposición, mediante la presentación de certificaciones e informes por parte de
operadores de telecomunicaciones, la realización planes de inspección y la elaboración
de un informe anual.
El Reglamento sobre el uso del dominio público radioeléctrico, establece que los
operadores que establezcan determinadas redes, entre ellas las redes de telefonía
móvil, tienen que elaborar un estudio detallado, realizado por técnico competente, que
indique los niveles de exposición radioeléctrica en áreas cercanas a sus instalaciones
radioeléctricas, en las que puedan permanecer habitualmente personas, y que este
estudio tiene que ser presentado ante el Ministerio de Economía y Empresa incorporado
en el proyecto que se tiene que presentar para solicitar la autorización de las
instalaciones radioeléctricas.
Asimismo, con carácter previo al inicio de emisiones, los operadores tienen que
obtener la autorización de puesta en servicio de las estaciones prevista en el Título IV
del mencionado reglamento sobre el uso del dominio público radioeléctrico, y para
otorgarla los servicios de inspección de la Secretaría de Estado para el Avance Digital
comprueban el cumplimiento de los niveles de emisiones en el caso de estaciones que
requieren de reconocimiento técnico, o los operadores tienen que presentar un
certificado de niveles de exposición realizado por un técnico competente en materia de
telecomunicaciones, en el caso de estaciones a las que sea aplicable el procedimiento
de certificación sustitutiva del reconocimiento técnico.
Además de lo anterior, de acuerdo con lo establecido en el “Dispongo” cuatro de
la Orden CTE/23/2002, de 11 de enero, por la que se establecen condiciones para la
presentación de determinados estudios y certificaciones por operadores de servicios de
radiocomunicaciones los operadores tienen que remitir al Ministerio de Economía y
Empresa, en el primer trimestre de cada año natural, una certificación emitida por
técnico competente de que se han respetado durante al año anterior los límites de
exposición establecidos en el anexo II del Reglamento que establece las restricciones a
las emisiones radioeléctricas y medidas de protección sanitaria frente a emisiones
radioeléctricas, aprobado por el Real Decreto 1066/2001.
Adicionalmente, el Ministerio lleva a cabo unos planes de inspección anuales. En
ellos se incluyen la realización de medidas en el entorno de una muestra de estaciones
radioeléctricas y una auditoria de las certificaciones presentadas por los operadores.
Asimismo, y debido a la importancia que otorga la normativa española a los
espacios sensibles (guarderías, centros de educación infantil, primaria, centros de
enseñanza obligatoria, centros de salud, hospitales, parques públicos, residencias o
centros geriátricos, etc) también se realizan trabajos específicos para comprobar los
niveles de exposición radioeléctrica en dichos lugares sensibles.
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Se concluye que la regulación actual sobre el uso del dominio público
radioeléctrico y control de los niveles de emisión es adecuada, incluye las decisiones
adoptadas por los organismos internacionales competentes e incorpora el principio de
precaución en la delimitación y fijación de los límites de exposición a las emisiones
radioeléctricas, garantizándose el oportuno y estricto control en su cumplimiento.
Hasta aquí la información recibida de la Secretaría de Estado para el Avance
Digital, a la que esta institución ha dirigido, con esta misma fecha, las siguientes
consideraciones:
“1. Lo primero que debe señalarse, es que la evaluación ambiental de planes
tiene un objeto distinto y está sujeta a un procedimiento diferente a de la evaluación
de impacto ambiental proyectos.
La Ley 21/2013 define con carácter general la evaluación ambiental como el
proceso a través del cual se analizan los efectos significativos que tienen o pueden
tener los planes y proyectos sobre el medio ambiente, antes de su adopción, aprobación
o autorización. Ese análisis incluye los efectos de aquellos sobre la población, la salud
humana, la flora, la fauna, la biodiversidad, la geodiversidad, la tierra, el suelo, el
subsuelo, el aire, el agua, el clima, el cambio climático, el paisaje, los bienes
materiales, incluido el patrimonio cultural, y la interacción entre todos los factores
mencionados.
Partiendo de la definición general, la Ley distingue entre la evaluación ambiental
estratégica, a la que deben someterse los planes, y la evaluación de impacto ambiental,
que procede respecto de los proyectos.
Para aclarar la cuestión, la Ley define qué debe entenderse por plan y qué debe
entenderse por proyecto.
El artículo 5.2 b) de la Ley define un plan como el conjunto de estrategias,
directrices y propuestas destinadas a satisfacer necesidades sociales, no ejecutables
directamente, sino a través de su desarrollo por medio de uno o varios proyectos. Por su
parte, en el artículo 5.3 b) de la Ley, un proyecto se define como cualquier actuación
que consista en: 1º la ejecución, explotación, desmantelamiento o demolición de una
obra, una construcción, o instalación, o bien 2º cualquier intervención en el medio
natural o en el paisaje, incluidas las destinadas a la explotación o al aprovechamiento
de los recursos naturales o del suelo y del subsuelo, así como de las aguas continentales
o marinas.
Definido el objeto de la evaluación, la Ley define la finalidad específica de una y
otra evaluación según recaiga sobre un plan o un proyecto. La evaluación ambiental
estratégica requiere incorporar los criterios de sostenibilidad en la toma de decisiones
estratégicas. Ello significa que en la elaboración del plan deben valorarse y tenerse en
cuenta los aspectos medioambientales, junto a los económicos y sociales, con el fin de
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alcanzar un elevado grado de protección ambiental y promover el desarrollo sostenible
(artículo 1 de la Ley 21/2013).
A través de la evaluación de proyectos, se garantiza una adecuada prevención de
los impactos ambientales concretos que se puedan generar, al tiempo que se establecen
las medidas necesarias de corrección o compensación de dichos impactos.
La distinción entre ambos tipos de evaluación tiene su reflejo en una diferente
tramitación. Así, el procedimiento para evaluar los planes se regula en el artículo 6 y en
el Capítulo I del Título II de la Ley 21/2013; y el de los proyectos, en el artículo 7 y en
el Capítulo II del Título II.
Centrándonos ahora en la evaluación ambiental estratégica, esta requiere, en
síntesis, la elaboración del estudio ambiental estratégico; la celebración de un trámite
de información pública y de consultas a las Administraciones públicas afectadas y
personas interesadas y una declaración ambiental estratégica en la que se incluyan las
determinaciones, medidas o condiciones que deban incorporarse en el plan que
finalmente se apruebe o adopte para garantizar su sostenibilidad.
2.
Hecha la distinción entre ambas formas de evaluación, para averiguar si el
Plan Nacional 5G debe someterse a evaluación ambiental debe comprobarse si cumple
los requisitos establecidos en la legislación.
1º Como se ha dicho, el artículo 5.2 b) de la Ley define un plan como el conjunto
de estrategias, directrices y propuestas destinadas a satisfacer necesidades sociales, no
ejecutables directamente, sino a través de su desarrollo por medio de uno o varios
proyectos. De la definición dada por esa Secretaría de Estado para el Avance Digital, a
través del informe de la Dirección General de Telecomunicaciones, y del contenido del
propio plan se deduce que el Plan Nacional 5G se ajusta a esta definición.
Así según la DG,
“El
Plan Nacional 5G tiene como objetivo situar a España entre
los países más avanzados en el desarrollo de esta nueva tecnología, de manera que
cuando la 5G alcance su madurez tecnológica y comercial, España esté lo mejor
preparada posible para aprovechar al máximo las oportunidades de este nuevo
paradigma tecnológico.
El Plan Nacional (…) es un documento que define y trata de impulsar una
estrategia de una política pública que va a provocar efectos beneficiosos para la
economía y sociedad españolas,...(…) Dicho Plan es únicamente un documento de
carácter general en el que se identifican los tipos de medidas, de carácter estratégico,
que se considera se deben a llevar a cabo para que España no quede retrasada en el
desarrollo de esta nueva tecnología, y pueda perder las oportunidades que
proporcionará en el futuro.
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Por ello, este Plan se enmarca en un contexto internacional en el que los
principales países europeos (Alemania, Francia, Reino Unido, etc.) y de otras regiones
del mundo (USA, Japón, Corea, etc.) están aprobando sus estrategias para el desarrollo
del 5G, y España no podía quedarse atrás en estos aspectos. Estas estrategias
nacionales, al igual que el Plan de acción 5G para Europa, y el Plan nacional 5G
publicado en España, constituyen documentos de referencia en cada uno de los países,
en los que se identifican las grandes medidas estratégicas a llevar a cabo para el
desarrollo del 5G, pero no se trata de medidas normativas específicas que deban ser
objeto para su aprobación y publicación de una evaluación específica y sobre un caso
concreto en lo que a su impacto en diferentes aspectos se refiere”.
Conforme a lo anterior, el Plan define los objetivos estratégicos, las medidas
estratégicas (entre ellas acciones para la gestión y planificación del espectro
radioeléctrico, puesta en marcha de proyectos piloto y desarrollo de instrumentos
legales que proporcionen seguridad jurídica para facilitar las inversiones en el
despliegue) y la hoja de ruta para el despliegue de las acciones clave. De lo anterior se
concluye que el Plan Nacional 5G se ajusta sin dificultad a la definición legal y es un
plan a los efectos de la Ley 21/2013, pues constituye un conjunto de directrices y
propuestas destinadas a satisfacer necesidades sociales, no ejecutables directamente.
2º El artículo 6.1 determina los planes que deben ser sometidos a evaluación
ambiental estratégica ordinaria conforme a lo siguiente:
-
Que se adopten o aprueben por una Administración pública.
En este caso, esa
Secretaría de Estado para el Avance Digital no ha informado de que el Plan haya
sido aprobado formalmente por el Consejo de Ministros mediante un acuerdo o
mediante una orden o resolución de un órgano del Ministerio de Economía y
Empresa. No obstante, no está del todo claro que la Ley 21/2013 exija un acto
de aprobación formal en sentido estricto, pues basta que el plan haya sido
“adoptado” por una Administración pública, lo cual ocurre en este caso, pues
como acaba de indicarse, y así lo reconoce la Dirección General de
Telecomunicaciones, el Plan es un documento de referencia elaborado y
difundido por el Ministerio, el cual define los pasos que han de darse y el
calendario que ha de cumplirse para el despliegue de la tecnología 5G.
Que su elaboración y aprobación venga exigida por una disposición legal o
reglamentaria o por acuerdo del Consejo de Ministros o del Consejo de Gobierno
de una comunidad autónoma.
Este precepto traspone el artículo 2 a) segundo
guión de la Directiva 2001/42/CE de evaluación ambiental de planes y
programas. Esta Directiva se refiere a los planes que sean exigidos por
disposiciones legales, reglamentarias o administrativas. Conforme a lo anterior,
debe interpretarse que las disposiciones que prevén la adopción de un plan no se
circunscriben al ámbito estatal o autonómico como dice la Ley 21/2013, sino que
su necesidad puede derivarse también de disposiciones o actos emanados de las
instituciones comunitarias. Según indica la Dirección General de
−
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Telecomunicaciones, el Plan Nacional 5G, es consecuencia de la necesidad de
cumplir con los objetivos marcados a nivel europeo en el Plan de Acción de 5G
para Europa aprobado por las instituciones comunitarias en abril de 2016 “como
estrategia para mejorar la competitividad europea en el desarrollo de esta
tecnología emergente, en el que se incluye diversos objetivos para los Estados
Miembros, entre ellos, la aprobación de planes de trabajo nacionales”.
Efectivamente, el Plan de Acción 5G para Europa fue adoptado por la Comisión
Europea mediante la Comunicación 2016 (588). Las comunicaciones son actos
atípicos propios del derecho derivado de la UE. Por tanto, el Plan Nacional 5G
entra dentro de la categoría de disposiciones a las que hace referencia la
Directiva y, por tanto, también cumple el requisito señalado.
-
Que los planes establezcan el marco para la futura autorización de proyectos
legalmente sometidos a evaluación de impacto ambiental y se refieran entre
otras materias a las telecomunicaciones, a la ordenación del territorio urbano y
rural, o del uso del suelo.
La materia objeto del Plan se encuadra dentro de la
categoría “telecomunicaciones” y obviamente establece el marco para la
autorización de proyectos, pues tal y como se desprende de la información
suministrada por la Dirección General de Telecomunicaciones, el Plan Nacional
5G de España prevé la realización de proyectos piloto para probar las nuevas
funcionalidades que ofrecerá la tecnología 5G. En particular, al amparo de Plan
Nacional 5G, se han convocado 2 proyectos piloto por la entidad pública Red.es,
que han sido adjudicados por dicha entidad mediante Resolución del 30 de abril
de 2019. Por tanto, el Plan sirve de marco para la autorización de proyectos.
La Ley establece otros requisitos alternativos para planes que también deben
someterse a evaluación, por ejemplo, que afecten de forma apreciable a espacios Red
Natura 2000.
A la vista de las dudas que pueden suscitarse sobre la concurrencia de los
requisitos necesarios para efectuar dicha evaluación, resulta significativo que esa
Secretaría de Estado no consultara en su momento al órgano ambiental acerca de la
procedencia de tramitar dicha evaluación. Debe recordarse que la Administración sirve
con objetividad los intereses generales y actúa de acuerdo con los principios de eficacia
y coordinación, con sometimiento pleno a la ley y al Derecho, lo cual habilita el órgano
sustantivo para consultar al órgano ambiental si existen dudas sobre la procedencia de
aplicar la Ley 21/2013, cuyos preceptos vinculan a todas las administraciones públicas.
El artículo 2 h) de la Ley establece un principio de colaboración activa entre los órganos
que intervienen en el proceso de evaluación; y según el artículo 3.1, las
Administraciones que puedan estar interesadas en el plan, debido a sus
responsabilidades medioambientales, serán consultadas sobre la información
proporcionada por el promotor y sobre la solicitud de adopción o aprobación de un plan.
Finalmente, la Ley prevé la posibilidad de que el órgano ambiental decida someter a
una evaluación simplificada un plan cuando se cumplan los requisitos del Anexo V de la
Ley 21/2013 entre los que se incluyen los riesgos para la salud humana o el medio
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ambiente y la magnitud y el alcance espacial de los efectos (área geográfica y tamaño
de la población que puedan verse afectadas). Para ello debe tener conocimiento del
Plan, el cual debe ser remitido por el órgano sustantivo y promotor del Plan.
También debe recordarse que la necesidad de someter el Plan Nacional 5G a este
tipo de evaluación se alegó por varias asociaciones en el trámite de información pública
del Plan. Esta institución no tiene constancia, pues esa Secretaría de Estado no ha
procedido a informar de ello, de cómo se han valorado dichas alegaciones ni si se ha
dado una respuesta motivada acerca de la manera en que se han tenido en cuenta en la
adopción del Plan. Hay que destacar que una de las finalidades de la evaluación
ambiental estratégica es garantizar la participación pública en la toma de decisiones y
garantizar que la variable ambiental se tiene en cuenta adecuadamente en ese proceso
(artículos 2 i) y k), 17.1 d) y siguientes de la Ley 21/2013).
Ello exige que esa Administración incluya el resultado de la información pública y
la manera en que se han tenido en consideración las alegaciones tanto en el análisis
técnico del expediente como en la declaración ambiental estratégica, en los términos
establecidos en los artículos 24 y 25 de la Ley 21/2013 y 3.2 y conexos de la Ley
27/2006 de acceso a la información, participación pública y acceso a la justicia en
materia de medio ambiente. Además, el órgano sustantivo debe publicar en el Boletín
Oficial del Estado, junto con la adopción del Plan, un extracto que incluya los siguientes
aspectos: 1º De qué manera se han integrado en el plan los aspectos ambientales; y 2º
Cómo se ha tomado en consideración en el plan, entre otras cuestiones, los resultados
de la información pública y de las consultas.
En el documento en el que resume el trámite de información pública, disponible
en la página web del Ministerio de Economía y Empresa, no se da respuesta a las
alegaciones planteadas sobre la necesidad de someter el Plan Nacional 5G a evaluación.
Así, aunque se haya celebrado un trámite de información pública, la ausencia de
valoración de alegaciones y de información al público de cómo se han tenido en cuenta
esas alegaciones, la participación pública en el proceso de toma de decisiones ha
resultado incompleta.
Tampoco esa Secretaría de Estado ha informado de que diera traslado al órgano
ambiental de esas alegaciones. Con esta forma de proceder también ha ignorado lo
establecido en el artículo 3.4 de la Ley 21/2013, según el cual, el órgano sustantivo
debe informar al órgano ambiental de cualquier incidencia que se produzca durante la
tramitación del procedimiento administrativo sustantivo de adopción de un plan que
tenga relevancia a los efectos de la tramitación de la evaluación ambiental.
3.
Las consideraciones anteriores conducen a la conclusión de que el Plan
Nacional 5G no se sometió a evaluación ambiental estratégica y que dicha decisión se
adoptó unilateralmente por el órgano sustantivo (y promotor del Plan) sin consultar con
el órgano ambiental sobre la procedencia de efectuar dicha evaluación, aunque el Plan
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podía cumplir los requisitos exigidos de la Ley 21/2013, en incluso podrían suscitarse
dudas en relación con la falta de aprobación formal.
Respecto a esta última cuestión (la necesidad de aprobación formal de los
planes) debe manifestarse que si bien no es irrazonable interpretar que los planes
deben ser aprobados por la Administración que lo elabora (u otra) para ser evaluados
ambientalmente, también es cierto que por la vía de no dictar una norma o un acto que
apruebe formalmente un plan, podría eludirse fácilmente la evaluación, incluso de
planes que cumplieran los demás requisitos señalados por la Ley 21/2013. En el caso del
Plan Nacional 5G se da la contradicción de que siendo indispensable para “situar
a
nuestro entre los países más avanzados en el desarrollo de esta nueva tecnología de
manera que cuando la 5G alcance su madurez tecnológica y comercial, España esté
preparada para aprovechar al máximo las oportunidades de este paradigma
tecnológico”,
no haya sido objeto de aprobación formal y que la Dirección General de
Telecomunicaciones afirme que carece de efectos vinculantes, aunque su contenido se
está cumpliendo.
En todo caso, existen planes estatales (por ejemplo, planes de infraestructuras),
con una naturaleza, finalidad y estructura similar al Plan Nacional 5G (aunque más
detallados y completos), que se han aprobado formalmente y que han sido sometidos a
evaluación ambiental estratégica. Esa Secretaría de Estado sin embargo, no ha
explicado las razones de la falta de aprobación formal del Plan Nacional 5G, pese a la
importancia que atribuye al cumplimiento de su contenido para alcanzar los objetivos
propuestos.
4.
En todo caso, tener en cuenta las consideraciones ambientales en la toma de
decisiones es una exigencia del desarrollo sostenible y, por tanto, los efectos
ambientales de las decisiones públicas deben valorarse aunque para ello no se siga un
procedimiento reglado. El artículo 3 del Tratado de la Unión Europea incluye entre sus
objetivos el establecimiento de "un nivel elevado de protección y mejora de la calidad
del medio ambiente". Y en el mismo sentido, el artículo 11 del Tratado de
Funcionamiento de la UE señala que "las exigencias de la protección del medio ambiente
deberán integrarse en la definición y en la realización de las políticas y acciones de la
Unión, en particular con objeto de fomentar un desarrollo sostenible". A la luz de lo
anterior, puede concluirse que la Secretaría de Estado no ha tenido en cuenta las
consideraciones ambientales a la hora de decidir y aprobar el Plan Nacional 5G.
Esta institución no puede deducir del contenido del Plan Nacional 5G si este
afecta o no apreciablemente al medio ambiente. Sin perjuicio de lo referido a las
emisiones radioeléctricas (sobre lo que se volverá más adelante), la ausencia de
información sobre los lugares de despliegue de nuevas infraestructuras, sobre posibles
afecciones a espacios protegidos, o al paisaje, o al uso del suelo, ponen en evidencia
que la variable ambiental no se ha tomado en consideración. Sin embargo, no puede
obviarse que propio Plan Nacional 5G señala que “el desarrollo de los servicios 5G
supondrá el despliegue masivo de nuevos elementos de red en el territorio español, ya
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sea en
nuevos emplazamientos
o en los emplazamientos que se utilizan para otras
tecnologías y servicios”. Por ello, hubiera sido deseable un mayor grado de definición de
la estrategia de despliegue del tecnología y, como se ha dicho, que se hubiera recabado
el criterio del órgano ambiental respecto a la necesidad de practicar una evaluación
reglada del Plan. Incluso en el caso de que la afección ambiental del Plan Nacional 5G
no sea significativa, la valoración de la variable ambiental debería haberse incluido en
el proceso de adopción del Plan y haberse tomado en consideración, al menos para
justificar que no era necesaria una evaluación ambiental estratégica, conforme a los
requisitos exigidos por la Ley 21/2013.
5.
Señalado lo anterior, existe escaso margen de maniobra para subsanar la falta
de evaluación y de valoración de los aspectos ambientales en la adopción del Plan
nacional 5G. Por un lado, el artículo 9 de la Ley 21/2013, determina la falta de validez
de los planes que han omitido la evaluación ambiental estratégica preceptiva. Sin
embargo, puesto que el Plan Nacional 5G no ha sido objeto de aprobación formal y
carece de efectos jurídicos vinculantes, la falta de validez pierde su sentido en este
caso. Además, el Plan diseña las directrices de actuación hasta 2020, de manera que el
ámbito temporal de la planificación está próximo a su fin. Dada esta situación, esta
institución solo puede concluir sobre este punto que el Plan Nacional no ha tenido en
consideración los aspectos ambientales del Plan y no los ha valorado ni siquiera a
efectos de justificar que no era exigible una evaluación reglada conforme a la Ley
21/2013.
6.
En relación con la evaluación de impacto ambiental de los proyectos piloto
adjudicados, debe señalarse que esa Secretaría de Estado no se ha referido en ningún
momento al artículo 7 de la Ley 21/2013 en el que se establecen los requisitos de
evaluación de impacto ambiental proyectos. Conforme a este artículo, deben ser objeto
de evaluación de impacto ambiental ordinaria los comprendidos en el anexo I; y deben
ser objeto de evaluación de impacto ambiental simplificada, entre otros, cualquier
proyecto que pueda afectar de forma apreciable a lugares de la Red Natura 2000 que no
esté incluido en el anexo I.
De la información disponible sobre los dos proyectos piloto adjudicados en
Andalucía y Galicia, no parece que se incluyan en alguno de los supuestos enumerados
en el anexo I de la Ley. Por otro lado parece que las actuaciones se van a desarrollar en
entornos urbanos, en parques tecnológicos, en instalaciones portuarias y otros entornos
altamente antropizados, de manera que es posible que los proyectos piloto no afecten
apreciablemente a lugares de la Red Natura 2000. No obstante, ello es una mera
suposición, dada la falta total de valoración de los efectos ambientales de los proyectos
por parte del órgano sustantivo o del órgano ambiental, incluso para justificar que dicha
evaluación no es necesaria, de acuerdo con lo exigido por la Ley 21/2013.
Debe destacarse que para justificar la falta de evaluación de los proyectos
piloto, esa Secretaría de Estado se refiere en todo momento a lo dispuesto en la Ley
9/2014 General de Telecomunicaciones y no a los requisitos exigidos en la Ley 21/2013.
12 de 17
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Tel.: (+34) – 91 432 79 00 Fax: (+34) – 91 308 11 58
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[email protected]
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Respecto a esta cuestión es necesario aclarar que la exención de
licencia ambiental
que
efectúa la Ley General de Telecomunicaciones respecto a los proyectos en esta materia
no alcanza al procedimiento de evaluación de impacto ambiental, que será obligatoria
cuando los proyectos reúnan los requisitos establecidos en la Ley 21/2013.
La legislación estatal en materia de evaluación ambiental es transposición de una
Directiva comunitaria de obligado cumplimiento que no ampara que las normas excluyan
una determinada categoría de proyectos del deber de evaluar si estos pudieran tener
efectos negativos y apreciables sobre el medio ambiente. Es decir, por aplicación de la
Ley de Telecomunicaciones no puede argumentarse
a priori
que ningún proyecto en la
materia tiene efectos apreciables sobre el medio ambiente y, que por tanto, en ningún
caso será exigible la evaluación que regula la Ley 21/2013. Al contrario, los proyectos
en materia de telecomunicaciones deberán someterse a evaluación de impacto
ambiental reglada si cumplen los requisitos establecidos en la Ley 21/2013; y no
deberán someterse si no los cumplen.
Otra cosa distinta es que, caso por caso, la Administración decida
motivadamente que un proyecto concreto no debe ser sometido a evaluación de
impacto ambiental antes de su autorización (aunque reúna los requisitos legales para
ello), cuando se dé alguno de los supuestos regulados en el artículo 8 de la Ley 21/2013,
es decir, proyectos en materia de defensa, emergencia civil, infraestructuras críticas
etcétera. Pero incluso en estos casos es preciso que el órgano sustantivo valore si es
necesario someter el proyecto a otra forma alternativa de evaluación y que dicha
valoración se ponga a disposición del público y se comunique a la Unión Europea antes
de su aprobación.
7.
En relación con el estado del conocimiento científico sobre los efectos de la
tecnología 5G en la salud, debe reiterarse que esta institución confía en la información
suministrada por las autoridades científicas y sanitarias. No obstante, también debe
señalarse lo siguiente:
1º Sin perjuicio de la Recomendación 1999/519CE del Consejo de Sanidad de la
UE, España es también miembro del Consejo de Europa y debe seguir las
recomendaciones que aprueba, entre ellas la Recomendación 1815 (2011) sobre los
peligros potenciales de los campos electromagnéticos y sus efectos sobre el medio
ambiente. En esa Recomendación se insta a los Estados miembros, entre otras cosas, a
tener en consideración los principios de precaución y ALARA (mantener los niveles de
exposición tan bajos como sea posible); a adoptar todas las medidas razonables para
reducir la exposición a los CEM, en particular de niños y jóvenes; a prestar especial
atención a las personas electrosensibles que sufren síndrome de intolerancia a los
campos electromagnéticos; a llevar a cabo los procedimientos de evaluación de riesgos
apropiados y mejorar los estándares de evaluación; y a mantener las instalaciones
eléctricas a una distancia segura de las viviendas. La Recomendación requiere por tanto
que determinados colectivos vulnerables tengan una consideración específica más allá
de los niveles de exposición establecidos para el conjunto de la población. Dicha
13 de 17
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atención específica no se encuentra ni en el Plan Nacional 5G ni en la adjudicación de
los proyectos piloto.
Si bien esta institución comparte el criterio de que no deben imponerse límites
arbitrarios, desautorizando o desconfiando de la regulación existente basada en el
conocimiento científico, tampoco la Administración ha justificado concluyentemente
que no deba atenderse la Recomendación del Consejo de Europa de prestar especial
atención a determinados colectivos vulnerables.
2º Esa Secretaría de Estado dice que, en lo que se refiere a los límites de las
emisiones radioeléctricas, estos límites no dependen de la tecnología utilizada (4G o
5G) sino de las características específicas de cada banda de frecuencias; y que las
bandas que se van a utilizar para la tecnología 5G van a ser las que ya se utilizan a nivel
masivo en España, con la única excepción de la banda de 26 GHz. Esta banda, según
afirma esa Administración, aún no ha sido adjudicada para el uso de 5G para servicios
comerciales masivos; y los organismos internacionales de normalización ya están
trabajando en una norma técnica que cubra el cálculo y procedimiento de medida de
emisiones en la banda de 26 GHz.
Esta información ratifica lo señalado por el Comité Científico sobre
Radiofrecuencias y Salud (CCARS) en su informe en esta materia para 2013-2016 en el
que se refiere expresamente a la ausencia de datos sobre límites de exposición de la
tecnología 5G en bandas superiores a 6GHz “pues
están aún en proceso de discusión,
definición y posterior estandarización, la cual no se espera cerrar antes del año 2020.”.
Dicho lo anterior, debe señalarse que si bien la utilización de la banda de 26 GHz
puede no ser masiva, como dice esa Secretaría de Estado, esta institución ha podido
comprobar que las bases reguladoras de la adjudicación de los proyectos piloto
contempla la utilización de la banda de 26 GHz y esta se valora “particularmente” en
los criterios de selección de proyectos (artículo 13 b) y anexo III) de la Orden
ECE/1016/2018, de 28 de septiembre, por la que se establecen las bases reguladoras de
la concesión de subvenciones a proyectos piloto de tecnología 5G).
Además, en los proyectos piloto hasta ahora adjudicados en Andalucía y Galicia,
según la información suministrada por Red.es (una entidad pública empresarial del
Ministerio de Economía y Empresa que depende de esa Secretaría de Estado) se prevé
que el despliegue de la tecnología 5G se realice en las bandas 3.7 y 26 GHz. Ello
significa que se va a utilizar una banda –la de 26 GHz- para la cual aún no se han fijado
los niveles de exposición seguros.
Este supuesto es el ámbito propio de la aplicación del principio de precaución o
cautela. Según este principio, cuando una actividad representa una amenaza o un daño
para la salud humana o el medio ambiente, hay que tomar medidas de precaución
incluso cuando la relación causa-efecto no haya podido demostrarse científicamente de
forma concluyente.
14 de 17
Paseo de Eduardo Dato, 31 – 28010 Madrid
Tel.: (+34) – 91 432 79 00 Fax: (+34) – 91 308 11 58
www.defensordelpueblo.es
[email protected]
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El principio de precaución se menciona en el artículo 191 del Tratado de
Funcionamiento de la Unión Europea con el fin de garantizar un elevado nivel de
protección del medio ambiente aunque su ámbito de aplicación es más amplio y se
extiende a la salud humana, animal y vegetal.
Por su parte, el Real Decreto 1066/2001, por el que se aprueba el Reglamento
que establece condiciones de protección del dominio público radioeléctrico,
restricciones a las emisiones radioeléctricas y medidas de protección sanitaria frente a
emisiones radioeléctricas, alude a este principio en el artículo 7, cuando impone al
Ministerio de Sanidad el deber de adaptar al progreso científico los límites de exposición
a las emisiones radioeléctricas, teniendo en cuenta el principio de precaución y las
evaluaciones realizadas por las organizaciones nacionales e internacionales
competentes.
La Comunicación de la Comisión sobre el recurso al principio de precaución (COM
(2000) 1 final de 2.2.2000), señala que las medidas basadas en el principio de
precaución deberán ser proporcionales al nivel de protección elegido, no
discriminatorias en su aplicación, coherentes con medidas similares ya adoptadas,
basadas en el examen de los posibles beneficios y los costes de la acción o de la falta de
acción, estar sujetas a revisión, a la luz de los nuevos datos científicos, y ser capaces de
designar a quién incumbe aportar las pruebas científicas necesarias para una evaluación
del riesgo más completa.
Obviamente, el análisis de estos aspectos y del potencial riesgo para la salud del
empleo de la tecnología 5G a través de la banda de 26 GHz excede las funciones de esta
institución y requiere la intervención de órganos y administraciones públicas distintas de
esa Secretaría de Estado, entre ellas las sanitarias. La disposición adicional décima de la
Ley de Telecomunicaciones prevé la creación de la Comisión Interministerial sobre
Radiofrecuencias y Salud que debe ser el órgano, a nivel estatal, apto para abordar
estas cuestiones de manera coordinada. La Comisión tiene por función asesorar e
informar a la ciudadanía, al conjunto de las administraciones públicas y a los diversos
agentes de la industria sobre las restricciones establecidas a las emisiones
radioeléctricas, las medidas de protección sanitaria aprobadas frente a emisiones
radioeléctricas y los múltiples y periódicos controles a que son sometidas las
instalaciones generadoras de emisiones radioeléctricas, en particular, las relativas a las
radiocomunicaciones.
Asimismo, dicha Comisión debe realizar y divulgar estudios e investigaciones
sobre las emisiones radioeléctricas y sus efectos y cómo las restricciones a las
emisiones, las medidas de protección sanitaria y los controles establecidos preservan la
salud de las personas, así como, a la vista de dichos estudios e investigaciones, realizará
propuestas y sugerirá líneas de mejora en las medidas y controles a realizar.
15 de 17
Paseo de Eduardo Dato, 31 – 28010 Madrid
Tel.: (+34) – 91 432 79 00 Fax: (+34) – 91 308 11 58
www.defensordelpueblo.es
[email protected]
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De la Comisión interministerial formarán parte en todo caso, además del órgano
competente en materia de telecomunicaciones, el Ministerio de Sanidad y el Instituto
de Salud Carlos III. Contará además con un grupo asesor o colaborador en materia de
radiofrecuencias y salud, con participación de comunidades autónomas, de la asociación
de entidades locales de ámbito estatal con mayor implantación y un grupo de expertos
independientes, sociedades científicas y representantes de los ciudadanos, para hacer
evaluación y seguimiento periódico de la prevención y protección de la salud de la
población en relación con las emisiones radioeléctricas, proponiendo estudios de
investigación, medidas consensuadas de identificación, elaboración de registros y
protocolos de atención al ciudadano.
Dicha Comisión aún no se ha constituido a pesar de haberlo sugerido esta
institución al entonces Ministerio de Sanidad, Servicios Sociales e Igualdad en el año
2017 y sin que dicho departamento haya ofrecido razones que justifiquen desatender el
mandato de la Ley. A la vista de las consideraciones expuestas, en particular el
despliegue de la tecnología 5G a través de una banda para la que no se han establecido
niveles de exposición a emisiones radioeléctricas seguras, su constitución resulta
ineludible, con el fin de que se pronuncie sobre la aplicación del principio de
precaución en este caso.
A juicio de esta institución no puede ignorarse que existe una preocupación
ciudadana por los efectos del despliegue de esta nueva tecnología y que sus
reclamaciones sobre los efectos de los campos electromagnéticos en la salud empiezan
a ser atendidas por los tribunales de justicia, los cuales reconocen, en virtud de los
informes médicos aportados, determinadas patologías por exposición a emisiones
radioeléctricas.
La Administración puede estar convencida de la inocuidad de las emisiones
cuando se respetan los valores de seguridad fijados por la Comisión Internacional para la
Protección ante Radiaciones No Ionizantes (ICNIRP), por debajo de los cuales no se han
reproducido efectos biológicos en las personas. Pero ello no le exime de poner en
marcha los mecanismos previstos en la legislación en materia de investigación,
asesoramiento, participación e información pública, ni de valorar y aplicar las medidas
de precaución necesarias para asegurarse de que el despliegue de la nueva tecnología
no suponga perjuicios para la salud, especialmente cuando aún no se han determinado
los niveles de exposición segura para una determinada banda de frecuencia, cuyo uso,
sin embargo, se ha autorizado.”.
En virtud de las consideraciones expuestas, y de conformidad con los artículos 28
y 30 de la Ley Orgánica 3/1981, de 6 de abril, el Defensor del Pueblo ha resuelto dirigir
a la Secretaría de Estado para el Avance Digital las siguientes resoluciones:
16 de 17
Paseo de Eduardo Dato, 31 – 28010 Madrid
Tel.: (+34) – 91 432 79 00 Fax: (+34) – 91 308 11 58
www.defensordelpueblo.es
[email protected]
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Las políticas de privacidad y el tratamiento de los datos de carácter personal se realizan conforme a lo dispuesto en el Reglamento (UE) 2016/679 del Parlamento Europeo y del Consejo de 27 de abril de 2016 relativo a la protección de las personas
físicas en lo que respecta al tratamiento de datos personales y a la libre circulación de estos datos (Reglamento general de protección de datos). Puede ejercer sus derechos de acceso, portabilidad, rectificación, supresión y limitación del tratamiento
ante el Defensor del Pueblo en C/ Zurbano 42, 28010 Madrid, así como reclamar ante la Agencia Española de Protección de Datos en www.agpd.es si entiende vulnerados sus derechos.
RECORDATORIO DE DEBERES LEGALES
“Someter los planes y proyectos en materia de telecomunicaciones a
evaluación ambiental estratégica y evaluación de impacto ambiental
respectivamente, cuando reúnan los requisitos establecidos en la Ley
21/2013 de evaluación ambiental”.
SUGERENCIAS
1. “Elaborar, conjuntamente con el Ministerio de Sanidad, Consumo y Bienestar
Social el proyecto de reglamento por el que debe regularse la Comisión
Interministerial sobre Radiofrecuencias y Salud y, tras cumplimentar los
trámites preceptivos, elevarlo al Consejo de Ministros para su aprobación.
2. Una vez constituida, someter a consulta de la Comisión la forma de proceder
respecto a la aplicación del principio de precaución en el desarrollo de
proyectos que impliquen el uso de la banda de 26 GHz, en tanto no se
determinen los límites seguros de exposición a emisiones radioeléctricas
exigibles para dicha frecuencia”.
Asimismo se ha solicitado a la Secretaría de Estado que informe de las medidas
adoptadas para evaluar los posibles efectos sobre la salud que pudieran derivarse de los
proyectos piloto en Andalucía y Galicia; si se ha consultado a dichas Comunidades
Autónomas sobre estos proyectos; y si se han adjudicado o se van a adjudicar otros
nuevos durante el ámbito de aplicación temporal del Plan Nacional 5G.
De la respuesta que a dichas resoluciones se reciba, se le informará, así como de
las actuaciones que procedan.
Le saluda muy atentamente,
Francisco Fernández Marugán
Defensor del Pueblo (e.f.)
El presente documento es una copia fiel de un documento sellado electrónicamente mediante un certificado emitido por la Fábrica Nacional de Moneda y Timbre para
actuaciones administrativas automatizadas.
17 de 17
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[email protected]
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BILAG 5
Faktaboks med overblik over Johansens industriarbejde
▪
1994/95:
Modtager forskningsmidler fra teleindustrien
–
Sonofon og Tele Danmark Mobil
–
til en
abonnentsdatabase, der anvendes til det såkaldte Interphone-studie.
Den danske del af studiet, ”The Danish
Cohort”, kritiseres for selve anvendelsen af kontrolgruppen, hvori erhvervsbrugere indgår sammen med borgere,
der ikke bruger mobiltelefon.
▪ 1994-2004:
Modtager midler fra Dansk Energi. Bestilt forskning vedrører skadeligheden af
højspændingsmaster og børn med bopæl tæt herpå samt de ansatte ved elselskaberne.
▪
1994-2007:
Modtager tre personlige honorarer fra COWI. Disse har også relation til højspænding.
▪
1994-2010:
Modtager fire personlige honorarer af ukendt størrelse fra Energinet.dk, en interesseorganisation
for danske energileverandører, heriblandt elselskaber. Hans honorarer uddeles for konsulentbistand til VVM-
rapporter om højspænding, fremgår det.
▪ 2006:
Modtager fornyet forskningsbevilling fra Energinet.dk. .
▪
2017, efterår:
Indgår ny kontrakt med COWI og orienterer SST herom. Emnet er rådgivning inden for
elektromagnetiske felter, som han også rådgiver Sundhedsstyrelsen om.
Kilde: Forskning.dk
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Contents lists available at
ScienceDirect
Toxicology Letters
journal homepage:
www.elsevier.com/locate/toxlet
Adverse health effects of 5G mobile networking technology under real-life
conditions
Ronald N. Kostoff
a,
*,
Paul Heroux
b
, Michael Aschner
c
, Aristides Tsatsakis
d,e
a
Research Affiliate, School of Public Policy, Georgia Institute of Technology, Georgia, United States
Toxicology and Health Effects of Electromagnetism, McGill University, Canada
c
Molecular Pharmacology, Einstein Center of Toxicology, Albert Einstein College of Medicine, United States
d
Laboratory of Toxicology, Medical School, University of Crete, Voutes, 71409 Heraklion, Crete, Greece
e
Department of Analytical, Toxicology, Pharmaceutical Chemistry and Pharmacognosy, Sechenov University, 119991 Moscow, Russia
b
G R A PHIC A L A B S TR A C T
A R TIC L E INFO
Keywords:
Electromagnetic fields
Wireless radiation
Non-ionizing radiation
Mobile networking technology
5G
Adverse health effects
Toxicology
Toxic stimuli combinations
Synergistic effects
Combined effects
Systemic effects
Real-life simulation
A B S TR A C T
This article identifies adverse effects of non-ionizing non-visible radiation (hereafter called wireless radiation)
reported in the premier biomedical literature. It emphasizes that most of the laboratory experiments conducted
to date are not designed to identify the more severe adverse effects reflective of the real-life operating en-
vironment in which wireless radiation systems operate. Many experiments do not include pulsing and mod-
ulation of the carrier signal. The vast majority do not account for synergistic adverse effects of other toxic stimuli
(such as chemical and biological) acting in concert with the wireless radiation. This article also presents evidence
that the nascent 5G mobile networking technology will affect not only the skin and eyes, as commonly believed,
but will have adverse systemic effects as well.
1. Introduction
Wireless communications have been expanding globally at an
exponential rate. The latest imbedded version of mobile networking
technology is called 4G (fourth generation), and the next version (called
5G- fifth generation) is in the early implementation stage. Neither 4G
⁎
Corresponding author.
E-mail addresses:
rkostoff@gmail.com
(R.N. Kostoff),
[email protected]
(A. Tsatsakis).
https://doi.org/10.1016/j.toxlet.2020.01.020
Received 12 December 2019; Received in revised form 16 January 2020; Accepted 23 January 2020
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R.N. Kostoff, et al.
nor 5G have been tested for safety in credible real-life scenarios.
Alarmingly, many of the studies conducted in more benign environ-
ments show harmful effects from this radiation. The present article
overviews the medical and biological studies that have been performed
to date relative to effects from wireless radiation, and shows why these
studies are deficient relative to safety. However, even in the absence of
the missing real-life components such as toxic chemicals and biotoxins
(which tend to exacerbate the adverse effects of the wireless radiation),
the literature shows there is much valid reason for concern about po-
tential adverse health effects from both 4G and 5G technology. The
studies on wireless radiation health effects reported in the literature
should be viewed as extremely conservative, substantially under-
estimating the adverse impacts of this new technology.
2. Wireless radiation/electromagnetic spectrum
This section overviews the electromagnetic spectrum, and deline-
ates the parts of the spectrum on which this article will focus. The
electromagnetic spectrum encompasses the entire span of electro-
magnetic radiation, including:
communications frequencies in this document.
3. Modern wireless radiation exposures
In ancient times, sunlight and its lunar reflections provided the bulk
of the visible spectrum for human beings (with fire a distant second and
lightning a more distant third). Now, many varieties of artificial light
(incandescent, fluorescent, and light emitting diode) have replaced the
sun as the main supplier of visible radiation during waking hours.
Additionally, EMF radiations from other parts of the non-ionizing non-
visible spectrum have become ubiquitous in daily life, such as from
wireless computing and telecommunications. In the last two or three
decades, the explosive growth in the cellular telephone industry has
placed many residences in metropolitan areas within less than a mile of
a cell tower. Future implementation of the next generation of mobile
networking technology, 5 G, will increase the cell tower densities by an
order of magnitude. Health concerns have been raised about wireless
radiation from (1) mobile communication devices, (2) occupational
exposure, (3) residential exposure, (4) wireless networks in homes,
businesses, and schools, (5) automotive radar, and (6) other non-io-
nizing EMF radiation sources, such as ‘smart meters’ and ‘Internet of
Things’.
4. Demonstrated biological and health effects from prior
generations of wireless networking technology
There have been two major types of studies performed to ascertain
biological and health effects of wireless radiation: laboratory and epi-
demiology. The laboratory tests performed provided the best scientific
understanding of the effects of wireless radiation, but did not reflect the
real-life environment in which wireless radiation systems operate (ex-
posure to toxic chemicals, biotoxins, other forms of toxic radiation, etc).
There are three main reasons the laboratory tests failed to reflect real-
life exposure conditions for human beings.
First, the laboratory tests have been performed mainly on animals,
especially rats and mice. Because of physiological differences between
small animals and human beings, there have been continual concerns
about extrapolating small animal results to human beings. Additionally,
while inhaled or ingested substances can be scaled from laboratory
experiments on small animals to human beings relatively straight-for-
wardly, radiation may be more problematic. For non-ionizing radiation,
penetration depth is a function of frequency, tissue, and other para-
meters. Radiation could penetrate much deeper into a small animal’s
interior than similar wavelength radiation in humans, because of the
much smaller animal size. Different organs and tissues would be af-
fected, with different levels of power density.
Second, the typical incoming EMF signal for many/most laboratory
tests performed in the past consisted of single carrier wave frequency;
the lower frequency superimposed signal containing the information
was not always included. This omission may be important. As
Panagopoulos states: “It is important to note that except for the RF/
microwave carrier frequency, Extremely Low Frequencies - ELFs
(0–3000 Hz) are always present in all telecommunication EMFs in the
form of pulsing and modulation. There is significant evidence in-
dicating that the effects of telecommunication EMFs on living organ-
isms are mainly due to the included ELFs…. While
∼50
% of the studies
employing simulated exposures do not find any effects, studies em-
ploying real-life exposures from commercially available devices display
an almost 100 % consistency in showing adverse effects”
(Panagopoulos,
2019).
These effects may be exacerbated further with
5 G: “with every new generation of telecommunication devices…..the
amount of information transmitted each moment…..is increased, re-
sulting in higher variability and complexity of the signals with the
living cells/ organisms even more unable to adapt” (Panogopoulos,
2019).
Third, these laboratory experiments typically involved one stressor
•
ionizing radiation (gamma rays, x-rays, and the extreme ultraviolet,
•
•
with wavelengths below
∼10
−7
m and frequencies above
∼3 ×
10
15
Hz);
non-ionizing visible radiation (wavelengths from
∼4 ×
10
−7
m to
∼7 ×
10
−7
m and frequencies between
∼4.2 ×
10
14
Hz and
∼7.7 ×
10
14
Hz);
non-ionizing non-visible radiation
short wavelength radio waves and microwaves, with wavelengths
between
∼10
−3
m and
∼10
5
m and frequencies between
∼3 ×
10
11
to
∼3 ×
10
3
Hz;
long wavelengths, ranging between
∼10
5
m and
∼10
8
m and fre-
quencies ranging between 3
×
10
3
and 3 Hz.
How are these frequencies used in practice?
•
The low frequencies (3 Hz – 300 KHz) are used for electrical power
•
•
•
•
line transmission (60 Hz in the U.S.) as well as maritime and sub-
marine navigation and communications.
Medium frequencies (300 KHz–900 MHz) are used for AM/FM/TV
broadcasts in North America.
Lower microwave frequencies (900 MHz – 5 GHz) are used for tele-
communications such as microwave devices/communications, radio
astronomy, mobile/cell phones, and wireless LANs.
Higher microwave frequencies (5 GHz – 300 GHz) are used for radar
and proposed for microwave WiFi, and will be used for high-per-
formance 5 G.
Terahertz frequencies (300 GHz – 3000 GHz) are used increasingly
for imaging to supplement X-rays in some medical and security
scanning applications (Kostoff
and Lau, 2017).
In the present study of wireless radiation health effects, the fre-
quency spectrum ranging from 3 Hz to 300 GHz is covered, with par-
ticular emphasis on the high frequency communications component
ranging from
∼1
GHz to
∼300
GHz. Why was this part of the spectrum
selected? Previous reviews of wireless radiation health effects found
that pulsed electromagnetic fields (PEMF) applied for relatively short
periods of time could sometimes be used for therapeutic purposes,
whereas chronic exposure to electromagnetic fields (EMF) in the power
frequency range (∼60 Hz) and microwave frequency range (∼1 GHz-
tens GHz) tended to result in detrimental health effects (Kostoff
and
Lau, 2013, 2017).
Given present concerns about the rapid expansion of
5G communications systems (which are projected to use mainly the
higher microwave frequencies part of the spectrum in the highest per-
formance (aka high-band) mode) in the absence of adequate and rig-
orous safety testing, more emphasis will be placed on the
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R.N. Kostoff, et al.
(toxic stimulus) and were performed under pristine conditions. This
contradicts real-life exposures, where humans are exposed to multiple
toxic stimuli, in parallel or over time (Tsatsakis
et al., 2016, 2017;
Docea et al., 2019a).
In perhaps five percent of the cases reported in the
wireless radiation literature, a second stressor (mainly a biological or
chemical toxic stimulus) was added to the wireless radiation stressor, to
ascertain whether additive, synergistic, potentiative, or antagonistic
effects were generated by the combination (Kostoff
and Lau, 2013,
2017; Juutilainen, 2008; Juutilainen et al., 2006).
Combination experiments are extremely important because, when
other toxic stimuli are considered in combination either with each other
or with wireless radiation, the synergies tend to enhance the adverse
effects of each stimulus in isolation. This was shown in several studies
that evaluated the cumulative effects of chronic exposure to low doses
of xenobiotics in combination (Kostoff
et al., 2018; Docea et al., 2018;
Tsatsakis et al., 2019a; Docea et al., 2019b; Tsatsakis et al., 2019b, c;
Fountoucidou et al., 2019).
For those combinations that include wire-
less radiation, combined exposure to toxic stimuli and wireless radia-
tion translates into much lower levels of tolerance for each toxic sti-
mulus in the combination relative to its exposure levels that produce
adverse effects in isolation. Accordingly, the exposure limits for wire-
less radiation when examined in combination with other potentially
toxic stimuli would be far lower for safety purposes than those derived
from wireless radiation exposures in isolation.
Thus, almost all of the wireless radiation laboratory experiments
that have been performed to date are flawed/limited with respect to
showing the full adverse impact of the wireless radiation that would be
expected under real-life conditions. Either 1) non-inclusion of signal
information or 2) using single stressors only tends to underestimate the
seriousness of the adverse effects from wireless radiation. Excluding
both
of these phenomena from experiments, as was done in the vast
majority of the reported wireless radiation health effects studies, tends
to amplify this underestimation substantially. Thus, the results reported
in the biomedical literature should be viewed as 1) extremely con-
servative and 2) the very low ‘floor’ of the seriousness of the adverse
effects from wireless radiation, not the ‘ceiling’.
In contrast to the controlled pristine environments that characterize
the wireless radiation animal laboratory experiments, the wireless ra-
diation epidemiology studies carried out to date typically involved
human beings who had been subjected to myriad known and unknown
stressors prior to (and during) the study. The real-life human exposure
levels from cell tower studies (reported by
Kostoff and Lau (2017))
that
showed increased cancer incidence were orders of magnitude lower
than those exposure levels generated in the recent highly-funded Na-
tional Toxicology Program animal laboratory studies (Melnick,
2019).
We believe the inclusion of real-world effects in the cell tower studies
accounted for the orders of magnitude exposure level decreases that
were associated with the increased cancer incidence. The laboratory
tests were conducted under controlled conditions not reflective of real-
life, while the epidemiology studies were performed in the presence of
many stressors, known and unknown, reflective of real-life. The myriad
toxic stimuli exposure levels of the epidemiology studies were, for the
most part, uncontrolled.
A vast literature published over the past sixty years shows adverse
effects from wireless radiation applied in isolation or as part of a
combination with other toxic stimuli. Extensive reviews of wireless
radiation-induced biological and health effects have been published
(Kostoff
and Lau, 2013, 2017; Belpomme et al., 2018; Desai et al., 2009;
Di Ciaula, 2018; Doyon and Johansson, 2017; Havas, 2017; Kaplan
et al., 2016; Lerchl et al., 2015; Levitt and Lai, 2010; Miller et al., 2019;
Pall, 2016, 2018; Panagopoulos, 2019; Panagopoulos et al., 2015;
Russell, 2018; Sage and Burgio, 2018; van Rongen et al., 2009;
Yakymenko et al., 2016; Bioinitiative, 2012).
In aggregate, for the high
frequency (radiofrequency-RF) part of the spectrum, these reviews
show that RF radiation
below the FCC guidelines
can result in:
•
carcinogenicity (brain tumors/glioma, breast cancer, acoustic neu-
romas, leukemia, parotid gland tumors),
•
genotoxicity (DNA damage, DNA repair inhibition, chromatin
structure),
•
mutagenicity, teratogenicity,
•
neurodegenerative diseases (Alzheimer’s Disease, Amyotrophic
Lateral Sclerosis),
•
neurobehavioral problems, autism, reproductive problems, preg-
•
nancy outcomes, excessive reactive oxygen species/oxidative stress,
inflammation, apoptosis, blood-brain barrier disruption, pineal
gland/melatonin production, sleep disturbance, headache, irrit-
ability, fatigue, concentration difficulties, depression, dizziness,
tinnitus, burning and flushed skin, digestive disturbance, tremor,
cardiac irregularities,
adverse impacts on the neural, circulatory, immune, endocrine, and
skeletal systems.
From this perspective, RF is a highly pervasive cause of disease!
The response from industry has been that no mechanism could ex-
plain the biological action of non-thermal and non-ionizing EM fields.
Yet, reports of clear perturbations of biological systems at levels near or
even below 1000
μW/m²
(Bioinitiaive, 2019) were explained by per-
turbations in electron and proton transfers supporting ATP production
in mitochondria (Sanders
et al., 1980; 1985)
exposed to RF or ELF
signals (Li
and Heroux, 2014).
To obtain another perspective on the full spectrum of adverse effects
from wireless radiation, a query was run on Medline to retrieve re-
presentative records associated with adverse EMF effects (mainly, but
not solely, RF). Over 5400 records were retrieved, and the leading
Medical Subject Headings (MeSH) extracted. The categories of adverse
impacts from both approaches match quite well. The adverse health
effects range from myriad feelings of discomfort to life-threatening
diseases.
The full list of MeSH Headings associated with this retrieval is
shown in Appendix 1 of (Kostoff,
2019).
The interested reader can as-
certain what other diseases/symptoms were included. The 5400+ re-
ferences retrieved are shown in Appendix 2 of (Kostoff,
2019).
5. What types of biological and health effects can be expected
from 5G wireless networking technology?
The potential 5G adverse effects derive from the intrinsic nature of
the radiation, and its interaction with tissue and target structures. 4G
networking technology was associated mainly with carrier frequencies
in the range of
∼1-2.5
GHz (cell phones, WiFi). The wavelength of
1 GHz radiation is 30 cm, and the penetration depth in human tissue is a
few centimeters. In its highest performance (high-band) mode, 5G
networking technology is mainly associated with carrier frequencies at
least an order of magnitude greater than the 4G frequencies, although,
as stated previously, “ELFs (0–3000 Hz) are always present in all tele-
communication EMFs in the form of pulsing and modulation”.
Penetration depths for the carrier frequency component of high-band
5G wireless radiation will be on the order of a few millimeters
(Alekseev
et al., 2008a, b).
At these wavelengths, one can expect re-
sonance phenomena with small-scale human structures (Betzalel
et al.,
2018).
Additionally, numerical simulations of millimeter-wave radia-
tion resonances with insects showed a general increase in absorbed RF
power at and above 6 GHz, in comparison to the absorbed RF power
below 6 GHz. A shift of 10 % of the incident power density to fre-
quencies above 6 GHz was predicted to lead to an
increase in absorbed
power between 3–370
% (Thielens
et al., 2018).
The common ‘wisdom’ presented in the literature and media is that,
if there are adverse impacts resulting from high-band 5 G, the main
impacts will be focused on near-surface phenomena, such as skin
cancer, cataracts, and other skin conditions. However, there is evidence
that biological responses to millimeter-wave irradiation can be initiated
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R.N. Kostoff, et al.
within the skin, and the subsequent systemic signaling in the skin can
result in physiological effects on the nervous system, heart, and im-
mune system (Russell,
2018).
Additionally, consider the following reference (Zalyubovskaya,
1977).
This is one of many translations of articles produced in the
Former Soviet Union on wireless radiation (also, see reviews of Soviet
research on this topic by
McRee (1979, 1980), Kositsky et al. (2001),
and
Glaser and Dodge (1976)).
On p. 57 of the pdf link, the article by
Zalyubovskaya addresses biological effects of millimeter radiowaves.
Zalyubovskaya ran experiments using power fluxes of 10,000,000
μW/
square meter (the FCC (Federal Communications Commission) guide-
line limit for the general public today in the USA), and frequencies on
the order of 60 GHz. Not only was skin impacted adversely, but also
heart, liver, kidney, spleen tissue as well, and blood and bone marrow
properties. These results reinforce the conclusion of Russel (quoted
above) that
systemic results may occur from millimeter-wave radia-
tion.
To re-emphasize, for Zalyubovskaya’s experiments, the incoming
signal was unmodulated carrier frequency only, and the experiment
was single stressor only. Thus, the expected real-world results (when
human beings are impacted, the signals are pulsed and modulated, and
there is exposure to many toxic stimuli) would be far more serious and
would be initiated at lower (perhaps much lower) wireless radiation
power fluxes.
The Zalyubovskaya paper was published in 1977. The referenced
version was classified in 1977 by USA authorities and declassified in
2012. What national security concerns caused it (and the other papers
in the linked pdf reference) to be classified for 35 years, until declas-
sification in 2012? Other papers on this topic with similar findings were
published in the USSR (and the USA) at that time, or even earlier, but
many never saw the light of day, both in the USSR and the USA. It
appears that the potentially damaging effects of millimeter-wave ra-
diation on the skin (and other major systems in the body) have been
recognized for well over forty years, yet today’s discourse only revolves
around the possibility of modest potential effects on the skin and per-
haps cataracts from millimeter-wave wireless radiation.
1) There may be ‘windows’ in parameter space where adverse effects
occur, and operation outside these windows would show a) no ef-
fects or b) hormetic effects or c) therapeutic effects. For example, if
information content of the signal is a strong contributor to adverse
health effects (Panagopoulus, 2019), then experiments that involve
only the carrier frequencies may be outside the window where ad-
verse health effects occur. Alternatively, in this specific example, the
carrier signal and the information signal could be viewed as a
combination of potentially toxic stimuli, where the adverse effects of
each component are enabled because of the synergistic effects of the
combination.
As another example, an adverse health impact on one strain of ro-
dent was shown for a combination of 50 Hz EMF and DMBA, while no
adverse health impact was shown on another rodent strain for the same
toxic stimuli combination (Fedrowitz
et al., 2004).
From a higher-order
combination perspective, if genetic abnormalities/differences are
viewed conceptually as potentially equivalent to a toxic stimulus for
combination purposes, then a synergistic three-constituent combination
of 50 Hz EMF, DMBA, and genetics was required to produce adverse
health impacts in the above experiment. If these results can be extra-
polated across species, then human beings could exhibit different re-
sponses to the same electromagnetic stimuli based on their unique ge-
netic predispositions (Caccamo
et al., 2013; De Luca et al., 2014).
1) Research quality could be poor, and adverse effects were over-
looked.
2) Or, the research team could have had a preconceived agenda, where
finding no adverse effects from wireless radiation was
THE
objective
of the study. For example, studies have shown that industry-funded
research of wireless radiation adverse health effects is far more
likely to show no effects than funding from non-industry sources
(Huss
et al., 2007; Slesin, 2006; Carpenter, 2019).
Studies in dis-
ciplines other than wireless radiation have shown that, for products
of high military, commercial, and political sensitivity, ‘researchers’/
organizations are hired to publish articles that conflict with the
credible science, and therefore create doubt as to whether the pro-
duct of interest is harmful (Michaels,
2008; Oreskes and Conway,
2011).
Unfortunately, given the strong dependence of the civilian
and military economies on wireless radiation, incentives for iden-
tifying adverse health effects from wireless radiation are minimal
and disincentives are many. These perverse incentives apply not
only to the sponsors of research and development, but to the per-
formers as well.
Even the Gold Standard for research credibility -
independent re-
plication of research results
- is questionable in politically, com-
mercially, and militarily sensitive areas like wireless radiation safety,
where the accelerated implementation goals of most wireless radiation
research sponsors (government and industry) are aligned. It is im-
perative that highly objective evaluators with minimal conflicts of in-
terest play a central role ensuring that rigorous safety standards for
wireless radiation systems are met before widescale implementation is
allowed.
7. Conclusions
Wireless radiation offers the promise of improved remote sensing,
improved communications and data transfer, and improved con-
nectivity. Unfortunately, there is a large body of data from laboratory
and epidemiological studies showing that previous and present gen-
erations of wireless networking technology have significant adverse
health impacts. Much of this data was obtained under conditions not
reflective of real-life. When real-life considerations are added, such as
1) including the information content of signals along with 2) the carrier
frequencies, and 3) including other toxic stimuli in combination with
6. What is the consensus on adverse effects from wireless
radiation?
Not all studies of wireless radiation have shown adverse effects. For
example, consider potential genotoxic effects of mobile phone radia-
tion. A study investigating “the effect of mobile phone use on genomic
instability of the human oral cavity's mucosa cells” concluded “Mobile
phone use did not lead to a significantly increased frequency of mi-
cronuclei” (Hintzsche
and Stopper, 2010).
Conversely, a 2017 study investigated buccal cell preparations for
genomic instability, and found “The frequency of micronuclei (13.66x),
nuclear buds (2.57x), basal (1.34x), karyorrhectic (1.26x), karyolytic
(2.44x), pyknotic (1.77x) and condensed chromatin (2.08x) cells were
highly significantly (p = 0.000) increased in mobile phone users”
(Gandhi
et al., 2017).
Also, a 2017 study to ascertain the “effect of cell
phone emitted radiations on the orofacial structures” concluded that
“Cell phone emitted radiation causes nuclear abnormalities of the oral
mucosal cells” (Mishra
et al., 2017).
Further, a 2016 study to “explore
the effects of mobile phone radiation on the MN frequency in oral
mucosal cells” concluded “The number of micronucleated cells/1000
exfoliated buccal mucosal cells was found to be significantly increased
in high mobile phone users group than the low mobile phone users
group” (Banerjee
et al., 2016).
Finally, a study aimed at investigating
the health effects of WiFi exposure concluded “long term exposure to
WiFi may lead to adverse effects such as neurodegenerative diseases as
observed by a
significant alteration on AChE gene expression
and some
neurobehavioral parameters associated with brain damage”
(Obajuluwa
et al., 2017).
There are many possible reasons to explain this lack of consensus.
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R.N. Kostoff, et al.
the wireless radiation, the adverse effects associated with wireless ra-
diation are increased substantially. Superimposing 5G radiation on an
already imbedded toxic wireless radiation environment will exacerbate
the adverse health effects shown to exist. Far more research and testing
of potential 5G health effects under real-life conditions is required be-
fore further rollout can be justified.
Transparency document
The
Transparency document
associated with this article can be
found in the online version.
Declaration of Competing Interest
The authors declare that they have no known competing financial
interests or personal relationships that could have appeared to influ-
ence the work reported in this paper.
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The International Commission on Non-Ionizing Radiation Protection: Conflicts of interest ,
corporate capture and the push for 5G
Klaus Buchner
and
Michèle Rivasi
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Table of Contents
Foreword by Klaus Buchner and Michèle Rivasi:
3-5
I - Introduction & Scope
6-19
II - Historic overview of ICNIRP and accusations of COI
20-34
III- Discussion & Controversies
35-46
IV
–
Conclusion
V
–
Portraits of ICNIRP Members
47-49
50-95
Annex I: Questions to ICNIRP
Annex II: Questions to WHO EMF Project
96
97
The International Commission on Non-Ionizing Radiation Protection: Conflicts of interest,
corporate interests and the push for 5G
Brussels June 2020
This report was commissioned, coordinated and published by two Members of the European
Parliament
–
Michèle Rivasi (Europe Écologie) and Klaus Buchner (Ökologisch-Demokratische
Partei), and financed by the Greens/EfA group in the European Parliament.
The report was written by Hans van Scharen with editing and additional research support
from Tomas Vanheste. Final Editing: Erik Lambert
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Foreword by Klaus Buchner and Michèle Rivasi
This report deals with an issue of which the importance cannot be overrated: the possible health
effects of Radiofrequency Radiation (RfR) or electro magnetic fields (EMF); It deals more specifically
with how the scientific debate has been hijacked by corporate interests from the Telecom industry.
After having read the reports of a journalistic collective called Investigate Europe, the many articles
from Microwave News as well as all the publications from independent scientists from around the
world, who for years have all been ringing alarm bells on adverse health effects from the use of
mobile phones and EMF, we decided that we needed to dig deeper into this strange, unknown to the
public but powerful scientific NGO
ased i Ge a
alled the I te ational
Commission on Non-
Io izi g Radiatio P ote tio ICNIRP .
The fi di gs of this epo t The I te atio al Co
issio o No
-Ionizing Radiation Protection:
Co fli ts of i te est a d the push fo G gi e us a u o fo ta le déjà-vu:
many facts and
processes that lead to the actual situation whereby European authorities
–
from the European
Commission to most of the member states
–
simply close their eyes for real scientific facts and early
warnings. We have seen exactly the same scenario in the debate on Tobacco, asbestos, climate
change and pesticides.
Also i it s latest guideli es f o Ma h this ea , ICNIRP assu es the o
ld that there is no scientific
evidence of adverse health effects from the radiation that comes with the new communication
technologies, within the limits it proposes. But at the same time a growing number of scientists and
also citizens are worried that EMFs do cause health problems. ICNIRP pretends to be scientifically
neutral, and free from vested interests of the Telecom industry. We show with this study that this is
pla i g ith the t uth o si pl a lie.
Already in 2011 Dr. Jacqueline McGlade, Executive Director of the European Environment Agency
said o
o ile pho es a d the pote tial head a e isk fo EMF: The European
Parliament has
responded (resolution of April 2009) to this public concern with a resolution on EMF in 2009 which,
among other things, called for lowering exposure to electromagnetic fields and for lower exposure
limits that would better protect the
pu li f o health haza ds. We sha e these e o
e datio s.
McGlade pleaded interim actions to protect public health, particularly for children on the basis of the
precautionary principle, as central to public policymaking where there is scientific uncertainty and
high health, environmental and economic costs in acting, or not acting, when faced with conflicting
evidence of potentiall
se ious ha . This is p e isel the situatio that ha a te ises EMF at this
point in its history. Waiting for high levels of proof before taking action to prevent well known risks
can lead to very high health and economic costs, as we have seen with asbestos, leaded petrol and
s oki g, said M Glade.
The EEA plea for a precautionary approach to policy making in this area, is based on an evaluation of
the e isti g e ide e a d o the lesso s f o ea lie haza ds, a al sed i the EEA
Late Lessons
from Early Warnings
p oje t. Da id Gee, EEA Se io Ad isor
on Science, Policy and Emerging
Issue and on the
d i e s of this p oje t said: Mo ile pho es ha e u e ous so ial, e o o i a d
e
e e i o e tal e efits , said. Ho e e , the e is sig ifi a t disag ee e t i the s ie tifi
community about whether mobile phone use increases the risk of head cancers. We recommend
using the precautionary principle to guide policy decisions in cases like this. This means that although
our understanding is incomplete, this should not prevent policy makers from taking preventative
a tio .
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In a recent discussion Gee stated that there are several striking similarities between
5G/radiofrequency radiatio
a d a of the te h ologies o su sta es that featu ed i the Late
Lesso s ase studies. Gee poi ted to
a lot of hubristic hype surrounded the introduction of the
new technology
.
Gee rightfully points to a marketing hype which
is idesp ead o
5G and a
failure to systematically and independently scrutinise the claimed benefits and costs of the new
technology . He sees a gross imbalance between research on developing and promoting the
technology and on anticipating and reducing potential harm to people and environments as well as
a failure to ensure independent research into health and environmental effects that can help
combat manufactured
dou t .
Gee was tough for the scientific community because scientists fail to acknowledge what they do not
know and to properly understand and embrace knowledge from other relevant disciplines .
Gee also sees
a
failure of scientists to be transparent about the paradigms, assumptions,
judgements and values used in academic science and in their evaluations of scientific evidence in
regulatory science. A failure of scientists and policymakers to appreciate complex and variable
realities; multi-causality; and the likelihood of inconsistent scientific results. A failure by
policymakers to understand the difference between the high strength of evidence needed to
establish robust scientific knowledge and the case specific appropriate strength of evidence needed
to justify timely preventive action.
Late lessons from early warnings, is indeed also a clear pattern that rises from this report. And there
have been more and more warnings (but unfortunately so far no lessons learned).
Also the Council of Europe adopted
i Ma
a st o g esolutio o the pote tial da ge s of
electromagnetic fields and their
effe t o the e i o e t i hi h it alled upo go e
e ts to
take all reasonable measures to reduce exposure to electromagnetic fields and said about ICNIRP:
It
is most curious, to say the least, that the applicable official threshold values for limiting the health
impact of extremely low frequency electromagnetic fields and high frequency waves were drawn up
and proposed to international political institutions (WHO, European Commission, governments) by
the ICNIRP, an NGO whose origin and structure are none too clear and which is furthermore
suspected of having rather close links with the industries whose expansion is shaped by
recommendations for maximum threshold values for the different frequencies of electromagnetic
fields .
In an article,
Pla etary electro ag etic pollutio : it is ti e to assess its i pact
, published in
The Lancet (December
2018) scientists from the Australian research group ORSAA state that out of
studies o EMFs, o less tha
pe e t fou d sig ifi a t iologi al effe ts o health effe ts .
Significant biological effects do not necessarily mean that human health will be harmed, but is an
important indicator for risk assessment and then for risk evaluation by regulators. To us the
atgument that that there is insufficient scientiifc evidence for regulators to act is factual not corect
and simply not true.
The International Agency for Research on Cancer (IARC), a global authority on cancer, concluded in
that adiatio f o
o ile pho es is a possi le head a e isk.
And recently an Advisory
Group has recommended
that IARC should reassess the cancer risks associated with non-ionizing
adiof e ue
adiatio ith high p io it . A o di g to the pa el s epo t, pu lished i The La et,
the group suggests that the new evaluation should take place between 2022 and 2024.
In 2012 a group of 29 independent scientists and health experts from around the world warned in an
i eless te h ologies a d
update of their
Bio Initiative 2007 Report
, a out possi le isks f o
electromagnetic fields
. Ho e e , the a k o ledge that so eti es, s ie e does ot keep pa e
with new environmental exposures that are by-products of useful things we want to buy and use in
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society. So, the deployment runs ahead of knowledge of health risks. It is an old story. This is the case
for EMF (electric
and magnetic fields)
a d RFR Radiof e ue
adiatio .
The Bio I itiati e epo t u de s o es the iti al eed to fa e diffi ult uestio s, ake id-course
corrections, and try to repair the damage already done in this generation, and to think about
p ote ti g futu e ge e atio s .
And they state that the existing public safety limits as formulated by the US regulator FCC and by
ICNIRP do not sufficiently protect public health against chronic exposure from very low-intensity
e posu es: If o id-course
corrections are made to existing and outdated safety limits, such delay
will magnify the public health impacts with even more applications of wireless-enabled technologies
exposing even greater populations around the
o ld i dail life.
In 2017, more than 200 doctors and scientists from various countries launched the, so-called
5G
Appeal
, that has since received more endorsements and whose mission statement starts with :
We
the u de sig ed s ie tists a d do to s … , e o
e d a o ato iu o the oll-out
of the
fifth generation, 5G, for telecommunication until potential hazards for human health and the
environment have been fully investigated by scientists
i depe de t f o i dust .
Since then there have been five replies on this Appeal by the European Commission, the last one
dati g f o De e e
. The fi st epl , the Co
issio states that the Co
issio is ot
aware of any conflicts of interests of members of international bodies such as ICNIRP or the
e e s of SCENIHR . O e of the
leading figures of the appeal
professor Lennart Hardell
stated
that this «does not represent the scientific evidence of inherent conflicts of interest both in ICNIRP
and SCENIHR. The European Commission seems to be ill-informed or even misinformed, as the EU
seems to take information mainly from these two fraudulent organisations, but not from
independent researchers. The EU does not seem to rely on sound science and thereby downplays the
RF-
elated isks.
It is clear from this report that ICNIRP itself does not have a sharp definition of conflicts of interest
(CoI
s , o does it ha e a ell-developed
policy to avoid these kinds of conflicts. It is a crying shame
that u de the p ete t of s ie tifi u e tai t ICNIRP, ut espe iall the Eu opea Co
issio a d
member states keep on failing to protect their citizens.
We very much agree with the title and content of the latest publication on Microwave News, which
reads
The Lies Must Stop, Disband ICNIRP - Facts Matter, Now More Than Ever
. There are
two major casualties in this polarised debate: the truth and public health. Both are too important
not to protect with all that we have. That is what we consider as our responsibility as elected
politicians .
By
MEP s
Michèle Rivasi (Europe Écologie) and Dr. Klaus Buchner (Ökologisch-Demokratische Partei)
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Introduction & Scope
In the last few decades, since the introduction, and rapid expansion, of new communication
technologies, there has been a proliferation of electromagnetic fields worldwide. A lot of
countries are now about to roll out 5G networks. The International Commission on Non-
Ionizing Radiation Protection (ICNIRP) assures the world that this can be done safely and that
there is no scientific evidence of adverse health effects within the limits it proposes. But at
the same time a growing number of scientists and also citizens are worried that EMFs do cause
health problems.
It is therefore high time to look into the workings of ICNIRP. If the European Commission and
national governments keep relying on this commission, as is currently the case, we must be
completely sure that it functions wholly independently and that there is no evidence of its
members being in situations of conflicts of interest.
ICNIRP is a non-governmental organisation (NGO) or association, registered in Munich,
specialising in non-ionizing radiation protection. One of the organisation's tasks is to
determine exposure limits for electromagnetic fields used by devices such as cellular phones.
On its website, ICNIRP states that it is a non-profit organisation with a scientific mission, and
that it is fo all e og ised as a official
collaborating non-state actor by the World Health
Organisation (WHO) and the International Labour Organisation (ILO). ICNIRP is consulted by
the European Commission and is linked to many organisations engaged in non-ionizing
radiation (NIR) protection
o ld ide th ough di e se olla o ati e p oje ts .
ICNIRP states that its ai is to p ote t people a d the e i o e t agai st adverse
effects
of NIR. To this e d, it de elops a d disse i ates s ie e-based
advice on limiting exposure
to non-ionizing radiatio
. ICNIRP o ks ith e pe ts f o all o e the o ld, f o a ide
variety of disciplines, including biology, epidemiology, medicine, physics, and chemistry.
ICNIRP s also states that its p ote tio ad i e is ased o u e t s ie tifi k o ledge a
out
the biological effects, and the action mechanisms, of radiation for the whole NIR frequency
range.
To a large extent, the Europea
Co
issio , as ell as the WHO, depe d o the e posu e
guida e a d safet ad i e gi e
ICNIRP. Fu the o e, a EU
member states look to
the EC and WHO for (European) advice on this issue. Therefore, it goes without saying that
ICNIRP has a significant role to play in ensuring the general public is protected against any
possible health risks related to electromagnetic fields (EMF).
In March 2019, in a comprehensive report,
How much is Safe?,
by Investigate Europe,
a
collective of investigative journalists from all over Europe, ICNIRP is described as follows:
ICNIRP is a pa ti ula l i flue tial g oup, as it ot o l e aluates adiatio a d health isk
research, but also provides guidelines for radiation safety limits that most countries use. It is
a private, German-registered organisation located outside Munich, behind a yellow door on
the premises of the German Federal office for radiation protection. Decisions on who to
invite in, are taken by ICNIRP itself.
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The report highlighted the close links that exist between ICNIRP and other important
organisations in the field of health protection.
Most European governments and radiation protection authorities rely mainly on these four
scientific bodies for advice on non-ionizing radiation protection:
-
-
-
-
The international commission on non-ionizing radiation protection, ICNIRP.
The EU Scientific Committee on Health, Environment and Emerging Risk, SCENIHR /
SCHEER.
The World
Health O ga isatio WHO s I te atio al EMF P oject.
The WHO Cancer Unit IARC, International Agency for Research on Cancer.
Investigate Europe
showed the close links between especially the first three
odies. The
groups, however, are to a remarkable deg
ee, staffed the sa e e pe ts, it stated. Of
13
ICNIRP scientists, six are members of at least one other committee. In the WHO group, this
applies fo si out of se e
e e s . The SCENIHR
Working Group on EMF
also counts
two ICNIRP-members.
I ie of the apid e pa sio of EMF s, i pa ti ula i the o te t of the pla ed
deployment of 5G networks in which telecom and media operators have huge financial and
economic vested interests, and given the evidence of closed circles of experts involved in
determining health guidelines in this field, critical scrutiny on the functioning of ICNIRP is
important and necessary.
New guidelines
In March 2020, ICNIRP published
its latest
Guidelines on Limiting Exposure to
Ele t o ag eti Fields
, desig ed fo the p ote tio of hu a s e posed to adiof e ue
electromagnetic fields (RF) in the range 100 kHz to 300 GHz. The guidelines cover many
applications such as 5G technologies, Wi-Fi,
Bluetooth, o ile pho es, a d ase statio s.
This publication replaces and supersedes earlier publications from 1998 and 2010. In a
press
release
from March 11th 2020, the then ICNIRP Chairman, Dr Eric van Rongen (now co-chair)
said: The e ele t o ag eti field guideli es ha e take se e
ears to develop and are
more appropriate than the 1998 guidelines for the higher frequencies that will be used for
5G in the future. We know parts of the community are concerned about the safety of 5G
and we hope the updated guidelines will help put people at ease. When we revised the
guidelines, we looked at the adequacy of the ones we published in 1998. We found that the
previous ones were conservative in most cases, and they would still provide adequate
p ote tio fo u e t te h ologies.
Va Ro ge s
main message was that when the new ICNIRP guidelines are followed 5G is
a solutel safe. He stated: The e guideli es p o ide ette a d o e detailed
exposure
guidance, in particular for the higher frequency range, above 6 GHz, which is of importance
to 5G, and future technologies using these higher frequencies. The most important thing for
people to remember is that 5G technologies will not be able to cause harm when these new
guideli es a e adhe ed to.
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So, this is how ICNIRP presents itself: an independent organisation that gives sound scientific
advice on safety guidelines with respect to non-ionizing radiation and that ensures citizens
remain safe.
However, this description raises doubts on two levels: Firstly, is ICNIRP really independent
and also, are its assurances that non-ionizing radiation is absolutely safe when their
guidelines are applied correct? Our report will focus on the questio
of ICNIRP s
independence, but first, we will briefly outline the current debate around the safety
guidelines.
The health debate
The possible adverse health effects of non-ionizing radiation, mainly microwave radiation
form mobile phones and other wireless devices/infrastructure, is a highly sensitive and
polarising issue. In some countries citizens and scientists plead for the application of the
p e- autio a p i iple i elatio to the olli g out of G et o ks, hilst asso iatio s
such as
ICNIRP maintain that
the ost i po ta t thi g fo people to e e e is that G
te h ologies ill ot e a le to ause ha
he these e guideli es a e adhe ed to.
In 2012 a group of 29 independent scientists and health experts from around the world
published an update of their
Bio Initiative 2007 Report,
a out possi le isks f o
i eless
technologies and electromagnetic
fields . The s ie tists, of hi h te holdi g a edi al
deg ee, still update thei atio ale fo Biologi all
-based Public Exposure Standards for
Electromagnetic Fields (Extremely
low frequency,
ELF and radiofrequency,
RF
assessi g
the latest scientific research and reporting on it. However, they acknowledge that
so eti es, s ie e does ot keep pa e ith e e i o e tal e posu es that a e
-
products of useful things we want to buy and use in society. So, the deployment runs ahead
of knowledge of health risks. It is an old story. This is the case for EMF (electric
and magnetic
fields)
and RFR (Radiofrequency radiation).
The Bio I itiati e epo t u de s o es the iti al eed to fa e diffi ult uestio s, ake id-
course corrections, and try to repair the damage already done in this generation, and to
thi k a out p ote ti g futu e ge e atio s .
And they state that the existing public safety limits as formulated by the US regulator FCC
and by ICNIRP do not sufficiently protect public health against chronic exposure from very
low-intensity
e posu es: If o id-course
corrections are made to existing and outdated
safety limits, such delay will magnify the public health impacts with even more applications
of wireless-enabled technologies exposing even greater populations around the world in
dail
life.
In an article,
Pla eta ele t o ag eti pollutio : it is ti e to assess its i pa t
, published
in
The Lancet Planetary Health
in December 2018, scientists (from the Oceania
Radiofrequency Scientific Advisory Association, ORSAA, and the Institute for Health and the
Environment, of the University at Albany) state that out of 2266 studies on EMFs, no less
tha
pe e t fou d sig ifi a t iologi al effe ts o health effe ts . Sig ifi a t iologi al
effects do not necessarily mean that human health will be harmed, but is an important
indicator for risk assessment and then for risk evaluation by regulators.
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The authors stated that it is high time for a wide-ranging debate on the rapid global
p olife atio of a tifi ial ele t o ag eti fields. The ost ota le is the la ket of
radiofrequency electromagnetic radiation, largely microwave radiation generated for
wireless communication and surveillance technologies, as mounting scientific evidence
suggests that prolonged exposure to radiofrequency electromagnetic radiation has serious
iologi al a d health effe ts.
Unfortunately, this mounting evidence did not result in policy changes, the authors from
ORSAA
o se e. Ho e e , pu li e posu e egulatio s i
ost ou t ies o ti ue to e
based on the guidelines of the
International Commission on Non-Ionizing Radiation
Protection
and Institute of Electrical and Electronics Engineers, which were established in the
1990s on the belief that only acute thermal effects are hazardous. Prevention of tissue
heating by radiofrequency electromagnetic radiation is now proven to be ineffective in
preventing biochemical and physiological interference .
For example, acute non-thermal exposure has been shown by NIH scientists, to alter human
brain metabolism, electrical activity in the brain and systemic immune responses. Chronic
exposure has been associated with increased oxidative stress and DNA damage, and cancer
risk. Laboratory studies, including large rodent studies by the US National Toxicology
Program and Ramazzini Institute of Italy, confirm these biological and health effects in vivo.
As we address the threats to human health from the changing environmental conditions due
to human activity, the increasing exposure to artificial electromagnetic radiation needs to be
i luded i this dis ussio .
The results of the National Toxicology Programme (NTP) the mentioned Lancet-authors
referred to, were presented at the end of 2018. The U.S. Food and Drug Administration
(FDA) nominated radio frequency radiation (RFR) used by cell phones for an NTP study
because of the widespread public use of cell phones and the limited knowledge about
potential health effects from long-term exposure. The study found that high exposure to RFR
(900 MHz) used by cell phones was associated with:
•
•
•
Clear evidence of tumours in the hearts of male rats. The tumours were malignant
schwannomas.
Some evidence of tumours in the brains of male rats. The tumours were malignant
gliomas.
Some evidence of tumours in the adrenal glands of male rats. The tumours were
benign, malignant, or complex combined pheochromocytoma.
However, ICNIRP criticised the NTP-study, saying that it did not prove a link between Radio
Frequency, Electro Magnetic Fields and carcinogenesis. But according to scientists like
Lennart Hardell, an oncologist, professor and researcher at the University hospital in Örebro
in Sweden, the ICNIRP rebuttal of the NTP-study was unfounded. The NTP-study leading
scientist Ronald Melnick recently also published a
comment on
the ICNIRP-note in which he
iti izes ICNIRP s i o e t state e ts a d false lai s .
James Lin, professor at the University of Illinois in Chicago and also editor of the online
journal,
Bioelectromagnetics,
published a remarkable and nuanced
review of the NTP-study
in late 2019. The review is remarkable because, from 2004 to 2016, James Lin was himself a
member of ICNIRP. As stated above, ICNIRP basically dismisses the NTP-study. However,
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basing his conclusions partly on the NTP-study, Lin now questions if the existing safety
guideli es a e still ade uate: A outsta di g uestio pe sists o the ade ua of these
guidelines for safe long-term exposure to RF radiation at or below 1.6 or 2.0 W/kg. Perhaps,
the ti e has o e to judi iousl eassess, e ise, a d update these guideli es.
Li s e ie is ua ed i so u h as he uses the pee
-review process to analyse the
conception
a d all possi le ethodologi al p o le s of the NTP-stud i depth: This
project is the largest NTP animal cancer study ever. It was nominated by the Food and Drug
Administration (FDA) in 1999. The supposedly 5-year project was sole sourced in 2004 to an
i dust ial esea h fi as the p oje t s p i ipal i estigato . The o k ega i
.
However, the project had been protracted for more than a dozen years with huge budget
o e u s, a d a esti ated e e tual p i e tag of $
illio .
Somewhat surprisingly, at the end of his review, Lin advocates for wireless radiation to
get
a more stringent cancer risk class":
No that the NTP e ie pa el has o luded that
there is clear evidence of carcinogenicity from long-term RF exposure in rats, is it
conceivable that IARC would upgrade its epidemiology-based classification of RF exposure to
the next higher levels of car
i oge i it to hu a s? Li see s to suggest that IARC should
put cell phone radiation in WHO-haza
d lass
a i oge i , i stead of toda s B possi l
carcinogenic).
Worldwide, there is rapidly growing concern and a proliferation of publications about EMF,
specifically concerning the out-roll of new generation 5G. On this subject, we will only cite a
2019 in-depth report
alled
5G Deployment: State of Play in Europe, USA, and Asia
1
. It
eads: I eased e posu e a esult, ot o l f o the use of u h highe f e ue ies i
5G, but also from the potential for the aggregation of different signals, their dynamic nature,
and the complex interfe
e e effe ts that a esult, espe iall i de se u a a eas. …
The 5G radio emission fields are quite different to those of previous generations because of
their complex beam-formed transmissions in both directions
–
from base station to handset
and fo
the etu .
The autho s state that ith G e a e e te i g u k o te ito . Although fields a e
highly focused by beams, they vary rapidly with time and movement and so are
unpredictable, as the signal levels and patterns interact as a closed loop system. This has yet
to be mapped reliably for real situations, outside the laboratory. (..) The problem is that
u e tl it is ot possi le to a u atel si ulate o easu e G e issio s i the eal o ld.
The debate on the safety of non-ionizing radiation is fascinating, heated and important, and
has been on-going for at least 30 years. This paper however does
not
go further into the
scientific debate on the possible levels of harm to public health caused by non-ionizing
radiation, mainly from mobile phones. We will focus on the independence of ICNIRP and the
possible existence of conflicts of interest of its members.
A study requested by the ITRE committee of the European Parliament, published in 2019 by
the Policy Department for Economic, Scientific and Quality of Life Policies - Directorate-
General for Internal Policies.
1
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The importance of funding
ICNIRP lai s it is f ee of ested i te ests . ICNIRP's fu di g elies o g a ts f o pu li
bodies. Additionally, ICNIRP members and ICNIRP SEG members may not be employed by
industry.
But ot ei g e plo ed i dust is
not, in itself, sufficient to avoid conflicts of interest.
It is also important to ascertain to what extent ICNIRP research activities may be funded by
industry.
It is a well-established fact that the source of funding for scientific research can have an
influence on the outcomes of research. A clear and precise explanation of how this is may
occur can be found on the website of UC Berkeley:
I a pe fe t o ld, o e ould 't atte —
all scientific studies (regardless of funding
source) would be completely objective. But of course, in the real world, funding may
introduce biases
—
for example, when the backer has a stake in the study's outcome. A
pharmaceutical company paying for a study of a new depression medication, for example,
might influence the study's design or interpretation in ways that subtly favour the drug that
they'd like to market. There is evidence that some biases like this do occur. Drug research
sponsored by the pharmaceutical industry is more likely to end up favouring the drug under
consideration than studies sponsored by government grants or charitable organisations.
Similarly, nutrition research sponsored by the food industry is more likely to end up
favouring the food
u de o side atio tha i depe de tl fu ded esea h.
This does ot lead to the o lusio that e should ig o e a
esea h fu ded
o pa ies o spe ial i te est g oups , Be kele sa s. But it is a easo fo the eed to
scrutinize studies funded by industry or special interest groups with extra care.
So, don't, for
example, brush off a study of cell phone safety just because it was funded by a cell phone
manufacturer
—
but do ask some careful questions about the research before jumping on the
bandwagon.
Are the results consistent with other independently funded studies? Does the
study seem fairly designed? What do other scientists have to say about this research? A little
scrutiny can go a long way towards identifying bias associated with funding
sou e.
A little s uti
is pe haps a u de state e t. I the
, the
Late lesso s f o ea l
a i gs
report produced by the European Environment Agency (EEA), a chapter written by
Lisa A. Bero, describes the various opinions on how to deal with private funding of scientific
research without compromising an independent non-biased outcome and/or publication of
that research.
For example, various researchers argue that it is logical for industry to fund research, in so
much as it is about their products that concerns exist. Former ICNIRP scientist Norbert
Leitgeb, professor at the Institute of Health Care Engineering at the Graz University of
Technology in Austria, told
Investigate Europe
that what is crucial is the putting in place of
effe ti e fi e alls to e su e that p i ate pa t e s a ot i te fe e ith esea
chers and
i flue e s ie tifi out o es o o lusio s .
That the source of funding has an important influence, is also something various ICNIRP-
researchers acknowledge. For example, in 2009 two scientists who are now members of the
ICNIRP-commission
–
Anke Huss and Martin Röösli
–
where co-authors of a systematic
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review
that sho ed that i dust
-sponsored studies were least likely to report results
suggesting effects
. The o luded that the o elatio et ee the sou e of fu di g a d
conflicts of interest are
i po ta t i this field of esea h.
in his evaluation of the NTP-study, another former ICNIRP-member, professor James Lin, also
pointed to the dominance
of the tele o i dust i the esea h: The FDA should e
applauded for nominating, and NIEHS/NTP should be lauded for having sponsored the
esea h a d o du ted the Cell Pho e Radio F e ue
Radiatio RFR Studies. It s
important for the U.S. government to step in to conduct such a research program, and not
leave the matter entirely to the cell phone industry. The wireless industry has had nearly
free reign to develop and roll out cellular mobile phones and related RF devices as they see
fit. … . Li goes o to uote figu es f o the s ste ati e ie : A s ste ati e ie of
59 published studies of controlled exposure to RF radiation with health-related outcomes
[10] showed that public agencies or charities funded 11 (19%), the wireless communications
industry funded 12 (20%), mixed sources (including industry) funded 14 (24%), and in 22
(37%) the
sou e of fu di g as ot epo ted.
This specific debate has been ongoing for many years, as
Investigate Europe
epo ts: At
least three studies over the years have documented that there is often a link between
conclusions of studies and the source of the money that paid for the research. Science
funded by industry is less likely to find health risks than studies paid for by institutions or
autho ities.
u h is safe?
by
Investigate Europe,
Lennart Hardell, an oncologist, professor and
In
Ho
researcher at the University hospital in Örebro in Sweden, a critical EMF researcher, warns
that although fu di g fo esea h ofte goes to u i e sities ith fi e alls put i pla e
between the individual scientist and the funder, the problem is, that researchers can come
to depend on this private funding to safeguard the future of their research.
Hardell carries out research on the possible links between long-term mobile use and brain
cancer and has published results that indicate that there are correlations between the two.
Hardell was a member of the IARC committee that researched EMF-effects, but is not a
member of (any) other committees concerned with the effects of non-ionizing radiation.
Investigate Europe:
A o di g to Ha dell, his esea h is fu ded th ough his sala f o the
hospital, as well as by funds raised by local cancer foundations and national organisations.
Of ou se, I ha e also o ked a lot o
f ee ti e , he sa s.
There are some ICNIRP-researchers who acknowledge that it is possible for the source of
funding to influence conclusions, but they say that they are very aware of this and cautious
to avoid it. For example, Gunnhild Oftedal, - associate professor at the Norwegian University
of Science and Technology, who specialises in research on the effects of electromagnetic
fields on humans, and is a member of ICNIRP
a d the efo e pa t of
the small international
network that determines what science to trust
said to
Investigate Europe
that toda e
are concerned about it. I have the impression that scientists are much more cautious about
receiving support from the industry
–
at
least di e t suppo t.
What a out the di e t fu di g e ei ed ICNIRP itself? ICNIRP states that its fu di g
stems from subsidies granted by national and international public institutions such as the
German Federal Ministry for the Environment, Nature Conservation, and Nuclear Safety
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(BMU), the European Union Programme for Employment and Social Innovation (EaSI) 2014-
2020 (EC - Directorate General Social Affairs), and the International Radiation Protection
Asso iatio IRPA .
O asio all , ICNIRP also
receives support to organise meetings or workshops from national
ministries or radiation protection agencies, such as the Australian Radiation Protection and
Nuclear Safety Agency (ARPANSA), and the Turkish Ministry of Health (MoH). Funding is
reported yea
l i the ICNIRP a ual epo ts . ICNIRP also a k o ledges that it e ei es
funding from national or international public organisations and via private donations. But
ICNIRP lai s that i o de to safegua d its i depe de e, o l do atio s f o p i ate
individuals or from businesses not related in any way to the field of non-ionizing radiations
can be accepted. For reasons of transparency, donations cannot be anonymous and are
listed i a ICNIRP do o s' epo t.
,150 in subsidies. The
According to the ICNIRP 2018
annual report,
it e ei ed €
Australian research group ORSAA points out that these kinds of funding sources are not
al a s as eut al as the a see : ICNIRP funding
partly comes from government
regulatory bodies, such as, for example, the Australian Radiation Protection & Nuclear Safety
Agency (ARPANSA). What is actually going on is best described as 'money laundering' by the
Telecom industry through government (ARPANSA) and onto WHO's International EMF
P oje t a d ICNIRP.
In Australia, as is the case for many countries worldwide, the government issues spectrum
licences to Telecom operators for large sums of money
–
often in the billions. In Australia,
this licensing is the remit of the industry regulator ACMA, the Australian Media
Communications Authority. ORSAA explains that ACMA also collects a separate levy, or tax,
from the wireless industry, money that is earmarked for scientific research on RF-EMR
health effe
ts: This has e ai ed a set a ou t of $ M pe a u si e
, despite the
assi e i eases i i eless i dust e e ues.
According to ORSAA, ACMA then diverts $300,000 to another government body, ARPANSA
(Australian Radiation Protection & Nuclear Safety Agency) for its public information
campaign, and $700,000 to the National Health & Medical Research Council (NHMRC). From
the $300,000 received annually by ARPANSA, a portion goes to the WHO's IEMFP (some
years ago this was around $50,000 a year), and finally, it appears that a portion goes to
ICNIRP. So, after a long trajectory, money from the Telecom industry does end up with
ICNIRP, which is cont
a to the state e t o the ICNIRP e site: O l do atio s f o
private individuals or from businesses not related in any way to the field of non-ionizing
adiatio s a e a epted.
Still a o di g to ORSAA, the o e that
the Australian NHMRC
receives in order to provide
grants for medical research has mostly gone to industry-friendly researchers who have direct
links with the wireless industry. For example, the largest recipient of these NHMRC research
funds is Prof. Rodney Croft, a psychology researcher at the University of Wollongong, who
held the role of Director of the Australian Centre for Electromagnetic Bio-effects Research
(ACEBR) for many years
2
. Rodney Croft has essentially been the head of RF-EMR health
research in Australia, despite his questionable qualifications for this health research role.
2
See also portrqit of Rodney Croft on pqge 50 of this report.
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Notably, he has led ICNIRP's RF-EMR exposure guidelines development team and now he has
been elected as the next Chairman of ICNIRP as from May 2020. Prof. Croft has received
ample direct industry funding in addition to his lucrative NHMRC grants, which should be
te ed i di e t i dust fu di g.
Finally, ICNIRP states on its website that all
its e pe ts a e e ui ed to o pl ith the
ICNIRP policy of independence and declare their perso
al i te ests. … These a e ke
elements to ICNIRP's commitment to independence and transparency, which ICNIRP believes
is fundamental to carrying out its
s ie tifi issio .
Whether those declarations of interests are really checked is something that the Italian
Vallisoleta a Asso iatio of people affe ted
o ile pho e a te as AVAATE
questioned
in their public statement from July 2015,
atta ki g ICNIRP: It is ha d to
understand whether ICNIRP investigates the Declarations filed by appointed members of
the ICNIRP Commission and Scientific Expert Committee, since in some cases these members
report that they work or have worked for these organisations but do not specify what they
have done or whether they
are paid. It is also hard to understand how ICNIRP controls the
content of the declarations by the appointed members of their Expert Committees, when in
most cases the most
contentious aspects of the biographical statement are not reported in
these state e ts.
The
itize s ehi d AVAATE also ask ho ICNIRP o t ols the o te t of the de la atio s
the appointed members of their Expert Committees when, at least in five cases, the persons
o e ed ha e ot sig ed thei state e ts .
Corporate capture
I the de ate o EMF a d possi le health effe ts, te s like o po ate aptu e of s ie tifi
research and
a ga e s ie e
are often used, and references to the tactics of the tobacco
industry are often made. According to several authors, these tactics also influence
organisations
like ICNIRP a d WHO s I te atio al EMF P oje t.
In the 2013
Late lesso s f o ea l a i gs
report produced by the European
Environment Agency (EEA), in collaboration with a broad range of external authors and peer
reviewers, these tactics are described in detail in the
hapte e titled To a o i dust
a ipulatio of esea h . The fo us is o the st ategies used the to a o i dust to
deny, downplay, distort and dismiss the growing evidence that, like active smoking, ETS
causes lung cancer and other effects in non-s
oke s. Autho Lisa A. Be o o e t ated o
the 'argumentation' that was used to accept, or reject, the growing scientific evidence of
harm. Who generated and financed the science used to refute data on adverse health
effects? What were the motivations? What kind of science and information, tools and
assu ptio s e e used to efute data o the ad e se health of to a o?
Be o sa s: The elease of illio s of i ternal
tobacco industry documents due to law suits in
the US has given insights into the inner workings of the tobacco industry and revealed their
previously hidden involvement in manipulating research. However, this insight is not
available for most corporate
se to s.
Bero also discusses the possibilities of 'full disclosure' of funding sources and special
interests in research and risk assessment in order to secure independence and prevent bias
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to a ds pa ti ula ie poi ts. She states that hile s oki
g bans are now being
introduced in more and more countries, other industries are drawing inspiration from
tobacco company strategies, seeking to maintain doubt about harm in order to keep
haza dous p odu ts i the a ketpla e.
With respect to the EMF-debate, according to Bero, public institutions or authorities should
adhere to the following:
he data o isk appea to e o t o e sial, use s of the data
investigate the sources of the controversy. Does the controversy exist only because the
findings of interest group-funded research are contrary to data collected by others? Is the
controversy supported primarily by evidence published in interest group-supported
pu li atio s? … Poli
ake s should appl these uestio s to all situatio s i hi h a
compan
has a i te est i
eati g o t o e s a out the isks of its p odu ts.
According to Bero, the tobacco industry's methods for influencing the design, conduct and
publication of research are similar to those of other corporate interests.
One of the leading researchers in the US who defends the viewpoint that the same tactics
are being used by Telecom companies is Theodora Scarato, Executive Director of the US
based
Environmental Health Trust
(EHT). As a policy analyst, Scarato manages and updates
the comprehensive EHT database on international policy that documents the 20+ nations
that have protective policies in place to reduce public exposure to cell phone and wireless
radiation.
Scarato and EHT claim that
Just as the To a o I dust
eated a Pla ook to defe d
cigarettes and manufacture doubt about the health effects of cigarettes, the Wireless
Industry seems
to have a fine-tu
ed the Pla ook of ad e tisi g, pu li
elations and
industry-funded science
to defend wireless products and falsely reassure the public that cell
pho es a d i eless p odu ts a e safe.
Ke to this pu li elations
effort are industry created resources, websites and materials
that communicate the myth of no proof of harm from wireless products. These are all part of
the Playbook to manufacture doubt that a problem exists. Examples of such propaganda
range fro
gloss
o hu es, Questio s a d A s e s o Hot Topi s su h as hild e a d
cell phones
, e sites o EMF a d Health a d esea h fo u s.
A d a o di g to S a ato, these ate ials a e paid fo , desig ed a d p epa ed
o
-
p ofit o ga isatio s that
are created by telecom and wireless companies pooling money
together. When citizens raise concerns about a particular product or when research comes
out indicating a health risk, companies can simply pull from these materials to respond as if
there are no
o e s .
These kind of tactics, used to influence science and risk assessment, also have their
repercussions for standard-setti
g odies like ICNIRP a d WHO s I te atio al EMF P oje t,
a o di g to s ie tifi esea he Do Mais h i his PhD thesis A
examination of the
manipulation of telecommunications standards by political, military, and industrial vested
i te ests at the e pe se of pu li health p ote tio : I a e e i easi gl glo alised
world the reliance on international organisations to set standards to protect public health
seems inevitable. Proposed internationalised sta
da ds su h as ICNIRP s e o
e datio s
act as an aid to economic development by not hindering trade that might conflict with
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stricter national standards (such as the Russia
Fede atio , the Cze h Repu li s fo e
standard and China for example). In the delicate trade-off between economic benefits and
ade uate health p ote tio , i te atio al o ga isatio s should ideall e ete all igila t
to ensure that their tasks are not co-opted by vested interest groups that are the producers
of risks to be regulated.
This appears to be a global issue. US researcher, Norm Alster, in
his report
Captu ed Age
describes what this kind of corporate capture can lead to by referring to the workings of the
FCC (Federal Communications Commission), which is the main official US institution that
deals with Telecom issues, and is sometimes
e tio ed i
iti ues of ICNIRP: That is a
term that comes up time and time again with the FCC. Captured agencies are essentially
controlled by the industries they are supposed to regulate. A detailed look at FCC actions—
and non-actions—shows that over the years the FCC has granted the wireless industry pretty
u h hat it has a ted .
As a esult, o su e safet , health, a d p i a , alo g ith o su e allets, ha e all
ee o e looked, sa ifi ed, o aided due to u he ked i dust i flue e. …)
Most
insidious of all, the wireless industry has been allowed to grow unchecked and virtually
u egulated, ith fu da e tal uestio s o pu li health i pa t outi el ig o ed. …
Industry control, in the case of wireless health issues, extends beyond Congress and
regulators to basic scientific research. And in an obvious echo of the hardball tactics of the
tobacco industry, the wireless industry has backed up its economic and political power by
stonewalling on public relations and bullying potential threats into submission with its huge
sta di g a
of la e s. … I dust
eha iou also
includes self-serving public relations
and hyper aggressive legal action. It can also involve undermining the credibility of, and
cutting off funding for, researchers who do not endorse cellular safety. It is these hardball
tactics that recall 20
th
centu
Big To a o ta ti s.
Conflicts of Interest
In 2017, almost 200 doctors and scientists from various countries launched the, so-called
5G
Appeal,
that has since received more endorsements and whose mission statement starts
with :
We the u dersig ed s ie tists a d do tors … , re o
e d a oratoriu o the roll-
out of the fifth generation, 5G, for telecommunication until potential hazards for human
health and the environment have been fully investigated by scientists independent from
i dustr .
Since then, as professor Hardell describes in
his article "Appeals that matter or not on a
moratorium on the deployment of the fifth generation, 5G, for microwave radiation"
published in January 2020, there have been five replies on this Appeal by the European
Commission, the last one dating from December 2019. The first reply, by the Commission
(from October 13, 2017 by the Directorate-General Health and Food Safety) states that
the
Commission is not aware of any conflicts of interests of members of international bodies such
as ICNIRP or the e ers of SCENIHR
.
Ho e e , a o di g to Ha dell, that does ot ep ese t the s ie tifi e ide e of i he e t
conflicts of interest both in ICNIRP and SCENIHR. The European Commission seems to be ill-
informed or even misinformed, as the EU seems to take information mainly from these two
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fraudulent organisations, but not from independent researchers. The EU does not seem to
rely on sound science and thereby downplays the RF-
elated isks.
Given the important effects of funding on research outcomes described above, there can be
no doubt that it is extremely important for ICNIRP to ensure it avoids any possibility of
conflicts of interests in the way that it, or any of its members, function. In its statutes, it
ites: No e e of
the Commission shall hold a position of employment that, in the
opi io of the Co
issio , ill o p o ise its s ie tifi i depe de e.
The u ial o ds he e a e
in the opinion of the Commissio
. The Commission evaluates
itself about possible conflicts of interest. There are no clear rules by which the Commission
judges if any of its members interests compromise its scientific independence. In its
statement on the declarations of interests ICNIRP writes:
The e aluatio of pe so al i teg it is e
omplex and might never be achievable in a
perfect way. It is the duty of the ICNIRP Commission to carefully consider and decide if the
declared interests potentially constitute a conflict of i
te est.
It is clear from this that ICNIRP itself does not have a sharp definition of conflicts of interest
CoI s , o does it ha e a ell-developed
policy to avoid these kinds of conflicts.
It is useful to refer to
a recent study
requested by the European Pa
lia e t s Petitio s PETI
committee which, as a key message, said
that EU i stitutio s a d age ies la k a o siste t
defi itio of o fli ts of i te est a d o
o ules o t a spa e
. This sa e stud also
stated that a ohe e t poli should e developed
for the required length of time between
working in the industry and being called to a committee among agencies with a similar
fu tio , i.e. isk assess e t .
In the online newsletter,
Politico,
the G eek MEP Ale is Geo goulis said: The e is a legal
inconsistency between the definitions of the conflicts of interest that should clearly cover
any conflicts between public and private functions, but also public functions with other
pu li fu tio s, The epo t e o
e ds lea la ifi atio s o hether
conflicts of
interest are potential or also perceived.
So, we will have to look at other, similar, organisations that have more stringent policies in
this field. The European Food and Safety Authority (EFSA) seems to be a good candidate. In
June 2017, EFSA,
afte a lo g histo of a usatio s of CoI s, sha pe ed its
definition and its
poli to a oid CoI s.
EFSA defines a conflict of interest
as a situatio he e a i di idual has a i te est that
may compromise or be reasonably perceived to compromise his or her capacity to act
independently and in the public interest in relation to the subject of the work performed at
EFSA .
This
defi itio is also so e hat oad a d ague. EFSA s solutio as to
set clear rules to
which its experts have to comply. For example: Research funding from the private sector
e efiti g EFSA s e pe ts should ot e eed % of the total esea h udget.
The EFSA-rules are minimum requirements. According to
Corporate Europe Observatory
they
are not strict enough to completely avoid conflicts of interest. So, it is reasonable to say that
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ICNIRP, that presents itself as an independent, scientific advisory board, should, at the very
least, comply with the EFSA rules.
In this paper, we will therefore:
* Give an overview of the history and all existing knowledge on the independence of, and
the conflicts of interest within, ICNIRP. These chapters provide the context in which we have
a closer look at the ICNIRP-members.
* Try to identify all the potential sources of conflicts of interest of ICNIRP-members. Such as:
research funding from the private sector; financial investments in, and employment by,
telecom business operators; consultancy work for the telecom industry.
* Try to find out if the ICNIRP-members comply to the EFSA-rules on conflicts of interest and
give an assessment on the independence of ICNIRP.
These are the ICNIRP experts whose professional backgrounds we will research (see the
portraits of each member in Part V):
As from December 2019, the composition of the ICNIRP Commission for the term of office
2020-2024 is
as below.
The new term of office starts in May 2020.
MEMBERS OF THE ICNIRP COMMISSION:
GUNDE ZIEGELBERGER (SCIENTIFIC SECRETARY), GERMANY
RODNEY CROFT (CHAIR), AUSTRALIA
ERIC VAN RONGEN (VICE-CHAIR) , THE NETHERLANDS
TANIA CESTARI, BRAZIL
NIGEL CRIDLAND, UNITED KINGDOM
GUGLIELMO D'INZEO, ITALY
AKIMASA HIRATA, JAPAN
ANKE HUSS, NETHERLANDS
KEN KARIPIDIS, AUSTRALIA
CARMELA MARINO, ITALY
SHARON MILLER, USA
GUNNHILD OFTEDAL, NORWAY
TSUTOMU OKUNO, JAPAN
MARTIN RÖÖSLI, SWITZERLAND
SOICHI WATANABE, JAPAN
MEMBERS WHO HAVE LEFT THE ICNIRP COMMISSION IN MAY 2020
Maria Feychting
Adèle Green
Zenon Sienkiewicz
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MEMBERS OF THE SCIENTIFIC EXPERT GROUP (SEG):
JACQUES ABRAMOWICZ - PG COSMETICS, PG ULTRASOUND
ANSSI AUVINEN - PG DATA GAPS
CHRISTIAN CAJOCHEN - PG SHORT WAVE LIGHT
JOSE GOMEZ-TAMES - PG HF DOSIMETRY REVIEW
PENNY GOWLAND - PG DATA GAPS
JOHN HANIFIN - PG SHORT WAVE LIGHT
JUKKA JUUTILAINEN - PG DATA GAPS
KEN KARIPIDIS - PG COSMETICS, PG DATA GAPS
MASAMI KOJIMA - PG LASER POINTERS
ILKKA LAAKSO - PG HF DOSIMETRY
ISABELLE LAGROYE - PG DATA GAPS
SARAH LOUGHRAN - PG SHORT WAVE LIGHT, PG HF GUIDELINES
JACK LUND - PG LASER GUIDELINES
SIMON MANN - PG HF DOSIMETRY
RÜDIGER MATTHES - PG HF DOSIMETRY
JOHN O'HAGAN - PG LASER GDL, PG LASER POINTERS, PG LED, PG SHORT WAVE
CHIYOJI OHKUBO - PG DATA GAPS
MARGARETHUS PAULIDES - PG HF DOSIMETRY
KENSUKE SASAKI - PG HF DOSIMETRY REVIEW
DAVID SAVITZ - PG ULTRASOUND
KARL SCHULMEISTER - PG DATA GAPS, PG LED, PG LASER GDL, PG POINTERS
DAVID H. SLINEY - PG LASER GDL, PG LASER POINTERS, PG LED, PG SHORT WAVE LIGHT
RIANNE STAM - PG COSMETICS
BRUCE STUCK - PG HF GDL, PG DATA GAPS, PG LED, PG LASER POINTERS, PG LASER GDL
JOHN TATTERSALL - PG HF GUIDELINES
TIM TOIVO - PG COSMETICS
ANDREW WOOD - PG DATA GAPS, PG HF DOSIMETRY
TONGNING WU
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I-
Historic overview of ICNIRP and accusations of COI
In this chapter, we give an overview of the history of ICNIRP as an organisation and examples
of accusations of Conflicts of Interests (COI) and other controversies concerning the
o ga isatio s o k. The autho s do ot a t to suggest that this o e ie is,
by any means,
complete or comprehensive.
About
ICNIRP s histo
, on its website, the organisation simply states that its beginnings go
back to 1973
he , du i g the
d International Congress of the International Radiation
Protection Association (IRPA), for the first time, a session on non-ionizing radiation
protection was organized. In 1977 the International Non-Ionizing Radiation Committee
(INIRC) was created. This Committee was the immediate forerunner of ICNIRP that was
chartered as an independent Commission in 1992 during the IRPA 7th International
Co g ess.
In a speech in Rio de Janeiro, in 2008, Paolo Vecchia, the Italian former ICNIRP-chair (2004-
, IRPA P eside t, Italia Ca lo Pol a i
-
2012),
explained in more detail:
I Ju e
1977), proposed "a possible role of IRPA in establishing criteria and standards in the field of
health protection against non-ionizing radiations" and the IRPA Executive Council decided to
set up a Working Group to review the health protection problems arising from different non-
io izi g adiatio NIR .
One could argue that IRPA itself, and then much later it
s spi
-off ICNIRP, came into
e iste e as a fall-out of the fi st US ato i o
testi g. O its e site, o the su je t of
its histo i al a kg ou d, IRPA states: Befo e the Se o d Wo ld Wa , adiatio p ote tio
had been a largely secondary concern of radiologists and radiological physicists. With the
concentration of effort under the
Manhattan Project
it was soon realised that this would
involve working with quantities and types of radiation and radioactive materials that had not
previously been envisaged. As a result, a distinct group of scientists within the project were
assig ed full ti e to hat as te ed "Health Ph si s".
In
an article from 2017
o the histo of of ICNIRP, at the o asio of it s
th
anniversary
fou de Mike Repa holi ote: Co e a out health isks f o e posu e to o
-ionizing
radiation (NIR) commenced in the 1950s after tracking radars were first introduced during
the Second World War. Soon after, research on possible biological effects of microwave
radiation in the former Soviet Union and the U.S. led to public and worker exposure limits
being much lower in Eastern European than in Western countries, mainly because of
diffe e t p ote tio philosophies. As e ill see fu the i this hapte this di ide et ee
Russia and the West on safety measures on non-ionizing radiation exists till today.
At the end of its conference in 1955, the US Atomic Energy Commission voted
overwhelmingly to form a professional Health Physics Society and the first IRPA Congress
was held in Rome between 5-10 September 1966. It is interesting to see that many of the 12
Executive Council Members of IRPA in 1966 remained in position for many years; a fact that
e hoes like a p elude to iti is that ICNIRP fu tio s like a old- o s et o k .
I
Co
20
, IRPA P eside t Pol a i i sisted that a separate
and independent International
issio o NIR P ote tio late ICNIRP should e esta lished…The ICNIRP ould look
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to IRPA as the sponsoring international scientific organization in a similar way that ICRP looks
to the International Congress of
Radiolog …. A d IRPA should o side oade i g its
i stitutio al autho it to i lude NIR .
So Carlo Polvani got what he wanted: the General Assembly amended the Constitution of
IRPA so that it ould also appl its o je ti es a d pu poses i the field
of non-ionizing
adiatio p ote tio . The the Ge e al Asse l eated a I te atio al NIR Co
ittee
[…] ith the o je ti e of de elopi g a kg ou d do u e ts a d i te atio all a epted
e o
e datio s . This e a e INIRC, set up i
, that e t on
to become ICNIRP, in
1992. Already four years earlier, Mike Repacholi (more on him later), a member of IRPA, had
begun writing the charter for ICNIRP which was signed in 1992.
But why elaborate so much on IRPA, before turning to ICNIRP itself? Critics often ask from
where ICNIRP got its self-acclaimed international and institutional authority? Well, partly
from IRPA, which still plays a role in the actual composition of ICNIRP. The IRPA Charter for
the creation of ICNIRP, from 1992, says: "The election of the members of the Commission
shall be made by the Commission from current members of the Commission and from
nominations submitted by the Commission itself, the Executive Council of IRPA and the IRPA
Associate Societies, with regard to an appropriate balance of expertise. Attention shall be
paid to geographical representation."
At the end of the 15th International Congress of IRPA, planned for 11-15 May 2020, in Seoul,
Korea, the new term of office of the new ICNIRP commission (2020-2024) would officially
start. This occurred, despite the
international congress in South-Korea
being postponed until
2021 due to the corona-crisis. This international congress counts
telecom companies of all
kinds among its sponsors
(platinum, silver, bronze as well as others). Since ICNIRP was born
from IRPA, and that, like any parent, IRPA still exerts a strong influence over ICNIRP, and
considering ICNIRP claims to function free of any vested interests, it seems important to us
to look more closely at IRPA.
And maybe also because of the actual role that IRPA wants to play in the ongoing debate
around safety and health in relation to EMF. Current IRPA-president, Roger Coates,
writes
that
a lot of effo t o e e e t ti es has go e i to p epa i g the IRPA Guida e fo
Engagement with the Public on Radiatio
a d Risk . This see s to e the t pi al t pe of
response given by bodies like IRPA, ICNIRP and others concerning public worries about
possible health effects:
let s e plai thi gs etter, e ause the pu li does t u dersta d
…that e er thi g is safe
. It is the same kind of response given in the past by the nuclear
sector when people started to become worried about nuclear safety issues (for example
after Chernobyl).
Some governments
–
at various levels
–
try to put into practice a guiding principle of
adiatio safet , alled ALARA , hi h sta ds fo As Lo As Reaso a l A hie a le . This
principle means that even when being subjected to a small dose, if receiving that dose has
no direct, practical or medical benefit, you should try to avoid it. IRPA-boss Roger Coates
states that the i te p etatio of hat is Reaso a le i the i ple e tatio of opti isatio
of
adiatio p ote tio is o e of the ke issues fo ou p ofessio a d is o e of IRPA s u e t
key themes. It is central to practical protection and is the dominant factor controlling
exposures in any well-de
eloped s ste of p ote tio . But hat does easo a le ea ?
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The e a e g o i g o e s ithi ou p ofessio that e a e gi i g
lo as a d i i isatio athe tha t ul ei g easo a le .
o e e phasis to as
On the subject of safety: before Roger Coates became IRPA-president he had
a life-long
career in the British nuclear industry:
he started working in 1975 at the Health Physics and
Safety Department at the Sellafield site of
British Nuclear Fuels plc (BNFL)
and did so for over
ea s,
holding radiation protection roles covering operations, environmental protection
and emergency planning. His responsibilities broadened to encompass nuclear safety,
together with conventional safety and environmental issues. He completed his industry
career as Director of Environment, Health and Safety for both BNFL and its British Nuclear
G oup su sidia . O e the ea s,
BNFL has had to face up to
quite
some issues
in the field
of safet a d as the su je t of a
damning report into the falsification of safety data at the
Sellafield reprocessing plant
at the sta t of this e tu .
This year,
on its website, IRPA published
the first new safety guidelines of ICNIRP since 1998,
of which ICNIRP-
hai Va Ro ge said, as e e tio ed ea lie :
The new guidelines
provide better and more detailed exposure guidance in particular for the higher frequency
range, above 6 GHz, which is of importance to 5G and future technologies using these higher
frequencies. The most important thing for people to remember is that 5G technologies will
ot e a le to ause ha
he these e guideli es a e adhe ed to.
Self-declared legitimacy
Since the signing of IRPA-charter in 1992, ICNIRP is based in Munich, Germany and registered
as a self-governed NGO (non-governmental organisation) that was formally recognized as
a offi ial olla o ati g o
-state actor by the World Health Organization (WHO) and the
I te atio al La ou O ga izatio ILO . ICNIRP is o sulted the Eu opea Co
issio
and is linked to many organizations engaged in NIR protection worldwide through diverse
collaborative projects.
As mentioned in the introduction of this report,
extensive reporting by
Investigate Europe,
in
March 2019 (updated on June 10
th
2020), showed that there are many close links between
ICNIRP and other leading organisations in the field of health protection. Many ICNIRP-
members are, or were, also members of one of these three scientific bodies (from which
most radiation safety authorities in Europe and governments, seek their advice) and it is
important to mention them again, because these are the bodies that guide government
policies in most countries:
-
-
-
The
EU Scientific Committee on Health, Environment and Emerging Risk, SCENIHR /
SCHEER.
The
World Health Organization (WHO) International EMF Project (IEMFP).
The
WHO Cancer Unit IARC, International Agency for Research on Cancer.
It is worth underlining, however, that IARC
does ot eall fit i to this ga g of fou
e ause
it has a much more critical and independent approach. IARC published a report in May 2011
which con
luded that adiof e ue
RF adiatio is possi l a i oge i to hu a s.
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The IARC cancer classification includes all sources of RF radiation, of which the long-term
exposure can come from mobile phone base stations, Wi-Fi access points, smart phones,
laptops and tablets.
However, IARC may now have a solid reputation as independent scientific body, some years
ago, IARC also got into trouble. Anders Ahlbom, senior professor of Epidemiology at the
Karolinska Institute in Stockholm, and a long standing, influential member of ICNIRP
(Commission Member and ICNIRP SCI working group (Epidemiology)), and ICNIRP Chairman
from 1996 until 2008, was also part of the IARC panel of experts in 2011. Ahlbom was, until
very recently, doing assessments of environmental health risks as chair of the Swedish
Radiation Safety Authority's (SSM), the scientific council on electromagnetic fields, as a
member of ICNIRP and of the EU advisory body SCENHIR.
But he was asked to step down from IARC after a journalist exposed him as being on the
oa d of his othe s o sulti g fi i B ussels, hi h helps lie ts o tele o s issues.
He
had not made IARC aware of this. As the Swedish investigative reporter, Mona Nielsson,
ote: Fu the o e, A de s Ahl o s othe , Gu a Ahl om,
was for a long time a
lobbyist for Swedish telecom giant Telia (previously TeliaSonera) in Brussels. At the same
ti e A de s Ahl o se ed as a i depe de t e pe t o se e al i po ta t e pe t pa els,
in Sweden as well as at the WHO and EU. At a meeting organized by the European
Commission in cooperation with GSM Association and Mobile Manufacturers Forum in
Brussels in 2004, Anders Ahlbom was an invited expert to speak on health effects, while his
brother Gunnar Ahlbom sat in the audience representing
TeliaSo e a.
There was, and is, more controversy and division on this topic within the WHO. In a 2017
article,
"A ha d ut to a k
,
professor Lennart Hardell draws attention to a
Fact Sheet
issued by WHO
i Ju e
, o l t o o ths afte the IARC s epo t adapti g
the cancer
lassifi atio of RF adiatio , hi h stated that to date, o ad e se health effe ts ha e
been
esta lished as ei g aused
o ile pho e use . A o di g to Ha dell, this state e t as
ot ased o s ie tifi e ide e at that ti e o a a i oge i effe t f o RF adiatio . A d
it was certainly a remarkable conclusion by WHO since IARC is a part of WHO, although
see i gl i depe de t . A d he goes o to o lude: Co side i g the WHO state e t of
'no adverse health effects' the aim might have been to undermine the IARC decision and give
the tele o i dust a ' lea ill' of health.
One of the main reasons for this schizophrenic approach within the WHO is to be found in
the figure of ICNIRP-fou
de , Mike Repa holi, a d the WHO s I te atio al EMF P oje t,
IEMFP) (see more below). At least
four ICNIRP-members
were, or are, also members of the
WHO-EMF Group.
In January 2019, in
the German newspaper Der Tagesspiegel,
investigative journalists
des i ed ICNIRP as a Ca tel , that s ste ati all efutes all studies that sho possi le
ha : A d o adiatio p ote tio age , o EU o
issio e a d o i iste ,
contradicts this. For European governments and their authorities, the 13 members of the
self-appointed Commission act as a kind of force majeure. But why? Why are all the warners,
even prominent figures like the panel of experts for the US Health and Safety Executive, not
hea d?
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The Investigative journalists
des i e a asto ishi g phe o e o : the e e s of ICNIRP
are simultaneously active in all the relevant institutions and thus have control over the
official discou
se. The
then go on to note that, legally speaking, ICNIRP is an association
that auto-controls itself and thus avoids dissenting opinions, but in the first instance, the
connection with the German state begins with the chosen address of ICNIRP which is the
same as the
German Federal Office for Radiation Protection (BfS).
Is it just a st a ge oi ide e that ICNIRP s se eta iat is lo
ated in the building of the BfS in
Munich. The scientific coordination for/of/within? ICNIRP has, for the last few years, been
the responsibility of a
BfS offi ial: Gu de Ziegel e ge . He p ede esso e e hai ed the
club until 2016. At the same time, the German government supports the NGO of scientists
with about 100,000 euro a year. The spokesperson rejects the impression that the private
organization is almost part of the German authority as "not applicable". The office only
supports the international network of research, she said. Moreover, the ICNIRP is officially
e og ised the WHO, hi h gi es it legiti a .
We have asked Mrs Ziegelberger via email if she would agree to answer our questions on
ICNIRP in writing, but we have, to this date, received no response (the ten questions can be
found in Annex I)
This self-declared sense of legitimacy was carefully created by the Australian scientist,
Michael Repacholi, who co-founded ICNIRP and also, a few years later, in 1996, the EMF
P oje t of the WHO offi iall the WHO s I te atio al EMF P oje t, IEMFP of hi h he
e a e the head. The WHO s I te atio al EMF P oje t IEMFP asi all ased itself
on
ICNIRP s guideli es a d doi g so ga e itself a ualit la el .
ICNIRP u der Michael Repacholi s chair a ship
Since 1978, the Australian biophysicist, Repacholi,
has been a member of the International
Non-Ionizing Radiation Committee (INIRC),
a part of the International Radiation Protection
Association (IRPA), and between 1988—1992 he was chairman of INIRC, which then became
into ICNIRP. Between 1996 and 2006, Repacholi called the shots at the WHO by creating, and
then leading, the WHO EMF Project, to study the health effects of electric- and magnetic-
field radiation (EMF).
So, almost simultaneously with his leadership of ICNIRP, Repacholi was able to set up the
EMF
P oje t of the WHO offi iall the WHO s I te atio al EMF P oje t, IEMFP i
,a d
became its head (see more below) until 2006. From the very beginning,
the WHO EMF
Project and ICNIRP have been intertwined,
as Louis Slesin wrote in
Microwave News.
Given
the central role of Repacholi, it might explain why, from very early on, ICNIRP was officially
e og ized the WHO. F o
u til toda , Repa holi has ee Me e E e itus of
ICNIRP and today, still has access to the organisation he founded.
As early as 1992, ICNIRP
adopted
Repa holi s
IRPA p oposal
that the only health issue
to address in standard setting was the short-term effects due to the absorption of RF/MW
e e g of suffi ie t po e to e o e ted to heat, ased o the IEEE s
(Institute for
Electrical and Electronic Engineers) Radiofrequency standard philosophy. Since then it seems
to be
a ed i sto e that ICNIRP o l e og ises the the al effe ts of adiatio as a
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serious concern. This is a crucial element to understand the position of ICNIRP, it was built
on the logics and thinking of electrical and electronic engineers and completely lacking
biomedical expertise.
In 1998, ICNIRP
pu lished its fi st Guideli es o li its of e posu e to ti e-varying
electric,
magnetic and electromagnetic fields (up to
GHz
, still largely produced under the
chairmanship of Repacholi.
A fierce and long-standing critic of the first ICNIRP guidelines was
Dr Neil Cherry,
Associate
Professor of Environmental Health.
In November 1999, Dr Cherry was invited by the Ministry
of Health/Ministry for the Environment of New Zealand to carry
out a peer-review of the
proposal to adopt the ICNIRP guidelines
for cell sites in New Zealand.
Che : The ICNIRP guidelines
were covered by a published assessment in 1998. This review
shows that the assessment had ignored all published studies showing chromosome damage.
It was highly selective, biased and very dismissive of the genotoxic evidence and the
epidemiological evidence of cancer effects and reproductive effects. The assessment gives
the strong impression of being predetermined in the belief that the only effects were from
high exposures that cause electric shocks and acute exposures that cause tissue heating. For,
example, they cite two studies saying that they do not show any significant increased effects
of Brain/CNS cancer from microwave exposures when the actual published papers, Grayson
(1996) and Beall et al. (1996), both do show significant increases of B
ai /CNS a e .
In September 2000, he
presented evidence
of Health Effects of Electromagnetic Radiation to
the Australian Senate Inquiry into Electromagnetic Radiation. The Inquiry Chairperson,
Se ato L Alliso , des i ed Che s
evidence as the only independent professional
evidence with no relation to industry. The conclusions from this evidence are strongly
contrasted with the position of Dr Michael Repacholi, the WHO, ICNIRP, the Australian
Radiation Laboratory and many other organisations around the world.
T e t ea s ago, Che said: This issue has ee so politi ized. The e a e t o ajo
casualties, the truth and public health. On these matters, I have no respect for the position
of ICNIRP, nor that of the WHO. The WHO position is taken solely by Dr Repacholi. ICNIRP is
a small self-appointed, self-promoted group that claims standing by having WHO
recognition. In other words, a body formed in part and led by Dr Repacholi, claims its
standing by being recognized by Dr Repacholi.
Che used ha sh o ds fo INCIRP u de Repa holi's hai a ship. The o siste tl
misquote and misrepresent the published research results. They reject all epidemiological
evidence because every single epidemiological study occurs with mean exposure levels and
orders of magnitude below their thermally-based standard. They are highly selective, using
only a small proportion of the available studies in order to construct and defend their own
case. They prefer author's conclusions that there are no effects, even when the data and
analysis in the paper clash with this and contradict it. They dismiss large, reliable and well-
defined studies as ill-defined and unreliable. They state that studies don't show significant
increases in CNS cancers when they actually do, even when the papers include significant
dose-response relationships. Both the WHO and ICNIRP, under Dr Repacholi's leadership,
have maintained the thermal view to the present, despite the large and ever-growing body
of scientific research that
fi l a d o lusi el halle ges this.
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He also a used Repa holi of ai tai i g lose li ks ith i dust . He ot
only appeared in
New Zealand in two court cases for industrial clients, in Vienna he was taken to an industry
sponsored press conference where he stated that there was no evidence that GSM cell
phones were hazardous to health. At the conference, he presented his paper on the Telstra
(Telstra
is Australia's largest mobile network operator and telecom company)
funded
project that showed that GSM cell phone radiation at quite low non-thermal levels, doubled
the cancer in mice. When challenged by the conference chairman, Dr Michael Kundi, Dr
Repacholi said that a study is not evidence until it is replicated. The conference rejected this.
A stud
is e ide e. Repli atio p o ides o fi atio a d esta lish e t.
The fact is that Repacholi has followed a remarkable career path, from member of IRPA and
working in an Australian hospital, to holding a dominant position in the international debate
on EMF risks. He also developed as a scientist, from
publishing a study
in 1997 on lymphoma
incidence in mice exposed to RF radiation, to becoming a consultant for telecom and power
companies ten years later.
I
, he pu lished
A History of the International Commission on Non-Ionizing Radiation
Protection (ICNIRP)
i the s ie tifi e ie
Health Physics,
i hi h he stated: ICNIRP s
guidelines have been incorporated into legislation or adopted as standards in many
countries. While ICNIRP has been subjected to criticism and close scrutiny by the public,
media, and activists, it has continued to issue well-received, independent, science-based
protection advice. This paper summarizes events leading to the formation of ICNIRP, its key
a ti ities up to
, ICNIRP s th a i e sa ea , a d its futu e halle ges.
It is quite revealing that Repacholi writes,
ICNIRP has ee su je ted to iti is a d lose
scrutiny by
the pu li , edia, a d a ti ists , a d et, fo gets to e tio ,
and also by
scientists.
Because, since the first publication of guidelines by ICNIRP in 1998, there has been
a never-ending stream of critical academics publishing harsh analysis on the scientific work
of ICNIRP. The issue is that Repacholi has not only been a dominant figure, but also a very
divisive figure, in the international EMF-debate and he has been able to make sure that
independent scientists who do not agree with the ICNIRP-dog
a of the al effe ts o l
have not become part of ICNIRP nor of the WHO EMF Project.
The fact that, in his article for the 25
th
anniversary of ICNIRP, Repacholi makes no mention of
the criticism and close scrutiny by scientists is quite telling. Because basically, the story of
ICNIRP and the ongoing controversy and ever deeper divisions within the scientific
community in the EMF-debate, started around the persona of Michael Repacholi himself.
Good scie ce a d the EMF Project IEMFP
As we have stated above, Repacholi was not only ICNIRP chairman, but also the leader of the
WHO EMF Project. In his
own words:
The WHO established the
International EMF Project
to provide a mechanism for resolving the many and complex issues related to possible
health effects of EMF exposure. The Project assesses health and environmental effects of
exposure to static and time varying electric and magnetic fields in the frequency range 0 -
GHz, ith a ie to the de elop e t of i te atio al guideli es o e posu e li its.
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In 1999, Repacholi published
the Proceedings of an International Seminar on EMF Risk
Perception and Communication
that took place in Canada. The event was not only
sponsored by the WHO, some government ministries and the Faculty of Medicine at the
University of Ottawa, but also by the Cellular Telephone Industry Association, the Canadian
Wireless Telecommunications Association and some electricity companies. The almost 300-
page do u e t pu lished Repa holi s I te atio al EMF P oje t pa t of the WHO s
Department of Protection of the Human Environment) kicks off with this statement:
Possi le health effe ts of e posu e to ele t o ag eti fields EMF ha e led to o e s
among the general public and workers that appear to go well beyond those that are
attributed to well-established risks. It is necessary to understand why this occurs and to deal
with it through an effective communications programme. People have the right to access
reliable, credible and accurate information about any health
isks f o EMF e posu e.
In his review,
"A hard nut to crack",
p ofesso Ha dell ites: Mi hael Repa holi
immediately set up a close collaboration between WHO and ICNIRP (being head of both
organizations) inviting the electric, telecom and military industries to meetings. He also
arranged for large part of the WHO EMF project to be financed by the telecommunication
industry's lobbying organisations; GSM Association and Mobile Manufacturers Forum, now
called
Mobile & Wireless Forum (MWF).
Ha dell states
that Repacholi acted like
a
representative for the telecom industry while responsible for the EMF health effects
depa t e t at the WHO
An investigative article in US magazine,
The Nation,
stated: Although Repa holi lai ed o
dis losu e fo s that he as i depe de t of o po ate i flue e,
in fact Motorola had
fu ded his esea h: While Repa holi as di e to of the WHO s EMF p og a , Moto ola
paid $50,000 a year to his former employer, the Royal Adelaide Hospital, which then
transferred the money to the WHO program. When journalists exposed the payments,
Repacholi denied that there was anything untoward about them because Motorola had not
paid hi pe so all .
According to
The Nation,
e e tuall , Moto ola s pa e ts e e u dled ith othe
industry contributions and funnelled through the Mobile and Wireless Forum, a trade
asso iatio that ga e the WHO s p og a $
,
a uall . I
, Repa holi helped
engineer a WHO statement
that EMF e posu es elo the li its e o
e ded i
international guidelines do not appear to have any known conse
ue e o health.
In a
Microwave News
article,
Repacholi claims that he always followed the WHO rules on
fu di g a d that, NO fu ds e e EVER se t to e. But the a ti le s autho , Louis
Slesin
goes
o to sa that this is fi a ial
legerdemain.
As
Microwave News
has previously
reported, Repacholi arranged for the industry money to be sent to the Royal Adelaide
Hospital in Australia, where he used to work. The funds were then transferred to the WHO.
Se e ea s ago, No Sa dle , a Moto ola spokes a , told us that, This is the p o ess fo
all the supporters of the WHO progra
. At the ti e, Moto ola as se di g Repa holi
$50,000 each year. That money is now bundled with other industry contributions and sent to
Australia by the Mobile Manufacturers Forum (MMF), which gives the project $150,000 a
ea .
A scientist who is very critical about the activities of Repacholi is American Professor Andrew
A. Marino (who used to work at the departments of Orthopedic Surgery, Neurology, and
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Cellula Biolog & A ato at the LSU Medi al S hool i Louisia a
ote: I
the
World Health Organization began what it said was a program to assess the scientific
evidence of possible health effects of EMFs. But the project was corrupted from the start
because it was controlled by the power- and cell-phone companies in the industrialized
countries. The companies designated Michael Repacholi as the project head. He had long
been a consultant and spokesman for power companies, so it was unrealistic to expect him
to conduct an open and honest inquiry, but his performance in office was even more
miserable than could have been anticipated based on his known conflict-of-i
te est.
Ma i o: While headi g the EMF
program at WHO, Repacholi dealt almost exclusively with
experts on the payroll of cell-phone and power companies. Scientists who disagreed with the
viewpoint of the EMF companies were excluded from the EMF evaluation process. The
public was also excluded from participation even though it was a major stakeholder in the
EMF debate. Only pro-i
dust spokes e e e hea d i Repa holi s sta
-chamber
processes, which ultimately resulted in reports and evaluations that exonerated the
companies from any responsibilit
fo hu a disease p odu ed thei EMFs.
Marino saw Repacholi at the Annual Meeting of the Bioelectromagnetics Society (BEMS) in
Cancu
, Me i o, i Ju e,
: The Mo ile Ma ufa tu e s Fo u , a o so tiu of the
o ld s ajo ell-phone
companies,
e e Gold Spo so s of the BEMS eeti g, a d the
leade s of BEMS, had i ited Repa holi to gi e a talk e titled Results f o
Yea s of
WHO
s I te atio al EMF P oje t, hi h he deli e ed at a ple a sessio of the eeti g.
Unsurprisingly, his talk was a paean to his EMF activities at WHO. He was proud of having
successfully stemmed the tide of concern regarding the link between environmental EMFs
and other human diseases, and of having defended the principle that man-made
environmental EMFs were harmless. He touted model legislation that he had drafted, and
said that he hoped it would be enacted by various governments so that the fact that
e i o e tal fields e e safe ould e e sh i ed i la .
I
Repa holi stepped do
as di e to of WHO s EMF
Project.
Not much later
Microwave News
a ou ed: It s Offi ial: Mike Repa holi Is a I
dustry
Co sulta t A d He s Al ead i Hot Wate : Just o ths afte lea i g his post as the head
of the EMF project at the World Health Organization (WHO), Mike Repacholi is now in
business as an industry consultant. The Connecticut Light and Power Co. (CL&P), a subsidiary
of Northeast Utilities, and the United Illuminating Co. (UI) have hired Repacholi to help steer
the Co e ti ut Siti g Cou il a a f o a st i t EMF e posu e sta da d.
To strengthen his testimony on behalf of the two electric utilities, Repacholi cited the
findings of an unfinished WHO report
—Environmental
Health Criteria (EHC)— on EMF risks.
Twenty invited experts drafted this report at a meeting in Geneva in October 2019. The final
version was expected to be made public months ago but it's still being edited by the WHO
staff.
According to Chris Portier, who chaired the expert EHC panel for the WHO, Repacholi has
misrepresented the group's conclusions: "The paraphrasing sometimes has gone a bit far
a d a e isleadi g . Po tie is the
associate director for risk assessment at the National
I stitute of E i o e tal Health S ie es NIEHS . see elo .
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Portier cites a couple of examples. For example, in a summary of the WHO report, Repacholi
states that the EHC panel concluded that "The epidemiological evidence cannot be used as a
asis fo sta da ds e posu e li its . Po tie eto ts, Su h a state e t is a su d, si e the
obviously can be used."
Repacholi has since also been involved in an
industry propaganda video
and
interviews
with
GSM Association and Hydro Quebec where he clearly speaks in favour of the
telecommunications and the power industries, respectively.
A year later, in 2007,
Microwave News
epo ted that Mike Repa holi has o e ealed that
up to half of the funds raised for his EMF Project came from industry. This admission was
made in an interview with
Resource Strategies Inc.
i a effo t, he states, to set the e o d
st aight. While Repa holi has a k o ledged i the past that he aised fu ds f o i dust ,
the extent of the industry support is much greater than anyone has previously suspected.
Repacholi has never disclosed how much money he received nor from whom. He insists that
the EMF P oje t as ot i flue ed i dust .
According to an e-mail seen by
Microwave News,
Repacholi touts the interview as an
e a ple of he e the p ess fi all got it ight :
Resource Strategies,
however, can hardly
be considered "the press" in the usual meaning of the term.
Resource Strategies
is a
corporate consulting firm that prepares briefing papers for clients, which are almost
exclusively in the wireless and electric utility businesses. Among them are
EPRI, FGF, GSM
Association
and
MMF.
All of these industry groups supported the EMF Project during
Repa holi s te u e. A d to i g it all full i le, the
WHO is also on
Resource Strategies
lie t list.
Some current ICNIRP members, such as the new chair, Rodney Croft, also declare doing work
for EPRI.
Researcher Don Maisch
wrote that Repacholi harmed the credibility of the WHO:
It is
acknowledged that in an ever increasingly globalized world the reliance on international
organisations to set standards to protect public health is an irrefutable fact of modern life. It
is also a fact that inter
atio al o ga izatio s ha ged ith this task eed to e ete all
igila t to e su e that thei o ga isatio s a e ot o-opted
by vested interest groups
–
as
exampled by Big Tobacco and WHO. However, when it comes to non-ionizing radiation
issues (in this case for power frequency health risk assessment) the evidence is clear that
Mi hael Repa holi has used his sta di g i oth WHO a d ICNIRP to sta k the WHO s
Environmental Health Criteria Task Group for power frequency exposures with
representatives of
the po e i dust i o t a e tio of WHO poli .
Maybe one of the most telling episodes in the professional life of Repacholi is his open fight
with his former boss, Gro Harlem Brundtland, who was director-general of the WHO. In
interviews and
a speech,
B u dtla d ad itted that she is ele t i all se siti e : I e e
place a mobile phone next to my head because in one second I would develop a bad
heada he.
Repacholi was not amused.
In 2012, several Norwegian newspapers reported
that the Fo e head of WHO s
EMF project and ICNIRP chairman says that Brundtland has
eated fea of o iles i the populatio . He offe ed to e a i e he , as if she had a
psychological problem.
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Very seldom were critical voices heard within the WHO. From the minutes of the Sixth
International Advisory Committee meeting in May 2001, we read that Russian professor
Yuo i G igo ie the o e f o the a g lette
e tio ed elo ta led a do u e t
outlining EMF activities in Russia, and the difficulties with standards harmonization
particularly because of the inadequate consideration of non-thermal effects by ICNIRP and
othe atio al autho ities .
Dr Paolo Vecchia, of the National Institute of Health in Italy, and later ICNIRP chair, reacted
to this sa i g that it is i po ta t
to be able to recognize what good science is. WHO
should be a reference point or clearinghouse for good science and good scientific review. It
is important to recognize that science and legal measures follow the technology
–
it is not
possible to do a mobile phone epidemiological study before the introduction of the
technology! Given the pace of new technological development it is not possible, even now,
to envisage the complete set
of e esea h that ill e eeded.
Vecchia also claimed to be personall
e o e ed a out defe si e s ie e , speaki g of
over-cautiousness and an over-e
phasis o u e tai ties. S ie tists should e o e
o fide t a out the state of a t . He
is now doing consultancy work and
speaks at Telecom-
conferences.
IEEE/ ICES
In 2008, Vecchia wrote:
Guideli es fo safe e posu
e to electromagnetic fields have also
been developed by other international organizations, in particular the Institute of Electrical
and Electronics Engineers (IEEE). Apart from some differences in terminology and numerical
values of the limits, these guidelines are based on the same methodological approach, the
sa e st u tu e, a d the sa e s ie tifi data ase as ICNIRP.
I his thesis o a e a i atio of the a ipulatio of telecommunications
standards by
political, military, and industrial vested interests
at the e pe se of pu li health p ote tio
ORSAA-member and scientist, Don Maisch, compares the ICNIRP and IEMFP with the
American based IEEE. It is interesting because while ICNIRP claims to be free from the
influence of private interests, IEEE/ICES has always openly had members of the military and
of the telecom industry among its ranks.
Mais h ites: O the pa t of oth IEMFP a d ICNIRP, a dis ega d fo thei o stated
principles on independence from industry and following questionable criteria for evaluating
science, suggests an agenda to cut off the scientific controversy over EMF human health
haza ds less tha s ie tifi ea s. It ould e a gued that IEEE s ope ly
industry and
military dominated standard-setting process is at least more honest than WHO / ICNIRP
as ue adi g as i depe de t s ie tifi oi es f ee of ested i te est a hi atio s.
Dariusz Leszczynski, Adjunct Professor at the University of Helsinki,
writes
about conflicts of
i te est o e i g ICES: ICES, e ui ale t of ICNIRP, p epa es safet e o
e datio s fo
the exposures of users by radiation emitted by cell phones. Unlike ICNIRP, anyone can apply
for membership of ICES and all members of ICES participate in the decision-making process.
Sou ds i e… Not a p i ate lu as ICNIRP he e pa ti ipatio is i itatio o ly
and the
invitees have to have the same opinion on radiation safety
–
this helps in reaching
u a i ous de isio s… But ICES has a othe p o le that aused e, e e of ICES fo a
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couple of years, to resign my membership in 2009. The problem is that the ICES membership
is
clearly dominated by scientists working or consulting for telecoms.
And in another
blogpost
Lesz z ski
ote: The e e ship of the IEEE-ICES-TC95
consists
predominantly of the industrial scientists and the committee is chaired by C.K. Chou since
the time he was employed by Motorola. This means that all safety standards being
developed by IEEE-ICES-TC95 are, in practice, developed by the industry scientists for the use
by the industry they are employed by. The industry scientists have the majority on the
committee and upper-hand in any process involving democratic voting. To me this is clear
Co fli t of I te ests .
In the portraits of ICNIRP chair, Croft, and co-chair, Van Rongen, we describe (from page 50)
how they worked on establishing closer relations between ICNIRP and ICES.
From
the minutes of a meeting by the IEEE/ICES TC95
working groups at a Motorola
headquarters, a few interesting things got clear: In 2017 Repacholi was still a member of the
ICES lite atu e s ste ati e ie
o ki g g oup . A d
ICES-chair Faraone Antonio from
Moto ola Solutio s p oudl a ou ed that
ICNIRP has dela ed
finalizing their conclusions
to gi e full o side atio of ICES s e o
e datio s .
Former Motorola employee Chou stated at the same meeting on the interaction with World
Health O ga izatio WHO EMF P oje t that i espo se to C-K
Chou, the WHO has agreed
to encourage international harmonization of RF Safety Limits, especially between ICNIRP and
ICES
And concerning the WHO EMF Project, Hardell
describes
how Repacholi recruited Emilie Van
Deventer to the WHO EMF Project in 2000, and to this day, she remains project manager at
WHO
fo the EMF p oje t: She has ee a lo g ti e e e of the i dust do i ated
organization
Institute of Electrical and Electronics Engineers (IEEE).
IEEE has prioritized
i te atio al lo i g effo ts fo de ades espe iall ai ed at the WHO. Ha dell states that
Van Deventer is an electrical engineer
and has no formal or earlier knowledge in medicine,
epidemiology or biology, so it is surprising that she was selected for such an important
position at the WHO. Hardell:
The e sa e ea she as e uited to the WHO EMF
Project,
Toronto University Magazine wrote
about Emilie van Deventer's work, stating that it
was 'invaluable' to industry: 'The software modelling done by teams like van Deventer's is
invaluable.' 'The industrial community is very interested in our research capabilities,' says
Van Deventer. 'It always needs to be working on the next generation of products, so it turns
to unive
sities to get the esea h do e .
The importance of this work is reflected in
the research funding
van Deventer and her team
received from the Natural Sciences & Engineering Research Council of Canada (NSERC),
Communications & Information Technology Ontario (CITO), and their major industrial
pa t e , No tel. We a e fulfilli g a e eal eed i the industry
today, which will only
increase as technology creates more opportunity. In the process, consumers will continue to
enjoy faster computers, lighter cell phones, smaller electronic organizers and the vast array
of other electronic gadgets the high-te
h o ld has to offe .
In 2016, during a
seminar at the SSI,
concerning health effects of EMF,
former
Swedish
investigative journalist, Mona Nilsson, asked both Emilie van Deventer, Head of the WHO
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EMF P oje t, a d E i a Ro ge , the the hai of the ICNIRP,
ho the itize s should
believe: them or the opinion of 220 scientists who signed an
Appeal
submitted to the United
Natio s a d the WHO? . Both Va Ro ge a d
Van Deventer
answered the question
without defending their position.
Apparently, neither Van Rongen or van Deventer are
willing to fully defend the reliability of the evaluation of science by ICNIRP, because as
Leszczynski points out, neither of them said that ICNIRP evaluation of science is reliable and
that the Appeal s o lusio s a e u elia le. This lea l de o st ates that the e is o
scientific consensus on the health effects of radiation emitted by wireless communication
devices. This situation should be taken into consideration when the WHO selects expert
group for preparation of the final version of the Environmental Health Criteria for RF-EMF.
Scientists with diverse scientific opinions should and must be appointed in order to facilitate
a u iased s ie tifi de ate.
We have sent questions to Van Deventer, but have, to date, received no answer.
Angry Russian letter
Although ICNIRP as e og ised as a offi ial olla o ati g o
-state actor by the World
Health Orga
izatio WHO a d the I te atio al La ou O ga izatio ILO , f o the ea l
days, ICNIRP has also been criticized for industry-bias and indisputable situations of conflict
of interest.
Hardell notes that the Ethical Board at the Karolinska Institute in Stockholm, Sweden,
o luded, al ead i
, that ei g a e e of ICNIRP a e a o fli t of i te est
that should be stated officially whenever a member from ICNIRP makes opinions on health
isks f o EMF.
Nevertheless, for the WHO, this does not appear to pose a problem. After
the IARC
publication
in 2011, the WHO announced a new 'formal risk assessment' in 2012, which was
launched in 2014 and was then open for public consultation until the end of 2014.
The WHO stated the d a i g of o lusio s f o the lite atu e a d the d afti g of these
chapters is the remit of a formal Task Group that will be convened by WHO at a later stage in
the p o ess.
Ha dell dis losed that it
turned out that of the six members in the WHO Core Group, four
a e a ti e e e s of ICNIRP a d o e is a fo e e e . I deed, i
a research paper
fo
, Sa ah J Sta ke o ludes that the
anticipated WHO Environmental Health
Criteria Monograph on Radiofrequency Fields, due in 2017, is being prepared by a core
group and additional experts, with 50% of those named, being, or having been, members of
AGNIR o ICNIRP Ta le .
In another
research paper,
f o
, Ha dell otes: It is st iki g ho ICNIRP has i filt ated
the WHO Monograph core group, making it less likely that the conclusions in that
Monograph will differ from
ICNIRP s o lusio s. A d a o di g to hi , o l o e pe so
see s to e i depe de t of ICNIRP a d se e al pe so s also ha e affiliatio s to othe
advisory groups, authorities and/or committees. Six of the 20 additional experts are
affiliated with ICNIRP
.
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In March 2017, professor Oleg A. Grigoriev, Chairman and Head of the Scientific Department
of Non-Ionizing Radiation, Federal Medical Biophysical Centre of Federal Medical Biological
Agency (RNCNIRP) of Russia
wrote an angry letter
to Maria Neira, Director of Public Health
and Environment at the WHO, in which
he ope l atta ks ICNIRP: It has just o e to ou
attention that the WHO RF Working group consists mainly from present and past ICNIRP
members. In general, the WG is not balanced and does not represent the point of view of
the majority of the scientific community studying effects of RF. In particular, the private self-
elected organization, ICNIRP, similar as majority of the current WHO RF WG members, does
not recognize the non-thermal RF effects, which represent the main concern of widespread
exposure to mobile communication and upholding guidelines from 1996, which are based on
RF the al effe ts o l .
The Russia s ie tist o ludes that the guideli es of ICNIRP a e i ele a t to the p ese t
situation when majority of population over the world is chronically exposed to non-thermal
RF from mobile communication. Based on multiple Russian studies and emerging number of
studies coming from other countries, the Russian equivalent of ICNIRP has consistently
warned against possible health effects from mobile communication. This point of view of
RNCNIRP (Russian radiation protection agency) is supported by hundreds of new
pu li atio s i ludi g ell k o
e e t RF studies i hu a a d a i als.
Apparently, this angry Russian letter, in addition to other outcries, did have some effect on
the WHO, because it
relaunched a Call for Expressions of Interest for systematic reviews
(2020)
fo a E i o e tal Health C ite ia Mo og aph : The Wo ld Health O ga izatio s
(WHO) Radiation Programme has an ongoing project to assess potential health effects of
exposure to radiofrequency electromagnetic fields in the general and working population. To
prioritize potential adverse health outcomes, WHO conducted a broad international survey
in 2018. Ten major topics were identified for which WHO will now commission systematic
e ie s to a al se a d s thesize the a aila le e ide e.
We wonder if this time the WHO will try to avoid conflicts of interests and whether, for
example, there will also be Russian experts and other non-ICNIRP affiliated scientists on the
panels of experts.
Investigate Europe
wrote that the conflicts in EMF research run deep:
Histo i all , s ie e
i this field has ee asso iated ith the tele o se to a d the ilita . ICNIRP s safet
limits primarily take into account the needs of the telecom industry, claims Dariusz
Leszczynski, former long-time researcher at the Finnish radiation protection agency. In 2011,
he sat on the committee of IARC, the cancer body of the World Health Organisation, when it
decided that EMF is
possi l a i oge i to hu a s. ICNIRP s goal is to set safet li its
that do not kill people, while technology works
– so so ethi g i et ee , sa s
Lesz z ski.
Dariusz Leszczynski, has written about
this many times
on his blog and has often referred to
an un
ala ed e pe t o positio : ICNIRP a , a d should, e o side ed as a p i ate
lu
he e, e e s of the e Mai Co
issio a e sele ted the embers
of the
outgoing Main Commission. It is a self-perpetuating and self-promoting German NGO that is
not accountable for its actions at all. Nobody controls it. Nobody supervises it. Nobody
checks it for conflicts of interests. Nobody checks it for the scientific accuracy. In all what
and how ICNIRP does, we, the general public, must rely on the self-assurances, from the
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ICNIRP, that all is in order. One may ask whether such self-assurances are sufficient when
ICNIRP is p epa i g ad iso ies e fo ed o
ld-wide by the WHO and applied by the
numerous governments and by the multi-
illio i dust .
The following Graphic
–
made by
Investigate Europe
shows the interlinkages between
renowned ICNIRP-members and other scientific bodies. These groups, are to a large extent
staffed the sa e e pe ts. Of ICNIRP s ie tists, si a e e e s of at least o e other
o
ittee. I the WHO g oup, this applies fo si out of se e ,
Investigate Europe
writes.
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III - Discussion & Controversies
An observation one could make based on what has been discussed above, is that ICNIRP is
simultaneously one of the most powerful and one of the least-known non-governmental
o ga isatio s NGO s i the o ld. Po e ful, e ause fo al ost th ee de ades, ICNIRP
has
enjoyed a monopoly in the regulation of exposure to EMFs through their guidelines thanks
to the stamp of approval of the WHO. For the past 30 years, and currently, this advice and
these guidelines, are to a large extent followed by governments all over the world. In every
annual report, by any major telecom company, you will find references to ICNIRP in any
discussion or statement on the safety of their mobile phones. ICNIRP garners huge influence
worldwide, functioning on a modest yearly budget of around 140.000 euro, and yet ICNIRP is
largely unknown by the general public.
ICNIRP presents itself, and is described by the European Commission and in the media, as an
independent commission that gives advice based on scientific evidence. Our research shows
that there are several reasons to question this (self)-image.
Biased composition
The composition of ICNIRP is very one sided. As one can read in the portraits of the members
of the ICNIRP commission and of the Scientific Expert Group (SEG), they all share the same
position on the safety issues: non-ionising radiation only poses a health threat at thermal
levels.
Prominent ICNIRP-members therefore denounce the findings of the
U.S. National Toxicology
Program (NTP) that showed rats and mice contracted cancer when exposed to telephone
radiation. In
a scientific publication,
Van Rongen and co-authors state, as we laid out in the
portrait of the former chair of the ICNIRP-
o
issio , that su sta tial li itatio s of the
NTP-study) preclude conclusions being drawn concerning RF EMFs
a d a i oge esis.
Professor Hans Kromhout of Utrecht University, who is leading a long-term study into the
effects of mobile phone use on human health, and who is chairman of a special committee
on Electromagnetic Fields of the leading Dutch Health Council, regrets the way INCIRP
i i alizes the o lusio s of the NTP stud .
You can see that certain groups are trying to
reason that away. But they are well-executed studies
, he said i
a Dutch newspaper.
According to Kromhout, a deep controversy divides the scientific community that researches
EMF: "Two camps have arisen in science, with the two groups shouting at each other from
thei t e hes. It has e o e i possi le to o du t a o al o e satio . This
observation is
also made
by ORSAA-scientists.
A d o e of these t o a ps, is ot ep ese ted at all i side ICNIRP. It ould see that the
Co
issio is o posed o l of o
-
elie e s, K o hout ote i a e ail to us. I the
Dutch newspaper, he had earlie
stated: It's a it of a opaque
club. How candidates are
elected is not clear. Call it self-indulgent. In that sense, it doesn't really have an independent
status."
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In more recent exchanges with us, he re-ite
ates that the use of the o d self-indulge t is
justified. He refers to the sentence in the
ICNIRP Charter:
The election of the members of
the Commission shall be made by the Commission from current members of the Commission
and from nominations submitted by the Commission itself, the Executive Council of IRPA and
the IRPA Associate Societies, with regard to an appropriate balance of expertise. Attention
shall e paid to geog aphi al ep ese tatio . The fi st pa t –
that it is the members of the
Commission who elect its new members
–
puts the Commission at risk of remaining a closed
circle made up only like-minded scientists.
3
The unbalanced composition of ICNIRP is further demonstrated by the lack of expert-
members with training and experience in medical and/or biological sciences. As one
researcher pointed out, of the outgoing ICNIRP commission only one member was trained in
medicine, and only three in biological sciences. Furthermore, the sole medical professional,
Adele Green, was not an expert researcher in RF-EMR (with a single original research article
back in 2005), but was specialised in UV-radiation and skin cancer. She also left ICNIRP in
May 2020. It seems a good thing she has been replaced by Dutch scientist, Anke Huss,
assistant
professor at the
Institute for Risk Assessment Sciences
(IRAS) at Utrecht University
(NL), who seems to be rather critical. Tania Cestari
has replaced Adele Green ICNIRP in May
2020,
although, like Green that she has collaborated with, her expertise seems to be on UV
radiation in dermatology. Interestingly, a search on the PubMed database showed that she
has no publications for radiofrequency or other EMFs so she is not an expert on wireless
radiation.
The system of cooptation of ICNIRP and the resulting excessively homogeneous composition
clearly favors such biases. In 2013, in his article "Not
Entirely Reliable : Private Scientific
Organizations and Risk Regulation - The case of Electromagnetic Fields",
Gabriel Domenech
Pascual, Professor Administrative Law at the University of Valencia, states in his conclusions :
"That lack of plurality tends to reduce both the quantity and the quality of the available
information that serves the basis of their judgments, to stifle critical dialogue, to exacerbate
the common biases and positions of their members and to produce extreme outcomes,
polarized in the direction of those biases and points of view."
We can safely say that
ICNIRP has been, and is still lacking people with a relevant medical
background and over represented by physical scientists, which may not be the wisest
composition when your remit is to offer advice on human health and safety to governments
around the world.
Dr. Chris Portier, former director of the National Center for Environmental Health and
international expert in the design, analysis, and interpretation of environmental health data
with a focus on carcinogenicity, writes to us that the ICNIRP Council and
SEG appea to ha e
a e
ide ala e of e pe ie e . Ho e e , hat the a e la ki g, a o di g to Po tie , is
representation by scientists who have a history of working in risk assessment for chemicals.
This leads to their having different risk assess
e t app oa hes tha the est of the a ea.
3
For a better understanding of IRPA and functioning of ICNIRP, we refer you to the historical section of this
report
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Po tie a gues that isk assess e t fo he i als is ell-established
and has been used for
a , a
ea s . This sta da d of assessi g isks of he i al su sta es,
governs how to
judge the quality of various types of scientific studies and how to incorporate them into the
final risk assessment decisions.
Po tie : I ha e lo g felt that e pe ts f o EMF-research
have been incorrectly arguing that
this exposure is different and must be handled separately. But ionizing radiation is handled
the sa e as as he i als i isk assess e t, h ot EMF? Po tie states that ICNIRP
ould e pa d thei e pe tise i epide iolog a d to i olog a d e pe ts ho u de sta d
the challenges of biomedical study design and interpretation in a general sense.
A d Po tie states that it ould also e good to ha e a fe s ie tists ho a e o e
outspoke a out pote tial isks. Po tie
ites that these i p o e e ts ould halle ge
ICNIRP
to e e a t a out thei dis issal of so e of the positi e fi di gs i esea h o
health effect of EMF, that do exist.
The composition of ICNIRP is also one sided in another sense: there is a lack of
representatives from the Middle East, Russia, China and India who have outstanding
research contributions in the RF research and also (in many cases) have more stringent
standards.
For Gabriel Domenech Pascual "this lack of plurality is not fortuitous at all, but caused by the
system used to elect the members of the ICNIRP. As everybody knows, cooptation tends to
produce homogeneous, conservative, immobile and not sufficiently innovative groups."
"This stands in sharp contrast with the principles underlying current European Union Law",
Domenech Pascual adds. "As stated in
the Communication from the Commission on the
collection and use of expertise,
pluralism is a determinant of the quality of the scientific
ad i e. The efo e, he e e possi le, a di e sit of ie poi ts
should be assembled. This
diversity may result from differences in scientific approach, different types of expertise,
different institutional affiliations, or contrasting opinions over the fundamental assumptions
underlying the issue. Depending on the issue and the stage in the policy cycle, pluralism also
entails taking account of multi-disciplinary and multi-sectorial expertise, minority and non-
conformist views".
Various EMF-experts have pointed out on many occasions in the past years that ICNIRP is
wrongfully dismissing certain scientific studies showing adverse health effects and sticking,
in an almost dog
ati a , to the o i tio that o
-ionising radiation poses no health
th eats a d the o l effe ts it has a e the al . T o leadi g e pe ts, K o
hout and Portier
confirm to us that ICNIRP is a closed, non-accountable and one-sided organisation. As
con
luded ea lie , a losed i le of like- i ded s ie tists has tu ed ICNIRP i to a self-
indulgent science club, with a lack of biomedical expertise as well as a lack of scientific
expertise in risk assessment and risk management philosophies (similar to those used for
io izi g adiatio a d fo he i als , hi h ight lead to tu el- isio .
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Will world safety standards really be safe?
Several ICNIRP-members are, or were, also members of the International Committee on
Electromagnetic Safety (ICES) of the IEEE. This is an organisation in which many people from
the media and telecom industry and from the military are actively and openly involved. The
former chair of the ICNIRP-commission was a member of an ICES-committee. As we
mentioned in his portrait, ICES thanked Van Rongen for improving the relationship between
ICES and ICNIRP and for his willingness to discuss the harmonisation of ICNIRP-guidelines and
IEEE-exposure limits. In its latest published annual report (2016), ICES states:
ICES ill
maintain its collaborative relationship with ICNIRP with the goal of setting internationally
harmonized safety limits for exposure to electromagnetic fields at frequencies below 300
GHz. This intera
tio ith ICNIRP is o side ed a ajo step fo a d.
In 2016 Van Rongen invited members of ICES to give their comment on the new guidelines
for HF Fields. And ICNIRP took these comments very seriously. In 2017 during the annual
meeting of ICES
it as stated that ICNIRP has dela ed fi alizi g thei o lusio s to gi e full
o side atio of ICES s e o
e datio s .
The new chair of the ICNIRP-commission Croft was also member of ICES until December
2015. Seven other ICNIRP-scientists - Guglielmo d'Inzeo, Akimasa Hirata, Jose Gomez-
Tames, Ilkka Laakso, Kensuke Sasaki, John Tattersall and Tongning Wu
–
were or are also
members of an ICES-committee.
This clearly shows that ICNIRP has been working very closely with IEEE/ICES on the creation
of the new RF safety guidelines that were published this year. And this implies that large
telecom-companies as Motorola and others, as well as US military, had a direct influence on
the ICNIRP guidelines, which are still the basis for EU-policies in this domain.
Kromhout comments that he was unaware of the fact that several ICNIRP-members also
participate in ICES/IEEE. ICES/IEEE is not one of the organisations that is mentioned as a
collaboration partner on the ICNIRP-website. On the subject of the IEEE, the Dutch professor
ites that this is ot eall a i depe de t o ga isatio he it o es to ele t o ag eti
fields and
health.
Portier sees the membership of ICES as a potential conflict of interest. He indicates as an
example that the declarations of interests of some ICNIRP-members mention membership in
ICES, but no mention of the travel costs associated with that membership being covered by
ICES:
This has t o o se ue es. T a el ost ei u se e t is a pe k a d it ould e
removed if the member fails to give the right answer, hence a potential Conflict of Interests.
Secondly, being a member in ICES gives industry access to the ICNIRP member which would
ot e a aila le to the ge e al pu li a d a thus ias opi io s.
A membership of and close cooperation of ICNIRP-members with ICES, which for several
years held its annual meeti
gs at a Moto ola s a h,
can be considered as a possible
conflict of interest. As described, during the current leadership of ICNIRP, these ties got even
lose
with the goal of setting internationally harmonized safety limits for exposure to
ele t o ag eti fields .
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Ties that bind
A lot of ICNIRP-scientists have also participated in research work that was funded, or partly
funded, by the telecom industry.
The International Agency for Research on Cancer (IARC) has a strict policy when it comes to
inviting scientists to assist it in the writing of the famous monographs
–
like the one from
2011,
that lassified adiof e ue
ele t o ag eti fields as, possi l a i oge i to
humans (Group2B), based on an increased risk for glioma, a malignant type of brain cancer
asso iated ith i eless pho e use. I the fi al
Monograph 2012 report, it is stated that
each scientist must disclose pertinent research, employment, and financial interests during
the past 3 years, unless that a grant from for example a company does not exceed more
tha % of total esea h udget: All g a ts that suppo t the e pe t s esea h o positio
and all consulting or speaking on behalf of an interested party on matters before a court or
go e
e t age
a e listed as sig ifi a t pe ti e t i te ests.
In our introduction, we wrote that the European Food and Safety Authority (EFSA) has
slightly less stringent member-selection c
ite ia:
Research funding from the private sector
e efiti g EFSA s e pe ts should ot e eed % of thei total esea h udget.
It seems that this percentage is not exceeded by most of the members of the ICNIRP-
commission and Scientific Expert Group, insofar as we can trust their Declarations of
Personal Interest. But these declarations are often not complete. Anssi Auvinen, for
e
a ple, e tio s that he e ei ed €
,000 from the Mobile Manufacturers Forum for
the Finnish section of the COSMOS-study. But he does not mention what percentage of his
total research budget that amount constitutes. And Maria Feychting, former vice-chair of the
ICNIRP-commission, did not mention any research support received from commercial
entities in her Declaration of Personal interest, although a lot of her research actually was, as
e sho ed i he po t ait, fu ded i dust . So e of the e e s DOI s a e also
somewhat out of date. For example, the last DOI available for Isabelle Lagroye, published on
the ICNIRP-website, is dated October 2015.
The majority of ICNIRP-scientists did perform research partly funded by industry. But is this
important information? As we argue in the introduction, we believe it is. Scientific
publications, co-authored by two ICNIRP-scientists
–
Anke Huss and Martin Röösli, confirm
the importance of funding. In 2006 and 2009 they did a systematic review of the effect of
the
source of funding in experimental studies of mobile phone use on health, and their
conclusion was that,
industry-sponsored studies were least likely to report results
suggesti g ad e se health effe ts .
And theirs is not the only study that showed this kind of bias. Portier agrees in writing to us
that this is a p o le : The e ha e ee u e ous studies
of the differences in reporting
from industry-funded research versus publicly-fu
ded esea h that suggest a st o g ias.
David O. Carpenter,
professor of Environmental Health Sciences at the University at Albany,
explains the mechanism behind this claim in the preface of the book
Corporate Ties That
Bind - An Examination of Corporate Manipulation and Vested Interest in Public Health:
O e
of the g
eatest p o le s i s ie tifi dis o e , he ites, is the pe e sio that a esult
due to conflicts of interest. While there are other possible bases for conflicts of interest,
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most are financial. Individual scientists may have financial conflicts of interest that influence
the design of the studies they perform so that they obtain a result similar to that which they,
or their funders, want. When funding for scientists comes from an organization or
corporation with desires to present a clean bill of health to the public, there is strong
motivation to give the funder what they want, if only to continue receipt
of fu di g.
The Australian researcher, Don Maisch, claimed in his PhD-thesis,
The Procrustean Approach:
Setting Exposure Standards for Telecommunications Frequency Electromagnetic Radiation
(2010), that the dismissal by ICNIRP of all studies that show health effects of non-ionizing
adiatio sho s the i flue e i dust e e ises o ICNIRP: Su h dis issal a , o the
surface, appear to be objective expert opinion, but an examination of ICNIRP
s isk
assessment processes finds, however, that power industry influence is endemic to the
process. This influence appears to be aimed at ensuring economic protection for the industry
against the need to spend enormous amounts of money on upgrading distribution networks
as well as the risks of litigation if more restrictive limits were ever put in force.”
According to Maisch, the essence is that the thermal limitations of the IEEE standards and
the ICNIRP RF
Guideli es a e said to e little o e than
an outdated artefact from a half-
century ago, maintained by a scientific elite who have long staked their scientific credibility
on maintaining that viewpoint. From their perspective, to retreat from that paradigm would
be to admit that they had it wrong
afte all.
Te ea s afte Mais h pu li atio a d a othe si ila iti
isms, ICNIRP still adheres to
the pa adig that the o l p o e effe ts a e the al. ICNIRP appea s to take i to a ou t
only the warming of tissue and uncontrolled muscle contractions, although they claim in the
ost e e t ad i e, that the also e aluated othe e ha is s , ites K o hout.
As many scientists and critical observers have pointed out, it seems as if ICNIRP members are
either oblivious or ignoring scientific studies that find possible adverse health effects where
there is an absence of heating. Even when some ICNIRP-members themselves acknowledge
that industry-funding of scientific research tends to have less positive findings, and publicly
funded studies
–
like the NTP-study
–
does find significant links between EMF and adverse
health effects, this does not seem to influence one iota the views of ICNIRP-members.
A mixed bag of responsibilities
In an e-mail we received from Lloyd Morgan, Senior Research Fellow of the
Environmental
Health Trust
and Director of the Central Brain Tumor Registry of the United States, is very
iti al of oth ICNIRP a d go e
e ts:
Who are ICNIRP? The International Committee on
Non-Ionising Radiation Protection (ICNIRP) are a private, self-appointed body or NGO who
together with the Advisory Group on Non-ionising Radiation (AGNIR) and Public Health
England (PHE), have somehow ended up effectively setting microwave radiation exposure
'safet ' sta da ds fo the populatio s of la ge pa ts of the o ld si e the
s, he ites.
What a azes e, a d si ultaneously
sickens me, is how did ICNIRP convince a large
number of "independent" nations to adopt ICNIRP's so called "standards"?
Morgan suspects that high-le
el pe so s i the go e
e t s ad i ist atio as a le to
have the legislation passed because almost no-one in the government understood what was
happe i g.
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ICNIRP only publishes guidelines. It is then up to national governments to decide if they pass
these guideli es i to la . A o di g to Llo d Mo ga , that pla es the u de o ea h
national gove
e t, should its itize s file a la suit .
Clearly, the Telecom sector as a whole, and the auctioning off of bandwidth and selling of
Telecommunication licenses, are an important source of cash income for governments. The
analogy with the Tobacco sector
has ofte ee
ade s hola s ho stud egulato
aptu e , ut the e is also
an important similarity between the tobacco and telecom sectors
in terms of their importance for State budgets.
The
auctioning off of Radio frequency spectrums
brings in billions of euros for European
countries. Telecom companies also earn billions of euros thanks to these spectrum
a uisitio s, si e o i g the ight to use a spe ifi adio f e ue
spe t u is
an
essential resource for telecommunication services such as mobile telephones, TV and radio
broadcasting, satellite and broadband communications.
a ou ed
The
European 5G Observatory
notes that,
Ge a s Fede al Net o k Age
that the 5G auction, which started in March 2019, ended with 6.55 billion euros offered in
total by the four bidders.
Deutsche Telekom
and
Vodafone
Germany criticized high prices of
it sa s:, f o
the ou t s au tio . I the
5G Action Plan
as adopted the EU i
September 2016, member states will be required to authorise the 700 MHz-band by 2020,
unless there are justified reasons for delaying it until mid-
at the latest , epo ts the
European 5G Observatory.
The O se ato also stated, i Ap il
, that e eptio al
circumstances caused by the Covid-19 epidemic have forced some countries in Europe to
postpone 5G auctions scheduled in the first months of 2020. Four EU countries, Austria,
France, Spain and Portugal have postponed spectrum auctions for 5G due to the Covid-19
epide i so fa .
The European Commission selected the consultancy firm,
Idate-digiworld
to carry out the
European 5G Observatory,
to monitor the rolling out of the 5 G Action Plan. IDATE-
DIGIWORLD is a smart-looking consultancy company and self-de
la ed Eu opea thi k-tank
for members, policy-
ake s a d pla e s of the digital t a sfo atio , ith so e of the
largest telecom operators and producers as its clients.
One of those
lie ts, is t a Tele o gia t, ut a go e
e tal egulato ,
Ofcom in the UK.
European 5G Observatory
epo ts that Of o
opened a consultation on human exposure to
Electromagnetic Field Emissions (EMF) in the UK. The consultation started on February 21th
2020 and
e ded o Ma
th
: The egulato p oposes to i lude a spe ifi o ditio
in telecom licences requiring
li e sees to o pl ith ICNIRP guideli es. {… At the sa e
time, Ofcom released the results collected close to 16 5G base stations in 10 cities across the
UK and to 60 GHz fixed wireless equipment in Liverpool. In all cases, the measured EMF
levels from 5G base stations were far below the ICNIRP Guidelines (the highest level was
approximately 1.5% of the relevant level); the 5G share of the total emissions level observed
as u e tl e lo .
To the uestio , Is ICNIRP espo si le? , Paolo Ve hia,
former Chairman for ICNIRP (2004-
2012)
answered very clearly at a conference in September 2008
that the ICNIRP guideli es
are neither mandatory prescriptio
s fo safet , the last o d o the
issue, nor are they
defe si e alls fo I dust o othe s. This state e t akes it lea that the de isio to
adopt these guideli es i to atio al legislatio as suffi ie t to p ote t pu li health is
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political. The possible misuse by governments of ICNIRP and its guidelines seems to be
another key question, that still needs looking into and answering.
On the other hand, ICNIRP presents itself as the provider of scientific truth. For example, in
a report
fo the I ish go e
e t, u de the headi g, Re o
e datio s I te atio al
Guideli es it states that the e should e st i t o plia e ith ICNIRP guideli es: The
ICNIRP guidelines on exposure limits have been recommended by the European Commission
to its Member States, and they provide science-based exposure limits that are applicable to
both public and occupational exposure from RF and ELF fields. They also provide sound
guidance on limiting exposure from mobile phones and masts, as well as for power-line
fields. The ICNIRP guidelines provide adequate protection for the public from any EMF
sources. While the guidelines were published in 1998, they are constantly under review and
still have appropriately protective limits. The guidelines are based on a weight of evidence
review from all peer-reviewed scientific literature and not on the conclusions of any single
s ie tifi pape .
Even as ICNIRP has been positioning itself during the last 25 years as the sole scientific truth
when it comes to possible relation between EMF and adverse health effects, it would not be
correct to hold this scientific NGO accountable if one day it would be undisputed that EMF
causes health problems. National governments have their own responsibility to protect their
itize s, just as the Eu opea Co
issio has, hi h afte all is the Gua dia of the T eat
a d the efo e should also take the legall i di g p e autio a p i iple i to a ou t.
The telecommunication industry applauds ICNIRP
In most policy fields, industry keeps reiterating that the limits scientific advisory committees
propose are too strict. But in the case of the exposure limits for non-ionizing radiation the
telecom industry seems very content with the norms ICNIRP proposes. In many reports over
the past twenty years, the Telecoms lobby in Europe has always referred to the safety
assurances published by ICNIRP.
In its Environmental Report of 2005, the European Telecommunications Networks
Ope
ato s Asso iatio ETNO
ote: Co e i g the Eu opea U io s legislati e a d
policy framework on EMF, ETNO has been in direct contact with EU institutions. The
association has provided a steady stream of facts and advice to legislative bodies in order for
the EU to base its Directive conce
i g i i u health a d safet e ui e e ts ega di g
the exposure of workers to the risks arising from physical agents (electromagnetic
fields o
a sound scientific basis as provided by the International Commission on Non-Ionising
Radiatio P ote tio ICNIRP .
Thirteen years later, the Boston Consulting Group, in a report
ith the o i ous title,
A
playbook for accelerating 5G in Europe
, pleads fo the ha o ized li its ICNIRP a d also
IRPA and the WHO EMF project) proposes, and criticizes governments that apply stricter
limits. Exactly the same point was made by ETNO in a public consultation by the European
Co
issio . ETNO as i fa ou of the ha o ised ICNIRP li its .
The same word,
harmonised,
comes back in a plea for
a ha o ised EU app oa h to G
se u it
that ETNO launched
o
Ja ua
. We the efo e el o e toda s
pu li atio of the G Se u it Tool o , p ese ted EU Me e States ith ENISA a d
the Eu opea Co
issio . Eu ope s de isio
-making on 5G should continue being based on
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facts, it should be proportionate to threats and build on a solid understanding of technology
reality. In this context, we invite National Governments to avoid disproportionate actions
that negatively impact the
i est e t li ate, a d hi h ould i tu ha
oth Eu ope s
competitiveness
a d its st ategi positio i G de elop e t.
ETNO argues that rules and regulations should not hamper but support European
i est e t a d i o atio , e ause egulato p essure
still risks holding back European
investment and innovation on many fro
ts … The speed of G ollout is sig ifi a tl slo ed
e essi e spe t u p i es a d halle gi g li e se o ditio s.
ETNO continues to explain the policy-
ish list: The oppo tu
ity of fully unleashing fibre
deployment awaits a pro-investment implementation of the European Electronic
Communications Code. Regulatory asymmetries, especially in the field of data, still hold back
European innovation. Market fragmentation still affects
Eu ope s full pote tial i et o k
investment. European institutions and national governments both have a major role to play
i e o i g su h a ie s.
Yet again, ETNO does not lobby for lowering the ICNIRP standards, these are not seen as part
of the egulato p essu e that ha pe s te h ologi al de elop e t. O the o t a
: the
o s ICNIRP p oposes a e the ha o ised li its that ETNO el o es.
All in all, the telecom-se
to see s to e uite pleased ith ICNIRP s positio i g. This is
deviating from the standard procedure in EU-policy making where a specific industry
concerned will on essential aspects always try to influence laws and regulations in their
favour through various ways of lobbying. Apparently in case of ICNIRP there is simply no
need to do so.
The Telecom Lobby
In order to promote a continuation of favourable policy-making, European telecom
companies have many lobby-meetings with the European Commission, and no doubt also at
national political levels. According to
the EU transparency Register,
ETNO has a
budget of
over one million euros for lobbying and representing
Eu ope s tele o o pa ies. With at
least seven registered lobbyists, ETNO had 70 registered lobby meetings with the European
Commission (EC) in 2
. ETNO s p i a pu pose is to de elop top-level
policy papers and
support members in promoting a positive policy environment allowing the EU
telecommunications sector to deliver best quality services to consumers and businesses. We
also organize some
of the ai Eu opea e e ts fo dis ussi g tele o a d digital poli .
But of course, the individual telecom companies also have lobbying budgets and lobbyists
representing them at the European institutions in Brussels.
Ericsson had a lobby budget
of
700.000 euros and five accredited lobbyist in 2019,
Telefonica had a lobbying budget of 1,8
million
euros and 6 lobbyists who covered no less than 83 meetings with the EC,
Deutsche
Telekom had a 1,5 million lobbying budget,
with 5 lobbyists and a total of 110 lobby
meetings with the EC.
In early December 2019,
a large delegation of CEOs from ETNO met with Margrethe
Vestager,
Executive Vice-P
eside t of the Eu opea Co
issio espo si le fo
Europe fit
for the Digital Age
. The delegatio i luded: Ti Hoettges
from
Deutsche Telekom,
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Stephane Richard from
Orange;
Thomas Arnolder from
Telekom Austria,
Salvatore Rossi
from
TIM,
Alexandre Fonseca from
Altice Portugal,
as well as the Chairman of ETNO, Steven
Tas, the Director General of ETNO, Lise Fuhr, and senior representatives from
Telefonica
and
Telenor.
At the end of January 2020, an important event was held, the
European 5G conference.
It
welcomed more
tha
delegates, ho dis ussed the
necessary next steps to ensure the
su ess of G i Eu ope .
Eric Van Rongen, at the time still ICNIRP-Chair, was among the
speake s ho p o ided the audie e ith i sightful ie s o thei a eas of e pe tise. The
purpose, apparently, was not to discuss the sagacity and safety of rolling out 5G, but rather
to ensure the success of 5G deployment.
It is important to note that the efforts of the telecom industry to influence regulatory
agencies often take illegal forms. Telecommunications companies are high
on the list
of the
companies that were penalised in the U.S. for corrupt practices. European companies like
Ericsson, Alstom
and
Telia
are in the top ten.
Also significant, is the fact that more and more
world leading insurance companies
are
backtracking from insuring telecom companies concerning the risks around EMF. In March
2019, in its
SONAR E e gi g
risk
i sights
epo t, o e of the o ld s la gest i su a e
companies,
Swiss Reinsurance Company
(Swiss Re), classified
u fo esee
consequences of electromagnetic
fields i to the highest isk lass, togethe
with endocrine disrupting chemicals.
The u i uit of ele t o ag eti fields EMF aises
concerns about potential implications for human health, in particular with regard to the use
of mobile phones, power lines or antennas for broadcasting. Over the last decade, the
spread of wireless devices has accelerated enormously. The convergence of mobile phones
with computer technology has led to the proliferation of new and emerging technologies.
This development has increased exposure to electromagnetic fields, the health impacts of
hi h e ai u k o .
The lobby power of the telecom-industry in Brussels, the decision-making heart of the EU, is
enormous. Yet the corporations involved do not have to lobby the guidelines and health
advice related to their technology, because
ICNIRP has ee p o idi g the safet
e tifi atio fo o e
ea s. At the sa e ti e the i surance
sector is not very assured
and does not want to pay possible litigation costs once telecom companies would get sued,
which is
happening more and more frequently.
The call for more independent scientific assessment in this area
Almost ten years ago, in May 2011, the Council of Europe adopted a report from Mr Jean
Huss on
The pote tial da ge s of ele t o ag eti fields a d thei effe t o the
en
i o e t
. It stated that the findings of scientific research on the possible risks of
electromagnetic fields were inconclusive and contradictory. In the light of the correlation
et ee o igi of fu di g a d the fi di gs it alled fo ge ui e i depe de
ce on the part
of the expert appraisal agencies and for independent, multidisciplinary and properly
balanced expert input. There must no longer be situations where whistle blowers are
discriminated against and renowned scientists with critical opinions are excluded when
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experts are selected to sit on expert committees or no longer receive funding for their
esea h.
In the meantime, not a lot seems to have changed. In a letter,
published this year in
Bioelectromagnetics,
three researchers - Steven Weller , Victor Leach and Murray May - of
the Aust alia O ea ia Radiof e ue
S ie tifi Ad iso Asso iatio ORSAA
ite:
Half a e tu of s ie tifi esea h i to the safet of
EMFs (from static to 300GHz) has not
resulted in any substantial policy advice changes. The question that we believe needs to be
asked is as follows: Is the continuing unchanged policy advice on EMFs occurring because
those who are trying to advocate change have no voice in the process and because the
process is domi
ated g oups ith self‐i te ests i
ai tai i g the status uo?
The th ee esea he s poi t to the fa t that adiof e ue
ele t o ag eti adiatio is a
oo i g ulti‐t illio
-dollar industry globally, and changing current prescribed safety levels
to more stringent standards would bring about unfavourable financial consequences and
affect industrial and military functions. In some countries, such as Australia, the regulator,
which has a health protection responsibility, also sells RF spectrum licenses, which
represents a clear conflict of interest. The very same agencies with responsibility for
providing safety advice to the public are also considered by some to have been captured by
the i dust .
The huge financial weight and power of the telecom companies is something the industry
itself also stresses.
I its epo t f o Ja ua
,
The State of Digital Communications
2020
,
ETNO
oasts that its Tele o
e e s a e th i i g a d usi ess is oo i g:
Telecom
is Eu ope s ajo te h olog usi ess, ith a € . illio pe ea alue added
a d t ai i g o the ise. … Of the Eu ope-based
companies figured in the 2019 Forbes
Digital 100 index, 11 are either telecoms operators or telecoms equipment vendors, and
o e tha half of the a e ETNO e e s.
Whethe o ot ICNIRP is aptu ed i dust , a e a ka le fa t is that the o ga isatio
that appea s to e the o ld s ost i po ta t od espo si le fo ad i e o o
-ionizing
radiation is a private organisation, not a public authority.
To e it see s ise if the EU a d atio al go e
e ts stop el i g o l o the ad i e of
ICNIRP. A o
ittee of its o is ot a u e essa lu u , Ha s K o hout ites. Whe
we ask him if it would seem to him more logical that it be a public organisation giving advice
on non-io
izi g adiatio , he a s e s: I o pletel ag ee.
But this is not what is happening in the heart of the European Union.
A o di g to ICNIRP s
website
there is a
contractual partnership
between the European Commission, which is the
Guardian of the Treaty, and thus also of the legally enshrined
precautionary principle.
It
states: The Eu opea Co
issio a d ICNIRP olla o atio o e the ea s, elies o a ual
or specific contracts, such as the Concerted Action within FP5 - Life Quality, Key action
Environment and Heath. ICNIRP also takes part, in consultation together with other
stakeholders, on the development of directives and liaises, upon request, with different EC
entities, such as the Scientific Committee on Emerging and Newly Identified Health Risks
(SCENIHR). Support to ICNIRP is provided by the European Commission through its
Directorate General Health and Safety at Work as part of an EC grant agreement, as laid
down
i the ICNIRP epo ts.
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Given the experience with ICNIRP of the past 25 years, the growing body of evidence that
there are serious concerns on adverse effects of EMF on public health and the huge
economic interests involved, it seems not very wise for the European Commission and
national governments to base their policies solely on the ICNIRP guidelines and advice.
Ch is Po tie ag ees sa i g that go e
e ts ha e o sa i the go e a e o
membership of ICNIRP. In addition, without their own review committees, governments do
not have their own experts to advise them about these topics. I believe it would be best if
such an entity was run by a trusted organization that has some form of government
o e sight.
Po tie s adds i
iti g to us: I ha e
een in the position of managing, running, chairing
and/or being a member of dozens of national and international committees. These were
always government committees or WHO-related entities. When run properly, governments
can get excellent advice on issues. There is usually a place for interested parties (industry,
concerned citizens) to express their opinions to these committee members at public forums.
And there are legal consequences to providing false information on Conflict of Interest
forms, etc. All of these reasons lead one to believe a government managed Commission
ould e ette .
We think that the call for more independent scientific assessment in this area is, for all the
arguments mentioned in the above, fully justified.
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IV - Conclusion
ICNIRP presents itself, and is described by the European Commission and in the media, as an
independent international commission that gives advice based on scientific evidence. We
believe that there are various reasons to question this (self)-image.
The composition of ICNIRP is very one sided. With only
one medically qualified person (but
not an expert in wireless radiation) out of a total of 14 scientists in the ICNIRP Commission
and also a small minority of members with medical qualifications in the Scientific Expert
Group, we can safely say that
ICNIRP has been, and is still, dominated by physical scientists.
This may not be the wisest composition when your remit is to offer advice on human health
and safety to governments around the world.
As one can read in the 45 portraits of the members of the ICNIRP commission and of the
Scientific Expert Group (SEG), they all share the same position on the safety issues: non-
ionising radiation poses no health threats and the only effects it has are thermal. ICNIRP
says "non-ionising radiation poses no health threats if it does not heat the tissue by more
than 1 °C", by which it admits that there are possible health effects, but only if exposure
levels to strong radiation are too high .
Over the past years, and on many platforms, various EMF-experts have stated that ICNIRP is
wrong to continue dismissing certain scientific studies showing adverse health effects
–
like
the American NTP-study - and is mistaken in its
al ost dog ati o i tio that o
-
ionising radiation poses no health threats and the only possible health effects it has are
thermal in case of strong radiation .
Even after much criticism from members of the global scientific community, ICNIRP still
adheres to the paradigm that the only proven effects (on health)
a e the al. ICNIRP
appears to take into account only the warming of tissue and uncontrolled muscle
contractions, although they claim in the most recent advice, that they also evaluated other
e ha is s , ites Dut h P ofesso Ha s K o hout, ho
is currently leading a long-term
study (in the Netherlands) into the effects of mobile phone use on human health, and who is
chairman of a special committee on Electromagnetic Fields of the leading Dutch Health
Council, which advises the Dutch government.
It seems
that a losed i le of like- i ded s ie tists has tu ed ICNIRP i to a self-
indulgent science club, with a lack of bio-medical expertise, as well as a lack of scientific
expertise in specific risk assessments. Thereby, creating a situation which might easily lead
to tu el- isio i the o ga isatio s s ope.
Two leading experts, Hans Kromhout and Chris
Portier, confirmed to us that ICNIRP is a closed, non-accountable and one-sided
organisation.
As many scientists and critical observers have pointed out, it seems that ICNIRP members
are either oblivious to, or are ignoring, scientific studies that find possible adverse health
effects in the absence of heating. Even though some ICNIRP-members have themselves
acknowledged that industry-funded scientific research tends to produce less findings
showing adverse health effects of EMF, whereas publicly funded studies
–
like the NTP-study
–
do find significant links between EMF and adverse health effects, this does not seem to
influence one iota the views of ICNIRP-members.
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The majority of ICNIRP-scientists have done, or are doing, research partly funded by
industry. Is this important? As we argue in the introduction, we believe it is. Scientific
publications, co-authored by two ICNIRP-scientists
–
Anke Huss and Martin Röösli, confirm
the importance of funding. In 2006 and 2009 they did a systematic review of the effects of
the source of funding in experimental studies of mobile phone use on health, and their
conclusion was that,
industry-sponsored studies were least likely to report results
suggesti g ad e se health effe ts . A d thei s is ot the o l stud that sho ed this, as
there have been numerous studies of the differences in reporting from industry-funded
research versus publicly-funded research that suggest a strong funding bias on the results.
In addition to the fact that certain members of ICNIRP, are simultaneously members of the
International Committee on Electromagnetic Safety (ICES) of the US-registered Institute of
Electrical and Electronics Engineers (IEEE), we have seen further evidence of a close
cooperation between ICNIRP and ICES, an organisation in which many people from the
media and telecom industries, as well as from the military, are actively and structurally
involved.
During
the current leadership of ICNIRP, these ties have become
e e lose
with
the goal of setting internationally harmonized safety limits for exposure to electromagnetic
fields .
This must surely be considered as a situation in which conflicts of interest are a real
possibility.
It is clear
from ICES minutes
that ICNIRP worked very closely with IEEE/ICES on the creation
of the new RF safety guidelines that were published in March 2020. And this implies that
large telecom-companies such as Motorola and others, as well as US military, had a direct
influence on the ICNIRP guidelines, which are still the basis for EU-policies in this domain.
Although there is a lot of lobby-power by the telecom sector in the European Union (both in
Brussels and in the member states),
the Eu opea Tele o
u i atio s Net o ks Ope ato s
Association (ETNO) does not lobby for lowering the ICNIRP standards, as these are not seen
as pa t of the egulato p essu e that ha pe s te h ologi al de elop e t. O the
o t a : the o s ICNIRP p oposes a e the ha o ised li its that ETNO el o es. All i
all, the telecom-se
to see s to e uite pleased ith ICNIRP s positioning.
This deviates
from the standard procedure in EU-policy making, where a specific industry concerned will,
on essential aspects, always try to influence laws and regulations in its favour through
various lobbying strategies. Apparently, in the case of ICNIRP, there is simply no need to do
so. At the same time, the insurance sector does not, at present, seem very reassured and
does not want to be put in a situation of having to pay potential litigation costs, if and when
telecom companies get sued, something that is happening more and more often.
Despite ICNIRP positioning itself, during the last 25 years, as the sole purveyor of scientific
truth when it comes to possible relation between EMF and adverse health effects, it would
not be right to hold this scientific NGO solely accountable if, one day, it were to become
undisputed that EMF do cause health problems. National governments, as well as the
European Commission, which is,
afte all, the Gua dia of the T eat ,
have a duty of care
and protection of their citizens, and therefore should also take the legally binding
p e autio a p i iple i to a ou t.
We think that the call for more independent scientific assessment in this area is, for all the
arguments mentioned above and in what follows, fully justified.
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That is the most important conclusion of this report: for really independent scientific advice
we cannot rely on ICNIRP. The European Commission and national governments, from
countries like Germany, should stop funding ICNIRP. It is high time that the European
Commission creates a new, public and fully independent advisory council on non-ionizing
radiation. The funds currently allocated to ICNIRP could be used to set up this new
organisation. And given the overall rise in R&D funding via Horizon Europe, with a foreseen
budget (for 2021-2027) of between 75 and 100 billion euros, funding should in no way
constitute an insurmountable hurdle to setting up this new, truly independent, body.
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V - PORTRAITS OF THE ICNIRP-MEMBERS
ICNIRP COMMISSION:
Gunde Ziegelberger (Scientific Secretary)
Biography
O ICNIRP s
website we read that Gunde Ziegelberger holds a PhD in Biology and after a
career at the Max-Planck-Institute, she joined the Federal Office for Radiation Protection
(BfS) in 2002, where she works on "Non-Ionizing Radiation". Since 2004 she also worked as
Scientific Secretary for ICNIRP- she replaced Rüdiger Matthes, who became a commission
member - and in that function, she is also a member of the ICNIRP Board together with the
Chair (see Croft) and Vice Chair (see Van Rongen).
ICNIRP s e site la ifies: The th ee
Board members represents ICNIRP externally and mostly in its relations with the
international and national partners and the press. The Scientific Secretariat is in charge with
some specific scientific projects mostly related to workshops and with all administrative and
operational tasks.
Position
In February 2019 Dr Ziegelberger gave a
short interview
in which she stated that when the
li it alues a e espe ted so fa s ie tifi fi di gs sho that hu a ei gs do t u a
isk
from electromagnetic radiation.
Ziegelberger functions as Scientific Secretary of ICNIRP, she co-authors many scientific
publications with ICNIRP-members. In September 2016 for example Ziegelberger was co-
author of
a publication
A
Closer Look at the Thresholds of Thermal Damage: Workshop
Repo t a ICNIRP Task G oup . The a ti le o ludes the o kshop –
co-organsied by the
WHO and financed by the European Commission, the Turkish Ministry of Health, the
International Radiation Protection Association (IRPA), the German Federal Ministry for the
Environment (BMUB), and the Finnish Radiation and Nuclear Safety Authority (STUK). The
o lusio sho s that the o kshop ill p o ide alua le i put i to
the revision of the
guidelines being
fo ulated ICNIRP fo li iti g hu a e posu e to RF fields. It as also
clear that only thermal (adverse) effects were discussed as was the case in the new ICNIRP
guidelines from 2020.
She co-authored as BfS -researcher
a study
within the ARIMMORA risk assessment which
concluded that
the elatio ship et ee e posu e
to the agent ELF-MF and risk of
childhood leukaemia
is o side ed o siste t ith IARC G oup B lassifi atio of possi l
carcinogenic to humans (Fig. 1). This category is the result of limited evidence of
carcinogenicity in humans and inadequate evidence of carcinogenicity in experimental
a i als.
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Possible conflicts of interest.
Although Ziegelberger plays an important role for ICNIRP, given her position in the board
and the fact that she works in an important department for radiation protection (BfS) of the
German government, we could not find any DOI.
Rodney Croft (chair as of May 2020)
Biography
Rodney Croft is a
psychology researcher
. He works as professor of Health Psychology at the
School of Psychology, University of Wollongong, Australia.
He joined the ICNIRP Biology Standing Committee in 2008 and the Main Commission in 2012,
to become chair in May 2020.
ICNIRP s e site states that his
research focuses on the delineation of human brain function,
as well as psychiatry more generally. He participates in a variety of national and international
scientific and government committees, was Executive Director of the Australian Centre for
Radiofrequency Bioeffects Research ((ACRBR 2004-2011) and is currently Director of the
Australian Centre for Electromagnetic Bioeffects Research.
In June 2011, Rodney Croft as Executive Director of ACRBR
announced that
the organisation
would cease operatio
s e ause it had een
unable to secure further funding to continue
its esea h a ti ities . But a of the ACRBR Di e to s ould e a le to o ti ue thei Rf
research but under the banner of the Bioelectromagnetics Research Group, part of the Brain
and Psychological Sciences Research Centre (BPsyC) at the Swinburne University of
Te h olog , hi h has fo a
ea s e lose ties to Telst a, Aust alia s iggest Tele o
company.
In August 2012 Croft received new funding when Australian Minister for Health, Tanya
Plibersek, announced the establishment of a new $2.5 million NHMRC Centre of Excellence:
the Australian Centre for Electromagnetic Bioeffects Research (ACEBR) to be based at the
University of Wollongong and led by Professor Croft. One of the central university partners
of the ACEBR research Swinburne University.
Position
Croft is a typical ICNIRP member and has been defending for years and from different
positions the point of view that there are no dangers associated with the use of mobile
phones. On the ABC Lateline program (April 4, 2009) Dr. Rodney Croft, then Director of
ACRBR, stated: The e eall has ee a lot of esea h do e to date a d the esea h has
e lea l sho that the e a e t a effe ts. With hild e , I eall do t think
there is
any eviden
e suggesti g that this ight e a p o le . The e is t a thi g to suggest that
e a ha e to e a little it o e autious.
Much earlier in 2003 the Australasian College of Nutritional and Environmental Medicine
(ACNEM)
published a paper
Do Mais h that detailed easo s h e t a p e autio s
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needed to be taken for children and cell phone use. The paper included a number of
statements of concern specific to this issue from scientific and medical organizations
internationally and concluded
ith the uestio : Is it o th the isk to o ti ue to allo
u est i ted ell pho e use
hild e .
In 2008 the
Russian National Committee on Non-Ionising Radiation Protection (RNCNIRP)
issued offi ial ad i e that the health of the p ese t ge e atio of hild e a d futu e
ge e atio s is u de da ge f o ell
phone use and therefore the committee has
recommended that cell phone use be restricted for people under 18 years of age.
C oft said i
: With hild e , I eall do t thi k the e is a e ide e suggesti g that
this ight e a p o le . The e is t anything
to suggest that we may have to be a little bit
o e autious A d to isuall a k up ACRBR s o hild e a d ell pho e use o the
ACRBR web site
pu lished
an animated image that included images of children happily
usi g ell pho es .
In 2009
a scientific review paper
with Van Rongen and Croft as first and second authors
espe ti el stated. Subjective
symptoms over a wide range, including headaches and
migraine, fatigue, and skin itches, have been attributed to various RF sources both at home
and at work. However, in provocation studies a causal relation between EMF exposure and
symptoms has not been demonstrated, suggesting that psychological factors such as the
conscious expectation of effe
t a pla a i po ta t ole i this o ditio . The a ti le
e tio s that all autho s a e eithe u e t o fo e e e s of the Sta di g Co
ittee
on Biolog
of the ICNIRP ut does ot e tio a thi g o fu di g of the stud .
During an
International Workshop on RF Measurements, Research Studies & Standards
Development
in 2018 Croft downplays scientific research that shows effect from EMF by
sa i g that Cou te ala i g is e essa to e a le app op iate i te p etatio of data a d
Co lusio s ust e ased o the s ie tifi lite atu e, ot just a data set .
In 2019, Croft and a researcher (expert in antipsychotics) were awarded 1.2 Million$ for a
project entitled "Exposures of mobile phone radiofrequency electromagnetic energy in
juveniles: effects on brain development and behaviours." Neither of the two researchers are
experts in the area of brain development, developmental psychology or juvenile behaviour.
Within ICNIRP, Rodney Croft was the chair of the Project Group that was tasked with
preparing the new ICNIRP Guidelines, published early 2020.
According to critics,
ICNIRP still
dismisses completely: the existence and significance of non-thermal effects, existence of the
risk of cancer in long term avid users of mobile phones,
IARC s lassifi atio of RF
as a
possible human carcinogen (the IARC monograph review of science was not included in list
of science reviews used by ICNIRP in preparation of the new guidelines).
Possible conflicts of interest
Just like his predecessor Van Rongen, Rodney Croft provides unpaid services to the IEEE ICES
SC/4 Standards committees, a US version of ICNIRP, with a broad number of representatives
from both military and telecom industry; ICES boasted
that the had at least t o e e s
of ICES as members of the new 13 person ICNIRP Project Group (PG) on HF guidelines (up to
300 GHz), of which the PG Chairman (Croft), is now very willing to work with ICES to develop
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science based safety standards. This will enhance the possibility of harmonizing international
RF safet sta da ds.
Croft also advises the EMF reference group, and a community group managed by the
Australian Government organization, ARPANSA. He receives
funding from the Electric Power
Research Institute EPRI
for a project investigating RF effects on EEG and thermoregulation.
To possi l a s e this uestio a ief e a i atio of ACEBR s S ie e & Wi eless
se i a Health & Futu e RF Te h ologies is a i di atio . I the se i a
acknowledge
e ts, the follo i g as stated: The ACEBR g atefull a k o ledges the
financial support of the National Health & Medical Research Council of Australia and Telstra
Co po atio , hi h has e a led SW
to u .
I Rod e C oft s i t odu tio to the p ese
tation by Mr. Mike Wood from the Australian
Mobile Telecommunications Association (AMTA) on "4G telecommunications technologies",
he said the follo i g, i pa t: Clea l hat e see he e is a hole lot of e te h ologies
which are going to come about. Ho
do e k o
hat s goi g to e ost ele a t to us?
Well, in the short term I think that our industry representatives are going to give the best
i di ato of this
Croft was appointed in 2014 an Associate Editor of the BEMS journal of the
Bioelectromagnetics Society (BEMS); The annual meetings of
BEMS are a heavily industry
sponsored event.
The
annual meeting celebrating
the Bioelectromagnetics Society (BEMS)
and the European Bioelectromagnetics Association (EBEA) was in 2015 in California (USA),
had sponsors including companies such as, the Electric Power Research Institute (EPRI),
Mobile Manufacturers Forum (MMF), Korean Institute of Electromagnetic Engineering
Society (Mobile EMF Consortium) and, GSM-ATM5.
Croft also held talks and
expert opinion
on behalf of industry and for
the Mobile
Manufacturers Forum,
a o so tiu of the o ld s ajo ell-phone
companies. At a 5G
Conference in Dubai In December 20, 2019, Croft held a lecture on behalf of ICNIRP
alongside ICES Chairman Jafar Keshvari and TC95 Chairman C-K. Chou.
He joined the conference organized by the Telecommunication Regulatory Authority (TRA) of
the United Arab Emirates held on December 8-9, 2019 in Dubai. Three presentations were
o RF e posu e safet li its: G RF safet o e s: Ne IEEE StdC . TM-
C-K.
Chou;
S ie tifi Basis of G E posu e Li its IEEE C . :
Sta da d
Jafar Keshvari,
a d E su i g G Safet ith the Ne ICNIRP Guideli es
kHz to
GHz
Rod e
Croft of ICNIRP.
Croft has also actively
collaborated in research with Ray McKenzie,
who is a manager at the
Mobile Carriers Forum (MCF) which is a special division of the Australian Mobile
Telecommunications Association (AMTA) dealing with the policy, regulatory, public
communications and health and safety aspects of the deployment of mobile networks in
Australia.
On his website Croft's disclosure statement says: Rodney Croft has consulted to a range of
organisations such as Shelharbour City Council, Department of Defence, Comcare and Optus.
According to
his ICNIRP declaration of interests
he received personal remuneration for
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providing data analysis services to Heptares Therapeutics Ltd, a pharmaceutical company.
And Croft received personal remuneration for providing advice to Australian Bureau of
Statistics (ABS) on effects of RF devices used by field staff on field staff, resulting from a
contract between University of Wollongong and ABS. He also received personal
e u e atio fo p o idi g ad i e to
Victorian Government on conducting
bioelectromagnetics research, resulting from a contract between University of Wollongong
a d Vi to ia Go e
e t .
As explained before in this report the Australian government receives billions from issuing
spectrum licences to Telecom operators. In Australia, this licensing is carried out by industry
regulator ACMA, the Australian Media Communications Authority. ACMA also collects a
separate levy or tax from the wireless industry, money that is earmarked for scientific
research on RF-EMR. ACMA then diverts $300,000 to the other government institution
ARPANSA (Australian Radiation Protection & Nuclear Safety Agency) for its public
information campaign) and $700,000 to the National Health & Medical Research Council
(NHMRC).
According to the Australian resea
h g oup ORSAA the o e that
the Australian NHMRC
receives in order to provide grants for medical research has mostly gone to industry-friendly
researchers who have direct links with the wireless industry. For example, the largest
recipient of this NHMRC research funds is Prof. Rodney Croft. He has essentially been the
head of RF-EMR health research in Australia, despite his questionable qualifications for this
health research role. Prof. Croft has
received ample direct industry funding
in addition to his
lucrative NHMRC grants,
hi h should e te ed i di e t i dust fu di g. C oft as the
only Australian who played a part in determining what NHMRC research on EMR and health
should be funded.
He used his international contacts at the WHO to get more Australian funding. This is how it
worked behind the scenes: Croft was invited
from Australia to the WHO for an expert
consultation
to determine which areas of medical research was needed; The Australian
NHMRC research on EMR then looked to the WHO guidelines (co-influenced by Croft and
ICNIRP or
hi-jacked as some critics say)
in order to decide their funding priorities (the 2010
WHO RF Research Agenda is the basis of funding for NHMRC research grants). Croft's
laboratory then received the funding and has continued to get most of the research money
over many years.
Croft had
good relations
with
an influential industry man, Dr K. Joyner.
Which researchers or
research groups have been granted the NHMRC funds has been influenced to a large extent
by Joyner, who was
Moto ola s Di e to of Glo al EME St ateg a d Regulato Affai s
and
also represented the Australian Mobile Telecommunications Association, an industry group,
on the telecommunications standards committee and the Mobile Manufacturers Forum ;
Notwithstanding these ties Joyner was a longstanding member of the Standards Australia
TE/7 Committee: Human Exposure to Electromagnetic Fields, and later on he was on the
ARPANSA committee that set the current Australian Radiofrequency/Microwave human
exposure standard. He was regarded by the cell phone companies as Australia's foremost
authority on the industry's position on health issues with EMR and has represented
Motorola and the Australian cell phone industry on several international standards-setting
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bodies. Joyner also had connections with Burson Marsteller, the PR firm representing the
cell phone industry in Australia.
In October 2003 Ken Joyner, the key Motorola representative gave a presentation at the
A ual Co fe e e of the Aust alia Radiatio P ote tio So iet alled: A Re ie of RF
Bioeffects Studies Relevant to the Use
of Mo ile Pho es Child e . Do Mais h ites i
an article
Moto ola s Mi k Mouse Re ie
: The Moto ola e ie s o lusio s as to a la k
of scientific evidence of possible harm to children using mobile phones ignores a large body
of expert opinion calling for a precautionary approach when it comes to children and mobile
pho e use.
As
reported in Microwave News (1999)
in Europe there was some discontent with scientists
ith Moto ola s i ol ement
with the EC research and telling European scientists how to
spend resea
h fu ds. As Do Mais h ites i Co po ate ties that i d: A E a i atio of
Co po ate Ma ipulatio a d Vested I te est i Pu li Health
: I Ja ua
,D .
Joyner announced that he was leaving his Director position at Motorola after 12 years and
was "looking for new opportunities to work in the telecommunications industry". In that
same year, Dr. Joyner was listed on the NHMRC's Peer Review Honour Roll which
acknowledged its many peer reviewers and external assessors who had exhibited "excellent
track records and wide-ranging expertise in Australian and international health and medical
research fields". However, under the section "Administering Institution/Employer" he was
listed as simply "consultant" and nothing about possible conflicts of interests. He later was
appointed as the sole non-radiation expert on the 14-member Victorian government's
Health department's Radiation advisory committee.
ORSAA alls this pu e
corruption at a huge cost to public health everywhere. This system of
funding and promoting an in-club of industry friendly researchers has kept a small number of
people in powerful positions within the WHO, ICNIRP, ARPANSA etc., influencing decision
maki
g fo ost of the o ld.
Eric van Rongen (Vice Chair ICNIRP-commission, until May 2020 chair)
Biography
Eric Van Rongen is a biologist. He is a staff member of the Dutch Health Council since 1992,
where he focuses on non-ionizing radiation.
Van Rongen is a member of ICNIRP since May 2001. In 2016, he became the chair of the
ICNIRP-commission. Since the beginning May 2020 he is no longer chair but vice-chair.
He also a member of the International Advisory Committee WHO EMF Project since 1995.
Van Rongen
did not publish
original research studies on EMF himself, only opinions or
review articles.
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Position
Van Rongen systematically, in scientific publications and in press articles, defends for more
than twenty years the point of view that there are no dangers associated with the use of
mobile phones. According to him, even for children there are no reasons to apply the
precautionary principle. In 2004 for example he published
an article
in which he stated: 'The
Health Council therefore sees no reason to recommend limiting the use of mobile phones by
children.'
He systematically criticizes all studies that seem to show that non-ionizing radiation poses a
problem. Recently the National Toxicologic Program (NTP) study on Cell Phone Radio
Frequency
concluded
that there was clear evidence of tumors in the hearts of male rats But
in an ICNIRP-publication Van Rongen and others
stated
that 'substantial limitations (of the
NTP-study) preclude conclusions being drawn concerning RF EMFs and carcinogenesis.'
Possible conflicts of interest
The WHO EMF project was severely
criticized
in 2007 for being for a large part financed by
the telecom industry, for example by the Mobile Manufacturers Forum (now
Mobile &
Wireless Forum),
a lobby organisation of the industry.
Since 2000 Van Rongen is a member of the International Committee on Electromagnetic
Safety (ICES) of the IEEE. This committee is dominated by people from industry and military.
The ICES chairman Jafar Keshvari works at Intel, the chairman of one of the main committees
C.K Chou at Motorola. ICES clearly is an industry lobby and standard setting organisation.
Maybe Van Rongen decided for that reason to become a 'non active member' according to
his
declaration of personal interests 2019.
In previous years there was some competition between ICNIRP and ICES/ IEEE
–
at the time
when the chair of ICES was still Dr. Ralf Bodemann, topshot of Siemens and Dr. B Jon
Klauenberg from US Air Force Research Laboratory was the chair of ICES working group
TC95. (Klauenberg was the US counterpart of former ICNIRP-chair Repacholi
to lead the
very start of the WHO EMF
i the
ies. A o di g to
an annual report of ICES
it was thanks
to the arrival in 2016 of Van Rongen as chair of ICNIRP that the relations with ICES improved
sig ifi a tl , as the e e ot so o dial efo e: I Ma
2016, there was a change of
leadership and some members of ICNIRP. The new ICNIRP Chairman and one of the new
members of the 14-member committee are also ICES members and ICNIRP is now willing to
discuss harmonization of the exposure limits found in IEEE Stds C95.1 TM -2005 and C95.6
TM -
a d the ICNIRP Guideli es.
The ICES annual report further mentions that thanks to the invitation to do so by Van
Rongen, ICES has been able to comment on the proposed new guidelines by ICNIRP. ICES
workgroup TC95 formed a 19-member task group to draft a document to comment on the
ICNIRP p oposed guideli es o ti e. ICES ill ai tai its olla o ati e elatio ship ith
ICNIRP with the goal of setting internationally harmonized safety limits for exposure to
electromagnetic fields at frequencies below 300 GHz. This interaction with ICNIRP is
o side ed a ajo step fo a d.
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A year later
during the annual meeting of ICES
in 2017
it as stated that ICNIRP has dela ed
fi alizi g thei o lusio s to gi e full o side atio of ICES s e o
e datio s . A d Van
Rongen gave a presentatio
sa i g that the e is
No evidence that HF-EMF causes such
diseases as cancer, no evidence that HF-EMF impairs health beyond effects that are due to
esta lished e ha is s of i te a tio .
Scientist Dariusz Leszczynski was a member of TC95, but resigned. He explained why on
his
blog:
My problem was that the membership of the IEEE-ICES-TC95 consists predominantly
of the industrial scientists and the committee is chaired by C.K. Chou since the time he was
employed by the Motorola. This means that all safety standards being developed by IEEE-
ICES-TC95 are, in practice, developed by the industry scientists for the use by the industry
the a e e plo ed .
According to
Leszczynski this is a clear conflict of interests.
The latest
minutes
of TC95 that ICES published on its website (August 2019) show that the
committee is still dominated by industry scientists.
In October 2019 Van Rongen
spoke
at the GSMA Europe EMF Forum. The GSM Association is
a lobby organisation that defends the interests of mobile operators worldwide. In 2018, he
also was a guest at the Forum. Then he
defended
ideas that GSMA received with pleasure:
"The ICNIRP limits provide a high level of protection for all people against known adverse
health effects. Dr van Rongen explained that there is no scientifically substantiated evidence
that radio signals cause diseases such as cancer and that ICNIRP had considered studies such
as that of the American National Toxicology Program."
In November 2019 Van Rongen
presented
the ICNIRP RF guideli es e isio at
d GLORE
(Global Coordination of Research and Health Policy on RF Electromagnetic Fields) conference
held on 4th
–
6rth of November in Lima, Peru. GLORE is an initiative to coordinate research
and policy initiated by Japan and Korea in 1997 and joined by Europe and then by USA,
Australia and Canada. Main speakers were also his ICES-colleagues Jafar Keshvari and TC95
Chairman C-K. Chou.
Van Rongen recently
assured
the Dutch press that there are no conflicts of interest inside
ICNIRP right now. He stated: 'In the past certain members maybe received co-funding from
the private sector, but currently no member has ties with the telecom sector.'
Of course, it depends on what you consider as a 'tie with industry', but his own involvement
in ICES is already shows that it is not true that 'currently no member had ties with the
telecom sector'. He also published articles together with researchers who did receive
industry funding, for example with Bernard Veyret, who is 'a member of the Scientific
Council of the French mobile operator Bouygues Telecom. His laboratory has received
research funds from the same operator.' This information can be found in the footnotes of
this article.
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Tania Cestari
Biography
Tania Cestari received her medical degree from the University of Rio Grande do Sul and
completed her medical Residency in Dermatology in Porto Alegre, Brazil and since 1995 she
works as Professor of Dermatology at the same university, where she studies predominantly
on clinical aspects and skin response. Dr Cestari has authored 112 scientific peer-reviewed
publications, 42 book chapters and joined the ICNIRP Commission in May 2020.
Position
Dr Cestari has been doing mainly research into skin allergies and dermatological problems;
We could not find any publication linked to EMF.
Possible conflicts of interest
I he De la atio
of Interests it is mentioned that she received research grants via the
Medical Foundation of her hospital from Pfizer, Abbvie Pharmaceutical and Vichy
Laboratoires for drug research.
Nigel Cridland
Biography
Nigel Cridland is Senior Group Leader at Public Health England. He joined what was to
become the Public Health England (PHE) already in 1990, where he specialised in non-
ionising radiation. He was member of the project team that wrote the European Commission
guide to implementation of the Artificial Optical Radiation Directive (2006) and leader of the
project team that developed the guide to implementation of the EMF Directive (2013).
He was Scientific Co-ordinator Mobile Telecommunications and Health Research (MTHR)
Programme 2001 - 2012. Cridland was a member of the Independent Expert Group on
Mobile Phones (2000). On
LinkedIn
he states that he was also member of the management
committee of the European COST 281 action Potential Health Implications from Mobile
Communications Systems.
Position
The
2000-report
of the Independent E
pe t G oup o Mo ile Pho es stated that the
balance of evidence to date suggests that exposures to RF radiation below NRPB and ICNIRP
guideli es do ot ause ad e se health effe ts to the ge e al populatio . But at the sa e
time,
it said: the gaps i k o ledge a e suffi ie t to justif a p e autio a app oa h .
The MTHR-programme (2001-2012) of which he was the Scientific Co-ordinator
concluded
that no association between cancer and mobile phone use was found. We can now be, said
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professor David Coggon, the chairman of the MTHR-p
og a
e, e u h o e o fide t
a out the safet of ode tele o
u i atio s s ste s. Cu iousl e ough the
authors
stated that: We see o eed fo eed fo fu the esea h i a of the a eas add essed
the
esea h that is su
a ised i this epo t.
Possible conflicts of interest
The MTHR-programme was funded by government and industry together, both for half of it.
The final report states that to ensure that any of the funding organisation could not
influence the outcome of the Programme an independent Programme Management
Committee was set up. But there can be doubts about the independence of its members.
From 2001 until 2007 Mike Repacholi (ICNIRP-founder, see the chapter on the history of
ICNIRP) was for example member of the committee.
Guglielmo d'Inzeo
Biography
O ICNIRP s e site it eads that Gugliel o d'I zeo is a P ofesso of "Bioele t o ag eti
Interaction" at "La Sapienza" University of Rome since 1990. He researched active and
passive microwave component design and bioelectromagnetism, mainly the interaction of
electromagnetic fields with biological tissues, the effects of microwaves and ELF fields on
biological samples and humans. He is author or co-author of more than seventy papers in
international refereed journals and books.
He became a member of the European Bioelectromagnetics Association EBEA in 1989, and
then President from 1993 to 1998. From 1992 to 2000 he was an Italian representative for
the
COST 244 and 244Bis projects
on "Biomedical Effects of Electromagnetic Fields". From
1998 to 2004 he chaired the Italian ICEmB (Inter-University Centre Electromagnetic Fields
and Biosystems). From 2001 to 2006 he was an Italian National representative in COST 281
p oje t Pote tial Health Effe ts f o E e gi g Wi eless Co
u i atio S ste s a d f o
2007 in COST BM0704 related project.
Position
He has ee a ti e i the IEEE si e the
ies, se ed as se eta –t easu e of the IEEE
Middle and South
hapte s a d as f o
2004 to 2009, also a member of the Technical
Committee 95 (TC95) of IEEE International Committee on Electromagnetic Safety (ICES), of
which Eric Van Rongen and Rodney Croft are also members. He published in the past 20
years
a number of studies in IEEE Transactions on Biomedical Engineering
and other IEEE
publications, in which several times ICNIRP-founder Mike Repacholi was heartily thanked for
his help.
In 2005 he was responsible for the Italian chapter of
the epo t Eu opea I fo atio
S ste o Ele t o ag eti Fields E posu e a d Health I pa ts
published on behalf of DG
SANCO (European Commission), which was coordinated by the Joint research Centre (JRC of
the EU ; Alo gside this p oje t the JRC de eloped du i g
-2004 the EIS-EMF project on
behalf of DG SANCO with the overall objective of promoting cooperation among policy
makers on public health and EMF risk communicatio
issues i the EU . What these p oje ts
basically reflect is the idea that concerns about possible health effect occur because people
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do not understand the issue well enough and that the concerns can be taken away by better
communication.
Possible conflicts of interest
As we stated before (see Van Rongen and Croft), ICES is dominated by people from industry
and military.
His declaration of personal interest 2019 is signed but only partly completed. d'Inzeo did
some paid consultancy for an Italian legal office called Trifirò & Partners and for a
Environmental Measurement Report Managers & Partners - Actuarial Services S.p.A in
Rome. His
DOI from 2016
mentions that he has bee
doi g o k fo the
Marconi
Foundation
. The Gugliel o Ma o i Fou datio states to p o ote esea h i the field of
telecommunications and carries out activities devoted to the knowledge and diffusion of
Gugliel o Ma o i s s ie tifi a ti it . The Ma o i Fou datio fu the states that
p ofessio al t ai i g a d tea hi g pla a ajo ole i its a ti ities a d that thei
esearch
focuses on two major fields: 1) mobile and personal communication systems, with a special
focus on radio access and propagation; and 2) the computer-assisted design of non-linear
i o a e de i es .
What is not declared in his DOI is that d'Inzeo, is
a director of the scientific committee
of
Elettra 2000, a consortium
of Marconi and other foundations. The self-declared aim of
Elett
a
is to sp ead k o ledge of Bioele t o ag eti s a d sta t a dialogue et ee
s ie e, politi s, i dust a d itize s, i ol i g ou g people a d s hools. A d Elett a
2000 promotes researches and studies related to specific areas of interest. In particular, the
consortium co-finances a number of national and international projects devoted to the study
of the effects of electromagnetic fields on human health, in order to provide an authoritative
scientific answer, fair and independent to the pro
le .
Elett a
p o ides
advice to enterprises
a d o s a ode fleet of i st u e ts fo
measuring ele
t o ag eti fields i oth lo a d high f e ue
hi h a e a aila le to
both institutional and private entities in order to promote the improvement of standards of
p ote tio a d safet of people a d e i o e t.
This paper from 2008 (The
Italian national electromagnetic field monitoring network)
is an
example of the kind of research projects that is financing. The conclusio
s eads: The
monitoring campaign, combined with the travelling communication campaign contributed to
create a different and more constructive approach to the problem by the citizens. This is
demonstrated by the analysis of the data press that shows criticality and greater negative
involvement in those areas where the monitoring campaign has been less efficient or less
i te se .
Furthermore, in 2019 an Italian journalist of Investigative Europe wrote the following in
Il
Fatto:
He has do e ultiplied s ientific
opinions for companies such as Vodafone,
participated in European projects - all funded by industry, such as Interphone, Cosmos,
Cefalo, and since the late 90s participates in the Efhran portal, where among the financiers
are Deutsche Telecom and the
Eu opea Asso iatio of GSM p odu e s.
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Akimasa Hirata
Biography
Akimasa Hirata is professor of Electrical and Electronic Engineering at the Nagoya Institute of
Technology and Director of Center of Biomedical Physics and Information Technology.
He also is an Administrative Committee Member and
Subcommittee Chairperson
(SC6 EMF
Dosimetry Modelling) in IEEE International Committee on Electromagnetic Safety (ICES). The
latest committee (also called TC95) is the one of which Eric Van Rongen and Rodney Croft
were also members.
Position
In November 2019 TC95 once again came to conclusion that the IEEE standards are safe. The
authors, among which Hirata,
wrote:
a The eight-of-evidence
provides no credible indication of adverse effects caused by
chronic exposures below levels specified in IEEE Std C95.1TM-2019.
b) No biophysical mechanisms have been scientifically validated that would link chronic
exposures below levels specified in IEEE Std C95.1TM-
to ad e se health effe ts.
Possible conflicts of interest
As we stated before (see Van Rongen and Croft), ICES is dominated by people from industry
and military.
Hirata conducted research
published
in
IEEE Transaction
in 2010 partly funded by KDDI
Foundation. KDDI Corporation is a Japanese telecommunications operator.
But according to
a recent publication
Hirata himself judges that he has no conflicting
interests.
Anke Huss
Biography
ICNIRP
s e site states that A ke
Huss is an assistant professor at the
Institute for Risk
Assessment Sciences
IRAS at Ut e ht U i e sit , the Nethe la ds. He esea h
focuses on
environmental and occupational exposure assessment to environmental factors including
electromagnetic fields and their health
.
Huss is also involved in the GERoNiMO project, cancer and neurodegenerative diseases such
as Pa ki so s disease, Alzhei e s o ALS i the NOCCA
Nordic Occupational Cancer Study)
and SNC (Swiss National Cohort) studies and on electromagnetic hypersensitivity. She is a
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member of the Dutch Health council, and the Scientific Council for Electromagnetic fields of
the Swedish Radiation Safety Authority (SSM).
Position
She is one of the rare members of ICNIRP who seems to be aware of an industry-bias; In the
ook
Overpowered: The Dangers of Electromagnetic Radiation (EMF) and What You Can do
about it
Ma ti Blank,
Anke Huss is quoted on Industry bias in research to the possible
health risks of EMF.
In a scientific paper Huss writes that 82% of the research funded by public agencies or
governments and 71% of the research jointly funded by industry and public sources, report
health effects from RF exposure. When the research is solely funded by industry only 33%
finds such a link.
Later Huss published another study
in which she and colleagues examined whether the
source of funding of 59 studies of the effects of low-level RF radiation has an effect on the
esults of studies. Of these studies,
% e e fu ded e lusi el
the
telecommunications industry, 11 (19%) were funded by public agencies or charities, 14 (24%)
had mixed funding (including industry), and in 22 (37%) the source of funding was not
epo ted. Huss et all o lude that the e is idesp ead o e ega di g the
possible
health effects associated with the use of cellular phones, mobile telephone base stations, or
broadcasting transmitters. Most (68%) of the studies assessed here reported biologic effects.
At present, it is unclear whether these biologic effects translate into relevant health hazards.
Reports from national and international bodies have recently concluded that further
research efforts are needed, and dedicated research programs have been set up in the
United States, Germany, Denmark, Hungary, Switzerland, and Japan. Our study indicates that
the interpretation of the results from existing and future studies of the health effects of
adiof e ue
adiatio should take spo so ship i to a ou t.
In 2010, she published
a follow up study
hi h o fi ed the p e ious fi di gs:
Of 75
additional studies 12% were industry-funded, 44% had public and 19% mixed funding;
funding was unclear in 25%. Previous findings were confirmed: industry-sponsored studies
were least likely to report results suggesting effects.
She also published in 2018
a eta‐a al sis
based on among
othe s epide iologi studies to
e a i e asso iatio s of o upatio al e posu e to e t e el ‐lo f e ue
ag eti fields
ELF‐MF
ith a ot ophi late al s le osis ALS .
Possible conflicts of Interests
Her DOI says she gets funding from US based EPRI for a study called TransExpo on leukaemia
in children. Ironically, she states that the contract does not mention complete independence
from the funder, but she explains clearly why the data will be analysed independently and
that the e is o a that the fu de s a ha e a i flue e o hat e epo t to the .
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Ken Karipidis
Biography
Ken Karipidis has been working as a scientist at the Australian Radiation Protection and
Nuclear Safety Agency (ARPANSA) since 2000. He is,
states ICNIRP, u e tl the assista t
director of the Assessment and Advice Section at ARPANSA where he is heavily involved in
the scientific and regulatory aspects of radiation protection from electromagnetic radiation
sou es.
He is member of the Scientific Expert Group since August 2015. In May 2020, he became
member of the ICNIRP Commission.
Position
In 2017 Karipidis published
an article
with the conclusion that the exposure to
radiofrequency radiation due to Wi-Fi in schools was very low. In
a letter
to the editor three
scientists criti
ized the stud as of little p a ti al use a d isleadi g .
Karapidis and Rodney Croft were part of a subcommittee established by ARPANSA to look at
EHS and the research in 2016/17. According to an ORSAA member present in these meetings
both Karipidis
a d C oft ig o ed li i al/ edi al e ide e i fa ou of poo l o du ted
p o o atio studies pe fo ed ps hologists, so e of ho
e e fu ded i dust .
At the end of 2018 Karipidis together with among others Rodney Croft published
a study
that
claimed to proof that in Australia there has been no increase in any brain tumour that can be
attributed to mobile phones. That study received a lot of
criticism
because it excluded the
group of people above sixty, which is the largest segment of the population with brain
tumours.
In August 2019 Karipidis advised 40,000 Australian doctors or general practitioners
via an
article
on the website of Royal Australian College of General Practitioners (RACGP) in which
he
a ted GPs a d thei patie ts to k o the e is o
evidence to support the concern that
5G technology, which uses radio waves and emits low-level
radiofrequency (RF)
electromagnetic energy (EME),
ill ause ha s to the pu li . He stated: The e s ee a
lot of research into whether radio waves cause adverse health effects, and the only
established health effects of radio waves are very high-power levels, where they raise
temperature. An everyday example of that is your microwave oven at home; inside the
microwave is very powerful radio waves which make the water molecules in the food
ou e e fast, heati g the up.
Possible conflicts of interest
In the introductory chapter, we wrote about the financial relationship between ARPANSA
and the telecom industry. ARPANSA every year has a meeting with the Australian
Telecommunications Association (AMTA), a lobby-organisation of the telecom industry.
Minutes
of this meeting made public after a Freedom of Information Request show that the
fu di g of esea h as also o the age da. I dust e ai s suppo ti e of o ti ued
fu di g, it sa s.
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Carmela Marino
Biography
Carmela Marino studied Biological sciences in Faculty of Sciences of "La Sapienza" University
of Rome. According to ICNIRP she is currently Head of the Unit of Radiation Biology and
Human Health, at Casaccia Research Center of Italian Agency for New Technologies, Energy
and Sustainable Economic Development (ENEA).
On behalf of ENEA she coordinated the research activity Subprogram 3
Interaction between
sources and biosystems
(MURST/ENEA-CNR Italian National Program
"Human and
Environmental Protection from
Ele tro ag eti E issio s
and was involved in
several
projects of the 5° and 6°FP, as member of steering Committee and Coordinator of research
unit.
Position
On the one hand Marino seems to agree with the official ICNIRP position; On the other hand
I Ma
, du i g ICNIRP s th I te atio al NIR Wo kshop i Edi u gh,
Marino held a
lecture
on the advantages, challenges and limits of experimental studies, in which she said
that the e is a la ge u e of studies ut ith o t o e sial esults a d also a li ited
number of studies in relation to particular
e dpoi ts. Ma i o asked he fello ICNIRP
members the rhetorical question, whether
these studies eall a le to gi e o lusi e
i fo atio ? ICNIRP s a s e to that uestio as a d is o.
Possible conflicts of interest
Her Declaration of Personal Interests does not mention anything. Notaby, not that since
April 2020 her university
holds a patent based on her research,
not mentioned in her DOI
2019, although the worldwide application for this patent was filed years ago.
Sharon Miller
Biography
Sharon Miller works at the Food and Drug Administration (FDA) as optical engineer since
1981. According to ICNIRP she served on numerous committees of the International
Commission on Illumination (CIE) and the International Organisation for Standardization
(ISO).
Position
Miller publications are mainly in the field of ultraviolet radiation and optical issues. It is
difficult to find scientific publications or public statements in which she says anything about
the safety of non-ionizing radiation.
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Possible conflicts of interest
In her Declaration of Personal Interest Miller does not state any possible conflict of interest
and we did not find any.
Gunnhild Oftedal
Biography
Gunnhild Oftedal is associate professor at the Norwegian University of Science and
Technology (NTNU). According to ICNIRP she is currently, working as Research Co-ordinator
at the Faculty of Information Technology and Electrical Engi
ee i g, NTNU. F o the ea l
1990s, she has been involved in research on health effects of EMF in the ELF and the RF
ranges, mainly with experimental human studies and observational studies.
She is member of international organisations in the field of non-ionising radiation and
participates in the work of WHO (Environmental Health Criteria project) on the health risk
assess e t o RF fields.
She was one of
the experts
on a government-commissioned study, published in 2012, of
possible health risks with radiation from mobile phones, base stations and wireless networks
in Norway.
Position
In 2004
she answered
on the questions if electromagnetic radiation from mobile phones
a ell affe t us i othe a s, too that s ie tists a e skati g o thi i e he dis ussi g
these issues. They know little about the cause-and-effect mechanisms involved, and hence
cannot eliminate the possibility that the effect of electromagnetic fields, however weak in
mobile phones,
a ause health p o le s .
But she sticks with the official ICNIRP position and
in a study
for the Norwegian government
she suggests that this app oa h is the ight o e: O l effe ts fo hi h the e as elia le
scientific evidence were used (by ICNIRP) as the basis for the exposure
est i tio s.
In another
recent stud
she o ludes that o e all, the e ide e poi ts to a ds o effe t
of
exposure. If physical effects exist, previous findings suggest that they must be very weak or
affect only few individuals with IEI-EMF. Given the evidence that the nocebo effect or
medical/mental disorders may explain the symptoms in many individuals with IEI-EMF,
additional research is required to identify the various factors that may be important for
developing IEI-EMF
a d fo p o oki g the s pto s.
As
writes Leszczynski
the o e o h pothesis a gues that people fi st e o e a a e, e.g.
from news and social media, of the possible health risks of EMF-emitting devices and then
worries about the possible health risk lead to develop symptoms, which they attribute to
EMF exposures.
Oftedal
denies in an article by IE
that the health debate is polarised:
I ou field it
is easy to
put people in two camps, but the landscape is much more nuan
ed . Also,
the closed culture
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at ICNIRP is ei g de ied: People ho de o st ate that the a e skilled a e asked to
o t i ute.
Possible conflicts of interest
I the stud o Mo ile
phone headache: a double blind, sham-controlled provocation
stud
o-financed
by The Research Council of Norway, Norwegian Post and
Telecommunication Authority, Statnett, Telenor, Norsk tele- og informasjonsbrukerforening
(NORTIB), Netcom. The study found no effects.
She is member of Bioelectromagnetics society (BEMS) according to the DOI and also of the
European Bioelectromagnetics Association (EBEA)
Tsutomu Okuno
Biography
Tsutomu Okuno worked for the National Institute of Occupational Safety and Health, Japan
from 1980 to 2015.
He became a member of the Scientific Expert Group in 2013 and is a member of the ICNIRP
Commission since 2016.
Position
Okuno was one of the authors of the ICNIRP
note
that criticized the NTP-study that showed
carcinogenicity in rats. For the rest, his work seems mainly to be on ultraviolet radiation, not
on radiofrequency radiation.
Possible conflicts of interest
In his Declaration of Personal Interest there do not seem to be sources of possible conflicts
of interest and we did not find information that contradicts this.
Martin Röösli
Martin Röösli is Professor for environmental epidemiology at
the Swiss Tropical- and Public
Health Institute
in Basel and leads the Environmental Exposures and Health Unit. His
background is situated in atmospheric physics and environmental epidemiology.
In the field of non-ionizing radiation Röösli did several exposure assessments and
epidemiological studies o
the health effe ts of ele t o ag eti fields i ludi g populatio
based studies dealing with cancer, neurodegenerative diseases and non-specific symptoms
of ill health .
He is the chair of
BERENIS,
a Swiss expert group advising the government on electromagnetic
fields and non-ionising radiation. He is a member of the advisory group of Cohort Study of
Mobile Phone Use and Health (COSMOS) and between 2015 and 2018 of the
the Scientific
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Council of the IARC,
specifically
SC52.
Since 2013 he is also a Member of the Editorial Board
of Bioelectromagnetics.
He is still a member of the Expert Group for the Swedish Radiation Safety Authority (SSM),
for which he gets 3000 Swiss francs yearly.
Relevant to this report Röösli was part of the Working Group of the IARC Monographs on the
Evaluation of Carcinogenic Risks to Humans Volume 102: Non-Ionizing Radiation, Part II:
Radiofrequency Electromagnetic Fields.
Position
Röösli has contributed to a study (see portrait of Anke Huss) which show that the funding of
scientific research into EMF can influence the findings. Nevertheless, he confirms the general
position of ICNIRP that no adverse health effects are proven.
In a
study
f o
Systematic review on the health effects of exposure to
adiof e ue
ele t o ag eti fields f o
o ile pho e ase statio s Röösli o ludes:
Ou e ie does ot i di ate a association
between any health outcome and
radiofrequency electromagnetic field exposure from MPBSs at levels typically encountered
i people s e e da e i o e t.
In a recent
5G report for the Swiss government
Röösli et all conclude that "No health effect
has been consistently proven," which he repeated
in an interview.
In an
annual report prepared for the Swedish Radiation Safety Authority
(April 2020) by a
nine-member panel of experts of which, ICNIRP vice-chair Eric Van Rongen and Röösli, which
according to
MicroWave News
is pu lished ea h ea as a a ual update ith the past
ea s ost i po ta t s ie tifi de elop e ts o the
health effects of EMFs and RF
adiatio states e
lu tl that o e esta lished ausal elatio ships et ee EMF
exposure and health risks
ha e ee ide tified. The a ual epo t si pl does ot e tio
the NTP epo t. The t o ICNIRP e e s a d their
seven colleagues made believe that the
NTP epo t does ot e ist. It s ot e tio ed, the e is o itatio . Nothi g at all. Fo the
record,
the NTP fi al epo t as eleased o No e e ,
.
Louis Slesin of
MicroWave News
ote: The e is a dis ussion
of the NTP findings in last
ea s S edish update. But that as ased o a ea lie NTP d aft he e the staff had opted
for a weaker desig
atio , so e e ide e of a e . Late , afte a i
-depth
public peer
review,
the NTP st e gthe ed the o lusio to lea e ide e of a e . That as the
headli e e s of
. Clea e ide e as a ga e ha ge ; lea i g it out of the a ual
update is a sure sign of bias. The NTP conclusion was now qualitatively different from the
earlier draft
—it ould ell ha e ee the title of the pa el s
update.
But van Rongen,
Röösli a d the othe s ig o ed it.
On January 7, 2020 prof. Lennart Hardell and supported by 22 scientists researching EMF
wrote a remarkably critical, open letter
to Mrs. Simonetta Sommaruga, President of the
Swiss
Co fede atio , i hi h the o lude: It is i pe ati e that the hai a d othe
experts evaluating scientific evidence and assessing health risks from RF radiation do not
have such clear conflicts of interests or bias as Martin Röösli has. Indeed, being a member of
ICNIRP and being funded by industry directly or through an industry funded foundation,
constitutes clear conflicts of interest. Furthermore, it is recommended that the
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interpretation of results from studies of health effects of radiofrequency radiation should
take spo so ship f o tele o i dust i to a ou t.
The group of scientists also point out to a strange contradiction in the positioning of Röösli:
Su p isi gl
the IARC classification from 2011
of RF-EMF
e posu e as lass B, possi l
carcinogenic to humans, was ignored in the background material to the new ICNIRP draft on
guidelines. Remarkably one of the ICNIRP commission members, Martin Röösli, was also one
of the IARC experts evaluating the scientific RF carcinogenicity in May 2011. Röösli did not
abstain from the IARC Group 2B classification and should be well aware of that decision, but
seems now to neglect that fact being an ICNIRP member. That may be due to the fact that
the IARC lassifi atio o t adi ts the s ie tifi asis fo the ICNIRP guideli es.
Hardell et al. suggest to the Swiss government that Mr. Martin Röösli should be released
from his duties as a scientist who is not objective and has substantial conflicts of interest. On
the letter Röösli reacted by saying: "It's not a scientific letter. It sounds like activists who do
not use scientific facts but who just attack people. It would be much more compelling if
Lennart responded to my criticism of him in a scientific way instead of derailing the debate
.
A recent
publication
of the COSMOS (October 2019) on the outcomes states reassuringly
that
usi g o ile pho es ost extensively
for making or receiving calls at baseline
reported weekly headaches slightly more frequently at follow-up than other users, but this
finding largely disappeared after adjustment for confounders and was not related to call-
time in GSM with higher RF-EMF exposure. (See also the portrait of Anissi Auvinen)
Possible conflicts of interests
Röösli does u paid o k fo the COSMOS stud , hi h e ei ed o side
able funding from
telecom companies. In the 2019-publication on this study for example, Nokia and mobile
et o k p o ide s TeliaSo e a a d Elisa a e e tio ed i the atego fu di g .
According to his DOI he gets 70,000 Swiss francs a year for the Berenis work, from the
Federal Office for the Environment.
He also received 16,000 francs for assisting in the
Working Group Mobile Phone and
Radiation
the Federal Office for the Environment of the Swiss government.
The Swiss Tropical and Public Health Institute in which he plays a leading role, has
a lot of
corporate clients
of which Swisscom, the biggest telecom company in Switzerland, of which
the Swiss government holds 51% of the shares.
In the
annual Report 2019
the institute
states that of the total budget of roughly 90 million Swiss francs, 78. 6 % was
o petiti el
a ui ed a d . % a e f o
Co e o t i utio s .
Studies selected or self-directed by Röösli, were directly funded by the (Research
Foundation
for Electricity and Mobile Communication)
of which
Martin Röösli is a member
since 2011, according to his CV on the website of the
S iss T opi al a d Pu li Health I stitute. FSM is a o
-profit-making foundation with the
purpose of promoting scientific research into the chances and risks of radio and electric
po e te h ologies that p odu e a d use ele t o ag eti fields . The
five founders of the
FSM
are:
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ETH Zurich, Swisscom, Salt, Sunrise, 3G Mobile (liquidated in 2011) and the current main
sponsors are Swisscom and Swissgrid. The sponsors are also represented in the FSM
Foundation Board with one delegate out of seven.
Soichi Watanabe
Biography
Watanabe is currently Director of the Electromagnetic Compatibility Laboratory of the
Natio al I stitute of I fo atio a d Co
u i atio s Te h olog NICT .
He was a member of ICNIRP Standing Committee III since 2004 and is a member of the
Commission since 2012.
He is a guest lecturer of several universities and at the Central Research Institute of Electric
Power Industry.
Position
All publications to which Watanabe contributed as author point in the same direction: no
effect. For example,
this article
about tumorgenenis in rats.
In 2019, he was co-author of
an article
hi h stated: To date, o ad e se health effe ts of
the EMF, linked to these applicatio
s, ha e ee esta lished.
Possible conflicts of interest
As a guest lecturer at the Central Research Institute of Electric Power Industry he receives a
s all a ou t a out €
fo ea h le tu e, o a ea .
He was co-author of the article with commission-member Hirata on the research funded
partly by KDDI Foundation.
MEMBERS WHO HAVE LEFT THE ICNIRP COMMISSION IN MAY 2020
Maria Feychting
Biography
Maria Feychting is a Professor of Epidemiology at the Institute of Environmental Medicine,
Karolinska Institutet, Stockholm, Sweden.
She joined the Commission in 2008 and was elected vice chair in 2012. She left the
Commission in May 2020.
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Position
Feychting was in charge of the Swedish part of the Interphone study which concluded that
there was no link between brain tumours and mobile phone use.
Feychting also conducted the Swedish part of the COSMOS-study, which in 2011 came to the
conclusion that there was no increase in glioma in the Nordic countries that could be
attributed to the use of mobile phones.
She recently repeated this point of view in
the media
in an article on the risks of 5G, which
were none according to her.
According to
this source
she criticized the NTP-study on false grounds.
Possible conflicts of interest.
In a 2019
study
i the o te t of COSMOS, she de la ed a de la atio of i te est as
hai a of the ICNIRP .
The telecom industry contributed
€ .
Interphone Study.
illio
to the fu di g total €
.
illio
i e
of the
A 2016
publication
on the Interphone Study once again mentioned industry funding by
among other the Mobile Manufacturers Forum.
The Swedish part of the COSMOS-study was
partly funded
by the telecom industry:
TeliaSonera, Telenor and Ericsson. In
her Declaration of Interests
for 2015 she declares that
he I stitute e ei ed a g a t f o i dust sou es hi h o stituted o o e than
4% of
he u it of epide iolog total i o e.
A 2011
study
was partly funded by the Swiss Research Foundation on Mobile
Communication, an
organisation
which is founded and funded by the telecom industry.
A 2012
study
was funded by the Electric Power Research Institute (EPRI), an organisation
funded by industry.
She did not mention these sources of funding in her
Declarations of Personal Interest.
Adèle Green
Biography
Green is an Australian epidemiological scientist at the Queensland Institute of Medical
Research, Australia and is the institute's Head of Cancer and Population Studies Group. She
specialised in UV and skin cancer causation,
harmful effects of UVR exposure in childhood
and the prevention of melanoma. Apart from various Australian research bodies, she was
also member of many committees at the International Agency for Research on Cancer (IARC)
and contributed to
the IARC monograph
that led to classification in
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Position
Although she focussed mostly on UV radiation, Green seemed to agree with her ICNIRP
colleagues on the ICNIRP position, for example
in this study
from 2005 where Green was first
author the research did not find
any consistent or biologically relevant effect of specific
radiation on cells.
And another study from 2009
Epidemiologic Evidence on Mobile Phones
and Tumor Risk,
o ludes sa i g that I
the last few years, the epidemiologic evidence
on mobile phone use and risk of brain and other tumors of the head has grown considerably.
In our opinion, overall the studies published to date do not demonstrate a raised risk within
approximately 10 years
of use fo a tu o of the ai o a othe head tu o . A d
despite certain methodologic shortcomings and limited data on long-te
use, the a aila le
data do not suggest a causal association between mobile phone use and fast-growing tumors
such as malig
a t glio a i adults, at least those tu o s ith sho t i du tio pe iods.
Conflicts of Interests
The declarations of interests
of D G ee ha e disappea ed f o the ICNIRP s e site. The
IARC Mo og aph e tio s that D G ee e ei ed esea h fu ds
not exceeding 5% of
total esea h suppo t f o L O éal hi h akes p odu ts i te ded to edu e the dose
f o sola adiatio .
Zenon Sienkiewicz
Biography
Sienkiewicz worked until his retirement in 2018 for Public Health England. There he led a
research group that investigates the effects of ionizing and non-ionizing radiation. Since
2011 he has been a member of ICNIRP. He was also external expert for the Scientific
Co
ittee o E e gi g a d Ne l Ide tified Health Risks SCENIHR epo t o Pote tial
health
effe ts of e posu e to ele t o ag eti fields EMF , adopted i Ja ua
.
Position
Sienkiewicz systematically defends the position that there is no proof for any harm caused
by non-ionizing radiation. In 2002, he said in the media: "The bottom line is there are no
known mechanisms by which mobile phone radiation can increase the risk of cancer."
Fifteen years later he still holds exactly the same position. In a 2017-article he stated that all
the e te si e esea h do e has ot ide tified a pu li health isks ith a deg ee of
e tai t . Mo eo e , it o luded that a i al studies i estigati g the a i oge i
potential of exposure to multiple RF frequencies should not be given a high priority for
esea h at this ti e.
Possible conflicts of interest
A remarkable fact in his latest
Declaration of Personal Interests
is that he has shares in
telecommunications multinational BT Group, one of the largest telecommunications
companies in the world from 2003 to the present day. The gain is very little: about 100
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pounds a year. But still: if you want to avoid the impression of conflicts of interest buying
shares in a telecom company does
t see to e a ise de isio .
He himself acknowledges this is a potential conflict of interest. Under
an article
published in
the State e t o the Co fli t of I te est is:
The authors declare that this work was
conducted in the absence of any commercial or financial relationships that could be
constructed as a potential conflict of interest,
except Sienkiewicz declares that he has owned
440 ordinary shares in BT Group, a communication services company.
In his
2015 Declarations of Interests
he de la es to ha e do e si e
P ovision
of
research and scientific advice to
UK go e
e t a d othe stakeholde s . It is ot spe ified
who those other stakeholders were, but it can be assumed those were not civil society
groups.
Also since 2009, he has been a consultant to the Rapid Response Group at the Japan EMF
Information Center, which is funded by "Japan Electrical Safety & Environment Technology
Laboratories, where he conducts reviews and analyses of recently published scientific
studies
He was between 2001 and 2012
member
of the Mobile Telecommunications Health
Research (MTHR)-programme. The programme did not find any association between
exposure to mobile telephone communication and an increased risk of developing cancer. In
the final report of the programme we read that that the core funding was provided in
approximately equal share by government and industry. He systematically defends the point
of view that there are no health risks associated with non-ionizing radiation. He was co-
author of the 2019 article which criticized the NTP-study.
SCIENTIFIC EXPERT GROUP
Jacques Abramowicz
Biography
Jacques Abramowicz is Professor of Obstetrics and Gynecology and the Director of the
Ultrasound Services at the University of Chicago.
He is a member of the Scientific Expert Group since May 2016.
Position
A a o i z is, sa s his pe so al page at Chi ago U i e sit ,
an expert in the use of
ultrasound for prenatal diagnosis of foetal anomalies and screening for early detection of
o a ia a e .
As far as we could find out, he did not perform research into the health effects of mobile
phone radiation.
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Possible Conflicts of Interest
In his declaration of personal interests Abramowi
z does t e tio possi le o fli ts of
interest and we did not find information that contradicts this.
Anssi Auvinen
Biography
Auvinen is currently a professor of Epidemiology at the School of Health Sciences, University
of Ta pe e i Fi la d. He is a e e of ICNIRP s S ie tifi E pe t G oup si e
. He
was also external expert for the Scientific Committee on Emerging and Newly Identified
Health Risks SCENIHR epo t o Pote tial health effe ts of e posu e to ele t o ag eti
fields EMF , adopted i Ja ua
.
Position
In harmony with all ICNIRP-members Auvinen criticizes research that seems to show an
association between health problems and mobile phone use.
Although there have been
individual reports of associations between MP-use and tumours, this research is not
o siste t a d o ala e does ot p o ide e ide e of a asso iatio , he a d his o-
authors
wrote
in 2008. His own research systematically shows no association between
health problems and non-ionizing radiation.
Auvinen participated in the Finish Cohort Study of Mobile Phone Use and Health (COSMOS).
A recent
publication
(October 2019) on the outcomes states reassuringly that
usi g
mobile
phones most extensively for making or receiving calls at baseline reported weekly headaches
slightly more frequently at follow-up than other users, but this finding largely disappeared
after adjustment for confounders and was not related to call-time in GSM with higher RF-
EMF exposure. Tinnitus and hearing loss were not associated with amount of call-ti
e. I
another
publication
on the COSMOS-outcomes (April 2020) an association between sleep
quality and mobile phone use is also not found.
Possible conflicts of interest
In his
Declaration of Interests
he submitted to ICNIRP he states that he in 2014 and 2015
e ei ed esea h €
,000 funding from the
Mobile Manufacturers Forum,
an international
organization founded in 1998 by leading manufacturers of mobile phones and radio
equipment, such as Alcatel, Ericsson, Mitsubishi Electric, Motorola, Nokia, Panasonic, Philips,
Sagem, Samsung, Siemens and Sony Ericsson.
The funding was for the COSMOS-study. In the 2019-publication on this study Nokia and
mobile network providers TeliaSonera and Elisa are mentioned in
the atego fu di g .
Another
recent article
states that Au i e e ei ed o sulti g fees f o
A o di g to his De la atio of I te est he e ei ed a fee of €
i
73
Epid Resea h I .
a d
. Not
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his declaration of interest is that he received lecture fees from pharmaceutical companies
Glaxo Smith Kline and MSD. Maybe one can argue that these companies do not operate in
the field of non-ionizing radiation. But to avoid conflicts of interests it seems wise to be
transparent about all fees and funding received from industry.
Christian Cajochen
Biography
ICNIRP s e site states that Cajo he studied atu al s ie es follo ed a
-y
postdoctoral stay at the Harvard Medical School in Boston, USA. He leads the Centre for
Chronobiology at the University of Basel and focusses on the influence of light on human
cognition, circadian rhythms and sleep, circadian related disturbances in psychiatric
disorders, and age-related changes in the circadian regulation of sleep and neurobehavioral
performance.
He serves as associate editor for established sleep-related scientific journals and is editor in
hief fo Clo ks&Sleep .
He started as a member of the Scientific Expert Group (SEG) in May 2018.
Position
As stated
Cajochen
focusses on the influence of lights and far as we could find out, he did
not perform research into the health effects of mobile phone radiation.
Possible conflicts of interest
I his DOI it is stated that he studies the effe ts of da LED o human
performance,
melatonin and sleep. Research studies in healthy human volunteers partially sponsored by
Toshi a Mate ials. I the pe iod f o
-2018 that accounts for 120.000 (we assume
eu o , he e Toshi a has the ight to e uest i e isio s to
the publication, so that no
Confidential Information is inadvertently disclosed or a delay of not more than 60 days to
allow for protection of any potentially patentable subject matter by filing of a patent
appli atio .
Toshiba does not focus on telecommunications, but rather on mainly infrastructure energy
and Electronic Devices.
Jose Gomez-Tames
Biography
Gomez-Tames is Research Associate Professor in Nagoya Institute of Technology.
He is also Working Group Chair of the Subcommittee on EMF Dosimetry Modelling of the
IEEE International Committee on Electromagnetic Safety from 2017.
Gomez-Tames is member of the Scientific Expert Group since 2018.
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Position
Gomez-Tames work is more on the modelling of non-ionizing radiation than on the health
effects.
Possible conflicts of interest
See Van Rongen and others on the role of IEEE/ICES.
In his
Declaration of Personal Interest
Gomez-Ta
es does t e tio othe sou es of
possible conflicts of interest and we did not find information that contradicts this.
Penny Gowland
Penny Gowland worked at the University of Nottingham School of Physics and Astronomy
until 2016 and is now retired. She did a PhD in Magnetic Resonance Imaging from the
Institute of Cancer Research in 1990.
A
o di g to ICNIRP s e site he o k at high field a d o
foetal development as led her
to take a strong interest in the interactions of EMF with the human body, and safety aspects
of MRI.
Penny Gowland is a member of the ICNIRP Scientific Expert Group (SEG) since March 2013.
Position
She de la ed i he DOI that he esea h i te ests a e i MRI: ut I a
a d p ofessio all i te ested i a
iologi al effe ts of EMFs.
also a ade i all
As stated Gowland focussed mainly on MRI and far as we could find out, she did not perform
research into the health effects of mobile phone radiation.
Possible conflicts of interest
According to the
organisation AVAATE
her previous Declaration of Interests, she reported
that she has held many research contracts with Phillips Electronics but without any money
involved. Gowland has been part of the MR safety working group of British Institute of
Radiology. According to the
British Institute of Radiology website,
Phillips and Siemens are
platinum sponsors.
In 2015 AVAATE also stated that the
European Society for Magnetic Resonance in Medicine
and Biology
(ESMRMB), organization mentions that Gowland was a member of several
committees, including the Committee on Security, and has received financial support from
companies like Hitachi, Philips, Siemens, Toshiba and General Electric.
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John Hanifin
Biography
John Hanifin is
laboratory director of the Light Research Program at
Thomas Jefferson
University.
He is a member of the Scientific Expert Group since May 2018.
Position
Hanifin is specialized in the effects of light. A recent publication he contributed to is for
example is about the effect on nurse and patient experience of the overnight use of blue
depleted illumination. He did not conduct research on the health effects of mobile
communications technologies.
Possible conflicts of interest
The Light Research Program
received
industry support from among others OSRAM, Philips
Lighting and Panasonic.
His
PhD-thesis
(2015) was also party funded by industry, by Philips Lighting, Apollo Lighting
and OSRAM.
Ha ifi s De la atio of Pe so al I te est sho s that
his laboratory earns about 5% of its
yearly income by conducting clinical research for Bios Lighting. It mentions that his
laboratory is obliged to submit a manuscript to the sponsor before publication for review
a d o
e t, ho e e Spo so shall ot exercise
editorial cont
ol o e the pu li atio .
The fact that the sponsor can review and comment the manuscript does not seem to be a
strong guarantee of independence.
Jukka Juutilainen
Biography
He is a retired professor emeritus of Radiation Biology and Radiation Epidemiology, and
Department Head of the Department of Environmental Science at the University of Eastern
Finland. Juutilainen teaches generic courses on environmental health and risk assessment, as
well as specific courses on non-ionizing and ionizing radiation
He is an Associate Editor of
Bioelectromagnetics,
effective immediately for which he was
nominated by the European Bioelectromagnetics Association (EBEA) a non-profit scientific
association with many current and former ICNIRP-members.
He was a member of the ICNIRP Standing Committee on Biology from 2004 until 2012 and
became a member of the Scientific Expert Group (SEG) in March 2013.
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Position
In 2007,
Microwave News
reported positively about a study published by
Juutilai e :
Every
now and then a new paper comes along that gives hope that one day we'll make sense of the
o fli ti g esults that ha e e o e the hall a k of EMF esea h.
The study
was
financed
partly by the cell phone industry
—the
MMF and the GSMA and although Juutilainen
suggested that needed a follow-up it never got one.
Another
study from 2007
o luded that the data did ot sho a effe ts of
radiofrequency electromagnetic fields on micronucleus frequency in erythrocytes. The
findings were consistent in two mouse strains (and in a transgenic variant of the second
strain), after 52 or 78 weeks of irradiation, at three SAR levels relevant to human exposure
from mobile phones, and
fo th ee diffe e t o ile pho e sig als. The stud as o-funded
by Nokia, Elisa Communications Corporation, Finland Benefon, Finland Sonera.
Juutilainen published
this study in 2009,
togethe
ith C oft a d Va Ro ge , o the Effe ts
of Radiofrequency Electromagnetic Fields on the
Hu a Ne ous S ste . The o lusio
as that
However, in provocation studies a causal relation between EMF exposure and
symptoms has never been demonstrated. There are clear indications, however, that
psychological factors such as the conscious expectation of effect may play an important role
i this o ditio .
Possible conflicts of interest
In his past ICNIRP Declaration of Interests, he stated that he has received research funding
from government organizations and foundations.
In his last non-sig
ed DOI he i di ates The Depa t e t of E i o e tal a d Biologi al
Sciences of the University of Eastern Finland (UEF) has received funding from the Electric
Power Research Institute (EPRI). Although EPRI is an independent, non-profit research
organization (and therefore not reported above in research support received from
commercial entities), this funding might be perceived as affecting my independence (Period:
2015-
.
According to AVAATE
he had u e ous esea h p og a s fu ded Nokia, Be efo ,
Sonera, Elisa,
FINNET, the GSM Asso iatio a d the Mo ile Ma ufa tu e Fo u . For
example, the national research programme on possible health effects of mobile phones in
Finland (from 1998 to 2003) which was coordinated by Juutilainen was mainly funded by
TEKES, National Technology Agency a governmental organisation, and also supported by
Nokia, Benefon, Sonera, Elisa, Radiolinja, Finnish 2G, Mobile Manufacturers Forum and the
GSM Association.
He has participated in conferences and publications funded in part by organizations with
interests in the telecommunications sector.
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Masami Kojima
Biography
Masami Kojima is a professor of Kanazawa Medical University. He is specialized in ocular
damage due to microwaves.
In the period 2001-2004 he was a consulting member for ICNIRP, since november 2014 he is
a member of the Scientific Expert Group.
Position
Koji a s esea h is ai l o the effe ts of i o a es
on the eye, often of rabbits. In his
publications, we found no direct statements about possible effects on the eye within the
ICNIRP-norms.
Possible conflicts of interest
He was co-author of the 2010 article partly funded by KDDI Foundation (see Hirata and
Watanabe).
His
Declaration of Personal Interest
does not mention other sources of possible conflicts of
interest and we did not find any.
Ilkka Laakso
Biography
He is Professor of Electromagnetics in Health Technologies at Aalto University, Finland and
focuses on theoretical and computational bioelectromagnetics at both extremely low and
adio f e ue ies. Laakso has ee
o i i g o putatio al ele t o ag eti s ith
edi al i age p o essi g a d iologi al eu o
odelli g. The pu pose of
this research is
to offer the medical and electrical engineering community new computational methods for
individual physical modelling of the human body.
A o di g to ICNIRP s e site he is the se eta of Su o
ittee of EMF Dosi et
Modeling (SC6) of the IEEE International Committee on Electromagnetic Safety and a
working group chairman si
e
.
Laakso became a member of the Scientific Expert Group (SEG) in 2016.
Position
A
study from 2009
(Assessment of the Computational Uncertainty of Temperature Rise and
SAR in the Eyes and Brain Under Far-Field
E posu e F o
to GHz a out the spe ifi
a so ptio ate SAR see s to suggest that the efe e e le els ICNIRP a d a i u
permissible exposure limits by IEEE seemed to be conservative in the sense that at the
reference le
els the te pe atu e ise i the e es a d ai as al a s less tha ◦C.
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Possible conflicts of interest
For IEEE/ICES see Van Rongen and others.
A o di g to his DOI fo ICNIRP he o s sto ks of a d is a oa d e e of Fieldsi O , a
consulting company in Finland that does computer simulations of electromagnetic fields,
including electromagnetic field exposure.
Isabelle Lagroye
Biography
Isabelle Lagroye
is a director of studies at the Ecole Pratique des Hautes Etudes (EPHE) and
o ks at Bo deau U i e sit . He esea h, states a e e t pu li atio , deals ai l ith
the biological and toxicological effects of non-i
asi e ele t o ag eti fields. She is
currently member of the Bruxelles-Capitale expert committee on non-ionising radiations.
She was member of an ICNIRP committee in the period 2009-2012 and was elected member
of the Scientific Expert Group in March 2013.
Position
In 2018 Lagroye together with two other scientists published an article in
European Scientist
in which she concluded that the NTP-stud consolidates current knowledge and reinforces
the fact that when effects of mobile radiofrequency fields can be observed, it is at exposure
levels that far exceeds the maximum permissible exposure values. In practice, these limits
cannot be reached with commonly used wireless communication technologies (relay
antennas, mobile phones, Wi-Fi
… .
This statement seems to be in contradiction with findings from her own research. A
recent
publication
of which Lagroye was co-autho
o ludes: Ho e e , e fou d that e posu e to
GSM-modulated 1800 MHz signals at 2 W/kg decreased the PMA maximal efficacy to
a ti ate oth RAS a d ERK ki ases' a ti it . So,
it influences the signaling between proteins.
This is an effect at 2 W/kg, while according to the new ICNIRP-norms health effects in head
and torso are only above 20W/kg and the norm is, with a safety factor of ten, 2W/kg.
Lagroye was also co-author of the
final report
of the Geronimo-project. In this report, we do
find indications for health effects. It says:
Results suggest that i eased RF dose to the
brain and longer mobile phone call time may
e asso iated ith isk of h pe a ti it a d o du t p o le s.
And:
a eta-analysis
among four birth cohorts (n=55,507) indicated that maternal cell
phone use during pregnancy may be associated with shorter pregnancy duration and
i eased isk fo p ete
i th Tsa a et al.,
, a epted A J Epide iol .
Interesting is also that research conducted by Lagroye seems to suggest non-thermal effects,
while ICNIRP states that thermal effects are the only ones for which there is scientific
evidence. In
this article
the autho s ite:
Altogether, our experimental findings provide
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evidence for dose-dependent effects of RF signals on the bursting rate of neuronal cultures
and suggest that part of the mechanism is non-thermal.
In 2009, she co-authored
a scientific paper
with Van Rongen and Croft which stated on the
effects
of radiofrequency electromagnetic fields on the human nervous system
that
the e
are clear indications, however, that psychological factors such as the conscious expectation
of effect may play an important role in this condition.
Possible conflicts of interest
The latest
Declaration of Personal Interest
of Lagroye that can be found on the ICNIRP-site
dates from 19 October 2015, almost five years ago. At that moment, she stated that she got
2,35% of the income of her research unit from a commercial partner, the Réseau de
T a spo t d Éle t i ité RTE).
A
study
published in 2010 which suggested that exposure to WiFi did not damage the brains
of young rats was funded by France Telecom and
La Fondation Santé et Radiofréquences,
an
organisation that is for the half funded by industry.
This organisation also partly funded several other studies to which she contributed, like
this
one
published in 2011 and
this one
published in 2012.
Another 2012
publication
was partly funded by Bouygues Telecom.
Sarah Loughran
Biography
ICNIRP s e site states that Lough a
is currently a researcher at the University of
Wollongong in the Australian Centre for Electromagnetic Bioeffects Research (ACEBR)
human neurophysiology research group, an NHMRC Centre of Research. She studied
physiology and psychology and got a PhD in cognitive neuroscience/psychophysiology at
Swinburne University of Technology,
investigating the effects of electromagnetic fields on
human sleep,
the electroencephalogram (EEG), and melatonin.
To this centre (ACEBR) also ICNIRP-chair Rodney Croft and ICNIRP-member Andrew Wood
are connected. Swinburne university and in particular
the Radiofrequency Dosimetry
Laboratory
is part of the ACEBR which has a very close relationship with and is co-funded by
Telstra, the biggest Telecom company in Australia. (See also portraits on Woods and Croft)
Loughran is also a member of the current World Health Organisation (WHO) RF
Environmental Health Criterion evaluation committee, and is on the board of directors for
the Bioelectromagnetics Society (BEMS). She is a member of the ICNIRP Scientific Expert
Group (SEG) since March 2013.
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Position
A
2005 study
by Loughran and Woods on the effects of EMF on human sleep demonstrated
that a sho t e posu e to o ile pho e-type
radiation has an effect on subsequent sleep
EEG, although no conclusions can be made regarding adverse health consequences as the
mechanisms
of the effe ts a e still u k o .
In 2007
Microwave News reports
that the a ilit of o ile pho e adiatio to affe t sleep is
emerging as a robust low-level effect. A team led by Bengt Arnetz has reported that a three-
hou e posu e to GSM adiatio at . W/Kg a hou efo e ed a dis upt sleep. This
study supported earlier findings of Peter Achermann of the University of Zurich and
Loughran at the time working at the Brain Sciences Institute at Swinburne University.
Because later findings of other studies got quite some media attention, Loughran, Peter
Achermann & Niels Kuster
published a statement
to temper the seriousness of the findings.
Loughran worked for some years in Switzerland, where several scientists like Kuster do
research on EMF and sleep.
The Nation
reported that
Niels Kuster, a Swiss engineer co-
authored in
The Lancet Oncology
a summary of
the WHO s fi di gs of
the Interphone study
hi h as lau hed the WHO s I te atio al Age
fo Ca e Resea h i
a d to
which two wireless trade associations contributed $4.7 million or 20 percent of the $24
million budget). Kuster had filed a conflict-of-interest statement affirming that his research
g oup had take
o e fo
a ious go e
e ts, s ie tifi i stitutio s a d
o po atio s. But afte his publication
The
La et issued a o e tio e pa di g o
Kuste s o fli t-of-interest
statement, noting payments from the Mobile Manufacturers
Forum, Motorola, Ericsson, Nokia, Samsung, Sony, GSMA, and Deutsche Telekom.
Nevertheless, Kuster participated in the entire 10 days of WHO-deli
e atio s.
In general,
Loughran (ACEBR) is in agreement with Croft.
In an interview
with
Computerworld:
There are people that are sufferi g a d es, it s
not due
to electromagnetic
e erg e posure, it s
more of a
psychosomatic
condition…
According to a 2017
study
IEI‐EMF p o ocation
case studies: A novel approach to testing
se siti e i di iduals of hi h Lough a is the se o d autho
the present experiment failed
to sho a relatio ship et ee RF‐EMF e posure a d a IEI‐EMF i di idual's s pto s
.
The
information on Electro hypersensitivity
f o the WHO s
EMF Project (see also History
chapter in this report) to which Loughran is connected has not been updated since 2005.
Possible conflicts of interest
In her DOI she declares for 2015 having received almost 16.000$ from
EPRI funding and
NPF
resear h I stitute, hi h a ou ted appro i atel for 5% of her la s i o e .
In a 2016
EPRI workshop
Lough a p ovided
an overview of the current state of knowledge
in the field of human laboratory studies, an assessment of the critical gaps in knowledge,
and recommendations for research priorities. Loughran and the session rapporteur, Rodney
Croft, University of Wollongong, led the workshop participants in a discussion of human
la o ato studies .
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See also portraits on Croft and Wood.
Jack Lund
Biography
Jack Lund was research physicist with the US Army Medical Research Command. There he
studied the effect of laser radiation on ocular tissue and the visual system. He retired in
2018.
He was an ICNIRP Consulting Expert from 2002 to 2012. He joined the Scientific Expert Group
in 2018.
Position
Jack Lund is an expert in laser safety issues. He did not publish article about the health
effects of mobile communication technologies and did not make, as far as we could find out,
make public statements about it.
Possible conflicts of interest
Lu ds
Declaration of personal interest
is o pletel e pt . We did ot fi d othe
information about possible conflicts of interest.
Simon Mann
Biography
According ICNIRP
s e site Si o Ma is a ha te ed ele t i al e gi ee a d heads the
Ph si al Dosi et Depa t e t at Pu li Health E gla d s Ce t e fo Radiatio , Che i al
and Environmental Hazards. Man is responsible for programmes of scientific work to
develop health-related advice on exposures to electromagnetic fields (EMFs) and optical
radiation across the UK.
He was secretary to the independent Advisory Group on Non-ionising Radiation (AGNIR), and
member of the IARC Working Group that evaluated the carcinogenic potential of
radiofrequency EMFs in 2011. He currently works with WHO EMF Project (see also history
part) to develop its Environmental Health Criteria monograph on radiofrequency fields.
He is also active in technical standardisation and is a UK delegate to the CENELEC TC106X
Committee.
During
a meeting of the WHO EMF Project
in 2013 Lindsay Martin from ARPANSA
–
(Australia) and Simon Mann (PHE - UK) were elected chair and vice chair respectively. In the
meeting J. Keshvari from International Committee on Electromagnetic Safety (ICES)and the
I te atio al Ele t ote h i al Co
issio IEC TC
said that Mai te a e o k is i
hand on several EMF exposure Standards. Harmonisation and avoiding duplication of effort,
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et ee CENELEC, IEEE a d ITU is e ou aged he e possi le. Kesh a i also
that IEEE/ICES has ee de elopi g a RF safet Sta da d fo NATO .
He is a member of the ICNIRP Scientific Expert Group since 2015.
Position
e tio ed
Mann is part of the close network of ICNIRP and WHO EMF scientists that claim there are no
real immediate health effects from EMF. For more on the WHO Project and EMF IEEE/ICES,
see the history part of this report and the portrait of Croft and Van Rongen.
Possible conflicts of interest
We ould ot fi d a e e t DOI o ICNIRP s e site:
the
li k to Ma
website is not functioning.
s DOI o ICNIRP s
However, he did not mention in his former Declaration of Interests statement submitted to
ICNIRP, that he has received research funding from the GSM association, the Mobile
Ma ufa tu e Fo u a d the UK s
Mobile Telecommunication and Health Research Program
(MTHR),
on which he still plays
a leading role.
According to AVAATE
MTHR
in the past
received funding from the Vodafone, a wireless company.
Since 2009 he has been a member of BEMS and the EBEA22.
Rüdiger Matthes
Biography
Rüdiger Matthes was from 1989 until his retirement in 2016 Head of the group "Non-Ionizing
Radiation (Dosimetry)" at the German Federal Office for Radiation Protection. He became
the Scientific Secretary of ICNIRP in 1993. He was Chairman of the Standing Committee on
Physics and Engineering (SCIII) from 2004 to 2008. He became Vice-Chair in 2008, and Chair
again in 2012. Since 2016 he is a member of the Scientific Expert Group.
Position
Matthes
defends the position
that there are no studies that prove the existence of non-
thermal health effects of non-ionizing radiation and that no plausible mechanism has been
described whereby these effects could take place. There is no evidence for a link between
cancer and the use of mobile phones,
he said
in 2010.
Matthes was one of the authors of a
recent ICNIRP-publication
in which ICNIRP explains the
principles for health protection on which its guidelines are based.
Possible conflicts of interest
In his
Declaration of Personal
Interests Matthes does not mention any possible conflict of
interest and we did not find any information that contradicts this.
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During
a meeting of the WHO EMF Project
in 2013
Matthes spoke on behalf of both BfS and
ICNIRP stati g that: E posu e e o
e datio s ha e ee de eloped se e al
organisations such as ICNIRP and IEEE/ICES, and there is good harmonisation between these
o fu da e tal li its.
John
O'Hagan
Biography
On
ICNIRP s e site it sa s that Joh O Haga heads the Lase a d Opti al Radiatio
Dosimetry Group at Public Health England. This research group covers all aspects of optical
radiation dosimetry, including both the beneficial and detrimental effects of optical radiation
on people.
He is Vice-President Standard of the International Commission on Illumination (CIE),
Co e o of the I te atio al Ele t ote h i al Co
issio Te h i al Co
ittee
Opti al
Radiation Safety and Laser Equipme
t Wo ki g G oup Non- ohe e t sou es , Chai a
of the B itish Sta da ds Co
ittee EPL/
Opti al Radiatio Safet a d Lase E uip e t
and is a member of a number of other national and international committees.
According to his DOI he was also a member of EU SCENHIR/SCHEER Working Group on
Potential risks to human health of Light Emitting Diodes (2016-2018) and is a Member of
WHO Core Group on NIR Basic Safety Recommendations.
He joined the ICNIRP Scientific Expert Group (SEG) in March 2013.
Position
In 2017 O
Haga o-wrote
a chapter in
Clay's Handbook of Environmental Health
in which
the general line of ICNIRP, SCENHIR and WHO EMF Project is repeated: no adverse health
effects.
Possible conflicts of interest
In his DOI he states
u de a ti ities P o isio of s ie tifi suppo t a d ad i e to
government and other stakeholders
, ut fails to e tio hi h stakeholde s.
In his statement, he says that he is the President of the Committee EPL/76 Optical radiation
safety and laser equipment, of BSI Standards Development (BSI is a company that sets rules
to help organizations worldwide achieve excellence). Organizations that work with this
committee include the Association of Industrial Laser Users, the Association of
Manufacturers of Domestic Appliances, GAMBICA Association Limited (a UK national
organisation representing the interests of companies in the instrumentation, control,
automation and laboratory technology industry) the Institute of Physics, the Institution of
Engineering and Technology, the Institution of Mechanical Engineers, and the Lighting
Industry Association.
He also reports that he is the Vice President of the CIE-UK National Illumination Committee
of Great Britain. This committee was established by the Illuminating Engineering Society of
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Great Britain, the Institute of Electronic and Electrical Engineers, the Institute of Gas
Engineers, and the NPL, in collaboration with industry and professional associations,
government departments and lighting technicians.
Chiyoji Ohkubo
Biography
Chiyoji Ohkubo is Director of the Japan EMF Information Center (JEIC). This organisation was
esta lished i Jul
to fa ilitate o
u i atio o EMF issues a o g go e
e t
agencies, industry, the media and the gene
al pu li .
In the period 2005-2007 he worked for the EMF WHO-project.
He is a member of Scientific Expert Group since March 2013.
Position
All his publications seem to fit into the same category: no effect. See for example
this study
in which the exposure of rats to RF EMF radiation did not alter their cerebral
microcirculation.
Possible conflicts of interest
For criticism of the WHO EMF Project see among others Van Rongen.
The Japan EMF Information Center,
writes Okhubo himself,
has ee fi a ed f o
do atio s stakeholde s a d go e
e tal fu ds. A i fo atio leaflet of the
o ga isatio sa s:
The JEIC is founded to present in a neutral way the positions of industry,
s ie e a d so iet , a d to dis uss the isk a al sis. It see s to e o oi ide e that
industry is mentioned first.
Ohkubo did
research
funded by the
Association of Radio Industries and Businesses (ARIB),
Japan.
Margarethus Paulides
Biography
Margarethus ('Maarten') Paulides obtained his MSc in Electrical Engineering at Eindhoven
University in 2002 and his PhD in Medical Electromagnetics
He works as Associate Professor, Department of Electrical Engineering, Electromagnetics, at
the university of Eindhoven as well as Associate Professor, Erasmus Medical Centre in
Rotterdam.
The outcome
of his research were novel devices,
patient-specific simulation technology and
pioneering data and knowledge for improving EMF exposure guidelines.
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Since 2015 he is board member of the Dutch National Antenna Research Framework (NARF).
From 2017, he serves in the Electromagnetics Committee of the Dutch Health Council that
advises the relevant ministers in the Netherlands on EMF related subjects. He also is a
Management Committee member and Workgroup leader in COST action CA17115.
He is a Member of the ICNIRP Scientific Expert Group (SEG) since 2017.
Position
Most of his research is focussed on applications in health monitoring, disease diagnosis and
therapy. We did not find much research on the health effects of radiofrequency radiation.
He did some research on thermal effects on tissue which resulted in this
2018 study
in which
the authors basically state that the protection levels of ICNIRP and IEEE are conservative and
safe:
To protect against any potential adverse effects to human health from localised
exposure to
adio f e ue
 kHz-  GHz ele t o ag eti fields RF EMF , i te ational
health organisations have defined basic restrictions on specific absorption rate (SAR) in
tissues. These exposure restrictions incorporate safety factors which are generally
conservative so that exposures that exceed the basic restrictions are not necessarily
ha ful.
Possible conflicts of interest
A o di g to the ICNIRP e site he also a ts as ad iso of sta t-up
companies aimed at
providing solutions for computer simulatio
a d i age guided i te e tio s .
His DOI further states that he does paid consultancy for a company Sensius.biz, which in fact
he co-fou
ded, fo a a ou t of
€. He also o s , % i sto ks of this o pa .
The same amount he got from a German company Sennewald Medizin Technic.
He e ei ed a
.
€ esea h G a t fo
Ge e al Ele t i Resea h Ce t e i Ge
.
€i
any.
ash
For the contracting company Phillips
he e ei ed a STW esea h g a t of
a d .
€ i ki d.
Kensuke Sasaki
Biography
Kensuke Sasaki is a Researcher of the National Institute of Information and Communications
Technology, Japan.
He is a member of Subcommittee of EMF Dosimetry Modelling of IEEE International
Committee on Electromagnetic Safety. He is also an expert for a committee of the
International Electrotechnical Commission.
He joined the Scientific Expert Group in November 2018.
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Position
Most publications of Sasaki are about how to measure the effects of non-ionizing radiation
and about the thermal effects of it on for example the eye. We did not find direct
statements about the health effects.
Possible conflicts of interest
For information about IEEE/ICES see Van Rongen.
Together with Hirata and Watanabe (see above) he conducted research
published
in
IEEE
Transaction
in 2010 partly funded by KDDI Foundation.
David Savitz
Biography
Savitz is currently Professor of Epidemiology and Obstetrics and Gynecology, at the American
Brown University.
His teachings and research is focussed mainly on epidemiologic methods and, reproductive,
environmental, a
d a e epide iolog a d he autho ed a ook e titled I te p eti g
Epide iologi E ide e .
He was a member of the ICNIRP Standing Committee on Epidemiology from 1997 until 2012
and then became a member of the ICNIRP Scientific Expert Group (SEG) in 2013.
Position
Given the fact that he has been connected to ICNIRP for 23 years we can safely assume that
he agrees with the position of this NGO on health effects of EMF.
Possible conflicts of interest
His Declaration of Interests statement to ICNIRP, says that he does paid consultancy but
o
-
ele a t to ICNIRP .
According
to AVAATE
this is ot eall t ue: He ga e
expert witness testimony
on behalf of
the defendants in a January 2012 lawsuit in Federal District court in Portland, Orego
.
A company AHM Wireless sued the Portland Public School System, because it called for the
removal of a Wi-Fi system in the schools. The testimony of Savitz was requested to assess
the expertise of plaintiffs' claims that the implementation of wireless devices and wireless
systems in the schools could possibly cause cancer or other adverse health effects.
In court, he states that the purpose of his contract with Battelle was to investigate
relationships between environmental agents and human health and that he had a variety of
sponsors, including some federal government agencies and other groups that he does not
recall at this time.
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Remarkably when he is asked about his ICNIRP membership he said that doesn´t
consider
himself to be really an active member and that he contributed all those years to just four
reports, together with Anders Ahlbom, who coordinated their advice work for ICNIRP and
whom had also recruited Savitz to join ICNIRP (in 2011 was asked to step down from IARC
panel after he was exposed
to e o the oa d of his othe s o sulti g fi , hi h
telecom clients).
Sa itz: M u de sta di g of the o ga ization
is really actually quite
limited. My role in it has been much narrower to participate in the evaluation of evidence
and the reporting of the results of that evaluation. I have not been involved in what's done
ith that e aluatio .
When the lawyer of the
pu li s hool asks So the o ga izatio , though, it's i ol ed ith
the protection of human beings from non-ionizing radiation; is
that o e t? Sa itz a s e s:
Agai ,
u de sta di g is ot u h deepe tha as ou des i ed it ased o the a e of
the organization. My understanding is that they evaluate evidence and make
recommendations that are intended to be protective of health.
When asked if he is paid to be part of scientific committees, he says that he remembers only
travel expenses being reimbursed by ICNIRP. He says he doesn´t even remember how many
scientific committees he belongs to. He wasn´t involved with what ICNIRP does in making
decisions after it receives the results of the evaluation carried out by the Standing
Committee on Epidemiology. He says that he has never read the ICNIRP Statutes, its mission,
etc. He maintains that he is hired to help evaluate a particular line of research. Also, when
asked if there was any relationship between ICNIRP and the WHO for the work in which he
contributed to, he said he did not know.
It almost seems as if Savitz does not want to be remembered too much about ICNIRP and
tries to distance himself from the NGO and its position. When the lawyer of the public
s hools asks ou ould ag ee the that e eed
protection from non-ionizing radiation; is
that o e t? , Sa itz a s e s: Well, that's ot so ethi g that I get i ol ed i the
technical
judgment of the sort of guidelines or regulations or decision-making. If you're asking,
obviously there are levels of exposure that I'm aware that can be harmful, so that I can
understand in a general way that it makes sense that there be conside
atio of egulatio .
AVAATE otes that he asked hethe he has ee paid out of fu ds a ui ed f o
companies and/or telecom consultants and law firms that represent these companies, he
replied that there are a few cases where he has done research funded by the electric utility
industry. However, he emphasized that the funders tried to isolate his work from the source
of
fu di g. He sa s he o e had do e a stud efo e ealizi g he e the o e a e f o .
Savitz also stated that he has done work sponsored by EPRI, as many ICNIRP members,
which is funded by the electrical power industry.
There is no record of these kind of data in the Declaration of interests that he submitted to
ICNIRP.
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Karl Schulmeister
Biography
Karl Schulmeister
is since 1994 head of the Laser, LED and Lamp Safety group at Seibersdorf
Laboratories in Austria. On his
LinkedIn profile
he des i es hi self as Consultant
on Laser
a d Opti al Radiatio Safet .
He was a member of the ICNIRP Standing Committee on Optical Radiation in the period
2008-2012 and joined the Scientific Expert Group in March 2013.
Position
Karl Schulmeister is specialized in optical radiation. He did not perform research on the
health effects of radiofrequency radiation.
Possible conflicts of interest
Seibersdorf
La o ato ies is a fi , ot a a ade i i stitutio . S hul eiste s g oup de i es,
according to his
Declaration of Interest,
about 10% of its income from paid consultancy.
Research for
an article
published in 2015 and
a white paper
published in 2016 received both
the support of the Laser Illuminated Projector Association, which
presents itself
as a si gle
i dust oi e i atio alizi g lase egulatio s .
David H. Sliney
Biography
Sliney
serves as chair
of the IES Photobiology Committee and holds a Ph.D. in biophysics and
medical physics from the University of London, Institute of Ophthalmology. He worked for
the US Army Public Health Center for 42 years, serving as Program Manager, Laser/Optical
Radiation Program, until retiring in 2007.
Het still acts as Safety Director, American Society for Lasers in Medicine and Surgery; And he
remains an associate faculty member of the Johns Hopkins School of Public Health,
Department of Environmental Science and Engineering, Baltimore, MD.
He served as member, advisor and chairman of numerous committees that are active in the
establishment of safety standards for protection against non-ionizing radiation (ANSI, ISO,
ACGIH, IEC, WHO, NCRP).
He has been an ICNIRP Commission Member from the very start in1992 until 2004 and as
Chairman of ICNIRP SCIV (optical radiation) from 1998 until 2004. He is a member of the
ICNIRP Scientific Expert Group (SEG) since November 2017.
Position
Sliney has been mainly focussing on safety and health issues of laser lights, UV light or other
sources, important for safety for medical staff who work with laser application in surgery
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and medicine. Also, scientists and military staff are risk groups for laser damage to the eye.
We could not find research on the health effects of radiofrequency radiation.
Which does not mean that he is not involved in the scientific debate. In 2013 for example he
participated in a webinar by the American Conference of Governmental Industrial Hygienists
(ACGIH) on electromagnetic radiation.
In
an article from 2017
on the history of of ICNIRP founder Mike Repacholi explicitly gives a
special thanks to long-term INIRC and ICNIRP member David Sliney for his help with
reviewing the article.
i the NATO S ie e Se ies
B.Jo Klaue e g
(US Air Force Research
In
a book
f o
Laboratory)
and also NATO-liaison, Sliney is
des i ed as D Da e Sli e a d a
e plo ee
ho se es o the ICNIRP . Klaue e g
who in the first years
led the WHO EMF Project
together with Repacholi,
is a prominent figure from the US Department of Defense (DOD)
a d des i es it as follo s: Be ause the US ilita se i es ope ates glo all a d ith
many different national partners, uniformity of the RFR exposure standards is a desirable
goal. He the des
ribe the various ways that the
DOD o t i utes to o ld ide sta da ds
ha o isatio . So, the DOD pa ti ipates i the WHO EMF p oje t fo e a ple th ough
active engagement of US Air Force Research Laboratory as well as US army personnel
providing service on the IEEE
. A d Sli e thus see s to e the US a
ep ese tati e i
ICNIRP.
Possible conflicts of interest
His DOI is signed in 2019 but does not mention much.
Rianne Stam
Biography
Rianne Stam is
senior scientist at the National Institute for Public Health and the
Environment (Bilthoven, the Netherlands) since 2007. There she performs risk assessments
and policy research on the biological effects and possible health risks of electromagnetic
fields (EMF).
She is a member of the Scientific Expert Group since March 2013.
Position
Stamm made in 2015 and
2019
overview reports of the long term effects of electromagnetic
fields
o the health of o ke s. The o lusio : S ie tifi esea h has ot et p o e a
links between the exposure of workers and the occurrence of cancer, disorders of the
nervous system or other illnesses in
the lo g te .
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Possible conflicts of interest
A o di g to he De la atio of Pe so al I te est Sta has o possi le o fli ts of i te est
and we did not find any information that contradicts this.
Bruce Stuck
Biography
Bruce E. Stuck He is now retired. He was from 1992-2010, the Director of the U.S. Army
Medical Research Detachment of the Walter Reed Army Institute of Research, where he had
espo si ilities fo the A
Medi al Depa t e t s lase a d adio f e ue
adiatio
biological effects research program. Until 2013 he was the Director of the Ocular Trauma
Research Division at the U.S. Army Institute of Surgical Research in San Antonio, Texas.
Since 2012 Stuck is a part-time independent consultant on non-ionizing radiation bioeffects.
He has been a member of ICNIRP SC IV since 1999 and of the Commission from 2004 until
2016. Stuck is now supporting the work of the Project Group as a SEG member.
Position
His research focussed on laser and radio frequency radiation biological effects and
establishes protection strategies (e.g. exposure limits or physical protection products) and
develops triage and treatment approaches for ocular injury from non-ionizing radiation and
shock wave exposures from blast . During his 32 years-experience in laser hazards research
experience he was author/co-author of numerous papers on ocular and cutaneous effects of
laser and radio frequency radiation. His primary interests are in the biological effects of
visible and infrared laser radiation on the retina and cornea and the assessment of laser-
induced eye injuries and their treatment.
Possible conflicts of interest
His DOI states that he is a
onsultant to Perfect Lens, LLC on a proprietary project under a
signed confidentiality agreement to provide advice and written assessment on biological
exposure limits as applied to their repetitively pulsed fem to second laser application for use
in medical application in the eye . He delivered oral and written reports on the device
hazard assessments. Income was less than 1% of personal income from his retirement
annuity in 2018 tax year.
John Tattersall
Biography
John Tattersall
is
scientist in the Defence Science and Technology Laboratory, a government
Agency which provides research and advice for the UK Ministry of Defence and other
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government departments. He also is Honorary Senior Lecturer in Clinical Neurosciences at
the University of Southampton.
He was a member of the IEEE International Committee on Electromagnetic Standards from
2012 until 2017.
He joined the Scientific Expert Group in March 2013.
Position
Twenty years ago, Tattersall did
research
that showed effects of RF Radiation on the brain of
rats.
New Scientist
wrote:
Last year, fears about mobiles affecting brain function received
fresh impetus thanks to work by John Tattersall and his colleagues at the Defence Evaluation
a d Resea h Age
s la s at Po to Do i Wiltshi e. Tatte sall e posed sli es of at ai
to microwave radiation. He found that it blunted their electrical activity and weakened their
responses to stimulation. Because the brain slices were taken from the hippocampus, a
structure with a role in learning, the results were seized upon as further evidence that
mobile
pho es ould s a le hu a
e o ies.
But according to
later research
these effe ts e e a tifi ial, a e e plai ed lo alised
heating produced by interaction of the RF fields with the recording and stimulating
ele t odes .
Tattersall was involved in the new guidelines that were published in 2020.
Possible conflicts of interest
For IEEE/ICES see Van Rongen and others.
Tim Toivo
Biography
Tim Toivo works as senior inspector for the Radiation and Nuclear Safety Authority STUK in
Helsinki, Finland. He is mainly involved in regulatory, research and expert work in the area of
safety issues of electromagnetic fields (EMF) and ultrasound.
He studied biomedical engineering at Tampere University of Technology 1996. And started
his work at STUK–Radiation and Nuclear Safety Authority in 1998 as a scientist in the unit of
non-ionizing radiation.
Part of his work is to inform users of EM fields and communicate with the general public
about safety issues. He participated in the preparation of the EU directive (EU 2013/35/EU)
as an expert for the Finnish delegation.
He is a member of the ICNIRP Scientific Expert Group (SEG) in February 2017.
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Position
Toi o as uoted i the ook Behi d the S ee : Nokia's su ess sto i a i dust of
navel-gazing executives and crazy frogs
: It is fai l eas to p o e that so ethi g is
hazardous, but it is extremely difficult to prove that something is totally safe under all
circumstances. It may take 20-30 years before any meaningful results are available from
people who have been exposed to low power radiation.
In 2009 STUK
pu lished a positio that hild e
s mobile phone use should be limited.
A publication in 2006
–
Epidemiological risk assessment of mobile phones and cancer:
Whe e a e i p o e?
-
together with Anssi Auvinen,
o luded that the ajo
opportunity to improve the quality of evidence is, however, through prospective studies. The
major limitation of epidemiological studies addressing the health effects of mobile phone
use is related to exposure assessment. These limitations are inherent in case–control
studies.
A 2008, in Vitro study of Pulsed 900MHz GSM Radiation on human Spermatozoa showed no
effect.
In
a 2009 publication
– Spe ifi a so ptio ate a d ele t i field easu e e ts I the ea
field of si o ile pho e ase statio a te as
- Toivo and colleagues seem to suggest that
the ICNIRP safet sta da ds a e e o se ati e: It as also sho that the ICNIRP asic
restriction for local exposure could be exceeded before the basic restriction for whole-body
e posu e if the dista e to the a te a is less tha
.
With several ICNIRP colleagues he published the
P og ess epo t: ICNIRP State e t o o
-
io izi g adiatio fo os eti pu poses
fo the IEEE. The o luded that fo os eti
devices using radiofrequency EMF and optical radiation, there is the potential that
occupational exposure limits can be exceeded if adequate protection measures are not
applied.
Possible conflicts of interest
Hid DOI states that he gets funds from ministries which go directly to the Radiation and
Nuclear Safety Authority STUK.
Andrew Wood
Biography
Wood is Professor in Bioelectromagnetic Research Group at Swinburne University of
Technology in Melbourne. He also is a Chief Investigator with the new Australian Centre for
Electromagnetic Bioeffects Research (a centre to which Rodney Croft and Sarah Loughran
are also connected).
Wood used to work at Telstra Research Labs and is now a leading researcher at
Swinburne
Radiofrequency Dosimetry Laboratory,
which is a part of the Bioelectomagnetic Research
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G oup. Telst a is Aust alia s la gest tele o
u i atio s o pa .
Swinburne university and
in particular the Radiofrequency Dosimetry Laboratory
has close relationship with and is co-
funded by Telstra, the biggest Telecom company in Australia.
The close working relationship between the Swinburne University and Telstra
is not new,
as
Do Mais h poi ted out: I fa t the Cha ello of S i u e U i e sit
, Mr. Bill Scales
(2005-
as p e iousl Telst a s G oup Ma agi g Di e to , Regulato , Corporate
and
Hu a Relatio s, a d Chief of Staff at Telst a. He as also Telst a s Di e to of IBM Glo al
Services Australia Ltd. and a Director of the Telstra Fou
datio .
Wood was a member of the Radiation Health Committee of the Australian Radiation
Protection and Nuclear Safety Agency (ARPANSA) for over ten years.
He is a member of the Scientific Expert Group since March 2013.
Position
Wood does not see dangers of 5G and
warns
fo ei g too autious: Wi eless te h ologies
bring enormous benefits, and being over-cautious would potentially deny these benefits to
eed o
u ities.
In a
recent article
he stated that studies which show health effects have a poor quality:
There are some comprehensive reviews of these, demonstrating that the quality of the
studies is very variable, and that, for example, results claiming to show increased genetic
damage or other biological effects are much more common in studies of low quality,
whereas higher-
ualit studies p edo i a tl sho o sig ifi a t effe ts.
Possible conflicts of interest
In a
2016 publication
that ga e a o e ie of the o k Wood s g oup pe fo
ed he and his
co-autho
s ote: O e its
-year history the Bioelectromagnetics Group has received
support from national competitive grants and from industry research support schemes. It
has been a node for both the Australian Centre for Radiofrequency Bioeffects Research
(ACRBR) and the Australian Centre for Electromagnetic Bioeffects Research (ACEBR—see
article in this edition). It has benefitted from industry collaboration and with national
egulato autho ities.
The close collaboration with industry we see time and again. Just like the actual chair of the
ICNIRP-commission Croft, Wood had actively collaborated with McKenzie,
who is a manager
at the Mobile Carriers Forum (MCF). See for more information the portrait of Croft.
In 2016, he published
an article
together with an employee of telecommunications company
Telstra.
He has done
contract work
on the issue of smart meters for the private company EMC
Technologies Pty Ltd.
According to his
Declaration of Personal Interest
he e ei es esea h suppo t f
om two
engineers employed by Telstra Corp and one by the Australian Mobile Telecommunications
Asso iatio .
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Tongning Wu
Biography
According to ICNIRP
s e site To g i g Wu is a se io e gi ee i the Chi ese A ade of
Information and Communications Technology. His research focusses on electromagnetic
dosimetry, anatomical modelling and biomedical applications of electromagnetic fields.
He is the member of International Advisory Committee (IAC) on Electromagnetic Fields of
WHO. He also participated in the IEC/IEEE workgroups on EMF safety. He is currently the co-
rapporteur of ITU-D Q7/2 (Strategies and policies concerning human exposure to
electromagnetic fields).
He became a member of the ICNIRP Scientific Expert Group (SEG) in 2019.
Position
Wu agrees with the general ICNIRP assessment that
to date, o ad e se health effe ts of
the EMF, li ked to these appli atio s, ha e ee esta lished. This as also o e of the
conclusions of
a stud Ele t o ag eti fields EMF e posu e
published in 2019.
In 2012 WU published
a stud o A la ge-scale
measurement of electromagnetic fields near
GSM base stations in Guangxi, China for risk communication
. The esults e e that i
general, the measurement mission promotes the science on EMF exposure among the
general public. Risk-related public behaviou
s ha e ee positi el i flue ed. The issio
also facilitates the cooperative
o fli t esolutio . It helps st e gthe the effe ti e ess of
isk o
u i atio .
Possible conflicts of interest
His DOI gives no information.
See Van Rongen and others on the role of IEEE/ICES.
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Annex I
Questio s put to ICNIRP s secretariat
1 - When will the ICNIRP Annual report 2019 be published?
2 - Are the 14 members of the Commission being paid for their work for ICNIRP (for
"representing ICNIRP externally and mostly in its relations with the international and
national partners and the press" as well as for their collaboration on specific Projects?)
3 - Same questions as n° 2 go for the Scientific Expert group and the Project Groups?
4 - If they are not paid, do you consider this as a normal practice that international
renowned experts work for free, especially given the importance and influence of the work
of ICNIRP?
5 -
ICNIRP itself lai s it is f ee of ested i te ests . ICNIRP's
budget relies on support
granted by public bodies; Why is the income not specified in your annual reports? Is it
possible to get specifications from which public bodies you get which amounts?
6 Who selects the 14 members of the Commission and how?
7 -
ICNIRP's statutes state: No ember
of the Commission shall hold a position of
employment that in the opinion of the Commission will compromise its scientific
independence'
Do we understand it correctly that basically the Commission evaluates itself about possible
conflicts of interest? What are the rules by which the Commission judges if interests of the
members compromise the scientific independence?
8-
I its state e t o the de la atio s of i te ests ICNIRP states: The e aluatio of pe so al
integrity is very complex and might never be achievable in a perfect way. It is the duty of the
ICNIRP Commission to carefully consider and decide if the declared interests potentially
o stitute a o fli t of i te est.
By which criteria or protocol are these considerations and decisions being made?
9- Do you consider the membership of IEEE ICES by some ICNIRP-members as a possible
conflict of interests?
10- How do you explain the fact that a private organisation like ICNIRP, which is not
accountable in democratic terms to anyone, has the position to de facto "determine" via
guidelines the EMF policies of most EU member states?
Several attempts to get a reaction to
these questions remained unanswered'
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Annex II
Questions put to [email protected]
On your website, you write: "Because disparities in EMF standards around the world has
caused increasing public anxiety about EMF exposures from the introduction of new
technologies, WHO commenced a process of harmonization of electromagnetic fields (EMF)
standards worldwide. With 54 participating countries and 8 international organizations
involved in the International EMF Project, it provides a unique opportunity to bring countries
together to develop a framework for harmonization of EMF standards and to encourage the
development of exposure limits and other control measures that provide the same level of
health protection to all people. "
1 - Is there a time schedule for this process of harmonization of electromagnetic fields (EMF)
standards worldwide?
2 - We see on your website that the last EMF -WHO meeting took place in 2018. Are there
any new meeting planned and if yes when?
3 - Do you know what IARC is currently working on and if so when will IARC publish an
update of the monograph?
https://publications.iarc.fr/Book-And-Report-Series/Iarc-Monographs-On-The-Identification-
Of-Carcinogenic-Hazards-To-Humans/Non-ionizing-Radiation-Part-2-Radiofrequency-
Electromagnetic-Fields-2013
4 - How do you consider the debate on "conflicts of interests" in this specific research area?
Would you agree that there has been and still is a lot of attention for this debate? Has his
debate been useful in narrowing the divide in the scientific community? What is in your view
the role of the WHO on this?
(see for example this recent letter published in "Bioelectromagnetics":
https://onlinelibrary.wiley.com/doi/full/10.1002/bem.22225 )
These questions remained unanswered
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The International Commission on Non-Ionizing Radiation Protection: Conflicts
of interest, corporate capture and the push for 5G
June 2020
www.michele-rivasi.eu
www.klaus-buchner.eu
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Habilitetserklæring
Opgavetype
Jeg skal bistå Sundhedsstyrelsen med/i?
Jeg skal tilknyttes råd/nævn/gruppe mv.
Mit speciale
Afgørelser, råd, undervisning mv
Sagkyndig
Ikke ioniserende stråling
Personoplysninger
Navn
Titel
Arbejdsplads/firma/institution
E-mail
Christoffer Johansen
Professor, overlæge
Onkologisk Klinik, Rigshospitalet
[email protected]
Oplysninger om personlige interesser m.m.
Spørgsmål 2.1 Jeg ejer aktier, anparter, andele eller
har en anden form for medejerskab i virksomheder,
der er underlagt Sundhedsstyrelsens
myndighedsudøvelse.
Spørgsmål 2.2 Jeg sidder i bestyrelsen, direktionen
eller lignende i en eller flere virksomheder eller
institutioner, der er underlagt Sundhedsstyrelsens
myndighedsudøvelse.
Spørgsmål 2.3 Jeg har indenfor de sidste 5 år været
ansat eller modtaget betaling for opgaver udført for
en eller flere virksomheder eller institutioner, der er
underlagt Sundhedsstyrelsens myndighedsudøvelse.
Spørgsmål 2.4 Jeg har patent på et eller flere
produkter inden for områder, der er underlagt
Sundhedsstyrelsens mynSpørgsmål 2.4 Jeg har
patent på et eller flere produkter inden for områder,
der er underlagt Sundhedsstyrelsens
myndidighedsudøvelse.
Spørgsmål 2.5 Jeg har personlige eller økonomiske
interesser i virksomheder, som kan blive kontraktpart
eller på anden måde indgå i et privatretligt forhold til
Sundhedsstyrelsen i forbindelse med den opgave,
som jeg udfører for Sundhedsstyrelsen.
Spørgsmål 2.6 Er en person i din nærmeste familie
ansat, medejer eller på anden måde tilknyttet
virksomheder eller institutioner, der er underlagt
Sundhedsstyrelsens myndighedsudøvelse.
Spørgsmål 2.7 Modtager din arbejdsplads
økonomiske bidrag fra virksomheder eller
institutioner, der er underlagt Sundhedsstyrelsens
myndighedsudøvelse?
Spørgsmål 2.8 Har du andre tilknytninger eller
omstændigheder, der kan være relevante for din
habilitet?
Nej
Nej
Nej
Nej
Nej
Nej
Nej
Ja
Sundhedsstyrelsen
Islands Brygge 67
2300 København S
Tel: +45 7222 7400
www.sundhedsstyrelsen.dk / [email protected]
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Oplysninger om personlige interesser m.m.
Spørgsmål 2.8 - Hvilke:
Jeg har gennem de sidste 20 år (1999, 2006 og
2010) udført en gennemgang og vurdering af
videnskabelig litteratur, der belyser sammenhængen
mellem eksponering for elektromagnetiske (EMF)
felter og helbreds effekter, for det rådgivende
ingeniørfirma COWI. Disse rapporter har jeg udført,
når COWI har rådgivet de firmaer, der står for
etablering af udvidelser eller vedligehold af de
netværk der distribuerer elektricitet i Danmark
gennem nye højspændingsledninger, transformer
stationer og lignende. Rapporterne er udformet som
en gennemgang af den videnskabelige litteratur med
fokus på undersøgelsernes kvalitet, fortolkningen af
resultaterne og betydning ud fra det evidens niveau,
der kan fortolkes på baggrund af de konkrete
videnskabelige artikel. Der indgår ingen
samfundsøkonomske, planlægningsmæssige eller
andre vurderinger i de rapporter jeg har skrevet - det
er udelukkende den videnskabelige kvalitet og
dermed resultaternes indflydelse på den evidens der
er for en sammenhæng mellem eksponering for EMF
og helbreds problemer. Rapporterne er offentlig
tilgængelige og indgår i det materiale som berørte
borgere kan få udleveret i forbindelse med
anlæggelse af de ovenfor anførte anlæg. Jeg har i
efteråret 2017 indgået en kontrakt med COWI om en
opdatering af denne rapport og i den forbindelse igen
orienteret Sundhedsstyrelsens Direktion om
kontrakten.
Underskriv din erklæring
Jeg har efter min bedste overbevisning ingen
yderligere uvedkommende interesser, som kan
påvirke mit objektive arbejde for Sundhedsstyrelsen.
Hvis der sker ændringer udfylder jeg straks en ny
erklæring, hvoraf ændringerne fremgår.
Udfyldt den
Valgt
30-08-2017
Sundhedsstyrelsen
Islands Brygge 67
2300 København S
Tel: +45 7222 7400
www.sundhedsstyrelsen.dk / [email protected]
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Europace (2019)
21,
219–229
doi:10.1093/europace/euy155
REVIEW
Electromagnetic interference in cardiac
electronic implants caused by novel electrical
appliances emitting electromagnetic fields in
the intermediate frequency range: a
systematic review
Sarah Driessen
1
*, Andreas Napp
2
, Kristina Schmiedchen
1
, Thomas Kraus
1
, and
Dominik Stunder
1
Research Center for Bioelectromagnetic Interaction (femu), Institute of Occupational, Social and Environmental Medicine, University Hospital, RWTH Aachen University,
Pauwelsstr. 30, 52074 Aachen, Germany; and
2
Department of Internal Medicine I (Cardiology, Angiology, Pneumology and Internal Intensive Care Medicine), University Hospital,
RWTH Aachen University, 52074 Aachen, Germany
Received 2 March 2018; editorial decision 5 June 2018; accepted 7 June 2018; online publish-ahead-of-print 9 July 2018
1
Electromagnetic fields (EMF) in the intermediate frequency (IF) range are generated by many novel electrical appliances, including electric
vehicles, radiofrequency identification systems, induction hobs, or energy supply systems, such as wireless charging systems. The aim of
this systematic review is to evaluate whether cardiovascular implantable electronic devices (CIEDs) are susceptible to electromagnetic in-
terference (EMI) in the IF range (1 kHz–1 MHz). Additionally, we discuss the advantages and disadvantages of the different types of studies
used to investigate EMI. Using the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement, we collected
and evaluated studies examining EMI in
in vivo
studies,
in vitro
studies (phantom studies, benchmark tests), and simulation studies. Our
analysis revealed that cardiac implants are susceptible to malfunction induced by EMF in the IF range. Electromagnetic interference may in
particular be provoked by security systems and induction hobs. The results of the studies evaluated in this systematic review further indi-
cate that the likelihood for EMI is dependent on exposure-related parameters (field strength, frequency, and modulation) and on implant-
as well as on lead-related parameters (model, type of implant, implant sensitivity setting, lead configuration, and implantation site). The
review shows that the factors influencing EMI are not sufficiently characterized and EMF limit values for CIED patients cannot be derived
yet. Future studies should therefore, consider exposure-related parameters as well as implant- and lead-related parameters systematically.
Additionally, worst-case scenarios should be considered in all study types where possible.
...................................................................................................................................................................................................
Keywords
Electromagnetic interference
•
Implantable cardioverter-defibrillator
•
Cardiac pacemaker
fields
•
Magnetic fields
•
Intermediate frequency
•
Systematic review
•
Electric
Introduction
In recent years, the number of patients that have been fitted with car-
diovascular implantable electronic devices (CIEDs) such as cardiac
pacemakers (PMs) or implantable cardioverter-defibrillators (ICDs)
has strongly increased. In the USA, while 9000 CIEDs were implanted
in 1990,
1
its number increased to 368 829 in 2009.
2
Over 4.2 million
primary CIED implantations were performed between 1993 and
2008.
3
In Europe, 547 586 PMs and 105 730 ICDs were implanted in
2016.
4
Additionally, novel CIEDs like leadless PMs, subcutaneous
ICDs, and heart failure devices are gaining more and more
importance.
* Corresponding author. Tel:
þ49
241 808 0749; fax:
þ49
241 808 2587.
E-mail address:
[email protected]
C
V
The Author(s) 2018. Published by Oxford University Press on behalf of the European Society of Cardiology.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/),
which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact
[email protected]
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220
At the same time, with the success of the CIED technology during
the past decades, exposure to external electric, magnetic, and elec-
tromagnetic fields (EMF) has increased, at least in the intermediate
frequency (IF) and radiofrequency (RF) range.
5–8
Electromagnetic
fields are used e.g. to transmit communication signals or arise along
power transmission lines. Other sources of EMF are electrical appli-
ances. Electromagnetic fields are classified according to their wave-
length and frequency. For example, power lines or electrical
household devices emit EMF with a lower frequency (LF) while mo-
bile phones, Wi-Fi, or microwave ovens produce EMF of a higher fre-
quency. Electromagnetic fields in the IF range are generated by many
novel electrical appliances, including electric vehicles, RFID (RF iden-
tification) systems, induction hobs, or energy supply systems, such as
wireless charging systems.
Cardiovascular implantable electronic devices are known to be sus-
ceptible to malfunction in the presence of strong EMF.
9–12
Many
researchers have studied electromagnetic interference (EMI), i.e. po-
tential, undesirable effects of EMF on the operation of CIEDs. The
EMF-Portal (www.emf-portal.org), the most comprehensive scientific
literature database on biological and health-related effects of EMF
provided by our institute currently comprises 639 records on EMI
(June 2017). The Manufacturer and User Facility Device Experience
(MAUDE) database of the American Food and Drug Administration
13
identified 2843 cases of malfunctions of medical devices induced by
EMI between January 2010 and March 2017. However, this may be an
underestimation of events as reporting of such incidents is not manda-
tory and some physicians may misjudge EMI episodes e.g. as atrial fi-
brillation. A survey of physicians in France showed that 16% of them
were concerned about patients who reported EMI at least once a
year, e.g. oversensing of noise signals due to EMF exposure is a phe-
nomenon regularly seen in daily practice.
14
Napp
et al.
9
demonstrated
the general mechanisms of effects in CIED caused by EMF, e.g. heating
of the implant or lead by RF fields or induction of electric currents
within the human body by LF fields leading to e.g. disturbance of the
sensing capabilities of the implant. Additionally, Beinart and
Nazarian
10
showed potential everyday sources of EMI and docu-
mented typical effects, e.g. damage to CIED circuitry, PM inhibition,
asynchronous pacing, or inappropriate ICD shocks.
Standard organizations have not proposed limit values to EMF expo-
sure for patients with CIEDs. The American National Standards
Institute (ANSI),
15,16
the International Commission on Non-Ionizing
Radiation Protection (ICNIRP),
17
and the European Union
18,19
did not
consider patients with CIEDs in their safety guidelines for the protec-
tion of humans exposed to EMF. Consequently, it is often difficult for
physicians and patients to identify sources of EMF which pose a risk
and to determine appropriate safety distances which should be
respected. In some cases, the applied safety measures in occupational
environments might result in a ban from workplaces for CIED carriers.
To date, no systematic analysis has been done for EMI in the IF
range (1 kHz–1 MHz). The aim of this systematic review is therefore
to evaluate whether CIEDs are susceptible to EMI in the IF range. In
particular, we consider the results from different types of studies
(in
vivo
and phantom studies, benchmark test) and outline their advan-
tages and disadvantages. Additionally, we identify the type of study
which is most appropriate to further investigate the various parame-
ters (implant setting, lead configuration, and individual parameters)
that influence the likelihood for EMI.
S. Driessen
et al.
Methods
Literature search strategy and general
information
As prescribed by the PRISMA (Preferred Reporting Items for Systematic
Reviews and Meta-analyses) statement,
20
we conducted a systematic lit-
erature search to identify relevant studies published from inception to
October 2016 using our thematically specialized open-access literature
database EMF-Portal (www.emf-portal.org). The EMF-Portal is the most
comprehensive scientific literature database on biological and health-
related effects of EMF and has been approved by the WHO as a refer-
ence database.
21
It has been publicly available for more than 15 years and
comprises currently 25 900 publications
22
(January 2018). Our search in
the EMF-Portal for the current systematic review was based in a first step
on the more general search term ‘electromagnetic interference’ (for a
link to the search string, see
Supplementary material online:
search strat-
egy). Additionally, we performed a more specific search in the frequency
range <10 MHz and in the category ‘electromagnetic interference’. The
lists of results were corrected for double publications.
Eligibility criteria and study selection
Articles were included when they reported experimental studies on EMI
with CIED in the frequency range of 1 kHz–1 MHz. We accepted bench-
mark tests, studies with phantoms,
in vivo
studies, and numerical simula-
tions. Only articles written in English or German and published in a peer-
reviewed journal were considered. There was no restriction regarding
the year of publication.
Excluded were studies that focused on CIED-programmer interfer-
ence, CIED-interference with further (cardiac) implant, EMI with other
implants (e.g. neurostimulator), or EMI induced by current application
(e.g. by medical devices). Furthermore, studies without specification of
the tested frequency range were excluded. Review articles, case studies,
editorials, commentaries, and unpublished or clearly not peer-reviewed
articles were also excluded.
Two authors independently (S.D. and D.S.) screened the studies for el-
igibility based on inclusion/exclusion criteria. Articles were screened in
two stages. First, titles and abstracts were reviewed to identify potentially
relevant articles. For those abstracts which met the inclusion criteria, the
full text was retrieved and independently reviewed in the second stage of
assessment. The two review authors made a joint decision about inclu-
sion of the articles.
Data extraction
The data from the studies included were extracted independently by two
authors (S.D. and D.S.). The extraction protocol was defined and agreed
upon before the start of the project. Extracted data included bibliographi-
cal data, study type (e.g. phantom,
in vivo
study), exposure parameters
(field source, i.e. electrical appliance, frequency, and field strength if pro-
vided), number of patients/CIED, CIED characteristics, and outcome (dis-
turbance). Additionally, for
in vivo
studies, implant settings and lead
polarities were extracted. Disagreements and uncertainties were dis-
cussed and resolved between the two review authors.
Results
The systematic literature search identified 389 articles that matched
the search criteria. After screening the title and abstract, 203 articles
were excluded for various reasons (e.g. secondary literature, not
dealing with EMI). The full text was obtained for the remaining 186
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Electromagnetic interference in CIEDs
221
distance from the patient to the security device (1.6–2.7 A/m, 50 cm
to the security gates)
33
and another study performed comprehensive
field measurements (14–310 A/m), but the field strength required to
induce EMI remained unclear.
34
The data of three studies showed that the acoustomagnetic EAS
system (58 kHz) could disturb PMs.
31,32,34
There was no evidence
that ICDs could be disturbed. However, only 38 ICD patients were
included in these studies compared with 265 PM patients (whereof
the PMs of 72 patients were disturbed). Electromagnetic interference
with PMs was also found with other security systems operating at
higher (120 kHz) or lower (10 kHz) frequencies.
33,35
Importantly, the
study by Wilke
et al.
33
provided evidence that PMs can be negatively
affected by security systems below the ICNIRP limits for the general
public (i.e. 21 A/m).
Two further studies did not observe EMI following exposure to
metal detectors
36
or EAS systems
23
; with the latter being one of the
two studies investigating ILRs. In a further study it remained unclear
whether EMI was induced by a 100 Hz or 1 kHz metal detector.
24
Three studies on potential EMI of induction hobs
25,26,31
showed
that the patients’ safety with CIEDs was guaranteed when minimum
distances were respected, i.e. no EMI was observed at distances of
20–35 cm. It was, however, not documented in these studies whether
disturbances occurred in closer proximity to the induction hobs.
Other devices such as an electromagnetic articulography device,
29
an ultrasonic dental scaler,
30
a magnetic endoscope imager,
27
or ava-
lanche transceivers
37
did not cause EMI under the used conditions.
Some dental devices appeared to have the potential to disturb PMs,
28
however, the frequency was provided only for one device and it is
unclear whether the other dental devices emitted EMF in the IF
range. The relevance of this data is, however, debatable for today’s
applications, because the study
28
was published in 1975.
Altogether, EMI in the IF range was revealed in 6 out of the 15
studies resulting in e.g. sensing anomalies (e.g. undersensing or over-
sensing),
31–34
asynchronous pacing,
33,34
increased pacing rate,
24,34
pacing inhibition,
24,32–35
and mode switch.
32
In McIvor
et al.
34
EMI
was accompanied by symptoms in patients, e.g. palpitations and
presyncope.
For a general risk assessment,
in vivo
studies with exposures to a
single device, such as avalanche transceivers
37
have only a limited sig-
nificance due to the lack of a proper dosimetry. Additionally, the ap-
plicability of the data to other exposure situations is limited. Studies
performed under standardized exposure set-ups, i.e. using e.g. a
Helmholtz coil or antenna settings are better suited, because EMF
can be homogenously generated and EMF at different frequencies
and field strengths can be applied systematically. That way, more gen-
eral data for various applications can be obtained.
articles to check for eligibility to be included in our analysis. Of these,
146 articles were excluded for the following reasons: frequency
range not provided or appropriate (n = 48), current application
(n = 35), case report (n = 21), CIED-implant interference (n = 15), no
CIED (n = 10), CIED-programmer interference (n = 4), or other rea-
sons (n = 13). Forty articles fulfilled the eligibility criteria and were in-
cluded in this review (see
Figure
1).
Of these, most studies (n = 15)
used combinations of several methods to investigate EMI (e.g. phan-
tom and benchmark), 13 studies used phantoms only, 10 articles in-
vestigated EMI in patients (in
vivo),
and one study used a benchmark
test only. Additionally, the search identified one simulation study (see
Figure
2).
Most of the studies investigated EMI on PMs only (n = 20), while
four studies considered ICDs only. Ten studies considered different
types of CIEDs [PMs, ICDs, and implantable loop recorder (ILR)].
Five studies did not use a CIED but a modified CIED case to measure
the induced voltage at its terminals. One study investigated EMI on
ILRs only.
23
In some studies, additional frequency ranges or electrical applian-
ces outside the IF range were investigated, but these data on EMI are
not considered in this review—if not stated otherwise.
Table
1
provides detailed information on the most important tech-
nical terms which are used in this review.
In vivo
studies
In
in vivo
studies, patients with CIEDs are directly exposed to EMF to
assess the electromagnetic compatibility of CIEDs. As such, individual
interference thresholds of the CIED can be determined for specific
exposure conditions.
In the current review, 10
in vivo
studies were evaluated which ex-
posed patients with CIEDs to EMF (Supplementary
material online,
Table S1).
Additional five studies used a combined methods approach,
i.e. they conducted also benchmark or phantom tests
(Supplementary
material online,
Table S3).
Altogether, potential EMI was investigated in 1084 patients that
had been fitted with CIEDs (769 PMs, 313 ICDs, and 2 ILRs). The nine
studies providing details on PM and ICD types included 369 single
chamber (217 PM, 152 ICD), 433 dual chamber (361 PM, 72 ICD),
and 42 resynchronization therapy devices (13 PM, 29 ICD). Eight of
the 15 studies included CIED carriers with both unipolar and bipolar
leads, whereas three studies
24–26
tested only patients with one lead
configuration (unipolar OR bipolar). Four studies did not provide any
details on lead configuration.
27–30
Eleven of the 15 studies left the
CIED sensitivity unchanged or investigated different sensitivities set-
tings (e.g. maximum, nominal), whereas two studies
29,31
tested under
maximum sensitivity only. Two studies did not provide any details on
sensitivity.
28,32
All included studies used real-life electrical appliance exposure
such as security systems [electronic article surveillance (EAS) systems
or metal detector gates,
n
= 8], medical devices (n = 4), induction
hobs (n = 3), or avalanche transceivers (n = 1). One study tested both
an EAS system and an induction hob (counted separately in each cat-
egory).
31
None of the included
in vivo
studies were performed under
a standardized exposure set-up, i.e. with e.g. a Helmholtz coil.
Furthermore, not all of the studies provided details on the field
strengths which actually occurred at the height of the implant (chest
area). At least, one study measured the magnetic field strength at a
Phantom studies
Phantoms simulate the human body or parts of the human body in-
cluding different tissue characteristics.
38
Experimental
in vitro
studies
using phantoms examine either directly the disturbance (EMI) of
CIEDs or they are used to determine the intracorporal voltage in-
duced by external EMF at the terminals of CIEDs. In phantoms, both
the response of CIEDs to different EMF and the impact of the lead
can be tested.
Potential EMI with CIEDs was investigated in 15 studies and five
studies measured the induced voltage. An additional five studies
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222
S. Driessen
et al.
Identification
Records identified through
database searching in the EMF-Portal
and additional records identified
through reference lists and reviews
(n = 389)
Screening
Total records screened in title
and abstract
(n = 389)
Records excluded after screening
of title and abstract (e.g. secondary literature, no
experimental study, language not
english or german, not peer-reviewed)
(n = 203)
Included
Eligibility
Full-text articles assessed
for eligibility
(n = 186)
Full-text articles excluded for the following
reasons (n = 146):
- Frequency range not given or
appropriate (n = 48)
- Current application (n = 35)
- Case report (n = 21)
- CIED-implant interference (n = 15)
- Other reasons (n = 13)
- No cardiac implant (n = 10)
- CIED-programmer interference (n = 4)
Articles included in the systematic review
(n = 40)
Figure 1
Flow diagram of literature search, eligibility, and inclusion process. Adapted from Moher
et al.
20
CIED, cardiovascular implantable elec-
tronic device; EMF, electromagnetic field.
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Electromagnetic interference in CIEDs
223
61.3 cm. There was no clear correlation between EMI and lead con-
figuration and no difference between maximum and nominal
sensitivity,
46
most likely due to the high intensity field strength of the
RFID system. Mattei
et al.
45
investigated typical exposure patterns of
RFID systems and identified EMI from 40 A/m at 125 kHz for a pulsed
signal and from 60 A/m for a continuous wave (CW) signal.
Two further studies on security systems showed that EMI was in-
duced by an anti-theft device of 120 kHz
33
and by different EAS sig-
nals (100 Hz–8 kHz, CW or pulsed
48
). Kainz
et al.
48
found that the
interference level of a pulsed signal was lower than that of a CW.
Two studies on induction hobs
25,49
revealed that EMI occurred
both as a function of the distance to the induction hob and depen-
dent on the presence/absence of the pot or the position of the pot.
However, the exact field strengths at specific distances were not
clear from both studies.
The data on security systems or induction hobs showed that some
devices in our everyday life may induce EMI in CIEDs and thus con-
firm the findings of
in vivo
studies.
Hikage
et al.
40
investigated 14 different WPT systems.
Electromagnetic interference occurred in 5 of the 12 WPT systems
for mobile application with modulated fields at a maximum distance
of < cm for PMs and at a distance of < cm for ICDs. The two WPT
_2
_1
systems for electric vehicle charging provoked no EMI. However, no
field strengths were provided and no details were shown which
WPT system caused which kind of EMI.
No EMI was induced under the specific study conditions for a
microtron device used for cancer therapy,
50
nor for an electromag-
netic navigational bronchoscopy device
51
or for a magnetically levi-
tated linear motor car
52
.
The four phantom studies on potential EMI using a standardized
exposure set-up
41–44
found that EMI depended on field frequency,
CIED type, and programmed sensitivity.
For a general risk assessment, the data of the evaluated phantom
studies on potential EMIs are limited as are the data of the discussed
in vivo
studies. Although there are many studies using a comprehen-
sive study design, the applicability of the data to other electrical appli-
ances or comparable exposure scenarios is limited due to the lack of
sufficient dosimetric data or a missing correlation of those data to
considered the development of a coupling model (Supplementary
material online,
Tables S2
and
S3).
In Babouri
et al.,
39
the phantom
served to validate detection levels recorded in benchmark tests.
Therefore, this study is discussed in the ‘Benchmark tests and test
in
air’
section.
Studies investigating electromagnetic interference
In the 15 studies on potential EMI, altogether, 185 CIEDs were inves-
tigated [100 PMs, 60 ICDs, and 25 PM/ICDs (not further specified
40
)].
Only 4 out of the 15 studies used a standardized exposure set-up,
e.g. a Helmholtz coil setting,
41–44
whereas the remaining 11 studies
investigated potential EMI in phantoms upon exposure to real-life
electrical appliances [RFID/security systems (n = 5), induction hobs
(n = 2), medical devices (n = 2), wireless power transfer (WPT) sys-
tems (n = 1), or a magnetically levitated linear motor car (n = 1)].
Only one study provided precise data on the correlation of EMI and
exposure characteristics.
45
The data of two studies
46,47
on RFID systems showed that the ma-
jority of the investigated PMs (67–83%) and ICDs (47–71%) could be
disturbed by different 134 kHz RFID systems at a distance of up to
Benchmark,
n
= 1
Simulation,
n
= 1
In vivo
studies
(in patients);
n
= 10
Combination of
different
methods;
n
= 15
Phantom studies;
n
= 13
Figure 2
Study types used for EMI investigation in the IF range.
EMI, electromagnetic interference; IF, intermediate frequency.
Table 1
Terms
Technical terms used in this review
Explanation
Disturbance of CIEDs’ operation by induction of intracorporal voltage caused by electric, magnetic, or EMF
EMF emitted by an electrical appliance, e.g. magnetic field (measured in T or A/m) or electric field (measured in
V/m)
Intracorporal voltage occurring at the terminals of a CIED induced by external EMF
Minimum field strength of an external EMF required to cause EMI
Noise signal that may disturb the regular operation of a CIED
Waveforms (CW, AM, PW, and pulses) of an external EMF or a disturbing/interfering signal; the waveform can
significantly influence the response of a CIED
Voltage of a disturbing/interfering signal which causes disturbance of CIEDs’ operation
Minimum detection levels of CIEDs defined in product standards, given in mV
....................................................................................................................................................................................................................
EMI
External EMF
Induced voltage
Interference thresholds
Disturbance/interfering signal
CW, AM, PW, and pulses
Detection level
Performance limits
A/m, Ampere/meter; AM, amplitude modulation; CIED, cardiovascular implantable electronic device; CW, continuous wave; EMF, electromagnetic fields; EMI, electromagnetic
interference; mV, millivolts; PW, pulsed modulation; T, Tesla; V/m, Volt/meter.
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224
EMI.
25,33,49
Likewise, phantom investigations with exposures to only a
single device, such as a magnetically levitated linear motor car
52
only
contribute in a limited way to a general risk assessment. The same
applies to studies using standardized conditions if EMI is not systemat-
ically tested for various frequencies and field strengths.
Determination of induced voltage
Besides the direct measurement of EMI, phantom studies can also
serve to determine the voltage induced by external EMF at the termi-
nals of CIEDs. The induced voltage is the critical measurement pa-
rameter for electromagnetic compatibility testing of CIEDs and can
be compared with international product standards, e.g. Ref.
53
These
CIED standards set performance limits up to 3 GHz with the objec-
tive of preventing malfunctions induced by EMF. The performance
limits increase linearly in the IF range (3 kHz–167 kHz) and vary be-
tween unipolar (9–500 mV) and bipolar (0.9–50 mV) testing.
53–55
The induced voltage was investigated in five studies.
Bassen
56
investigated different iPods but the induced voltage was
below the noise level of their measurement instruments. They con-
cluded that no EMI would be expected.
Irnich and Bernstein
57
investigated 11 induction hobs and the in-
duced voltage was between 6 and 800 mV dependent on the distance
and the position of the pot. The combination of their phantom study
with a benchmark test showed that 14.8% of PMs would be disturbed
under worst-case conditions and never at a minimum distance of
35 cm to the thorax. These results confirm the findings of phantom
studies on EMI
25,49
and the findings of
in vivo
studies
25,26,31
in that in-
duction hobs appear to be safe at a specific distance.
Seckler
et al.
58
investigated a WPT system and compared the data
with a standardized exposure set-up using Helmholtz coils (111 kHz,
both systems). Under the standardized exposure condition the per-
formance limit (i.e. 333 mV for CIEDs with unipolar leads and
33.3 mV for bipolar leads) was already exceeded at 11
mT
and thus
below the ICNIRP limit
17
of 27
mT;
whereas with the WPT system,
the limits—even with the WPT system touching the phantom—
were not exceeded. This comprehensive study approach demon-
strates the significant difference between the voltage induced by a ho-
mogenous field of Helmholtz coils and by inhomogenous fields of an
electronic device. Moreover, this study highlights the importance to
characterize the emitted field patterns (e.g. CW and AM) and dosi-
metric data of electronic devices.
Mattei
et al.
59
used an antenna design at 125 kHz to emulate RFID
systems and measured a maximum induced voltage for a unipolar
lead of 62.2 mV and 19.8 mV for a bipolar lead, thus indicating that
the performance limits (i.e. 375 mV for CIEDs with unipolar and
37.5 mV for bipolar leads) were not exceeded under the specific ex-
posure conditions. In a later study by the same authors,
45
however,
EMI was detected and thus, the performance limits seemed to be
exceeded by exposure of RFID systems (see section ‘phantom stud-
ies—Studies investigating electromagnetic interference’). Exceeding
of the performance levels under consideration of EAS-similar expo-
sure scenarios was also demonstrated by numerical simulations of
Leitgeb
et al.
60
who calculated induced voltages between 3.2- and
13.5-fold above the performance limits in the IF range (60 kHz–
5 kHz, respectively) under worst-case conditions (Supplementary
material online,
Table S5).
S. Driessen
et al.
Gustrau
et al.
61
identified induced voltages at the PM terminals of
0.126 mV–131 mV (1 kHz–1 MHz, at 1 A/m, i.e. 1.26
mT).
Gustrau
et al.,
61
Seckler
et al.,
58
and Mattei
et al.
59
found a dependence of the
induced voltage on lead configuration.
Coupling model
A further motivation to perform phantom studies, is the develop-
ment of a coupling model (transfer function). Transfer functions dem-
onstrate the relationship between the strength of an external EMF
and the induced intracorporal voltage at the terminals of a CIED. The
transfer functions of the five studies included were determined by nu-
merical or analytical approaches based on data gained in phantom
studies or benchmark tests.
Hedjiedj
et al.
62
developed a transfer function based on a simple
phantom and found detection levels from >55/104 mV at 10/25 kHz
for a sensitivity level of 0.7 mV. The authors also included benchmark
tests and reported detection levels in two out of five PMs of >150/
130 mV at 10/25 kHz for a sensitivity level of 1 mV.
In two comprehensive studies, Andretzko
et al.
presented a nu-
merical model for the determination of transfer functions between
electric fields
63
or magnetic fields
64
and the induced voltage. The
results obtained by numerical simulation were in agreement with ex-
perimental data from benchmark tests and phantom studies. The de-
tection levels increased with increasing PM sensitivity values;
additionally, the interference thresholds depended on the loop area
formed by the CIED with its lead, i.e. for a large (300 cm
2
) loop area
interference threshold occurred from 20
mT
and for a standard loop
area (225 cm
2
) from 26
mT
(unipolar lead).
In a further study by the same research group,
43
the realistic lowest
interference thresholds were calculated and given with 33.36
mT
(25 kHz) or 79.18
mT
(10 kHz), respectively, for unipolar lead settings
(200 cm
2
). However, the coupling model was not validated and tests
in air
and tests with a phantom yielded different results. The result of
this study together with the results of the other three studies suggest
that the detection levels of the considered CIEDs were significantly
above the performance limits recommended by international prod-
uct standards,
53
thus indicating compliance with the proposed stand-
ards, although the applied magnetic fields (30–85.4
mT)
exceeded the
limit value recommended by ICNIRP (i.e. 27
mT).
43,64
Whether the
transfer function presented by this research group could serve as a
solid basis for the calculation of induced voltages from external EMF
should be validated by comprehensive realistic data obtained from
benchmark tests, phantom, and
in vivo
studies.
Finally, in a study by van Wijk van Brievingh
et al.,
65
the authors
calculated—according to their coupling model—interference thresh-
olds between 0.1 and 100 A/m (i.e. 0.126–126
mT)
for 100 Hz and
250 kHz. However, no specific values for induced voltages were
provided.
In general, the data of these five studies indicate that interference
thresholds depend on the loop area formed by the CIED with its
lead, on the frequency of the applied external EMF, the sensitivity set-
ting of the CIED and the device itself and thus confirm the findings of
several other phantom studies. Universal transfer function therefore,
may provide a helpful tool to estimate induced voltages under specific
conditions (e.g. lead type) and in dependence of specific exposure
scenarios (frequency and field strength).
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Electromagnetic interference in CIEDs
225
Potential EMI provoked by EAS systems was also found in
in vivo
stud-
ies e.g. Refs
31,32,34,35
and in phantom studies e.g. Refs
46,47
. The
strengths of external EMF were only provided for EAS systems used
in Dodinot
et al.
35
and for signals used in Kainz
et al.
48
where interfer-
ence thresholds were reached from 1.13 mT and approximately
15 A/m
peak-to-peak
, respectively. Additionally, the study by Lucas
et al.
66
indicated that unipolar PMs were affected more often than bi-
polar PMs.
Finally, Corbett
et al.
27
investigated a medical magnetic endoscope
imager and did not find EMI with different CIEDs. The same result
was obtained in their experiment with patients (see
In Vivo
Studies
section).
Benchmark tests and tests
in air
Manufactures of CIEDs are obligated to test their implants for com-
pliance with product standards in order to obtain approval for the
European market (CE marking) or from the Food and Drug
Administration (FDA) for the US market. Regarding electromagnetic
compatibility performance limits as well as test methodologies
(benchmark tests) are defined in ISO 14117:2012
53
for the US mar-
ket and in EN 45502-2-1:2004
55
(PMs) and EN 45502-2-2:2008
54
(ICD) for the European market. In benchmark tests disturbance sig-
nals are fed directly into the pace/sense channel of the CIED by gal-
vanic coupling in order to analyse the CIED’s response and detection
levels. The simple methodology is a major advantage of benchmark
tests. Cardiovascular implantable electronic devices of different man-
ufacturers and with different settings can be tested and evaluated by
any number of various disturbance signals. However, a disadvantage
of benchmark tests is that individual parameters of the patient or the
lead are not considered and the data cannot be transferred to exter-
nal EMF of e.g. a certain electrical appliance.
Although benchmark tests are a well-accepted method, many
researchers preferred to perform tests
in air.
In such tests, implants
are equipped with leads and located within the exposure area of a
standardized set-up or close to a specific electrical appliance, compa-
rable to phantom studies but without a phantom. Thus, potential EMI
can be correlated with field strengths of an external EMF. In the cur-
rent review, benchmark tests were used in six studies, whereas tests
in air
were performed in seven studies (Supplementary
material on-
line,
Tables S3
and
S4).
Andretzko
et al.
64
conducted both benchmark
tests and tests
in air
(counted in each category separately).
Altogether, in the 12 studies included interference was evaluated in
>286 PMs (exact number not given in van Wijk van Brievingh
et al.
65
),
in one ICD and in three ILRs. The results of benchmark studies gener-
ally indicated compliance with the performance limits set by product
standards. Additionally, the results of some benchmark tests and tests
in air
showed the dependence of potential EMI on frequency, the
CIED and its sensitivity level.
39,64,66
In 4 of the 12 studies included, benchmark tests or tests
in air
were
combined with other methods in order to establish a transfer func-
tion.
62–65
These studies are discussed in detail in the ‘Phantom
Studies—Coupling Model’ section. Nevertheless, due to the data of
these studies it can be summarized that the lowest detection levels
were found from 55 mV (10 kHz)
62
and 95 mV (25 kHz)
64
depending
on the sensitivity level of the PM.
64
Comparable detection levels
were also found in an earlier study by the same research group
39
combining benchmark tests and phantom investigations.
A further publication with tests
in air
43
reported interference
thresholds from 1.09
mT
at 10 kHz (single-chamber PM) and from
0.54
mT
at 25 kHz (dual-chamber PM); however, this was found un-
der artificial loop conditions (90 turns-lead).
Irnich and Bernstein
57
performed benchmark tests in order to in-
vestigate the impact of a typical signal of induction hobs (24 kHz) and
reported detection levels below the performance limits. It has to be
noted, however, that the data was recorded for an older PM model
which was released before 1998.
Three out of four studies performing tests
in air
on security sys-
tems found that EMI was caused by different EAS systems and EAS
signals.
35,48,66
Only the study by de Cock
et al.
23
did not report EMI.
Discussion
The aim of this systematic review was to evaluate whether CIEDs are
susceptible to EMI in the IF range generated by many novel electrical
appliances, including electric vehicles, induction hobs, or wireless
charging systems.
Forty articles fulfilled the eligibility criteria and were included in
this review. Most of the studies investigated EMI on PMs only
(n = 20), while four studies considered ICDs only. Ten studies consid-
ered PMs, ICDs, and ILRs. Five studies did not use a CIED but a modi-
fied CIED case to measure the induced voltage at its terminals. One
study investigated EMI on ILRs only.
23
There is only limited data on EMI with CIEDs in the IF range and
only a few of the evaluated studies correlated the documented EMI
with exposure data (e.g. Refs
33,45,58
). Likewise, the studies that did
not report EMI, rarely provided detailed data on exposure
conditions.
26,29,31,41,42,51
More than one-third of the studies investigated CIEDs which were
exposed to security systems, including EAS, metal detectors, and
RFID (n = 15), and five studies investigated potential EMI in the prox-
imity of induction hobs. Single studies also investigated other elec-
tronic appliances, such as iPods,
56
a magnetically levitated linear
motor car,
52
WPT systems,
40,58
or avalanche transceivers.
37
There is evidence that EMF sources of everyday life such as secu-
rity systems may induce EMI.
31–34,45,46
Also, induction hobs appear to
provoke EMI in close proximity.
25,26,31,49
For other electronic appli-
ances, EMI or exceeding of performance levels was found only for
WPT systems.
40,58
However, it cannot be concluded that the other
investigated electrical appliances that did not reveal any EMI adhere
to safety standards in general, because some studies investigated only
a few CIEDs or a few patients (7 ICD
51
or 3 PM, 1 ICD
52
) or the ex-
posure parameters were insufficiently described.
37,56
We evaluated benchmark tests, simulation, phantom, and
in vivo
studies. As shown in
Table
2,
the studies evaluated in this review used
different methods (e.g. phantom and benchmark) to investigate EMI
for various electrical appliances. For RFID/EAS systems, EMI was con-
sistently reported in
in vivo
studies, phantom studies, and benchmark
tests, whereas for induction hobs and wireless charging systems, EMI
was found only in phantom studies.
Clinical relevance
Previous studies have shown that oversensing of noise signals due to
EMF exposure occurs in everyday life and physicians caring for CIED
patients are regularly confronted with EMI.
14,67,68
In the studies
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2259378_0206.png
226
S. Driessen
et al.
Table 2
Types of studies used for EMI investigation in different electrical appliances
In vivo
studies
Phantom studies
X
39,41–44,58,61–65
X
23,31–35
O
23,24,36
O
25,26,31
O
28–30
X
33,45–48,59
O
48
X
25,49,57
X
40,58
O
50,51
O
27
Benchmark tests and tests
in air
O
39,43,62–65
X
23,35,48,66
O
23,48
O
57
O
40
Simulation
O
43,61,63,64
O
60
Electrical appliance
Standardized exposure set-up
RFID/EAS systems
Metal detector
Induction hobs
Wireless charging systems
Different medical devices (articulography device,
dental devices, microtron device, navigational
bronchoscopy device, and magnetic
endoscope imager)
Different iPods
Avalanche transceivers
Magnetically levitated linear motor car
....................................................................................................................................................................................................................
O
56
O
37
O
52
EAS, electronic article surveillance; EMI, electromagnetic interference; O, no EMI was found in this category; RFID, radiofrequency identification; X, EMI was reported for this
study type in at least one study.
included in this review sensing anomalies (e.g. undersensing, over-
sensing),
31–34
asynchronous pacing,
33,34
increased pacing rate,
24,34
pacing inhibition,
24,32–35
and mode switch
32
were reported.
Oversensing in the atrial channel can be misinterpreted by CIEDs
as atrial fibrillation and cause a change in the pacing mode to either
VVI(þR) or DDI(þR) mode, which results in atrioventricular dysyn-
chrony. The event may remain unnoticed and has no clinical conse-
quence if the interference is brief. However, in the case of extended
atrioventricular dysynchrony, patients with a high ventricular pacing
percentage may develop the pacemaker syndrome, including symp-
toms of palpitations, dizziness, and reduced physical capacity.
69
Additionally, inappropriate mode switch episodes could lead physi-
cians to initiate therapeutic oral anticoagulation if the episodes are
not correctly identified as EMI. If atrial oversensing occurs and if
mode switch is disabled, inappropriate ventricular pacing may be trig-
gered up to the upper tracking rate.
9
Oversensing in the ventricular channel may result in pacing inhibi-
tion with subsequent severe bradyarrhythmias, (near-)syncope, or
asystole in PM-dependent patients.
70
Additionally, sustained ventricu-
lar oversensing in ICD patients may lead to inappropriate shock deliv-
ery. Inappropriate shocks are not only painful and can result in
psychological distress but they can be potentially proarrhythmic and
are associated with adverse overall survival.
71
In the case of strong
EMF exposure, PMs/ICDs may switch to noise mode with asynchro-
nous pacing (VOO/DOO).
72
In noise mode, the subsequent loss of
sensing of the intrinsic signal prevents the detection of the underlying
intrinsic rhythm faster than the pacing frequency resulting in a risk of
T-wave stimuli as well as the perception of ventricular arrhythmias.
Thus, anti-tachycardia therapy of ICDs would be withheld with po-
tential lethal consequences.
Precautionary methods
Cardiologists can reduce the risk of EMI for CIED patients by evaluating
and programming the sensitivity settings. The lowest possible sensitivity
should be selected, which still ensures an appropriate sensing of intrin-
sic signals. Features like automatic capture measurement or adaptive
sensitivity control may lead to inappropriate automatic reprogramming
of the sensitivity and should therefore, be switched off in patients with
foreseeable strong EMF exposure or documented EMI. In the case of
ICDs, defibrillator testing with ventricular fibrillation induction may be
necessary to evaluate appropriate sensing of fibrillation waves with sen-
sitivity settings lower than the manufacturer’s recommendations.
Prolonged detection intervals and elevation of the VT/VF zones as
mentioned in several studies
73–75
may prevent inappropriate shocks
without impairing the outcome of the patients.
Programming to VVI mode is an additional option to prevent atrial
oversensing which usually occurs before the ventricular channel is af-
fected due to the small intrinsic atrial signals and the corresponding
high sensitivity setting (poor signal-to-noise ratio). Therefore, to be
able to programme a lower sensitivity it is important to achieve a sta-
ble anchoring of the lead with good sensing amplitudes during the im-
plantation procedure.
In a systematic investigation on the CIED’s lead location, we found
that a medial position and horizontal orientation of a bipolar lead’s
distal end as well as a short lead’s tip-to-ring spacing makes CIEDs
less susceptible to EMI.
76
We, therefore, recommend the implanta-
tion of true bipolar leads and programming the sensing configurations
appropriately in all patients, if possible. When changing the sensing
configuration or in case of pre-existing unipolar leads, physicians, and
patients should be aware of a higher likelihood of EMI.
Patients with recent EMI events, should first be advised to maintain
a greater distance (usually >30 cm) to the source of EMF, followed by
a careful evaluation of the technical integrity of the CIED. In addition,
an in-depth analysis of the situation of EMI including field measure-
ments, e.g. at the workplace, should be performed and a history of
earlier device disturbances should be obtained. Furthermore, remote
monitoring of devices may be of great help for early EMI detection.
Research needs
For future studies, we recommend using standardized exposure set-
ups and to conduct different types of studies in order to achieve a
comprehensive risk assessment for patients with CIEDs.
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2259378_0207.png
Electromagnetic interference in CIEDs
227
Individual parameters, including height or physique, which are also
affecting the interference threshold,
77
can however, neither be con-
sidered in phantom studies nor in benchmark tests. Therefore,
in vivo
studies should be performed in which patients with CIEDs are di-
rectly exposed to EMF and in which individual interference thresh-
olds of the CIED can be determined for specific exposure conditions.
Data obtained from
in vivo
studies need no additional validation and
can be transferred directly to real-life exposure situations. Therefore,
results from benchmark tests and phantom studies should always be
validated by
in vivo
studies. A disadvantage of
in vivo
studies is, how-
ever, that they are time-consuming and that a large number of
patients has to be tested to identify patient-related, CIED-related,
and lead-specific predictors.
The combination of benchmark tests, phantom, and
in vivo
studies
allows the development of a coupling model (transfer function).
Transfer functions demonstrate the relationship between the
strength of an external EMF and the induced intracorporal voltage at
the terminals of a CIED. A solid transfer function which serves as the
basis for the calculation of the induced voltages from various external
EMF can be derived by using comprehensive data obtained from the
different types of studies. Establishing a transfer function is necessary
to define limit values.
It is of great importance to define limit values for patients with
CIEDs because the current EMF limit values (e.g. ICNIRP,
17
27
mT
and 21 A/m for 3 kHz–10 MHz) proposed for the general public may
be exceeded by everyday electrical appliances emitting EMF in the IF
range. According to Leitgeb
et al.,
60
EAS systems may exceed the lim-
its by a factor of 13 compared with ICNIRP’s recommendation pub-
lished in 2010
17
and even by a factor of 60 with regard to ICNIRP’s
recommendation published in 1998.
78
Induction hobs may also ex-
ceed ICNIRP limit values in close proximity and depending on the po-
sition of the pot.
25
This does not suggest that the general public
(including people with CIEDs) is automatically at risk but caution is
warranted for worst-case exposure scenarios.
60
Vice versa, compli-
ance with ICNIRP does not suggest that the safety of patients with
CIEDs is guaranteed, because ICNIRP does not consider people fit-
ted with electronic implants in their recommendation. Furthermore,
the results of single studies in the present review provide evidence
that EMI may even be induced below the proposed ICNIRP limit val-
ues.
33,58
Thus, the establishment of limit values for patients with
CIEDs will contribute to estimate which electronic appliances can be
considered safe for CIEDs carriers and which distances to various
electronic appliances should be respected in order to prevent EMI.
Exposure set-up and characterization
Only 11 of the 40 studies included in this review used a standardized
exposure set-up, e.g. a Helmholtz coil or an antenna setting, while
most of the studies conducted experiments with a single electronic
appliance. For a general risk assessment, however, studies with single
device exposure have only a limited value, often due to a lack of a
proper dosimetry. In contrast, under standardized conditions, EMF of
a defined frequency and field strength can be generated and applied.
In such a setting, it is possible to determine exactly the exposure
parameters for which EMI is likely or unlikely to be induced. When
conducting studies with single devices a complete dosimetry should
be performed such that the results are applicable to different expo-
sure scenarios, including new technologies. It is important to charac-
terize the field strength and distribution as well as the frequency and
modulation (i.e. waveform such as CW vs. pulses) of EMF sources in
the vicinity of the patient or implant. This view is supported by
McIvor
et al.
34
and Seidman
et al.
47
who noted that the field strength,
frequency and modulation are the crucial parameters for EMI. From
their findings, McIvor
et al.
34
further concluded that susceptibility to
interference was enhanced by the 60 Hz pulsed signal. Additionally,
Hikage
et al.
40
found that EMI were more likely when CIEDs were ex-
posed to pulsed signals with a repetition time close to the physiologi-
cal heart rhythm.
Different types of studies
Beyond the use of standardized exposure set-ups and the characteri-
zation of the exposure parameters, we recommend performing
benchmark tests, phantom, and
in vivo
studies. The combination of dif-
ferent types of studies will help to systematically evaluate the influ-
ence of CIED-, lead-, and patient-related factors. However, it has to
be noted that each type of study has several advantages and
disadvantages.
Benchmark tests are highly suited for investigating the influence of
different CIED types and sensitivity settings. The disturbance signals
are fed directly into the pace/sense channel of the CIED by galvanic
coupling in order to analyse the CIED’s response and detection lev-
els. Several studies included in this review have shown that the likeli-
hood for disturbance depends on the CIED type (i.e. PM or ICD,
model
41,46,47
) and CIED sensitivity settings.
32,66
The simple method-
ology is a major advantage of benchmark tests. However, a disadvan-
tage is that individual parameters of the patient or the lead cannot be
considered.
The influence of the lead can best be examined in phantom studies.
Additionally, with phantom studies, the intracorporal voltage induced
by external EMF in the CIED-lead system can also be determined.
The induced voltage is an important measurement parameter for
electromagnetic compatibility testing of CIEDs because it can directly
be compared with the performance limits set in international product
standards, e.g. Ref.
53
Several studies included in this review have
shown that the likelihood for EMI depends on the lead parameters
(bipolar and unipolar
42
), lead configuration (i.e. loop area formed by
implant housing with its lead wire), and implantation site.
58,59
In clini-
cal practice, the susceptibility of CIEDs to EMI has been reduced by
using bipolar instead of unipolar leads. However, bipolar leads are still
susceptible to interference in the presence of strong EMF.
76
Conclusion
There are several studies investigating EMI of CIEDs by novel electri-
cal appliances emitting EMF in the IF range. However, the current
data do not allow a general risk assessment for CIED carriers regard-
ing common or future potential interferers, especially due to the lack
of a proper dosimetry in most of the studies or the missing correla-
tion of dosimetric data with EMI. The findings were only consistent
for security systems and induction hobs for which EMI in CIEDs could
be demonstrated in close proximity to the appliances. The results of
the studies evaluated in this systematic review and the results of stud-
ies on EMI in other frequency ranges indicate that the likelihood for
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2259378_0208.png
228
EMI is dependent on exposure-related parameters (field strength,
frequency, modulation) and on implant- as well as on lead-related
parameters (model, type of implant, implant sensitivity setting, lead
configuration, and implantation site). To better characterize the fac-
tors influencing EMI, future studies should consider all these factors
systematically by conducting different types of studies. Benchmark
test and phantom studies should be performed according to interna-
tional standards.
53–55
Concerning
in vivo
studies, where no compara-
ble recommendations exist, good experiences
70,72
were had in co-
operation between cardiologists with profound knowledge in elec-
trophysiology and electrical engineers with profound knowledge in
exposure set-ups.
Additionally, worst-case scenarios should be considered in all
study types where possible (i.e. unipolar sensing, maximum sensitiv-
ity, atrium sensing, sustained pacing of the CIED, left-sided implanta-
tion, lateral lead’s tip position, vertical lead’s tip orientation,
homogeneous field exposure, and thorax perpendicular to the mag-
netic field exposure). That way, it might be possible to derivate EMF
limit values for CIED patients in the future.
S. Driessen
et al.
Supplementary material
Supplementary material
is available at
Europace
online.
Funding
This work was supported by the European Research Group on
Environment and Health in the Transport Sector (EUGT) e.V., Germany.
Conflict of interest:
A.N. received travel grants by Biotronik, Boston
Scientific, Medtronic, and St. Jude Medical (now Abbott). All other
authors have no conflict of interest.
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ONCOLOGY LETTERS 20: 15, 2020
COMMENT
Health risks from radiofrequency radiation, including 5G,
should be assessed by experts with no conflicts of interest
LENNART HARDELL and MICHAEL CARLBERG
The Environment and Cancer Research Foundation, SE-702 17 Örebro, Sweden
Received April 8, 2020; Accepted June 19, 2020
DOI: 10.3892/ol.2020.11876
Abstract.
The fifth generation, 5G, of radiofrequency (RF)
radiation is about to be implemented globally without inves-
tigating the risks to human health and the environment.
This has created debate among concerned individuals in
numerous countries. In an appeal to the European Union (EU)
in September 2017, currently endorsed by >390 scientists
and medical doctors, a moratorium on 5G deployment was
requested until proper scientific evaluation of potential nega-
tive consequences has been conducted. This request has not
been acknowledged by the EU. The evaluation of RF radiation
health risks from 5G technology is ignored in a report by a
government expert group in Switzerland and a recent publi-
cation from The International Commission on Non-Ionizing
Radiation Protection. Conflicts of interest and ties to the
industry seem to have contributed to the biased reports. The
lack of proper unbiased risk evaluation of the 5G technology
places populations at risk. Furthermore, there seems to be a
cartel of individuals monopolizing evaluation committees,
thus reinforcing the no-risk paradigm. We believe that this
activity should qualify as scientific misconduct.
Introduction
Most politicians and other decision-makers using guidelines
for exposure to radiofrequency (RF) radiation seem to ignore
the risks to human health and the environment. The fact that
the International Agency for Research on Cancer (IARC) at
the World Health Organization (WHO) in May 2011 classified
RF radiation in the frequency range of 30 kHz to 300 GHz
to be a ‘possible’ human carcinogen, Group 2B (1,2), is being
ignored. This has been recently exemplified in a hearing at the
Tallinn Parliament in Estonia (3).
An important factor may be the influence on politicians
by individuals and organizations with inborn conflicts of
interests (COIs) and their own agenda in supporting the
no-risk paradigm (4,5). The International Commission on
Non-Ionizing Radiation Protection (ICNIRP) has repeatedly
ignored scientific evidence on adverse effects of RF radiation
to humans and the environment. Their guidelines for expo-
sure are based solely on the thermal (heating) paradigm and
were first published in ICNIRP 1998 (6), updated in ICNIRP
2009 (7) and have now been newly published in ICNIRP
2020 (8), with no change of concept, only relying on thermal
effects from RF radiation on humans. The large amount of
peer-reviewed science on non-thermal effects has been ignored
in all ICNIRP evaluations (9,10). Additionally, ICNIRP has
successfully maintained their obsolete guidelines worldwide.
COIs can be detrimental, and it is necessary to be as
unbiased as possible when assessing health risks. There are
three points that should be emphasized. Firstly, the evidence
regarding health risks from environmental factors may not
be unambiguous, and therefore informed judgements must be
made. Furthermore, there are gaps in knowledge that call for
experienced evaluations, and no conclusion can be reached
without value judgements. Secondly, paradigms are defended
against the evidence and against external assessments by social
networks in the scientific community. Thirdly, the stronger the
impact of decisions about health risks on economic, military
and political interests, the stronger will stakeholders try to
influence these decision processes.
Since the IARC evaluation in 2011 (1,2), the evidence on
human cancer risks from RF radiation has been strengthened
based on human cancer epidemiology reports (9-11), animal
carcinogenicity studies (12-14) and experimental findings on
oxidative mechanisms (15) and genotoxicity (16). Therefore,
the IARC Category should be upgraded from Group 2B to
Group 1, a human carcinogen (17).
The deployment of the fifth generation, 5G, of RF radiation
is a major concern in numerous countries, with groups of citi-
zens trying to implement a moratorium until thorough research
Correspondence to:
Dr Lennart Hardell, The Environment and
Cancer Research Foundation, Studievägen 35, SE-702 17 Örebro,
Sweden
E-mail: [email protected]
International Commission on Non-Ionizing Radiation Protection,
Scientific Committee on Emerging and Newly Identified Health Risks,
Swedish Radiation Safety Authority, 5G, electromagnetic field, appeals,
moratorium, microwave radiation, radiofrequency electromagnetic
field, health risks, non-ionizing radiation guidelines, conflicts of interest
Key words:
Switzerland, European Union, World Health Organization,
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HARDELL and CARLBERG: RADIOFREQUENCY RADIATION AND CONFLICTS OF INTERESTS
on adverse effects on human health and the environment has
been performed. An appeal for a moratorium, currently signed
by >390 international scientists and medical doctors, was sent
to the European Union (EU) in September 2017 (18), currently
with no EU response (19). Several regions have implemented a
moratorium on the deployment of 5G motivated by the lack of
studies on health effects, for instance Geneva (20).
In the present article, the current situation in Switzerland is
discussed as an example (21). Additionally, the ICNIRP 2020
evaluation is discussed (8).
Evaluation of health risks in Switzerland
Several Swiss citizens have brought to our attention that
Associate Professor Martin Röösli is the chair of two impor-
tant government expert groups in Switzerland (directeur),
despite possible COIs and a history of misrepresentation of
science (22,23). These groups are Beratende Expertengruppe
NIS (BERENIS; the Swiss advisory expert group on elec-
tromagnetic fields and non-ionizing radiation) (24), and the
subgroup 3, the Mobile Communications and Radiation Working
Group of the Department of the Environment, Transport,
Energy and Communications/Eidgenössisches Departement
für Umwelt, Verkehr, Energie und Kommunikation, evaluating
RF-radiation health risks from 5G technology (25,26).
The conclusions made in the recent Swiss government
5G report are biased and can be found here (27,28). This 5G
report concluded that there is an absence of short-term health
impacts and an absence or insufficient evidence of long-term
effects [see Table 17 (Tableau 17) on page 69 in the French
version (27) and Table 17 (Tabelle 17) on page 67 in the
German version (28)].
Furthermore, it was reported that there is limited
evidence for glioma, neurilemmoma (schwannoma) and
co-carcinogenic effects, and insufficient evidence for effects
on children from prenatal exposure or from their own mobile
phone use. Regarding cognitive effects, fetal development and
fertility (sperm quality), the judgement was that the evidence
on harmful effects is insufficient. These evaluations were
strikingly similar to those of the ICNIRP (see Appendix B in
ICNIRP 2020; 8). Other important endpoints, such as effects on
blood-brain barrier, cell proliferation, apoptosis (programmed
cell death), oxidative stress (reactive oxygen species) and gene
and protein expression, were not evaluated.
According to Le Courrier November 19, 2019, Martin
Röösli presented the conclusion in an interview in the
following way: ‘Sur
l'aspect sanitaire pur, «le groupe de
travail constate que, jusqu'à présent, aucun effet sanitaire
n'a été prouvé de manière cohérente en dessous des valeurs
limites d'immissions fixées», résume Martin Röösli, profes-
seur d'épidémiologie environnementale à l'Institut tropical et
de santé publique suisse’
(29). [Regarding
the health issue,
the working group concludes that, until now, no health effect
has been consistently proven below the given exposure limits,
summarizes Martin Röösli, professor in environmental epide-
miology at the Swiss Tropical and Public Health Institute].
This Swiss evaluation is scientifically inaccurate and
is in opposition to the opinion of numerous scientists in
this field (18). In addition, 252 electromagnetic field (EMF)
scientists from 43 countries, all with published peer-reviewed
research on the biologic and health effects of nonionizing
electromagnetic fields (RF-EMF) have stated that:
‘Numerous
recent scientific publications have shown
that RF-EMF affects living organisms at levels well below
most international and national guidelines. Effects include
increased cancer risk, cellular stress, increase in harmful free
radicals, genetic damages, structural and functional changes
of the reproductive system, learning and memory deficits,
neurological disorders, and negative impacts on general well-
being in humans. Damage goes well beyond the human race,
as there is growing evidence of harmful effects to both plant
and animal life’
(30).
We are concerned that the Swiss 5G report may be influ-
enced by ties to mobile phone companies (COIs) by one or
several members of the evaluating group.
COIs
Funding from telecom companies is an obvious COI. Martin
Röösli has been a member of the board of the telecom funded
Swiss Research Foundation for Electricity and Mobile
Communication (FSM) organization and he has received
funding from the same organization (31-33).
It should be noted that the FSM is a foundation that serves
formally as an intermediate between industry and researchers.
According to their website, among the five founders of FSM
who ‘provided
the initial capital of the Foundation’
four are
telecommunications companies: Swisscom, Salt, Sunrise,
3G Mobile (liquidated in 2011). The fifth founder is ETH
Zurich (technology and engineering university). There are
only two sponsors, Swisscom (telecommunications) and
Swissgrid (energy), who ‘support
the FSM with annual dona-
tions that allow for both the management of the Foundation
and research funding’
(34).
The same situation applies to being a member of
ICNIRP (Table I) (35). In 2008, the Ethical Council at
Karolinska Institute in Stockholm stated that being a member
of ICNIRP is a potential COI. Such membership should
always be declared. This verdict was based on activities by
Anders Ahlbom in Sweden, at that time a member of ICNIRP,
but is a general statement (2008-09-09; Dnr, 3753-2008-609).
In summary: ‘It
is required that all parties clearly declare ties
and other circumstances that may influence statements, so
that decision makers and the public may be able to make solid
conclusions and interpretations. AA [Anders Ahlbom] should
thus declare his tie to ICNIRP whenever he makes statements
on behalf of authorities and in other circumstances’
(translated
into English).
COIs with links to industry are of great importance; these
links may be direct or indirect funding for research, payment
of travel expenses, participation in conferences and meetings,
presentation of research, etc. Such circumstances are not
always declared as exemplified above. A detailed description
was recently presented for ICNIRP members (22).
ICNIRP
ICNIRP is a non-governmental organization (NGO) based in
Germany. Members are selected via an internal process, and
the organization lacks transparency and does not represent the
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ONCOLOGY LETTERS 20: 15, 2020
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Table I. Members of the WHO core group and additional experts of the Environmental Health Criteria Document 2014 (54), EU
SCENIHR 2015 (52), the SSM 2015-2020 (93) and ICNIRP commission or the Scientific Expert Group 1992-2020 (94).
Members
Emilie van Deventer
Simon Mann
Maria Feychting
Gunnhild Oftedal
Eric van Rongen
Maria Rosaria Scarfi
Jukkka Juutilainen
Denis Zmirou
Theodoros Samaras
Norbert Leitgeb
Anssi Auvinen
Heidi Danker Hopfe
Kjell Hansson Mild
Mats Olof Mattsson
Hannu Norppa
James Rubin
Joachim Schüz
Zenon Sienkiewicz
Olga Zeni
Anke Huss
Clemens Dasenbrock
Lars Klaeboe
Martin Röösli
Aslak Harbo Poulsen
a
WHO, 2014
X
X
X
X
X
X
X
X
SCENIHR, 2015
SSM, 2015-2020
X
(X)
b
ICNIRP, 1992-2020
X
a
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
c
X
X
X
WHO Observer in the main commission (95);
b
2002-2011;
c
2020-2024. The table is based on members of WHO, SCENIHR and SSM during
the defined time period(s). No other individuals among those within WHO or SCENIHR were found in the list of SSM participants. A total
of 15 additional experts in WHO were not members of SCENIHR, SSM or ICNIRP. SCENIHR, Scientific Committee on Emerging and
Newly Identified Health Risks; SSM, Swedish Radiation Safety Authority; WHO, World Health Organization; EU, European Union; ICNIRP,
International Commission on Non-Ionizing Radiation Protection.
opinion of the majority of the scientific community involved
in research on health effects from RF radiation. Independent
international EMF scientists in this research area have declared
that: ‘In
2009, the ICNIRP released a statement saying that it
was reaffirming its 1998 guidelines, as in their opinion, the
scientific literature published since that time has provided no
evidence of any adverse effects below the basic restrictions
and does not necessitate an immediate revision of its guidance
on limiting exposure to high frequency electromagnetic fields.
ICNIRP continues to the present day to make these assertions,
in spite of growing scientific evidence to the contrary. It is
our opinion that, because the ICNIRP guidelines do not cover
long-term exposure and low-intensity effects, they are insuf-
ficient to protect public health’
(30).
ICNIRP only acknowledges thermal effects from RF
radiation. Therefore, the large body of research on detrimental
non-thermal effects is ignored. This was further discussed in a
peer-reviewed scientific comment article (3).
In 2018, ICNIRP published ‘ICNIRP
Note: Critical
Evaluation of Two Radiofrequency Electromagnetic Field
Animal Carcinogenicity Studies Published in 2018’
(36). It is
surprising that this note claims that the histopathological evalu-
ation in the US National Toxicology Program (NTP) study on
animals exposed to RF radiation was not blinded (12,13). In
fact, unfounded critique of the NTP study had already been
rebutted (37); however, this seems to have had little or no
impact on this ICNIRP note casting doubt on the findings of the
animal study: ‘This
commentary addresses several unfounded
criticisms about the design and results of the NTP study that
have been promoted to minimize the utility of the experimental
data on RFR [radiofrequency radiation] for assessing human
health risks. In contrast to those criticisms, an expert peer-
review panel recently concluded that the NTP studies were
well designed, and that the results demonstrated that both
GSM- and CDMA-modulated RFR were carcinogenic to the
heart (schwannomas) and brain (gliomas) of male rats’
(37).
In contrast to the opinion of the 13 ICNIRP commission
members, the IARC advisory group of 29 scientists from
18 countries has recently stated that the cancer bioassay in
experimental animals and mechanistic evidence warrants
high priority re-evaluation of the RF radiation-induced
carcinogenesis (38).
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HARDELL and CARLBERG: RADIOFREQUENCY RADIATION AND CONFLICTS OF INTERESTS
ICNIRP draft.
On July 11, 2018, ICNIRP released a draft on
guidelines (39) for limiting exposure to time-varying electric,
magnetic and electromagnetic fields (100 kHz to 300 GHz).
It was open for public consultations until October 9, 2018.
Appendix B was based on assessment of health risks based on
a literature survey (39).
Surprisingly, the IARC classification of RF-EMF exposure
as Group 2B (‘possibly’ carcinogenic to humans) from 2011
was concealed in the background material to the new ICNIRP
draft on guidelines. Notably, one of the ICNIRP commission
members, Martin Röösli (40), was also one of the IARC experts
evaluating the scientific RF carcinogenicity in May 2011 (41).
He should be well aware of the IARC classification. The IARC
classification contradicts the scientific basis for the ICNIRP
guidelines, making novel guidelines necessary and providing
a basis to halt the rollout of 5G technology.
Therefore, the ICNIRP provides scientifically inaccurate
reviews for various governments. One issue is that only
thermal (heating) effects from RF radiation are considered,
and all non-thermal effects are dismissed. An analysis from
the UK demonstrates these inaccuracies (4), also discussed in
another article (5). All members of the ICNIRP commission
are responsible for these biased statements that are not based
on solid scientific evidence.
ICNIRP release of novel guidelines for RF radiation.
On
March 11, 2020, ICNIRP published their novel guidelines for
exposure to EMFs in the range of 100 kHz to 300 GHz, thus
including 5G (8). The experimental studies demonstrating a
variety of non-thermal biological/health effects (9,10) are not
considered, as in their previous guidelines (6,7). Additionally,
the ICNIRP increased the reference levels for the general
public averaged over 6 min for RF frequencies >2-6 GHz (those
that will be used for 5G in this frequency range), from
10 W/m
2
(Tables 5 and 7 in ref. no. 6) to 40 W/m
2
(Table 6 in
ref. no. 8), which paves the way for even higher exposure levels
to 5G than the already extremely high ones.
Background dosimetry is discussed in Appendix A of the
ICNIRP 2020 guidelines (8). The discussion on ‘Relevant
Biophysical Mechanisms’ should be criticized. The only
mechanism considered by ICNIRP is temperature rise, which
may also occur with 5G exposure, apart from the established
non-thermal biological/health effects (42,43). It is well known
among experts in the EMF-bioeffects field that the recorded
cellular effects, such as DNA damage, protein damage,
chromosome damage and reproductive declines, and the vast
majority of biological/health effects are not accompanied
by any significant temperature rise in tissues (44-47). The
ion forced-oscillation mechanism (48) should be referred to
as a plausible non-thermal mechanism of irregular gating of
electrosensitive ion channels on cell membranes, resulting in
disruption of the cell electrochemical balance and initiating
free radical release and oxidative stress in the cells, which in
turn causes genetic damage (15,49). The irregular gating of
ion channels on cell membranes is associated with changes in
permeability of the cell membranes, which ICNIRP admits in
its summary (8).
Health risks are discussed in Appendix B of the ICNIRP
2020 guidelines (8). Again, only thermal effects are consid-
ered, whereas literature on non-thermal health consequences
is disregarded (9,10,50). In spite of public consultations on the
draft, the final published version on health effects is virtually
identical to the draft version, and comments seem to have been
neglected (19). In the following section, Appendix B on health
effects (8) is discussed.
Appendix B starts with: ‘The
World Health Organization
(WHO) has undertaken an in-depth review of the literature
on radiofrequency electromagnetic fields (EMFs) and health,
which was released as a Public Consultation Environmental
Health Criteria Document in 2014... Further, the Scientific
Committee on Emerging and Newly Identified Health
Risks (SCENIHR), a European Commission initiative, also
produced a report on potential health effects of exposure to
electromagnetic fields (SCENIHR 2015), and the Swedish
Radiation Safety Authority (SSM) have produced several
international reports regarding this issue (SSM 2015, 2016,
2018). Accordingly, the present guidelines have used these
literature reviews as the basis for the health risk assessment
associated with exposure to radiofrequency EMFs rather than
providing another review of the individual studies’.
In the last 11 years since its previous ICNIRP 2009
statement (7), ICNIRP has not managed to conduct a novel
evaluation of health effects from RF radiation. However, as
shown in Table I, several of the present ICNIRP members
are also members of other committees, such as the EU
Scientific Committee on Emerging and Newly Identified
Health Risks (SCENIHR), the Swedish Radiation Safety
Authority (SSM) and the WHO, thus creating a cartel of
individuals known to propagate the ICNIRP paradigm on RF
radiation (4,5,22,51). In fact, six of the seven expert members of
the WHO, including Emelie van Deventer, were also included
in ICNIRP (5,7). Therefore, Emilie van Deventer, the team
leader of the Radiation Programme at WHO (the International
EMF Project), is an observer on the main ICNIRP commis-
sion, and SSM seems to be influenced by ICNIRP. Among the
current seven external experts (Danker-Hopfe, Dasenbrock,
Huss, Harbo Polusen, van Rongen, Röösli and Scarfi), five are
also members of ICNIRP, and van Deventer used to be part
of SSM.
As discussed elsewhere (5), it is unlikely that a person's
evaluation of health risks associated with exposure to RF
radiation would differ depending on what group the person
belongs to. Therefore, by selecting group members, the final
outcome of the evaluation may already be predicted (no-risk
paradigm). Additionally, we believe that this may compromise
sound scientific code of conduct.
The SCENIHR report from 2015 (52) has been used to
legitimate the further expansion of the wireless technology
and has been the basis for its deployment in a number of
countries. One method, applied in the SCENIHR report, to
dismiss cancer risks involves the selective inclusion of studies,
excluding studies reporting cancer risks and including some
investigations with inferior epidemiological quality. The report
has been heavily criticized by researchers with no COI (53): ‘In
January of 2015, the Scientific Committee on Emerging and
Newly Identified Health Risks (SCENIHR) published its final
opinion on (P)otential health effects of exposure to electro-
magnetic fields... SCENIHR has not answered the question it
was appointed to investigate. The Committee has answered a
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different question, limiting its conclusions to whether certainty
or causal effect is established, instead of possibility of health
risks... Overall, SCENIHR has not conducted a scientific
review process for judging possible health risks. This results
in erroneous and deceptive conclusions by failing to conclude
such possible health risks do exist. Evidence that SCENIHR
has presented clearly and conclusively demonstrates that
EMF health risks are possible, and in some cases are estab-
lished. The Committee is obligated to draw to the attention of
the European Commission that EMF is a new and emerging
problem that may pose an actual or potential threat’.
Regarding the SSM, only yearly updates are available and
no overall evaluations are made. Therefore, no thorough review
is presented. Over the years, the ICNIRP has dominated this
committee (Table I). Therefore, it is unlikely that the opinion
of the SSM will differ from that of the ICNIRP.
In 2014, the WHO launched a draft of a Monograph on
RF fields and health for public comments (54). It should be
noted that the WHO issued the following statement: ‘This
is a
draft document for public consultation. Please do not quote
or cite’.
ICNIRP completely ignored that request and used the
aforementioned document. The public consultations on the
draft document were dismissed and never published.
In addition to van Deventer, five of the six members (Mann,
Feychting, Oftedal, van Rongen, and Scarfi) of the Core
Group in charge of the WHO draft were also affiliated with
ICNIRP, which constitutes a COI (Table I). Scarfi is a former
member of ICNIRP (5). Several individuals and groups sent
critical comments to the WHO on the numerous shortcom-
ings in the draft of the Monograph on RF radiation. In
general, the WHO never responded to these comments and
it is unclear to what extent, if any, they were even consid-
ered. Nevertheless, the final version of the WHO ‘in-depth
review’ has never been published. Instead, WHO made a call
on October 8, 2019 (Emelie van Deventer), for systematic
reviews to analyze and synthesize the available evidence:
‘Through
this Call, WHO invites eligible teams to indicate
their interest in undertaking a systematic review on one (or
more) of the following topics: SR1 - Effect of exposure to RF
on cancer (human observational studies); SR2 - Effect of
exposure to RF on cancer (animal studies); SR3 - Effect of
exposure to RF on adverse reproductive outcomes (human
observational studies); SR4 - Effect of exposure to RF on
adverse reproductive outcomes (animal and in vitro studies);
SR5 - Effect of exposure to RF on cognitive impairment
(human observational studies; SR6 - Effect of exposure to
RF on cognitive impairment (human experimental studies);
SR7 - Effect of exposure to RF on symptoms (human observa-
tional studies); SR8 - Effect of exposure to RF on symptoms
(human experimental studies; SR9 - Effect of exposure to RF
on biomarkers of oxidative stress; SR10 - Effect of exposure
to heat from any source and pain, burns, cataract and heat-
related illness’.
The authors of the present article were part of a team that
applied to review SR1- human cancer. On December 20, 2019,
the following reply was received from the WHO Radiation
Programme: ‘After
careful review, we have decided to choose
another team for this systematic review’.
Transparency is of importance for the whole process.
Therefore, a query was sent to the WHO requesting informa-
tion regarding the following points: ‘Who
did the evaluation of
the groups that answered the call? What criteria were applied?
How many groups had submitted and who were these? Which
groups were finally chosen for the different packages?’.
In
spite of sending the request four times, January 2, January 3,
April 7 and April 30, 2020, there has been no reply from
WHO. This appears to be a secret process behind closed doors.
These circumstances have also been reported in Microwave
News (55).
It is important to comment on the current ICNIRP evalu-
ation. Notably, on February 27, 2020, two weeks before the
ICNIRP publication, the WHO Team on Public Health,
Environmental and Social Determinants of Health issued a
statement on 5G mobile networks and health: ‘To
date, and
after much research performed, no adverse health effect
has been causally linked with exposure to wireless tech-
nologies’
(56). This statement is not correct based on current
knowledge (4,5,9-11,17,19) and was without a personal signa-
ture. The lack of research on 5G safety has been previously
discussed (19). Furthermore, there is no evidence that can
‘causally link’ an adverse effect to an exposure. Causality is
no empirical fact, it is an interpretation.
In the following section, only one (cancer) of the eight
different end points in the ICNIRP publication (8) is discussed,
since it deals with our main research area.
viii) Cancer.
‘In
summary, no effects of radiofrequency EMFs on the
induction or development of cancer have been substantiated.
Summary
The only substantiated adverse health effects caused by
exposure to radiofrequency EMFs are nerve stimulation,
changes in the permeability of cell membranes, and effects
due to temperature elevation. There is no evidence of adverse
health effects at exposure levels below the restriction levels in
the ICNIRP (1998) guidelines and no evidence of an interac-
tion mechanism that would predict that adverse health effects
could occur due to radiofrequency EMF exposure below those
restriction levels’.
Comments
The ICNIRP draft (39) has been previously described to some
extent (19). The published final version on health effects is
virtually similar to the draft. It cannot be taken at face value as
scientific evidence of no risk from RF radiation. One example
is the following statement (p. 41): ‘…a
set of case-control
studies from the Hardell group in Sweden report significantly
increased risks of both acoustic neuroma and malignant
brain tumors already after less than five years since the start
of mobile phone use, and at quite low levels of cumulative call
time’.
This allegation is not correct according to our publication
for glioma (11). In the shortest latency group >1-5 years, the
risk of glioma was not increased (odds ratio (OR), 1.1; 95% CI,
0.9-1.4) for use of wireless phones (mobile phone and/or cord-
less phone). There was a statistically significant increased risk
of glioma per 100 h of cumulative use (OR, 1.011; 95% CI,
1.008-1.014) and per year of latency (OR, 1.032; 95% CI,
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HARDELL and CARLBERG: RADIOFREQUENCY RADIATION AND CONFLICTS OF INTERESTS
1.019-1.046) (11). These published results are in contrast to the
ICNIRP claims.
Regarding acoustic neuroma, the corresponding detailed
results are reported in our previous study (57). The shortest
latency period >1-5 years yielded an OR of 1.2 (95% CI,
0.8-1.6) for use of wireless phones; the risk increased per 100
h of cumulative use (OR, 1.008; 95% CI, 1.002-1.014) and
per year of latency (OR, 1.056; 95% CI, 1.029-1.085) (57).
Therefore, the allegation by ICNIRP is false.
It is remarkable that ICNIRP is uninformed and that their
writing is based on a misunderstanding of the peer-reviewed
published articles as exemplified above. Additionally, our
studies (11,57) and another study by Coureau
et al
(58),
as well as the IARC evaluation from 2011 (1,2), are not
included among the references. Several statements by
ICNIRP are made without any scientific references. On
the other hand, the Danish cohort study on mobile phone
use (59) is included, in spite of the fact that it was judged
by IARC (1,2), as well as in our review (60), to be unin-
formative. A biased article written by authors including
ICNIRP members, used to ‘prove’ the no-risk paradigm
for RF radiation carcinogenesis (23), is cited by ICNIRP.
Notably, the article has not undergone relevant peer-review
and we believe that it should not have been published in its
current version. The shortcomings in the aforementioned
article are discussed in the following sections. As discussed
below, another claim (23) is incorrect regarding increased
risk of brain tumors associated with use of wireless phones:
‘However,
they are not consistent with trends in brain
cancer incidence rates from a large number of countries or
regions, which have not found any increase in the incidence
since mobile phones were introduced’.
The criticism of the ICNIRP draft guidelines from 2018
by the EMF call (61) can also be applied to the current
ICNIRP publication. The call has been signed by 164
scientists and medical doctors, as well as 95 NGOs: ‘The
International Commission on Non-Ionizing Radiation
Protection (ICNIRP) issued draft Guidelines on 11th July
2018 for limiting exposure to electric, magnetic and elec-
tromagnetic fields (100 kHz to 300 GHz).1 These guidelines
are unscientific, obsolete and do not represent an objective
evaluation of the available science on effects from this form
of radiation. They ignore the vast amount of scientific find-
ings that clearly and convincingly show harmful effects at
intensities well below ICNIRP guidelines.2 The guidelines
are inadequate to protect humans and the environment.
ICNIRP guidelines only protect against acute thermal effects
from very short and intense exposure. The guidelines do not
protect against harmful effects from low-intensity and long-
term exposure, such as cancer, reproductive harm, or effects
on the nervous system, although these effects are convinc-
ingly shown to appear from chronic exposure at intensities
below ICNIRP limits.2,3
ICNIRP's mandate to issue exposure guidelines needs
to be seriously questioned. ICNIRP is not independent of
industry ties as it claims.12,13 Its opinions are not objective,
not representative of the body of scientific evidence, but are
biased in favor of industry. It is obvious from their reluctance
to consider scientific findings of harm that ICNIRP protects
industry, not the public health, nor the environment.
We ask the United Nations, the World Health Organization,
and all governments to support the development and consider-
ation of medical guidelines16, that are independent of conflict
of interests in terms of direct or indirect ties to industry, that
represent the state of medical science, and that are truly
protective’.
In the recent report on ICNIRP published by two Members
of the European Parliament it is concluded: ‘That
is the most
important conclusion of this report: For really independent
scientific advice we cannot rely on ICNIRP. The European
Commission and national governments, from countries like
Germany, should stop funding ICNIRP. It is high time that
the European Commission creates a new, public and fully
independent advisory council on non-ionizing radiation’
(22).
Other examples of scientific misrepresentation
Published article.
This section discusses an article with conclu-
sions not substantiated by scientific evidence, representing a
biased evaluation of cancer risks from mobile phone use and
is an example of lack of objectivity and impartiality (23). The
aforementioned report was used by ICNIRP 2020 (8) to vali-
date that no risks have been found for brain and head tumors.
Therefore, the article should be discussed in further detail.
The aforementioned article has numerous severe scientific
deficiencies. One is that the results on use of cordless phones as
a risk factor for brain tumors are not discussed. In fact, detailed
results on cordless phones in studies by Hardell
et al
(11,57)
are omitted.
When discussing glioma risk, all results on cumulative use
of mobile phones, as well as ipsilateral or contralateral use
associated with tumor localization in the brain, are omitted
from the figures in the main text. Some results in the article by
Röösli
et al
(23), such as cumulative use, can be found in the
Supplementary Material, although the increased risk among
heavy users is disregarded (11,57,58,62). In Supplementary
Figure 4, all odds ratios regarding long-term (≥10 years)
use of mobile phones are above unity (>1.0) for glioma and
neuroma (23). No results are provided for ipsilateral mobile
phone use (same side of tumor localization and mobile phone
use), which is of large biological importance. Results on cumu-
lative use, latency and ipsilateral use are especially important
for risk assessment and have shown a consistent pattern of
increased risk for brain and head tumors (11,57).
In the aforementioned article, recall bias is discussed
as the reason for increased risk (23). The studies by
Hardell
et al
(11,57) included all types of brain tumors. In one
analysis, meningioma cases in the same study were used as the
‘control’ entity (11), and still a statistically significant increased
risk of glioma was identified for mobile phone use (ipsilateral
OR, 1.4; 95% CI, 1.1-1.8; contralateral OR, 1.0; 95% CI, 0.7-1.4)
and for cordless phone use (ipsilateral OR, 1.4; 95% CI, 1.1-1.9;
contralateral OR, 1.1; 95% CI, 0.8-1.6). If the results were
‘explained’ by recall bias, similar results would have been
obtained for both glioma and meningioma. Thus, this type
of analyses would not have yielded an increased glioma risk.
Also, for acoustic neuroma a statistically significant increased
risk was found using meningioma cases as ‘controls’ (57).
Therefore, the results in the studies by Hardell
et al
(11,57)
cannot be explained by a systematic difference in assessment
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of exposure between cases and controls. These important
methodological findings were disregarded by Röösli
et al
(23).
In the analyses of long-term use of mobile phones, a
Danish cohort study on mobile phone use is included (59),
which was concluded to be uninformative in the 2011 IARC
evaluation (1,2). A methodological shortcoming of the afore-
mentioned study was that only private mobile phone subscribers
in Denmark between 1982 and 1995 were included in the
exposure group (59). The most exposed group, comprising
200,507 corporate users of mobile phones, were excluded and
instead included in the unexposed control group consisting of
the rest of the Danish population. Users with mobile phone
subscription after 1995 were not included in the exposed group
and were thus treated as unexposed at the time of cut-off of the
follow up. No analysis of laterality of mobile phone use in rela-
tion to tumor localization was performed. Notably, this cohort
study is now included in the risk calculations, although Martin
Röösli was a member of the IARC evaluation group and
should have been aware of the IARC decision. The numerous
shortcomings in the Danish cohort study, discussed in detail
in a peer-reviewed article (60), are omitted in the article by
Röösli
et al
(23).
Regarding animal studies, a study by Falcioni
et al
(14) at
the Ramazzini Institute on RF radiation carcinogenesis is only
mentioned as a reference, but the results are not discussed. In
fact, these findings (14) provide supportive evidence on the
risk found in human epidemiology studies (3), as well as the
results in the NTP study (12,13).
Furthermore, for incidence studies on brain tumors, the
results are not presented in an adequate way. There is a lot
of emphasis on the Swedish Cancer Register data (63,64), but
the numerous shortcomings in the reporting of brain tumor
cases to the register are not discussed. These shortcomings
have been presented in detail in a previous study (63), but are
disregarded by Röösli
et al
(23).
There is clear evidence from several countries regarding
increasing numbers of patients with brain tumors, such as in
Sweden (63,64), England (65), Denmark (66) and France (67).
The article by Röösli
et al
(23), does not represent an
objective scientific evaluation of brain and head tumor risk
associated with the use of wireless phones, and should thus be
disregarded. By omitting results of biological relevance and
including studies that have been judged to be uninformative,
the authors come to the conclusion that there are no risks:
‘In
summary, current evidence from all available studies
including in vitro, in vivo, and epidemiological studies does
not indicate an association between MP [mobile phone] use
and tumors developing from the most exposed organs and
tissues’.
Röösli
et al
(23), disregard the concordance of increased
cancer risk in human epidemiology studies (11,57,58,62)
animal studies (12-14,68,69) and laboratory studies (15,16,37).
It is unfortunate that the review process of the aforementioned
article has not been of adequate quality. Finally, there is no
statement in the article of specific funding of this particular
work, which is not acceptable. Only a limited number of
comments on general funding are provided. It is not plausible
that there was no funding for the study. We believe that, due to
its numerous limitations, the aforementioned article should not
have been published.
CEFALO.
In 2011, a case-control study on mobile phone use
and brain tumor risk among children and adolescents termed
CEFALO was published (70). The study appears to have been
designed to misrepresent the true risk, since the following
question regarding cordless phone use was asked: ‘How
often
did [child] speak on the cordless phone in the first 3 years
he/she used it regularly?’.
There are no scientific valid reasons to limit the investiga-
tion to the first 3 years. The result is a misrepresentation and
a wrong exposure classification, since Aydin
et al
(70) will-
ingly omitted any increase in the child's use of and exposure
from cordless phone radiation after the first 3 years of use.
This unscientific treatment of cordless phone exposure was
not mentioned in the article other than in a footnote of a table
and in the methods section (70); however, no explanation was
provided: ‘Specifically,
we analyzed whether subjects ever
used baby monitors near the head, ever used cordless phones,
and the cumulative duration and number of calls with cord-
less phones in the first 3 years of use’.
Since previous studies have demonstrated that these phone
types, in addition to mobile phones, increase brain tumor
risk (11,57), we believe that the exclusion of a complete expo-
sure history on the use of cordless phones represents scientific
misconduct.
In a critical comment the authors of the present study
wrote: ‘Further
support of a true association was found in
the results based on operator-recorded use for 62 cases and
101 controls, which for time since first subscription >2.8
years yielded OR 2.15 (95% CI 1.07-4.29) with a statisti-
cally significant trend (P = 0.001). The results based on
such records would be judged to be more objective than
face-to-face interviews, as in the study that clearly disclosed
to the interviewer who was a case or a control. The authors
disregarded these results on the grounds that there was no
significant trend for operator data for the other variables
- cumulative duration of subscriptions, cumulative dura-
tion of calls and cumulative number of calls. However, the
statistical power in all the latter groups was lower since
data was missing for about half of the cases and controls
with operator-recorded use, which could very well explain
the difference in the results’
(71).
Our conclusion was that: ‘We
consider that the data
contain several indications of increased risk, despite low
exposure, short latency period, and limitations in the study
design, analyses and interpretation. The information certainly
cannot be used as reassuring evidence against an association,
for reasons that we discuss in this commentary’
(71).
This is in contrast to the authors that claimed that the study
was reassuring of no risk in a press release from Martin Röösli,
July 28, 2011: ‘Kein
erhöhtes Hirntumorrisiko bei Kindern und
Jugendlichen wegen Handys... Die Resultate sind beruhigend’
[‘No
increased brain tumour risk in children and adolescents
for mobile phone users... The results are reassuring’]
(72).
A similar press release was issued by Maria Feychting at the
Karolinska Institute in Stockholm stating: ‘Reassuring
results
from first study on young mobile users and cancer risk… The
so called CEFALO study does not show an increased brain
tumor risk for young mobile users’
(73). Considering the results
and the numerous scientific shortcomings in the study (70), the
statements in these press releases are not correct.
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8
Discussion
HARDELL and CARLBERG: RADIOFREQUENCY RADIATION AND CONFLICTS OF INTERESTS
There is no doubt that several individuals included in Table I
are influential, being members, as well as having consulting
assignments, in several organizations, such as ICNIRP,
BERENIS, the SSM, the Program Electromagnetic Fields
and Health from ZonMw in the Netherlands, and the Rapid
Response Group for the Japan EMF Information Center (74).
In fact, there appears to be a cartel of individuals working
on this issue (75). Associate Professor Martin Röösli has had
the chance to provide his view on the content of the present
article relating to him. The only message from him was in
an e-mail dated January 16, 2020: ‘Just
to be clear, all my
research is funded by public money or not-for -profit funda-
tions [foundations]. I think you will not help an important
debate if you spread fake news’.
Obviously, as described in
the present article, his comment is not correct considering his
funding from the telecom industry (76,77).
As shown in Table I, few individuals, and mostly the same
ones, are involved in different evaluations of health risks from
RF radiation and will thus propagate the same views on the
risks in agencies of different countries associated with the
ICNIRP views (4,5). Therefore, it is unlikely that they will
change their opinions when participating in different organi-
zations. Furthermore, their competence in natural sciences,
such as medicine, is often low or non-existent due to a lack of
education in these disciplines (2). Therefore, any chance for
solid evaluations of medical issues is hampered. Additionally,
it must be concluded that if the ‘thermal only’ dogma is
dismissed, this will have wide consequences for the whole
wireless community, including permissions for base stations,
regulations of the wireless technology and marketing, plans to
roll out 5G, and it would therefore have a large impact on the
industry. This may explain the resistance to acknowledge the
risk by ICNIRP, EU, WHO, SSM and other agencies. However,
the most important aspects to consider are human wellbeing
and a healthy environment. Telecoms can make profit in a
variety of ways, and wireless is just one of them. They have
the capacity to maintain profits by using different techniques,
such as optical fiber, that will provide more data with less RF
radiation exposure. Particularly when considering the liability,
they are incurring in their misguided insistence of wireless
expansion that may ultimately catch up to them in the form of
lawsuits, such as those previously experienced by asbestos and
tobacco companies (78,79).
A recent book describes how deception is used to capture
agencies and hijack science (80). There are certain tools that
can be used for this. One is to re-analyze existing data using
methods that are biased towards predetermined results (23).
For example, this can be performed by hiring ‘independent
experts’ to question scientific results and create doubt (81,82). As
clearly discussed in a number of chapters of the books (80-82),
front groups may be created to gain access to politicians and
to influence the public with biased opinions. Other methods
may involve intimidating and harassing independent scientists
that report health risks based on sound science, or removing all
funding from scientists who do not adhere to the no-risk pro-
industry paradigm. Another tool would be economic support
and courting decision makers with special information sessions
that mislead them on science and mask bribery (3,5,19,80-82).
An industry with precise marketing goals has a big advan-
tage over a loose scientific community with little funding.
Furthermore, access to regulatory agencies and overwhelming
them with comments on proposed regulations is crucial (3).
To counteract all these actions is time consuming and not
always successful (19). Nevertheless, it is important that these
circumstances are explored and published in the peer-reviewed
literature as historical notes for future use.
Based on the Swiss and ICNIRP experiences, some recom-
mendations can be made. One is to include only unbiased and
experienced experts without COIs for evaluation of health risks
from RF radiation. All countries should declare a moratorium
on 5G until independent research, performed by scientists
without any ties to the industry, confirms its safety or not. 2G,
3G, 4G and WiFi are also considered not to be safe, but 5G
will be worse regarding harmful biological effects (42,83,84).
The authors of the present article recommend an educational
campaign to educate the public about the health risks of RF
radiation exposure, and safe use of the technology, such as the
deployment of wired internet in schools (85), as previously
recommended by the European Council resolution 1815 in
2011 (86) and The EMF Scientist Appeal (87). Additionally,
it is recommended that the government takes steps to mark-
edly decrease the current exposure of the public to RF
radiation, (88,89). Notably, DNA damage has been identified
in peripheral blood lymphocytes using the comet assay tech-
nique, and in buccal cells using the micronucleus assay, in
individuals exposed to RF radiation from base stations (90).
Finally, an alternative approach to the flawed ICNIRP safety
standards may be the comprehensive work of the European
Academy for Environmental Medicine (EUROPAEM) EMF
working group that has resulted in safety recommendations,
which are free from the ICNIRP shortcomings (50). Recently, the
International Guidelines on Non-Ionising Radiation (IGNIR)
have accepted EUROPAEM safety recommendations (91). The
Bioinitiative group has recommended similar safety standards
based on non-thermal EMF effects (92). WHO and all nations
should adopt the EUROPAEM/Bioinitiative/IGNIR safety
recommendations, supported by the majority of the scientific
community, instead of the obsolete ICNIRP standards.
In conclusion, it is important that all experts evaluating
scientific evidence and assessing health risks from RF radia-
tion do not have COIs or bias. Being a member of ICNIRP and
being funded by the industry directly, or through an industry-
funded foundation, constitute clear COIs. Furthermore, it is
recommended that the interpretation of results from studies on
health effects of RF radiation should take sponsorship from the
telecom or other industry into account. It is concluded that the
ICNIRP has failed to conduct a comprehensive evaluation of
health risks associated with RF radiation. The latest ICNIRP
publication cannot be used for guidelines on this exposure.
Acknowledgements
The authors would like to thank Mr. Reza Ganjavi for valuable
comments.
Funding
No funding was received.
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ONCOLOGY LETTERS 20: 15, 2020
9
Availability of data and materials
Data sharing is not applicable to this article, as no datasets
were generated or analyzed during the present study.
Authors' contributions
LH and MC contributed to the conception, design and writing
of the manuscript. Both authors read and approved the final
manuscript.
Ethics approval and consent to participate
Not applicable.
Patient consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
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83. Di Ciaula A: Towards 5G communication systems: Are there
health implications? Int J Hyg Environ Health 221: 367-375, 2018.
84. Russell CL: 5 G wireless telecommunications expansion:
Public health and environmental implications. Environ Res 165:
484-495, 2018.
85. Hedendahl LK, Carlberg M, Koppel T and Hardell L: Measurements
of radiofrequency radiation with a body-borne exposimeter in
Swedish schools with Wi-Fi. Front Public Health 5: 279, 2017.
86. Council of Europe: The potential dangers of electromagnetic
fields and their effect on the environment. Resolution 1815, 2011.
http://assembly.coe.int/nw/xml/XRef/Xref-XML2HTML-en.asp?fileid
=17994. Accessed July 6, 2020.
87. EMFscientist: Welcome to EMFscientist.org. https://www.
emfscientist.org/. Accessed July 6, 2020.
88. Koppel T, Ahonen M, Carlberg M, Hedendahl LK and Hardell L:
Radiofrequency radiation from nearby mobile phone base
stations-a case comparison of one low and one high exposure
apartment. Oncol Lett 18: 5383-5391, 2019.
89. Hardell L, Carlberg M, Hedendahl LK, Koppel T and Ahonen M:
Environmental radiofrequency radiation at the Järntorget Square in
Stockholm Old Town, Sweden in May, 2018 compared with results
on brain and heart tumour risks in rats exposed to 1.8 GHz base
station environmental emissions. World Acad Sci J 1: 47-54, 2019.
90. Gulati S, Yadav A, Kumar N, Kanupriya, Aggarwal NK, Kumar R
and Gupta R: Effect of GSTM1 and GSTT1 polymorphisms on
genetic damage in humans populations exposed to radiation from
mobile towers. Arch Environ Contam Toxicol 70: 615-625, 2016.
91. International Guidelines on Non-Ionising Radiation: Guidelines.
IGNIR's latest independent guidelines on EMF exposure are
available now to download and use. https://ignir.org/?page_id=8.
Accessed July 6, 2020.
92. Bioinitiative: Bioinitiative 2012. A rationale for biologically-
based exposure standards for low-intensity electromagnetic
radiation. https://bioinitiative.org/. Accessed July 6, 2020.
93. Swedish Radiation Safety Authority: Publications. https://www.
stralsakerhetsmyndigheten.se/en/publications/?area=Magnetf%
c3%a4lt+och+tr%c3%a5dl%c3%b6s+teknik. Accessed July 6,
2020.
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Structure and Membership. https://www.icnirp.org/en/about-
icnirp/structure-membership/index.html. Accessed July 6, 2020.
95. International Telecommunication Union: van DEVENTER
Tahera Emilie. https://www.itu.int/en/ITU-T/Workshops-and-
Seminars/emf/201307/Pages/vanDEVENTERTaheraEmilie.aspx.
Accessed July 6, 2020.
This work is licensed under a Creative Commons
Attribution-NonCommercial-NoDerivatives 4.0
International (CC BY-NC-ND 4.0) License.
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INSURANCE FOR ARCHITECTS & ENGINEERS
ProSurance
TM
A&E
Policy Document
Contents
Preamble
Insuring Clauses
How Much We Will Pay
Your Deductible
Definitions
Exclusions
General Conditions
Statutory Conditions
Privacy Notice
Ontario Commercial Liability Notice
Complaints Procedure
Subscription Notice
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2012 CFC Underwriting Ltd, All Rights Reserved
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CFC Underwriting Limited
85 Gracechurch Street
London EC3V 0AA
United Kingdom
T: +44 (0) 207 220 8500
F: +44 (0) 207 220 8501
E: [email protected]
W: www.cfcunderwriting.com
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PREAMBLE
This Policy is a contract of insurance between you and us. Your Policy contains all the details of the cover that we provide, subject always to our
receipt of the Premium. This Policy consists of and must be read together with the Declarations and any Endorsements. This Policy is not complete
unless it is signed and a Declarations page is attached.
The Sections of this policy are identified by BLUE LINES across the page with WHITE UPPER CASE PRINT. Clause headings in blue UPPER CASE
PRINT are for information only and do not form part of the cover given by this Policy. Other terms in bold lower case print are defined terms and
have a special meaning as set forth in the DEFINITIONS section and elsewhere. Words stated in the singular shall include the plural and vice versa.
However, this protocol does not apply to the STATUTORY CONDITIONS and subsequent Sections.
IMPORTANT: INSURING CLAUSES 1 and 2 provide cover on a claims made basis. Under these INSURING CLAUSES a claim must be
first
made
against the company named as the Insured in the Declarations or any subsidiary during the period of the policy and notified to us during the period of
the policy to be covered.
In consideration of the Premium and in reliance upon the information that you have provided to us prior to commencement of this insurance and
which is deemed to form the basis of this insurance:
1
INSURING CLAUSES
INSURING CLAUSE 1: ERRORS & OMISSIONS
SECTION A: PROFESSIONAL LIABILITY
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim
first
made against the company named as the Insured in the
Declarations or any subsidiary and notified to us during the period of the
policy arising out of any:
a)
negligent act, error or omission, negligent misstatement or negligent
misrepresentation;
b) breach of any contractual term implied by law concerning necessary
quality, safety or
fitness,
or your duty to use reasonable care and
skill;
c) breach of warranty of authority, breach of duty, breach of trust,
breach of confidence, misuse of information or breach of privacy;
d) libel, slander or defamation;
e) dishonesty of your directors, partners, officers or employees
provided that we maintain all rights of subrogation to recover such
legal costs and expenses from any director, partner, officer or
employee if they are found guilty of such a dishonest act; or
other act, error or omission giving rise to civil liability to your clients
f)
but not any breach of contract save as specified above;
committed by you or on your behalf in the course of your business
activities. We will also pay costs and expenses on your behalf.
b)
any enforcement action in connection with the containment, clean-
up, removal or treatment of such pollution or contamination.
We will also pay costs and expenses on your behalf.
SECTION E: LOSS OF DOCUMENTS
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim
first
made against the company named as the Insured in the
Declarations or any subsidiary and notified to us during the period of the
policy arising out of destruction of, damage to, loss or mislaying of your
documents or documents in your care, custody or control. We will also
pay costs and expenses on your behalf.
SECTION F: COMPUTER VIRUS AND HACKING
ATTACK
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim
first
made against the company named as the Insured in the
Declarations or any subsidiary and notified to us during the period of the
policy as a direct result of:
a)
any third parties’
financial
losses arising directly from a hacking attack
or virus that has emanated from or passed through your computer
systems, or
b) any third parties’
financial
losses arising directly from their inability
to access your computer systems in the way in which you have
authorised them to as a direct result of your computer systems’
failure or impairment due to a hacking attack or virus, or
c) any third parties’
financial
losses arising directly from the loss or theft
of your data or data for which you are responsible or held to be
responsible arising directly from a hacking attack or virus.
We will also pay costs and expenses on your behalf.
SECTION B: BREACH OF CONTRACT
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim by a client
first
made against the company named as the Insured
in the Declarations or any subsidiary and notified to us during the period
of the policy arising out of any breach of client contract. We will also pay
costs and expenses on your behalf.
SECTION G: LOSS MITIGATION
We agree to pay any reasonable costs necessarily incurred by you with
our prior written consent in respect of measures taken by you for the
sole purpose of avoiding or mitigating a claim or potential claim for which
you would be entitled to indemnity under INSURING CLAUSE 1 of this
Policy had such measures not been taken.
SECTION C: INTELLECTUAL PROPERTY RIGHTS
INFRINGEMENT
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim
first
made against the company named as the Insured in the
Declarations or any subsidiary and notified to us during the period of the
policy arising out of your infringement of any intellectual property right
in the course of your business activities. We will also pay costs and
expenses on your behalf.
SECTION H: PAYMENT OF WITHHELD FEES
We agree to pay your withheld fees with our prior written consent in the
event that your client brings or threatens to bring a claim against you that
would be covered under INSURING CLAUSE 1, SECTIONS A or B for
an amount greater than your withheld fees if you attempt to recover the
withheld fees from them. Prior to payment of your withheld fees you must
obtain written confirmation from your client that they will not bring a
claim against you if you agree not to pursue them for your withheld fees
and provide it to us.
SECTION D: POLLUTION LIABILITY
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim
first
made against the company named as the Insured in the
Declarations or any subsidiary and notified to us during the period of the
policy arising out of:
a)
pollution or contamination of the atmosphere, or of any water, land,
buildings or other property;
ALL SECTIONS
We will not make any payment on your behalf under any SECTION of
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Authority
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this INSURING CLAUSE in respect of any claim arising directly or
indirectly out of injury or damage:
a)
from products or workmanship; or
b) that did not occur directly as a result of your business activities.
We will make these payments regardless of fault.
2
INSURING CLAUSE 7: COMMERCIAL PROPERTY
We agree to reimburse you up to the amount insured shown in the
Declarations for:
a) the cost of repairing damage occurring during the period of the
policy to your office buildings, including landlord’s
fixtures
and
fittings,
walls, gates and fences, yards, car parks and pavements,
piping, ducting, cables, wires and associated control gear and
accessories on the premises and extending to the public mains but
only to the extent of your responsibility;
b) damage occurring during the period of the policy to contents of
every description contained in your office;
c) damage occurring during the period of the policy to contents of
every description kept at the home of your directors, officers,
partners or employees in the course of your business activities;
d) damage occurring during the period of the policy to contents of
every description temporarily elsewhere, including while in transit;
e) the necessary and reasonable costs you incur following damage
occurring during the period of the policy to glass which belongs to
you or for which you are legally responsible for:
i)
temporary boarding up;
ii) repair of window frames or removal or replacement of
fixtures
and
fittings
in the course of replacing the glass;
iii) replacement lettering or other ornamental work and alarm foil
on glass;
f)
damage occurring during the period of the policy to money held in
the course of your business activities:
in the office during business hours, in transit or in a Bank Night Safe;
g)
h) in the office outside business hours in a locked safe;
i)
at the home of your directors, officers, partners or employees;
j)
damage occurring during the period of the policy to the personal
belongings of your employees or visitors to the office provided they
are not covered under any other insurance;
k) the reasonable cost of compiling the documents, books of account,
drawings, card index systems or other records including
film,
tape,
disc, drum, cell or other magnetic recording or storage media for
electronic data processing that you need to continue your business
activities if these items have been lost or distorted as a direct result
of damage covered under this INSURING CLAUSE;
the costs you incur to replace locks and keys necessary to maintain
l)
the security of your office or safes following theft of keys involving
force and violence occurring during the period of the policy;
m) the amount of any rent for the office which you are legally obliged
to pay for any period during which the office or any part of it is
unusable as a result of damage covered under this INSURING
CLAUSE.
We also agree to pay:
a) costs and expenses on your behalf;
b) compensation as shown in the Declarations if any of your directors,
officers, partners or employees who are aged between 16 and 70 on
the Inception Date shown in the Declarations suffers an injury in the
course of your business activities in a robbery or attempted robbery
and suffers:
death, permanent total disablement, loss of a limb or loss of
i)
sight as a direct result of the injury within one year of the date
of its occurrence;
ii) temporary total disablement. The compensation for temporary
total disablement will be the amount shown in the Declarations
per week, for a maximum of 104 weeks.
However, we will not pay compensation under more than one heading in
the Declarations for the same injury.
INSURING CLAUSE 2: EMPLOYEE BENEFITS LIABILITY
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim
first
made against the company named as the Insured in the
Declarations or any subsidiary and notified to us during the period of the
policy arising out of any negligent act, error or omission committed by
you or on your behalf in the administration of your employee benefit
program. We will also pay costs and expenses on your behalf.
Furthermore, we agree to pay on your behalf any costs and expenses
necessarily incurred with our prior written consent in respect of measures
taken by you with the object of avoiding or mitigating a claim for which
you would be entitled to indemnity hereunder had such measures not
been taken.
INSURING CLAUSE 3: THIRD PARTY LIABILITY
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim arising out of accidental injury or damage occurring during the
period of the policy in the course of your business activities. We will also
pay costs and expenses on your behalf.
However, we will not make any payment on your behalf under this
INSURING CLAUSE in respect of any claim:
a) which is covered under INSURING CLAUSE 1, or would be covered
under INSURING CLAUSE 1 but for the exhaustion of the limit of
liability or aggregate limit of liability of INSURING CLAUSE 1;
b) arising directly or indirectly out of any product.
INSURING CLAUSE 4: PRODUCTS LIABILITY
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim arising out of accidental injury or damage occurring during the
period of the policy in the course of your business activities in connection
with any product. We will also pay costs and expenses on your behalf.
However, we will not make any payment on your behalf under this
INSURING CLAUSE in respect of any claim which is covered under
INSURING CLAUSE 1, or would be covered under INSURING CLAUSE
1 but for the exhaustion of the limit of liability or aggregate limit of liability
of INSURING CLAUSE 1.
INSURING CLAUSE 5: TENANTS’ LEGAL LIABILITY
We agree to pay on your behalf all sums which you become legally obliged
to pay (including liability for claimants’ costs and expenses) as a result of
any claim arising out of accidental damage to premises leased to, hired by,
on loan to or held in trust by you or otherwise in your care, custody or
control occurring during the period of the policy in the course of your
business activities. We will also pay costs and expenses on your behalf.
However, we will not make any payment on your behalf under this
INSURING CLAUSE in respect of any claim:
a) which is covered under INSURING CLAUSE 1, or would be covered
under INSURING CLAUSE 1 but for the exhaustion of the limit of
liability or aggregate limit of liability of INSURING CLAUSE 1;
b) arising directly or indirectly out of any product.
INSURING CLAUSE 6: MEDICAL EXPENSES
We agree to pay medical expenses for injury caused by an accident
occurring during the period of the policy:
on premises you own or rent;
a) on ways next to premises you own or rent; or
b) because of your business activities;
provided that:
c) the injured person, at the time of the accident, is not entitled to
benefits under any workers compensation or disability benefits law
or similar law; and
d) the medical expenses are incurred and notified to us within one year
of the date of the accident; and
e) the injured person submits to examination, at our expense, by
physicians of our choice as often as we reasonably require.
INSURING CLAUSE 8: BUSINESS INTERRUPTION
We agree to reimburse you up to the amount insured shown in the
Declarations for your loss of income, extra expense, loss of research and
development expenditure , project delay costs and accounts receivable
resulting solely and directly from an interruption to your business activities
caused by:
a) insured damage to your office or contents of every description or
to any other property used by you at your office;
b) insured damage to property in the vicinity of your office which
prevents or hinders your access to your office;
c) insured damage at the premises of one of your suppliers, other than
a supplier of water, gas, electricity or telephone services;
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2012 CFC Underwriting Ltd, All Rights Reserved
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d)
e)
failure in the supply of water, gas, electricity, or telephone services
to your office for more than 24 consecutive hours caused by insured
damage to any property;
your inability to use your office due to restrictions imposed by a
public authority following:
i)
ii)
iii)
iv)
a murder or suicide;
an occurrence of a notifiable human disease;
injury traceable to food or drink consumed at your office;
vermin or pests at your office.
3
HOW MUCH WE WILL PAY
The maximum amount payable by us for all claims, losses, damage, costs
and expenses and medical expenses shall not exceed the amounts shown
in the Declarations in respect of each INSURING CLAUSE unless limited
below.
However, solely with respect to any claims under this Policy that shall and
must be governed by Quebec law on the scope of our liability, we agree
to pay costs and expenses in addition to the Limits of Liability stated in
the Declarations.
Where more than one claim or loss arises from the same original cause
or single source or event all such claims or losses shall be deemed to be
one claim or loss and only one limit of liability shall be payable in respect
of the aggregate of all such claims or losses.
Where cover is provided under multiple SECTIONS of INSURING
CLAUSE 1 only one Limit of Liability shall be payable in respect of that
claim.
In respect of INSURING CLAUSES 1 to 5 we may at any time pay to you
in connection with any claim the amount of the aggregate limit of liability
or limit of liability (after deduction of any amounts already paid). Upon
such payment being made we shall relinquish the conduct and control of
and be under no further liability in connection with such claim except for
the payment of costs and expenses incurred prior to the date of such
payment (unless the aggregate limit of liability or limit of liability is stated
to be inclusive of costs and expenses).
In respect of INSURING CLAUSE 7 only:
At our option, we will pay for any damaged property on the following
a)
basis:
i)
for the office, the cost of rebuilding or replacing the damaged
property;
for contents of every description, the cost of repair or
replacement as new.
If, at the time the damage occurs, the amount insured is less than
85% of the total value of the office or contents of every description
insured, the amount we will pay will be reduced in the same
proportion as the amount insured bears to the total value of the
office or contents of every description insured.
The amount insured for the office and contents of every description
will be adjusted monthly in line with any increase in nationally
published indices. We will not reduce the amount insured without
your consent.
ii)
b)
c)
In respect of INSURING CLAUSE 8 the amount we will pay will be:
a) the difference between your actual income during the indemnity
period and the income it is estimated you would have earned during
that period or, if this is your
first
trading year, the difference between
your income during the indemnity period and during the period
immediately prior to the loss, less any savings resulting from the
reduced costs and expenses you pay out of your income during the
indemnity period; and
b) any additional costs and expenses;
c) any project delay costs during the indemnity period, including the
total value of any milestone payments that were due in the indemnity
period but will no longer be received by you either during the
indemnity period or at any point in the future due to permanent
termination of the project;
d) any research and development expenditure irrevocably lost during
the indemnity period; and
e) any accounts receivable, provided you keep a record of all amounts
owed to you and keep a copy of the record away from your office.
YOUR DEDUCTIBLE
We shall only be liable for that part of each and every claim, loss or
medical expenses (which for the purpose of this clause shall be deemed
to include all costs and expenses incurred) which exceeds the amount of
the Deductible stated in the Declarations. Where more than one claim,
loss or medical expenses arises from the same original cause or single
source or event all such claims, losses or medical expenses shall be
deemed to be one claim, loss or medical expenses and only one
Deductible will apply.
If any expenditure is incurred by us which by virtue of this clause is your
responsibility then you shall reimburse such amount to us on our request
or where possible we will deduct such amount from any payment we make
to you.
DEFINITIONS
1. “Accounts receivable”
means:
all sums due to you from customers, provided you are unable
a)
to effect collection thereof as the direct result of insured
damage to records of accounts receivable;
b) interest charges on any loan to offset impaired collections
pending repayment of such sums made uncollectible by such
insured damage;
c) collection expense in excess of normal collection cost and
made necessary because of insured damage.
2. “Administration”
means:
a) counseling employees, including their dependants and
beneficiaries, with respect to your employee benefit program;
b) handling records in connection with your employee benefit
program;
c) effecting enrolment or termination of any employee’s
participation in a plan included in your employee benefit
program;
d)
interpreting your employee benefit program.
3. “Aggregate limit of liability”
means the maximum amount payable as stated in the Declarations
by us in respect of all claims, or in respect of all accidents giving rise
to medical expenses.
4. “Amount insured”
means the maximum amount payable by us as shown in the
Declarations in respect of each of INSURING CLAUSES 7 and 8.
The amount applies to each incident of loss or damage occurring
during the period of the policy provided always that after the
first
incident of loss or damage you comply with our recommendations
to prevent any further incidents of loss or damage.
5. “Breach of client contract”
means your unintentional breach of a written contract relating to
the performance of your business activities for a client.
6. “Business activities”
means:
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a)
b)
in respect of INSURING CLAUSE 1, the business activities as
stated in the Declarations.
in respect of all other INSURING CLAUSES, the business
activities as stated in the Declarations and shall include, for the
purpose of those business activities:
i)
the ownership, repair and maintenance of your property;
ii) provision and management of canteen, social, sports and
welfare organisations for the benefit of your directors,
officers, partners or employees and medical,
fire fighting,
and security services;
iii) attendance at conferences and tradeshows as either an
exhibitor or visitor.
c)
interest on that part of any judgment we pay that accrues
after entry of the judgment and before we have paid,
offered to pay, or deposited in court the part of the
judgment that is within the limit of liability.
in respect of INSURING CLAUSES 7 and 8, the costs and
expenses incurred by you or on your behalf in establishing that
you have sustained a loss or damage and the quantum of such
loss or damage or the costs and expenses incurred by you or
on your behalf in mitigating any such loss or damage.
in respect of INSURING CLAUSE 7 only, the necessary and
reasonable costs and expenses you incur to remove debris
from the premises or the area immediately adjacent, following
damage covered under this INSURING CLAUSE.
iii)
4
d)
7. “Claim”
means a demand received by you for money or services, including
the service of suit or institution of arbitration proceedings. “Claim”
shall also mean a threat or initiation of a suit seeking injunctive relief
(meaning a temporary restraining order or a preliminary or
permanent injunction).
8. “Client”
means any third party with whom you have a written or implied
contract in place for the supply of your business activities in return
for a fee.
9. “Contents of every description”
means the contents of your office used in connection with your
business activities which are owned by you or for which you are
legally responsible, including:
a)
computer and ancillary equipment (including monitors,
keyboards, printers and software), television and video
equipment, photographic, photocopying, surveying and
telecommunications equipment;
b) documents, briefs, manuscripts, plans, business books,
computers systems records and programs;
c) goods held in trust, stock and samples;
d) wines, spirits and tobacco kept for entertainment purposes;
e) works of art or precious metals;
f)
fixed
glass in windows, doors and fanlights, glass showcases,
glass shelves, mirrors and sanitary
fixtures
and
fittings;
heating oil for the office contained in
fixed
tanks in the open
g)
at the address shown in the Declarations;
h) tenant’s improvements, decorations,
fixtures
and
fittings
including, if attached to the building, external signs, aerials and
satellite dishes;
i)
pipes, ducting, cables, wires and associated control equipment
at the address shown in the Declarations and extending to the
public mains.
“Contents of every description” does not include money or the
personal belongings of your employees or visitors to the office.
10. “Costs and expenses”
means:
a)
in respect of INSURING CLAUSES 1 (SECTIONS A to F only)
and 2,
i)
your legal costs and expenses in the defence or
settlement of any claim made against you, and
ii) your legal costs and expenses in the defence of any
criminal claim made against you, provided that we
maintain all rights of subrogation to recover such legal
costs and expenses from any director, officer, partner or
employee if they are found guilty of such a criminal act,
and
iii) the cost of bonds to release attachments but without any
obligation to furnish these bonds, and
iv) interest on that part of any judgment we pay that accrues
after entry of the judgment and before we have paid,
offered to pay, or deposited in court the part of the
judgment that is within the limit of liability.
b) in respect of INSURING CLAUSES 3 to 5,
i)
your legal costs and expenses in the defence or
settlement of any claim made against you, and
ii) the cost of bonds to release attachments but without any
obligation to furnish these bonds, and
Subject to all costs and expenses being incurred with the Claims
Managers’ written consent (such consent not to be unreasonably
withheld).
If costs and expenses are shown in the Declarations to be in addition
to the aggregate limit of liability or limit of liability in respect of any
of INSURING CLAUSES 1 to 5, and if a payment in excess of the
amount of indemnity available hereunder has to be made to dispose
of any claim or number of claims, our liability for such costs and
expenses shall be such proportion thereof as the amount of
indemnity available hereunder bears to the amount required to
dispose of such claim or claims.
Costs and expenses are always included in the amount insured in
respect of INSURING CLAUSES 7 and 8.
11. “Damage/damaged”
means direct physical damage to, or destruction of, or loss of
possession of, or loss of use of, tangible property. In respect of
INSURING CLAUSES 1, 3 and 4 damage does not include damage
to or destruction of, or loss of possession of, or loss of use of, or
corruption of, data.
12. “Documents”
means deeds, wills, agreements, maps, plans, records, books, letters,
certificates, forms, computer programmes or information stored,
written or punched into card or tape or magnetic discs or tapes or
any other data media and documents of any nature whatsoever,
whether written, printed or reproduced by any other method (other
than bearer bonds, coupons, banks notes, currency notes and
negotiable instruments).
13. “Employee”
means any person employed by the company named as the Insured
in the Declarations, or any subsidiary. Employee does not include
any director, officer or partner of the company named as the Insured
in the Declarations, or any subsidiary.
14. “Employee benefit program”
means group automobile insurance, group homeowners insurance,
group life insurance, group dental insurance, group health insurance,
profit sharing plans, pension plans, early retirement offerings,
employee investment subscription plans, Workers’ Compensation,
Unemployment Insurance, Social Security, Disability Benefit
Insurance, travel, savings or vacation plans or any similar benefit
programs.
15. “Extra expense”
means the necessary and reasonable extra costs and expenses you
incur in order to continue your business activities during the
indemnity period.
16. “Hacking attack”
means any malicious or unauthorised electronic attack including but
not limited to any fraudulent electronic signature, brute force attack,
phishing, denial of service attack, that has been initiated by any third
parties or by any employees and that is designed to damage, destroy,
corrupt, overload, circumvent or impair the functionality of
computer systems, software and ancillary equipment.
17. “Income”
means your total income from your business activities.
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18. “Indemnity period”
means the period beginning at the date of the damage, or the date
the restriction is imposed, and lasting for the period during which
your income or expenditure is affected as a result of such damage
or restriction, but for no longer than the number of months shown
in the Declarations.
19. “Injury”
means:
a)
in respect of INSURING CLAUSE 1 death, bodily injury, mental
injury, illness or disease;
b) in respect of all other INSURING CLAUSES:
death, bodily injury, mental injury, illness, disease, shock,
i)
mental anguish or humiliation; and
ii) false arrest, detention or imprisonment; and
iii) malicious prosecution; and
iv) wrongful entry into, or eviction of a person from, a room,
dwelling or premises that the person occupies.
20. “Insured damage”
means damage to property provided that:
the damage is covered under INSURING CLAUSE 7; or
a)
b) an insurer has paid the claim, or has agreed to pay the claim,
under any other insurance covering such damage.
21. “Intellectual property right”
means any intellectual property right including but not limited to
trademarks, trade secrets, broadcasting rights, domain names,
metatags and copyrights but does not include patents.
22. “Limit of liability”
means the maximum amount payable by us as stated in the
Declarations in respect of each claim or loss, or in respect of each
accident giving rise to medical expenses.
23. “Loss of a limb”
means loss by physical separation of a hand at or above the wrist, of
a foot at or above the ankle, and includes total and irrecoverable
loss of use of a hand, arm or leg.
24. “Loss of sight”
means total and irrecoverable loss of sight.
25. “Loss”
means direct
financial
loss sustained by you.
26. “Money”
means cash, bank and currency notes, cheques, travellers’ cheques,
postal orders, money orders, crossed bankers’ drafts, current
postage stamps, savings stamps and certificates, trading stamps, gift
tokens, customer redemption vouchers, company sales vouchers,
credit card counterfoils, travellers tickets and contents of franking
machines, all belonging to you.
27. “Medical expenses”
means reasonable expenses for:
a)
first
aid administered at the time of an accident;
b) necessary medical, surgical, x ray and dental services, including
prosthetic devices;
c) necessary ambulance, hospital, professional nursing and funeral
services.
28. “Office”
means the office space (including any outbuildings) you occupy at the
address shown in the Declarations as more fully described in the
application form.
29. “Period of the policy”
means the period between the Inception Date shown in the
Declarations and the Expiry Date shown in the Declarations or until
the Policy is cancelled in accordance with
GENERAL
CONDITION
10 of this Policy.
30. “Permanent total disablement”
means disablement which entirely prevents the injured person from
attending to any business or occupation for which he is reasonably
suited by training, education or experience for 24 calendar months
and at the expiry of that period being beyond hope of improvement.
31. “Project delay costs”
means any additional costs and expenses incurred by you as a direct
result of a delay to a project, including the interest charges incurred
from any reasonable loan required as a result of a delayed milestone
payment.
32. “Product”
means any tangible property (including containers, packaging, labelling
or instructions, but explicitly excluding any software, data, or source
code) after it has left your custody or control which has been
designed, specified, formulated, manufactured, constructed, installed,
sold, supplied, distributed, treated, serviced, altered, processed,
cleaned, renovated or repaired by you or on your behalf in the
course of your business activities.
33. “Research and development expenditure”
means your expenditure on research and development less the cost
of reusable materials consumed for the purposes of the research and
development.
34. “Subsidiary”
means any company which the company named as the Insured in the
Declarations controls through:
a)
holding 50% or more of the voting rights, or
b) having the right to appoint or remove 50% or more of its board
of directors; or
c) controlling alone, pursuant to a written agreement with other
shareholders or members, 50% or more of the voting rights
therein.
35. “Temporary total disablement”
means disablement which entirely prevents the injured person from
attending to his business or occupation.
36. “Third party”
means any person or company who is not a director, officer, partner
or employee of the company named as the Insured in the
Declarations, or any subsidiary.
37. “Virus”
means any malicious software code including but not limited to any
logic bomb, Trojan horse or worm that has been introduced by any
third parties or by any employees and that is designed to damage,
destroy, corrupt, overload, circumvent or impair the functionality of
computer systems, software and ancillary equipment.
38. “We/our/us”
means the Underwriters named in the Declarations.
39. “Withheld fees”
means any contractually due fee that your client refuses to pay you,
but excludes any part of the fee that represents your profit or mark-
up or liability for taxes.
40. “Workmanship”
means any physical workmanship in manufacture, fabrication,
construction, erection, installation, assembly, alteration, servicing,
remediation, repair, demolition or disassembly (including any
materials, parts or equipment furnished in connection therewith) by
you.
41. “Wrongful act”
means any act or event the subject of INSURING CLAUSE 1 of this
Policy for which you have purchased coverage.
42. “You/your”
means:
a)
the company named as the Insured in the Declarations, or any
subsidiary, and
b) any past, present or future employee, trainee, director, officer
or partner of the company named as the Insured in the
Declarations or any subsidiary.
5
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Authority
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EXCLUSIONS
We will not
a)
make any payment on your behalf for any claim, or
b) incur any costs and expenses, or
c) reimburse you for any loss, damage, legal expenses, fees or
costs sustained by you, or
d) pay any medical expenses:
9. Double insurance
for which you are entitled to indemnity under any other insurance
except for:
a)
any additional sum which is payable over and above such other
insurance, or
b) any contribution that we are obliged to make by law and that
contribution shall be in proportion to the respective limits of
liability or amounts insured of the Policies.
6
EXCLUSIONS RELATING TO OTHER INSURANCES:
1. Marine and aviation
arising directly or indirectly from the ownership, possession or use
by you or on your behalf of any aircraft, hovercraft, offshore
installation, rig, platform or watercraft.
2. Auto
arising directly or indirectly from the ownership, possession or use
by you or on your behalf of any motor vehicle or trailer other than
injury or damage:
a)
caused by the use of any tool or plant forming part of or
attached to or used in connection with any motor vehicle or
trailer;
b) occurring beyond the limits of any carriageway or thoroughfare
and caused by the loading or unloading of any motor vehicle
or trailer;
c) arising out of the use of any motor vehicle or trailer
temporarily in your custody or control for the purpose of
parking;
provided always that we will not make any payment on your behalf
or incur any costs and expenses in respect of any legal liability for
which compulsory insurance or security is required by legislation or
for which a government or other authority has accepted
responsibility.
3. Project-specific insurance
arising out of any projects for which you have purchased project
specific insurance.
4. Product guarantee
for costs incurred in the repair, alteration, reinstatement, inspection,
reconditioning or replacement of any product or part thereof and
any
financial
loss consequent upon the necessity for such repair,
alteration, reinstatement, inspection, reconditioning or replacement,
other than in respect of INSURING CLAUSE 1 when you are legally
obliged to pay these sums to a client.
5. Product recall
arising directly or indirectly from the recall of any product or part
thereof except for claims made under INSURING CLAUSE 1 where
you are legally liable for these costs to a third party as the direct
result of a wrongful act committed or alleged to have been
committed by you.
6. Employment practices
arising out of or resulting from any employer-employee relations,
policies, practices, acts, omissions, any actual or alleged refusal to
employ any person, or misconduct with respect to employees.
7. Employers’ liability
arising directly or indirectly out of injury to your directors, officers,
partners or employees.
However, this EXCLUSION shall not apply to employees on whose
behalf contributions are required to be made by you under the
provisions of any Workers’ Compensation Law in respect of whom
liability has been denied by any Workers’ Compensation authority.
8. Directors’ and Officers’
arising out of any personal liability incurred by your directors or
officers when they are acting in that capacity or managing you, or
arising from any statement, representation or information regarding
your business contained within any accounts, reports or
financial
statements.
EXCLUSIONS RELATING TO THE CONDUCT OF
YOUR BUSINESS:
10. Benefit laws
arising directly or indirectly out of your failure to comply with the
mandatory provisions of any law concerning workers compensation,
unemployment insurance, social security, disability benefits or
pension benefits.
11. Circumstances known at inception
arising out of any circumstances or occurrences which could give
rise to a claim, loss or damage under this Policy or any accidents
giving rise to medical expenses of which you are aware, or ought
reasonably to be aware, prior to the Inception Date of this Policy,
whether notified under any other insurance or not.
12. Computer failure
in respect of INSURING CLAUSES 7 and 8 only, arising directly or
indirectly from loss or distortion of your data or damage to your
electrical or mechanical plant resulting from a failure of your
computer or ancillary equipment (including monitors, keyboards,
printers or software), television or video equipment, photographic,
photocopying, surveying or telecommunications equipment.
However, we will reimburse you up to the amount insured for
damage occurring during the period of the policy to your office
computer and ancillary equipment, but only if your office computer
and ancillary equipment is subject to a manufacturer’s guarantee or
a maintenance contract providing free parts and labour in the event
of a breakdown.
13. Contractual
fines
and penalties
for
fines
and penalties arising from your breach of contract, including
any liquidated damages, service credits or associated penalties arising
from your failure to perform under a service level agreement
14. Employee benefit program advice
arising directly or indirectly from:
a)
advice given to any person to participate or not to participate
in any plan included in your employee benefit program;
b) the failure of any investment to perform as represented by you.
15. ERISA
arising out of or resulting from your acts related to any pension,
healthcare, welfare, profit sharing, mutual or investment plans, funds
or trusts; or any violation of any provision of the Employee
Retirement Income Security Act of 1974, or any amendment to the
Act or any violation of any regulation, ruling or order issued pursuant
to the Act.
16. Failure to ensure feasibility of contracts
arising from any contract where before entering into or amending
the contract you failed to take reasonable steps to ensure that you
could fulfil all your obligations in accordance with the terms of the
contract.
17. Faulty workmanship
arising from damage to your property or office caused directly or
indirectly by misuse, inadequate or inappropriate maintenance, faulty
workmanship, defective design, the use of faulty materials or whilst
being cleaned, worked on or maintained.
18. Hazardous devices
arising directly or indirectly from any product which with your
knowledge is intended for incorporation into the structure,
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machinery or controls of any aircraft, other aerial device, military
vehicle, hovercraft, waterborne craft or any medical equipment.
19. Legal Action
where action for damages is brought in a court of law outside the
territories specified in the Declarations, or where action is brought
in a court of law within those territories to enforce a foreign
judgement whether by way of reciprocal agreement or otherwise.
20. Limiting recovery rights
arising directly or indirectly out of your failure to take reasonable
steps to ensure that our rights of recovery against any third party
are not unduly restricted or
financially
limited by a specific term in
any contract or agreement.
21. Patents
arising out of the actual or alleged infringement of any patent or
inducing the infringement of any patent.
22. Retroactive Date
in respect of INSURING CLAUSES 1 and 2 only, arising out of any
actual or alleged wrongful act or negligent act, error or omission
committed before the date specified as the Retroactive Date in the
Declarations.
23. RICO
for or arising out of any actual or alleged violation of the Organised
Crime Control Act of 1970 (commonly known as the Racketeer
Influenced and Corrupt Organisation Act or RICO), as amended, or
any regulation promulgated thereunder or any similar federal, state
or local law, whether such law is statutory, regulatory or common
law.
24. SEC
for or arising out of the actual or alleged violation of the Securities
Act of 1933, the Securities Exchange Act of 1934, or any similar state
or federal law, or any amendment to the above laws or any violation
of any order, ruling or regulation issued pursuant to the above laws.
25. Unjust enrichment
in respect of INSURING CLAUSE 1 only, for that part of any claim
that results in you being in a better
financial
position as a direct result
of your wrongful act than you would have been if you had not
committed the wrongful act.
26. Water ingress (applicable to British Columbia only)
arising out of, or relating directly or indirectly to, in whole or in part,
the infiltration of precipitation into the building envelope of a building
located in the Province of British Columbia, or into a multi-unit
building located in the Province of British Columbia.
For the purposes of this exclusion the following definitions are added
to the Policy:
Multi-unit building means a building containing more than one unit,
whether that unit is used for residential, industrial or any other
purpose.
Building envelope means the assemblies, components, and materials
of a building which are intended to separate and protect the interior
space of a building from the adverse effects of exterior climactic
conditions.
Infiltration of precipitation means, but is not limited to, the actual,
alleged, threatened, or possible infiltration, migration, presence,
accumulation, condensation or dispersal of water or moisture on,
in, or into the building envelope.
27. Wilful or dishonest acts of directors
in respect of INSURING CLAUSES 1 and 2 only, arising out of any
wilful, malicious, reckless or dishonest act or omission by any
director, partner or officer of the company named as the Insured in
the Declarations or any subsidiary, unless such person had already
ceased to be a director, partner or officer of the company named as
the Insured in the Declarations and all subsidiaries at the time of
their
first
wilful, malicious, reckless or dishonest act or omission, or
unless specifically covered under INSURING CLAUSE 1 SECTION
A (e). We will not provide any cover for any director, partner or
officer of the company named as the Insured in the Declarations or
any subsidiary who commits, condones or ignores any dishonesty.
7
GENERAL INSURANCE EXCLUSIONS:
28. Antitrust
for or arising out of any actual or alleged antitrust violation, restraint
of trade, unfair competition, false, deceptive or unfair trade practices,
violation of consumer protection laws or false or deceptive
advertising unless insurable under the applicable law.
29. Asbestos
arising from or contributed to by the manufacturing, mining, use,
sale, installation, removal, distribution of or exposure to asbestos,
materials or products containing asbestos, or asbestos
fibres
or dust,
unless arising directly from a wrongful act committed by you:
a)
on or after 1st January 1990, or
b) on or after the date specified as the Retroactive Date in the
Declarations,
c) whichever is the later, in the course of your business activities.
30. Associated companies
a) in respect of any claim made by any company
firm
or
partnership in which the company named as the Insured in the
Declarations has an executive or
financial
interest, unless such
claim emanates from an independent third party; or
b) in respect of any claim made by any company
firm
partnership
or individual which has an executive or
financial
interest in the
company named as the Insured in the Declarations or any
subsidiary, unless such claim emanates from an independent
third party; or
c) arising out of or resulting from any of your activities as a
trustee, partner, officer, director or employee of any employee
trust, charitable organization, corporation, company or
business other than that of the company named as the Insured
in the Declarations or any subsidiary; or
d) in respect of any claim made by or on behalf of the company
named as the Insured in the Declarations or any subsidiary.
31. Earthquake
in respect of INSURING CLAUSES 7 and 8 only, caused by
earthquake, except for:
a) ensuing loss or damage which results directly from
fire,
explosion, smoke or leakage from
fire
protective equipment;
or
b) ensuing damage to contents of every description while in
transit.
32. Electromagnetic
fields
directly or indirectly arising out of, resulting from or contributed to
by
electromagnetic
fields,
electromagnetic
radiation,
electromagnetism, radio waves or noise.
33. Flood
in respect of INSURING CLAUSES 7 and 8 only, caused by
flood,
including waves, tides, tidal waves, or the rising of, the breaking out,
or the overflow, of any body of water whether natural or manmade,
but this EXCLUSION does not apply to:
a) ensuing loss or damage which results directly from
fire,
explosion, smoke or leakage from
fire
protective equipment;
or
b) ensuing damage to contents of every description while in
transit.
34. Fines
for
fines,
penalties, civil or criminal sanctions and for punitive,
multiple or exemplary damages unless insurable under the applicable
law.
35. Insolvency
arising out of or relating directly or indirectly from your insolvency
or bankruptcy, or the insolvency or bankruptcy of any third party.
Furthermore, no coverage is provided under INSURING CLAUSE 8
if you become insolvent or bankrupt.
36. Land or water
arising directly or indirectly from damage to land or water within or
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below the boundaries of any land or premises presently or at any
time previously owned or leased by you or otherwise in your care,
custody or control.
37. Miscellaneous property exclusions
in respect of INSURING CLAUSES 7 and 8 only, arising directly or
indirectly from:
a)
wear and tear, inherent defect, rot, vermin or infestation, or
any gradually operating cause;
b) dryness or humidity, being exposed to light or extreme
temperatures, unless the damage is caused by storm or
fire;
c) coastal or river erosion;
d) theft from an unattended vehicle unless the item is out of sight;
e) frost, other than damage due to water leaking from burst pipes
forming part of the permanent internal plumbing provided the
office is occupied and in use;
f)
arising directly or indirectly from unexplained loss or
disappearance or inventory shortage of your property;
g)
a hacking attack or virus.
38. Nuclear
arising directly or indirectly from or contributed to by :
a)
ionising radiations or contamination by radioactivity from any
nuclear fuel or from any nuclear waste from the combustion
of nuclear fuel;
b) the radioactive, toxic, explosive or other hazardous properties
of any explosive nuclear assembly or nuclear component
thereof.
39. Pollution
arising directly or indirectly out of :
a)
pollution or contamination of the atmosphere, or of any water,
land, buildings or other property;
b) any enforcement action in connection with the containment,
clean-up, removal or treatment of such pollution or
contamination;
but this EXCLUSION shall not apply in respect of :
i)
INSURING CLAUSE 1, SECTION D; or
ii) INSURING CLAUSES 7 and 8 to the backing up of sewers,
sumps, septic tanks or drains.
40. Toxic mould / fungus
arising directly or indirectly from any loss, injury, damage, costs or
expenses, including, but not limited to, losses, damage, costs or
expenses related to, arising from or associated with clean-up,
remediation, containment, removal or abatement, caused directly or
indirectly, in whole or in part, by:
a) any fungus, mould, mildew or yeast, or
b) any spore or toxins created or produced by or emanating from
such fungus, mould, mildew or yeast, or
c) any substance, vapour, gas, or other emission or organic or
inorganic body or substance produced by or arising out of any
fungus, mould, mildew or yeast, or
d) any material, product, building component, building or
structure, or any concentration of moisture, water or other
liquid within such material, product, building component,
building or structure, that contains, harbours, nurtures, or acts
as a medium for any fungus, mould, mildew, yeast or spore or
toxins emanating therefrom,
regardless of any other cause, event, material, product or building
component that contributed concurrently or in any sequence to that
loss, injury, damage, cost or expense.
However, this EXCLUSION shall not apply in respect of INSURING
CLAUSE 1 where the loss, injury, damage, costs or expenses arose
directly from a wrongful act committed by you in the course of your
business activities.
For the purposes of this EXCLUSION the following definitions are
added to the Policy:
Fungus includes, but is not limited to, any plants or organisms
belonging to the major group Fungi, lacking chlorophyll, and including
moulds, rusts, mildews, smuts and mushrooms.
Mould includes, but is not limited to, any superficial growth produced
on damp or decaying organic matter or on living organisms, and fungi
that produced moulds.
Spore means any dormant or reproductive body produced by or
arising from or emanating out of any fungus, mould, mildew, plants,
organisms or microorganisms.
41. Trade Debt
arising out of or in connection with any trading losses or trading
liabilities incurred by any business managed or carried on by you, or
any loss of your profit arising from the loss of any client, account or
business.
42. War and terrorism
directly or indirectly caused by, resulting from or in connection with
any of the following regardless of any other cause or event
contributing concurrently or in any other sequence to the claim, loss,
damage, costs and expenses or medical expenses;
a)
war, invasion, acts of foreign enemies, hostilities or warlike
operations (whether war be declared or not), civil war,
rebellion, insurrection, civil commotion assuming the
proportions of or amounting to an uprising, military or usurped
power; or
b) any act of terrorism.
For the purpose of this EXCLUSION an act of terrorism means an
act, including but not limited to the use of force or violence or the
threat thereof, of any person or groups of persons, whether acting
alone or on behalf of or in connection with any organisations or
governments, committed for political, religious, ideological or similar
purposes including the intention to influence any government or to
put the public, or any section of the public, in fear.
This EXCLUSION also excludes claims, losses, damage, costs and
expenses or medical expenses of whatsoever nature directly or
indirectly caused by, resulting from or in connection with any action
taken in controlling, preventing, suppressing or in any way relating
to a) or b) above.
This EXCLUSION does not apply to any claim or loss arising directly
from a hacking attack or virus.
8
GENERAL CONDITIONS
1. What you must do in the event of a claim or loss
Should any director, partner, or senior executive officer of the
company named as the Insured in the Declarations and any subsidiary
become aware of any claim, loss or damage or of any situation that
could give rise to a claim or loss or should an allegation, complaint
or claim be made or intimated against you, the following obligations
must be complied with by you:
a)
You must not admit liability for or settle or make or promise
any payment in respect of any claim, loss or damage which may
be covered under this Policy. Neither must you incur any costs
or expenses in connection with such a claim, loss or damage
without our written consent. However, you should arrange for
any urgent repairs following damage covered under INSURING
CLAUSE 7 to be done immediately. Before any other repair
work begins we have the right to inspect your damaged
property. We will notify you if we intend to do this.
The Claims Managers, as specified in the Declarations, must be
notified as soon as is reasonably possible if during the period
of the policy:
i)
you suffer any loss or damage that could be covered by
this Policy or any allegation, complaint or claim is made
or intimated against you, whether verbal or made in
writing.
ii) any director, partner, or senior executive officer of the
company named as the Insured in the Declarations and
any subsidiary become aware of the intention of any
person to make a complaint allegation or claim against
you, whether verbal or in writing. Once notice has been
b)
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iii)
iv)
made to us, we will regard any subsequent claim that may
arise as notified under this Policy.
you become aware of an action of yours that could give
rise to a loss, allegation, complaint or claim being made
or intimated against you. Once notice has been made we
will regard any subsequent claim that may arise as notified
under this Policy.
you discover reasonable cause for suspicion of fraud or
dishonesty whether this could give rise to a claim under
this Policy or not and we shall not be liable under this
Policy for any claim or loss sustained in consequence of
any fraudulent or dishonest act or omission committed
after the date of such discovery.
or any other claims under this insurance and the Policy will be
treated as if it had not been effected.
4. Agreement to pay claims
We have the right and duty to take control of and conduct in your
name the investigation settlement or defence of any claim. We shall
also pay on your behalf costs and expenses incurred with our prior
written consent (subject to the Limits of Liability and applicable
Deductible shown in the Declarations) provided that we shall not
a) pay for the costs and expenses of any part of a claim that is
not covered by this Policy.
b) incur any costs and expenses in the defence of any claim unless
there is a reasonable prospect of success, taking into account
the commercial considerations of the costs of defence.
We shall always endeavour to settle any claim through negotiation,
mediation or some other form of alternative dispute resolution and
shall pay on your behalf the amount so agreed by us and the claimant.
If we cannot settle by such means, we shall pay the amount which
you are found liable to pay either in court or through arbitration
proceedings, subject always to the limit of liability shown in the
Declarations.
If you refuse to consent to a settlement that we recommend and
that the claimant will accept, you must then defend, investigate or
settle the claim at your own expense. As a consequence of your
refusal, our liability for any claim shall not be more than the amount
that we could have settled the claim for had you consented, plus any
costs and expenses incurred prior to the date of such refusal.
5. Innocent non-disclosure
We will not seek to avoid the Policy or reject any claim on the
grounds of non-disclosure or misrepresentation except where the
non-disclosure or misrepresentation was reckless or fraudulent or
you failed to conduct a full inquiry prior to providing the information
that forms the basis of this insurance. In the event that we seek to
avoid the Policy or reject any claim on this basis the burden of
proving otherwise rests solely with you.
6. Your duty to advise us of changes
If you become aware that any of the information that you have given
us in the Application Form or elsewhere in connection with your
application for this insurance has materially changed then you must
advise us as soon as is practicable. In this event, we reserve the right
to amend the terms, conditions or premium of the Policy.
7. Risk management conditions
If we attach any additional conditions to your Policy regarding any
risk survey or risk management timetable or any other similar
conditions then it is your responsibility to ensure that these
conditions are complied with by the deadlines shown in the
conditions.
8. Our rights of recovery
If any payment is made under this Policy in respect of a claim, loss or
damage and there is available to us any of your rights of recovery
against any other party then we maintain all such rights of recovery.
We shall not exercise these rights against any past, present or future
employee, director, officer or partner of the company named as the
Insured in the Declarations or any subsidiary, unless such payment
is in respect of any wilful, malicious or dishonest acts or omissions.
You must do nothing to impair any rights of recovery. At our request
you will bring proceedings or transfer those rights to us and help us
to enforce them. Any recoveries shall be applied as follows:
a)
first,
to us up to the amount of our payment on your behalf
including costs and expenses;
b) then to you as recovery of your Deductible or other amounts
paid as compensation or costs and expenses.
9. Waiver of subrogation
Notwithstanding
GENERAL CONDITION
8 above we agree to
waive our rights of subrogation against a responsible third party
client of yours but only if you and your client have entered into a
contract that contains a provision requiring us to do this.
9
We have nominated the Claims Managers to accept notice on our
behalf.
Due to the nature of the coverage offered by this Policy, any
unreasonable delay by any director, partner, or senior executive
officer of the company named as the Insured in the Declarations and
any subsidiary in notifying the Claims Managers of (i), (ii), (iii) or (iv)
above could lead to the size of the claim, loss or damage increasing
or to our rights being restricted. We shall not be liable for that
portion of any claim that is due to any unreasonable delay in any
director, partner, or senior executive officer of the company named
as the Insured in the Declarations and any subsidiary notifying the
Claims Managers of any claim, loss or damage in accordance with
this
GENERAL CONDITION.
c)
We will expect you to provide us with full and accurate
information about any matter that you notify to us under your
obligations set out above. Once notice has been made you
must give the Claims Managers all the assistance and
information that is reasonably required. You must follow their
advice and do anything that they reasonably require you to do
to avoid, minimise, settle or defend any claim, loss or damage.
If you think a crime has been committed you must report it to the
appropriate law enforcement authorities. You must also permit the
Claims Managers and any other parties that are appointed by the
Claims Managers to notify the appropriate law enforcement
authorities of any claim, loss or damage where this action is deemed
necessary, and you must comply with the advice given by such
authorities.
If any of your computer or ancillary equipment is lost or stolen while
it is temporarily removed from the office, we will not make any
payment unless you report the loss to the police within 48 hours
after you become aware of it.
2. Continuous cover
If you have neglected, through error or oversight only, to report a
claim made against you during the period of a previous renewal of
this Policy issued to you by us, then provided that you have
maintained uninterrupted insurance of the same type with us since
the expiry of that earlier Policy, then, notwithstanding EXCLUSION
11, we will permit the matter to be reported under this Policy and
will indemnify you, provided that:
a) the indemnity will be subject to the applicable aggregate limit
of liability or limit of liability of the earlier Policy under which
the matter should have been reported or the aggregate limit
of liability or limit of liability of the current Policy, whichever is
the lower;
b) we may reduce the indemnity entitlement by the monetary
equivalent of any prejudice which has been suffered as a result
of the delayed notification;
c) the indemnity will be subject in addition, to all of the terms,
CONDITIONS, DEFINITIONS and EXCLUSIONS, other than
the aggregate limit of liability or limit of liability, contained in
this current Policy.
3. Fraudulent claims
If you notify us of any claim knowing that claim to be false or
fraudulent in any way, we shall have no responsibility to pay that claim
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2012 CFC Underwriting Ltd, All Rights Reserved
CFC A&E CAN V1.7
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10. Cancellation
This Policy may be cancelled:
a)
by you at any time on request; or
b) by us if we give you 30 days written notice, or
c) by us if we give you 15 days written notice, should any amount
in default not be paid within 15 days of the due date shown in
the Debit Note that accompanies this Policy.
If you give us notice of cancellation in accordance with a) above, the
earned Premium shall be computed at pro rata to the number of
days that the Policy is in effect subject to a minimum amount of 30%
of the Premium.
If we give you notice of cancellation in accordance with b) or c)
above, the Premium shall be computed at pro rata to the number of
days that the Policy is in effect.
The Policy Administration Fee shall be deemed fully earned upon
inception of the Policy.
11. Prior subsidiaries
In respect of INSURING CLAUSE 1 only, should an entity cease to
be a subsidiary after the Inception Date of this Policy, cover in
respect of such entity shall continue as if it was still a subsidiary, until
the termination of this Policy, but only in respect of any claim or loss
that arises out of any act, error or omission committed by that entity
prior to the date that it ceased to be a subsidiary.
12. Mergers and acquisitions
During the period of the policy, if the company named as the Insured
in the Declarations or any subsidiary
a)
purchases assets or acquires liabilities from another entity in
an amount greater than 10% of the assets of the company
named as the Insured in the Declarations as listed in its most
recent
financial
statement; or
b) acquires another entity whose annual revenues are more than
10% of the annual revenues of the company named as the
Insured in the Declarations for their last completed
financial
year;
then you shall have no coverage under this Policy for any claim, loss
or damage that arises directly or indirectly out of the purchased or
acquired entity unless the company named as the Insured in the
Declarations gives us written notice prior to the purchase or
acquisition, obtains our written consent to extend coverage to such
additional entities, assets or exposures, and agrees to pay any
additional premium required by us.
If during the period of the policy the company named as the Insured
in the Declarations consolidates or merges with or is acquired by
another entity, then all coverage under this Policy shall terminate at
the date of the consolidation, merger or acquisition unless we have
issued an endorsement extending coverage under this Policy, and the
company named as the Insured in the Declarations has agreed to any
additional premium and terms of coverage required by us.
13. Extended reporting period
In respect of INSURING CLAUSES 1 and 2 only, an Extended
Reporting Period of 60 days following the Expiry Date as shown in
the Declarations shall be automatically granted hereunder at no
additional premium. Such Extended Reporting Period shall cover
claims
first
made and reported to us during this 60 day Extended
Reporting Period but only in respect of any act, error or omission
committed prior to the date of cancellation or non-renewal, and
subject to all other terms, conditions and exclusions of the policy.
No claim shall be accepted by us in this 60 day Extended Reporting
Period if you are entitled to indemnity under any other insurance,
or would have been entitled to indemnity under such insurance but
for the exhaustion thereof.
14. Optional extended reporting period
In respect of INSURING CLAUSES 1 and 2 only, in the event of:
a)
cancellation or non-renewal of this Policy by us, or
b) cancellation or non-renewal of this Policy by you because you
have ceased to trade as the direct result of the retirement or
death of all of your directors, officers or partners;
then you shall have the right, upon payment of the Optional
Extended Reporting Period Premium shown in the Declarations in
full and not proportionally or otherwise in part, to have issued an
endorsement providing a 365 day Optional Extended Reporting
Period from the cancellation or non-renewal date. Such Optional
Extended Reporting Period shall cover claims
first
made against the
company named as the Insured in the Declarations or any subsidiary
and notified to us during this Optional Extended Reporting Period
but only in respect of any claim arising out of any act, error or
omission committed prior to the date of cancellation or non-
renewal, and subject to all other terms, conditions and exclusions of
the policy.
In order for you to invoke the Optional Extended Reporting Period
option, the payment of the Optional Extended Reporting Period
Premium shown in the Declarations for this Optional Extended
Reporting Period must be paid to us within 15 days of the date of
the non-renewal or cancellation.
At the commencement of this Optional Extended Reporting Period
the entire premium shall be deemed earned and in the event that
you terminate the Optional Extended Reporting Period for any
reason prior to its natural expiration, we will not be liable to return
any premium paid.
The right to the Extended Reporting Period or the Optional
Extended Reporting Period shall not be available to you where:
Cancellation or non-renewal by us is due to non-payment of
a)
premium, or
b) Cancellation or non-renewal by us is due to your failure to pay
such amounts in excess of the applicable Limit of Liability or
within the amount of the applicable Deductible as is required
by this Policy in the payment of claims.
At the renewal of this Policy, our quotation of different premium,
Deductible or Limit of Liability or changes in policy language shall
not constitute non-renewal by us for the purposes of granting this
Optional Extended Reporting Period.
In no event shall the granting of the Extended Reporting Period or
the Optional Extended Reporting Period increase our Limit of
Liability, including costs and expenses, as shown in the Declarations.
15. Choice of law
This Policy shall be interpreted under, governed by and construed in
all respects in accordance with the law of the jurisdiction of the place
of registration of the company named as the Insured in the
Declarations and for this purpose, we and you agree to submit to
the exclusive jurisdiction of the courts within the territorial limits
and jurisdiction of the place of registration of the company named
as the Insured in the Declarations.
In any action to enforce our obligations under this Policy we can be
designated or named as “Lloyd’s Underwriters” and such designation
shall be binding on Lloyd’s Underwriters liable under this Policy as if
we had each been individually named as defendant. Service of such
proceedings may validly be made upon the Attorney In Fact in
Canada for Lloyd’s Underwriters, whose address for such service is
1155, rue Metcalfe, Suite 2220, Montreal, Quebec, H3B 2V6.
10
STATUTORY CONDITIONS
1. Misrepresentation
If a person applying for insurance falsely describes the property to
the prejudice of the Insurer, or misrepresents or fraudulently omits
to communicate any circumstance that is material to be made known
to the Insurer in order to enable it to judge of the risk to be
undertaken, the contract is void as to any property in relation to
which the misrepresentation or omission is material.
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2012 CFC Underwriting Ltd, All Rights Reserved
CFC A&E CAN V1.7
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2. Property of others
Unless otherwise specifically stated in the contract, the Insurer is not
liable for loss or damage to property owned by any person other than
the Insured, unless the interest of the Insured therein is stated in the
contract.
3. Change of interest
The Insurer is liable for loss or damage occurring after an authorized
assignment under the Bankruptcy Act or change of title by succession,
by operation of law, or by death.
4. Material change
Any change material to the risk and within the control and knowledge
of the Insured avoids the contract as to the part affected thereby,
unless the change is promptly notified in writing to the Insurer or its
local agent; and the Insurer when so notified may return the unearned
portion, if any, of the premium paid and cancel the contract, or may
notify the Insured in writing that, if he desires the contract to
continue in force, he must within
fifteen
(15) days of the receipt of
the notice, pay to the Insurer an additional premium; and in default
of such payment the contract is no longer in force and the Insurer
shall return the unearned portion, if any, of the premium paid.
5. Termination
1. This contract may be terminated:
a)
by the Insurer giving to the Insured
fifteen
(15) days’ notice
of termination by registered mail or
five
(5) days’ written
notice of termination personally delivered;
b) by the Insured at any time on request.
2. Where this contract is terminated by the Insurer:
a)
the Insurer shall refund the excess of premium actually paid
by the Insured over the pro rata premium for the expired
time, but in no event, shall the pro rata premium for the
expired time be less than any minimum retained premium
specified; and
b) the refund shall accompany the notice unless the premium
is subject to adjustment or determination as to amount, in
which case the refund shall be made as soon as practicable.
3. Where this contract is terminated by the Insured, the Insurer
shall refund as soon as practicable the excess of the premium
actually paid by the Insured over the short rate premium for the
expired time, but in no event shall the short rate premium for
the expired time, be deemed to be less than any minimum
retained premium specified.
4. The refund may be made by money, postal or express company
money order or cheque payable at par.
5. The
fifteen
(15) days mentioned in clause (1) (a) of this condition
commences to run on the day following the receipt of the
registered letter at the post office to which it is addressed.
6. Requirements after loss
1. Upon the occurrence of any loss of or damage to the insured
property, the lnsured shall, if the loss or damage is covered by
the contract, in addition to observing the requirements of
Conditions 9, 10 and 11:
a)
forthwith give notice thereof in writing to the Insurer;
b) deliver as soon as practicable to the Insurer a proof of loss
verified by a statutory declaration,
i)
giving a complete inventory of the destroyed and
damaged property and showing in detail quantities,
costs, actual cash value and particulars of amount of
loss claimed,
ii) stating when and how the loss occurred, and if
caused by
fire
or explosion due to ignition, how the
fire
or explosion originated, so far as the Insured
knows or believes,
iii) stating that the loss did not occur through any wilful
act or neglect or the procurement, means or
connivance of the Insured,
iv) showing the amount of other insurance and the
names of other Insurers,
v) showing the interest of the lnsured and of all others
in the property with particulars of all liens,
encumbrances and other charges upon the property,
showing any changes in title, use, occupation,
location, possession or exposures of the property
since the issue of the contract,
vii) showing the place where the property insured was
at the time of loss,
c) if required give a complete inventory of undamaged
property and showing in detail quantities, cost, actual cash
value;
d) if required and if practicable, produce books of account,
warehouse receipts and stock lists, and furnish invoices and
other vouchers verified by statutory declaration, and
furnish a copy of the written portion of any other contract.
2. The evidence furnished under Clauses 1 (c) and (d) of this
condition shall not be considered proofs of loss within the
meaning of Statutory Conditions 12 and 13.
7. Fraud
Any fraud or wilfully false statement in a statutory declaration in
relation to any of the above particulars, vitiates the claim of the
person making the declaration.
8. Who may give notice and proof
Notice of loss may be given, and proof of loss may be made, by the
agent of the Insured named in the contract in case of absence or
inability of the Insured to give the notice or make the proof, and
absence or inability being satisfactorily accounted for, or in the like
case, or if the Insured refuses to do so, by a person to whom any part
of the insurance money is payable.
9. Salvage
1. The Insured in the event of any loss or damage to any property
insured under the contract, shall take all reasonable steps to
prevent further damage to any such property so damaged and to
prevent damage to other property insured hereunder including,
if necessary, its removal to prevent damage or further damage
thereto.
2. The Insurer shall contribute pro rata towards any reasonable and
proper expenses in connection with steps taken by the Insured
and required under subparagraph 1 of this condition according to
the respective interests of the parties.
10. Entry, control, abandonment
After loss or damage to insured property, the Insurer has an
immediate right of access and entry by accredited agents sufficient to
enable them to survey and examine the property, and to make an
estimate of the loss or damage, and after the Insured has secured the
property, a further right of access and entry sufficient to enable them
to make appraisal or particular estimate of the loss or damage, but
the Insurer is not entitled to the control or possession of the insured
property, and without the consent of the Insurer there can be no
abandonment to it of insured property.
11. Appraisal
In the event of disagreement as to the value of the property insured,
the property saved or the amount of the loss, those questions shall
be determined by appraisal as provided under the Insurance Act
before there can be any recovery under this contract whether the
right to recover on the contract is disputed or not, and independently
of all other questions. There shall be no right to an appraisal until a
specified demand therefor is made in writing and until after proof of
loss has been delivered.
12. When loss payable
The loss is payable within sixty (60) days after completion of the proof
of loss, unless the contract provides for a shorter period.
13. Replacement
1. The Insurer, instead of making payment, may repair, rebuild, or
replace the property damaged or lost, giving written notice of its
intention so to do within thirty days after receipt of the proofs
of loss.
2. In that event the Insurer shall commence to so repair, rebuild or
replace the property within forty-five (45) days after receipt of
the proofs of loss, and shall thereafter proceed with all due
diligence to the completion thereof.
vi)
11
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2012 CFC Underwriting Ltd, All Rights Reserved
CFC A&E CAN V1.7
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14. Action
Every action or proceeding against the Insurer for the recovery of
any claim under or by virtue of this contract is absolutely barred
unless commenced within one year next after the loss or damage
occurs.
15. Notice
Any written notice to the Insurer may be delivered at, or sent by
registered mail to, the chief agent or head office of the Insurer in the
12
PRIVACY NOTICE
By purchasing insurance from certain Underwriters at Lloyd's, London
(“Lloyd's”), a customer provides Lloyd’s with his or her consent to the
collection, use and disclosure of personal information, including that
previously collected, for the following purposes:
• the communication with Lloyd’s policyholders
• the underwriting of policies
• the evaluation of claims
• the detection and prevention of fraud
• the analysis of business results
• purposes required or authorised by law
For the purposes identified, personal information may be disclosed to
Lloyd’s related or affiliated organisations or companies, their
agents/mandataries, and to certain non-related or unaffiliated
organisations or companies.
Further information about Lloyd’s personal information protection policy
may be obtained from the customer's broker or by contacting Lloyd’s on
514 861 8361 or through [email protected].
ONTARIO COMMERCIAL LIABILITY NOTICE
Notice to Insureds:
Pursuant to the
Freedom Of Information And Protection Of Privacy Act, R.S.O. 1990,
c.F.31 (as amended)
Important
The notice below applies to insurance contracts containing non-
automobile legal liability coverages in provinces where statistical data
relating to such contracts must be reported to the Superintendent of
Insurance.
Legal authority for collection
Insurance Act, R.S.O. 1990, c.I.8, section 101(1).
Principal purpose for which personal informtion is intended to be used
Information collected by insurers from insureds or supplied to insurers
pertaining to the attached document will be used:
• to compile aggregate statistical data to be used in monitoring trends
in the insurance industry;
• to develop statistical exhibits to be used in monitoring the insurance
industry;
• to respond to requests for customized statistical information on the
insurance industry;
• to respond to inquiries on statistical information made to Office of
the Superintendent of Insurance; and
• to use and disclose such information for purposes which are
consistent with the previous clauses.
The Public Official who can answer questions about the collection is:
Manager, Statistical Services
Financial Services Commission of Ontario
5160 Yonge Street, 17th Floor
Box 85
North York, Ontario M2N 6L9
Telephone: (416) 250-7250
Fax: (416) 590-7070
FOI (11/1999)
COMPLAINTS PROCEDURE
If you have a complaint with any aspect of your Lloyd’s insurance, please
refer to the broker/agent who arranged your policy for you.
OR
You may contact the General Insurance OmbudService (GIO) who will
contact Lloyd’s on your behalf. The GIO can be reached at:
GIO - Atlantic Provinces
(902) 429-2730
Toll-free: 1-800-565-7189
Website: www.gio-scad.org
GIO - British Columbia & Yukon
(604) 684-3635
Toll-free: 1-877-772-37777
Website: www.gio-scad.org
GIO - Ontario
(416) 362-9528
Toll-free: 1-800-387-2880
Website: www.gio-scad.org
GIO - Prairies, Northwest Territories & Nunavut
(780) 423-2212
Toll-free: 1-800-377-6378
Website: www.gio-scad.org
Province of Québec
GIO
(514) 288-6015
Toll-free: 1-800-361-5131
Website: www.gio-scad.org
OR
Autorité des marchés
financiers
(l’Autorité)
Québec City (418) 525-0311
Montréal
(514) 395-0311
Toll-free: 1-866-526-0311
E-mail:
[email protected]
GIO – Alberta
(780) 421-8181
Toll-free: 1-888-421-4212
Website: www.gio-scad.org
For more information or to submit the facts of your insurance-related
dispute, please visit the GIO website at www.gio-scad.org.
Should you be dissatisfied with the outcome of your broker’s resolution
or with the GIO’s / l’Autorité’s assistance, please submit your written
complaint to:
Lloyd’s Canada Inc.
Broker Management Services
1155 rue Metcalfe, Suite 2220
Montreal, Quebec H3B 2V6
Tel:
1-877-4LLOYDS
Fax:
(514) 861-0470
E-mail:
[email protected]
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2012 CFC Underwriting Ltd, All Rights Reserved
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Your written complaint will be forwarded to Lloyd’s Complaints
Department in London which ensures that Lloyd’s Underwriters and their
representatives deal with claims and complaints in an acceptable manner.
It acts as an impartial mediator. When undertaking a review this
Department takes account of general legal principles, good insurance
practice, and whether all events surrounding a given case have been
considered fairly.
If you are dissatisfied with Lloyd’s
final
letter, you may ask the GIO to
arrange for mediation. Mediation is not available until Lloyd’s has issued
its
final
letter of position on your complaint.
In Québec you may also avail yourself of the services of l’Autorité who
will study your
file
and may recommend mediation, if it deems this action
appropriate and if both parties agree to it.
GIO - Alberta can be contacted where a policyholder is not satisfied with
the basis on which a premium for basic coverage for a private passenger
vehicle was determined, or considers that an insurer, directly or indirectly,
has taken an adverse contractual action with respect to insurance for basic
coverage.
13
SUBSCRIPTION NOTICE
IN CONSIDERATION OF THE INSURED having paid or agreed to pay
each of the INSURERS named in the List of Subscribing Companies
forming part hereof, or to INSURERS whose names are substituted
therefor or added thereto by endorsement, hereinafter called “THE
INSURERS”, the Premium set against its name in the List of Subscribing
Companies (attached hereto),
THE INSURERS SEVERALLY AND NOT JOINTLY agree, each for the
Sum(s) Insured or Percentage(s) and for the Coverage(s) Insured set
against its name in the List of Subscribing Companies, and subject always
to the terms and conditions of this Policy, that if a loss occurs for which
insurance is provided by this Policy at any time while it is in force, they
will indemnify the INSURED against the loss so caused; the liability of
each insurer individually for such loss being limited to that proportion of
the loss payable according to the terms and conditions of this Policy which
the Sum Insured or the amount corresponding to the Percentage set
against its name in the List of Subscribing Companies, or such other sum
or percentage as may be substituted therefor by endorsement, bears to
the total of the sums insured or of the amounts corresponding to the
percentages of the sums insured respectively set out against the coverage
concerned on the Declarations page(s).
Wherever in this Policy, or in any endorsement attached hereto, reference
is made to “The Company”, “The Insurer”, “This Company”, “we”, “us”,
or “our”, reference shall be deemed to be made to each of the Insurers
severally.
This policy is made and accepted subject to the foregoing provisions, and
to the other provisions, stipulations and conditions contained herein,
which are hereby specially referred to and made a part of this Policy, as
well as such other provisions, agreements or conditions as may be
endorsed hereon or added hereto.
IN WITNESS WHEREOF THE INSURERS through their representative(s)
duly authorized by them for this purpose have executed and signed this
Policy.
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2012 CFC Underwriting Ltd, All Rights Reserved
CFC A&E CAN V1.7
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A&E
INSURANCE FOR ARCHITECTS & ENGINEERS
CFC Underwriting Limited
85 Gracechurch Street
London EC3V 0AA
United Kingdom
T: +44 (0) 207 220 8500
F: +44 (0) 207 220 8501
E: [email protected]
W: www.cfcunderwriting.com
CFC Underwriting Limited is Authorised and Regulated by the Financial
Conduct
Authority
©1999-2011 CFC Underwriting Ltd, All Rights Reserved
CFC A&E CAN V1.7
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See discussions, stats, and author profiles for this publication at:
https://www.researchgate.net/publication/279863242
Oxidative mechanisms of biological activity of low-intensity radiofrequency
radiation
Article  in  Electromagnetic
Biology and Medicine · July 2015
DOI: 10.3109/15368378.2015.1043557 · Source: PubMed
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including:
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National University for Food Technologies
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Indiana University Bloomington
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Sumy State University, Sumy, Ukraine
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ISSN: 1536-8378 (print), 1536-8386 (electronic)
Electromagn Biol Med, Early Online: 1–16
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2015 Informa Healthcare USA, Inc. DOI: 10.3109/15368378.2015.1043557
REVIEW ARTICLE
Oxidative mechanisms of biological activity of low-intensity
radiofrequency radiation
Igor Yakymenko
1
, Olexandr Tsybulin
2
, Evgeniy Sidorik
1
, Diane Henshel
3
, Olga Kyrylenko
4
and Sergiy Kyrylenko
5
1
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Institute of Experimental Pathology, Oncology and Radiobiology of NAS of Ukraine, Kyiv, Ukraine,
2
Department of Biophysics, Bila Tserkva National
Agrarian University, Bila Tserkva, Ukraine,
3
School of Public and Environmental Affairs, Indiana University Bloomington, Bloomington, IN, USA,
4
A.I.Virtanen Institute, University of Eastern Finland, Kuopio, Finland, and
5
Department of Structural and Functional Biology, University of
Campinas, Campinas, SP, Brazil
Abstract
This review aims to cover experimental data on oxidative effects of low-intensity radio-
frequency radiation (RFR) in living cells. Analysis of the currently available peer-reviewed
scientific literature reveals molecular effects induced by low-intensity RFR in living cells; this
includes significant activation of key pathways generating reactive oxygen species (ROS),
activation of peroxidation, oxidative damage of DNA and changes in the activity of antioxidant
enzymes. It indicates that among 100 currently available peer-reviewed studies dealing with
oxidative effects of low-intensity RFR, in general, 93 confirmed that RFR induces oxidative
effects in biological systems. A wide pathogenic potential of the induced ROS and their
involvement in cell signaling pathways explains a range of biological/health effects of low-
intensity RFR, which include both cancer and non-cancer pathologies. In conclusion, our
analysis demonstrates that low-intensity RFR is an expressive oxidative agent for living cells
with a high pathogenic potential and that the oxidative stress induced by RFR exposure should
be recognized as one of the primary mechanisms of the biological activity of this kind of
radiation.
Keywords
Cellular signaling, cancer, free radicals,
oxidative stress, radiofrequency radiation,
reactive oxygen species
History
Received 10 January 2015
Accepted 12 April 2015
Published online 7 July 2015
Introduction
Intensive development of wireless technologies during the last
decades led to a dramatic increase of background radio-
frequency radiation (RFR) in the human environment. Thus,
the level of indoor background RFR in industrialized
countries increased 5,000-fold from 1985 to 2005 (Maes,
2005). Such significant environmental changes may have a
serious impact on human biology and health. As a proof of
such impact, a series of epidemiological studies on the
increased risk of tumorigenesis in ‘‘heavy’’ users of wireless
telephony exists (Hardell et al., 2007, 2011; Sadetzki et al.,
2008; Sato et al., 2011). Some studies indicate that long-term
RFR exposure in humans can cause various non-cancer
disorders, e.g., headache, fatigue, depression, tinnitus, skin
irritation, hormonal disorders and other conditions (Abdel-
Rassoul et al., 2007; Buchner & Eger, 2011; Chu et al., 2011;
Johansson, 2006; Santini et al., 2002; Yakymenko et al.,
2011). In addition, convincing studies on hazardous effects of
RFR in human germ cells have been published (Agarwal
et al., 2009; De Iuliis et al., 2009).
All abovementioned studies dealt with the effects of low-
intensity RFR. This means that the intensity of radiation was
far below observable thermal effects in biological tissues, and
far below safety limits of the International Commissions on
Non-Ionizing Radiation Protection (ICNIRP) (ICNIRP,
1998). To date, molecular mechanisms of non-thermal effects
of RFR are still a bottleneck in the research on the biological/
health effects of low-intensity RFR, although recently many
studies have been carried out on metabolic changes in living
cells under low-intensity RFR, and comprehensive reviews
were published (Belyaev, 2010; Consales et al., 2012; Desai
et al., 2009; Yakymenko et al., 2011). In the present work, we
analyze the results of molecular effects of low-intensity RFR
in living cells and model systems, with a special emphasis on
oxidative effects and free radical mechanisms. It might seem
paradoxical that, despite being non-ionizing, RFR can induce
significant activation of free radical processes and overpro-
duction of reactive oxygen species (ROS) in living cells. We
believe that the analysis of recent findings will allow
recognition of a general picture of the potential health effects
of already ubiquitous and ever-increasing RFR.
Address correspondence to Prof. Igor Yakymenko, Laboratory of
Biophysics, Institute of Experimental Pathology, Oncology and
Radiobiology of NAS of Ukraine, Vasylkivska str. 45, Kyiv, 03022
Ukraine. E-mail: [email protected]
Radiofrequency radiation
RFR is a part of electromagnetic spectrum with frequencies
from 30 kHz to 300 GHz. RFR is classified as non-ionizing,
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which means that it does not carry sufficient energy for
ionization of atoms and molecules. A part of RFR with the
highest frequencies (300 MHz to 300 GHz) is referred to as
microwaves (MWs). MW is RFR with the highest energy,
which can potentially generate the highest thermal effects in
the absorbing matter.
The main indexes of RFR are (i) frequency (Hz); (ii) inten-
sity or power density (PD) of radiation (W/m
2
or
mW/cm
2
); (iii)
its modulated or non-modulated nature; and (iv) continuous or
discontinuous pattern of radiation. For the absorbed RFR
energy, a parameter of specific absorption rate (SAR) is used
(W/kg). The most common digital standard of RFR for mobile
communication is still GSM (Global System for Mobile
communication), which utilizes frequencies at about 850, 900,
1800 and 1900 MHz. This radiation is frequency modulated,
with channel rotation frequency of 217 Hz, and belongs to the
radiation of the pulsed mode (Hyland, 2000).
As to the international safety limits, the ICNIRP recom-
mendations restrict intensity of RFR to 450–1000
mW/cm
2
(depending on the frequency of radiation) and the SAR value
to 2 W/kg, as calculated for human heads and torsos (ICNIRP,
1998). These indexes were adopted by ICNIRP based on the
behavioral response of laboratory rats, which were exposed to
gradually increased intensities of RFR to determine the point
at which the animals became thermally distressed
(Gandhi et al., 2012).
Low-intensity RFR is referred to as radiation with
intensities which do not induce significant thermal effects in
biological tissues. Accordingly, any intensity of RFR under
the ICNIRP limits can be referred to as low-intensity. In this
paper we will analyze only the effects of low-intensity RFR.
Physical/biophysical effects of low-intensity RFR
in living cells
RFR, especially MW, can produce thermal effects in matter
due to interaction with charged particles, including free
electrons, ions or polar molecules, inducing their oscillations
in electromagnetic field. The thermal effect of MW can be seen
when warming food in the microwave. The effect strongly
depends on the intensity of radiation and is mostly negligible
under low-intensity RFR conditions. On the other hand, energy
of RFR/MW is insufficient not only for the ionization
of molecules, but even for activation of orbital electrons.
Hence, RFR was often assessed as a factor producing only
thermal effects. Nevertheless, evident biological effects of
low-intensity RFR promoted research on physical mechanisms
of non-thermal biological effects of this kind of radiation.
A biophysical model of a forced-vibration of free ions on
the surface of a cell membrane due to external oscillating
electromagnetic field (EMF) was proposed (Panagopoulos
et al., 2000, 2002). According to the authors, this vibration of
electric charges can cause disruption of the cellular electro-
chemical balance and functions.
A ‘‘moving charge interaction’’ model was proposed for
low-frequency EMF (Blank and Soo, 2001). The authors
explained activation of genes and synthesis of stress proteins
under EMF exposure due to interaction of the field with
moving electrons in DNA (Blank and Soo, 2001; Goodman
and Blank, 2002). They also demonstrated that EMF
increased electron transfer rates in cytochrome oxidase and
accelerated charges in the Na,K-ATPase reaction. Moreover,
they demonstrated acceleration of the oscillating Belousov–
Zhabotinski reaction in homogeneous solutions due to the
application of low-frequency EMF (Blank and Soo, 2003).
An ability of low-strength magnetic fields to trigger onset-
and offset-evoked potentials was demonstrated (Marino et al.,
2009). Effectiveness of a rapid magnetic stimulus (0.2 ms) has
led the authors to a conclusion on direct interaction between
the field and ion channels in plasma membrane. A plausible
mechanism of overproduction of free radicals in living cell
due to electron spin flipping in confined free radical pairs in
magnetic field of RFR was proposed (Georgiou, 2010).
A significant effect of low-intensity RFR on ferritin, an
iron cage protein present in most living organisms from
´
bacteria to humans, was revealed (Cespedes and Ueno, 2009).
Exposure of ferritin solution to low-intensity RFR signifi-
cantly, up to threefold, reduced iron chelation with ferrozine.
The authors explained that magnetic field of RFR plays a
principle role in the observed effect, and that this effect is
strongly non-thermal. The non-thermal mechanism of the
interaction of RFR magnetic fields with ferritin is supposedly
mediated by an inner super-paramagnetic nanoparticle
(9H
2
O
Â
5Fe
2
O
3
with up to 4500 iron ions), which is a
natural phenomenon intrinsic to the cells. It results in
reduction of input of iron chelates into the ferritin cage.
The authors underlined the potential role of ferritin malfunc-
tion for oxidative processes in living cell due to the
participation of Fe
2+
ions in the Fenton reaction, which
produces hydroxyl radicals. In this respect, it is interesting to
point to the results of an
in vitro
study with RFR exposure of
´
rat lymphocytes treated by iron ions (Zmyslony et al., 2004).
Although RFR exposure (930 MHz) did not induce detectable
intracellular ROS overproduction, the same exposure in the
presence of FeCl
2
in the lymphocyte suspensions induced a
significant overproduction of ROS.
Another set of studies indicates on a possibility of changes
in protein conformation under RFR exposure. Thus, low-
intensity 2.45 MHz RFR accelerated conformational changes
in
b-lactoglobulin
through excitation of so-called collective
intrinsic modes in the protein (Bohr and Bohr, 2000a, 2000b),
which suggests a principal ability of RFR to modulate the
non-random collective movements of entire protein domains.
Similarly, a frequency-dependent effect on intrinsic flexibility
in insulin structure due to applied oscillating electric field was
demonstrated (Budi et al., 2007). Moreover, macromolecular
structure of cytoskeleton was significantly altered in fibro-
blasts of Chinese hamster after the exposure to modulated
RFR of the GSM standard (Pavicic and Trosic, 2010). Thus, a
3 h exposure of fibroblasts to modulated RFR (975 MHz) led
to significant changes in the structure of microtubules and
actin microfilaments, which have polar cytoskeleton struc-
tures, while non-polar vimentin filaments reportedly stayed
unchanged. Taking into account an extensive regulatory
potential of cytoskeleton on cell homeostasis, these data could
obviously add to the nature of the biological effects of RFR.
It was shown that ornithine decarboxylase (ODC) can
significantly change its activity under low-intensity RFR
exposure (Byus et al., 1988; Hoyto et al., 2007; Litovitz et al.,
1993, 1997; Paulraj et al., 1999).
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In addition, so-called ‘‘calcium effects’’ under RFR
exposure in living cells have been demonstrated (Dutta
et al., 1989; Paulraj et al., 1999; Rao et al., 2008), which
include a significant increase in intracellular Ca
2+
spiking.
Taking into account that calcium is a ubiquitous regulator of
cellular metabolism, these data point to a possibility that non-
thermal RFR can activate multiple Ca
2+
-dependent signaling
cascades.
Finally, an ability of low-intensity MW to dissociate water
molecules was demonstrated in model experiments years ago
(Vaks et al., 1994). In these experiments, MW of 10 GHz with
radiated power 30 mW produced a significant level of H
2
O
2
in
deionized water (and also in MgSO
4
solution) under stable
temperature conditions. According to the authors, a kinetic
excitation of liquid water associates C(H
2
O) upon the
absorption of MW leads to subsequent viscous losses due to
friction between moving clusters of water molecules. It results
in partial irreversible decomposition of water, including
breaks of intramolecular bonds (H–OH) due to a mechan-
ochemical reaction, and generation of H

; OH

; H
+
and OH
À
groups. Among these, the hydroxyl radical (OH

) is the most
aggressive form of ROS, which can break any chemical bond
in surrounding molecules (Halliwell, 2007). The authors
assessed that this type of mechanochemical transformation in
water could be responsible for 10
À4
–10
À8
relative parts of the
total MW energy absorbed. Given the fact that the water
molecules are ubiquitous in living cells, even a subtle chance
for dissociation of water molecules under low-intensity
RFR exposure could have a profound effect on tissue
homeostasis. It is of note here that one OH

radical can
initiate irreversible peroxidation of many hundreds of macro-
molecules, e.g. lipid molecules (Halliwell, 1991). Taken
together, these data show that non-thermal RFR can be
absorbed by particular charges, molecules and cellular
structures, and in this way can potentially induce substantial
modulatory effects in living cell.
Generation of reactive oxygen species under RFR
exposure in living cells
NADH oxidase of cellular membrane was suggested as a
primary mediator of RFR interaction with living cells
(Friedman et al., 2007). Using purified membranes from
HeLa cells, the authors experimentally proved that the
exposure to RFR of 875 MHz, 200
mW/cm
2
for 5 or 10 min
significantly, almost threefold, increased the activity of
NADH oxidase. NADH oxidases are membrane-associated
enzymes that catalyze one-electron reduction of oxygen into
superoxide radical using NADH as a donor of electron, thus
producing powerful ROS. This enzyme has been tradition-
ally known due to its role in induction of oxidative burst in
phagocytes as a part of immune response. Yet, later the
existence of non-phagocytic NAD(P)H oxidases was
revealed in various types of cells, including fibroblasts,
vascular and cardiac cells (Griendling et al., 2000).
Obviously, the presence of superoxide-generating enzyme
in many types of non-phagocytic cells points to the
considerable regulatory roles of ROS in living cells. On
the other hand, an ability of low-intensity RFR to modulate
the activity of the NADH oxidase automatically makes this
factor a notable and potentially dangerous effector of cell
metabolism. Notably, the authors pointed out that the
acceptor of RFR is different from the peroxide-generating
NADPH oxidases, which are also found in plasma mem-
branes (Low et al., 2012).
The other powerful source of ROS in cells is mitochondrial
electron transport chain (ETC), which can generate super-
oxide due to breakdowns in electron transport (Inoue et al.,
2003). It was demonstrated that generation of ROS by
mitochondrial pathway can be activated under RFR exposure
in human spermatozoa (De Iuliis et al., 2009). The authors
revealed a dose-dependent effect of 1.8 GHz RFR exposure on
ROS production in spermatozoa, particularly in their
mitochondria. The significantly increased level of total ROS
in spermatozoa was detected under RFR with SAR
¼
1 W/kg,
which is below the safety limits accepted in many countries. It
was demonstrated recently in our laboratory that the exposure
of quail embryos
in ovo
to extremely low-intensity RFR
(GSM 900 MHz, 0.25
mW/cm
2
) during the initial days of
embryogenesis resulted in a robust overproduction of super-
oxide and nitrogen oxide radicals in mitochondria of embry-
onic cells (Burlaka et al., 2013). It is not clear yet which
particular part of ETC is responsible for the interaction with
RFR. To date, three possible sites of generation of superoxide
in ETC have been shown: the ETC complex I (Inoue et al.,
2003), complex II (Liu et al., 2002), and complex III (Guzy
and Schumacker, 2006). A significant inverse correlation
between mitochondrial membrane potential and ROS levels in
living cell was found (Wang et al., 2003). As the authors
underlined, such a relationship could be due to two mutually
interconnected phenomena: ROS causing damage to the
mitochondrial membrane, and the damaged mitochondrial
membrane causing increased ROS production.
In addition to the well-established role of the mitochondria
in energy metabolism, regulation of cell death is a second
major function of these organelles. This, in turn, is linked to
their role as the powerful intracellular source of ROS.
Mitochondria-generated ROS play an important role in the
release of cytochrome c and other pro-apoptotic proteins,
which can trigger caspase activation and apoptosis (Ott et al.,
2007). A few reports indicate on activation of apoptosis due to
low-intensity RFR exposure. In human epidermoid cancer KB
cells, 1950 MHz RFR induced time-dependent apoptosis (45%
after 3 h) that is paralleled by 2.5-fold decrease of the
expression of ras and Raf-1 and of the activity of ras and Erk-
1/2 (Caraglia et al., 2005). Primary cultured neurons and
astrocytes exposed to GSM 1900 MHz RFR for 2 h demon-
strated up-regulation of caspase-2, caspase-6 and Asc (apop-
tosis associated speck-like protein containing a card) (Zhao
et al., 2007). Up-regulation in neurons occurred in both "on"
and "stand-by" modes, but in astrocytes only in the "on"
mode. We should underline that, in that study an extremely
high biological sensitivity to RFR was demonstrated, as a cell
phone in the ‘‘stand-by’’ position emits negligibly low-
intensity of radiation (up to hundredths
mW/cm
2
).
Based on the analysis of available literature data, we
identified altogether 100 experimental studies in biological
models which investigated oxidative stress due to low-
intensity RFR exposures. From these 100 articles, 93 studies
(93%) demonstrated significant oxidative effects induced by
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I. Yakymenko et al.
Electromagn Biol Med, Early Online: 1–16
low-intensity RFR exposure (Table 1–3), while 7 studies (7%)
demonstrated the absence of significant changes (Table 4).
The total number includes 18
in vitro
studies, 73 studies in
animals, 3 studies in plants and 6 studies in humans. Majority
of the research was done on laboratory rats (58 studies, with
54 positive results), while 4 studies out of 6 in humans were
positive. From the
in vitro
studies, 17 were positive (94.4%),
including 2 studies on human spermatozoa and 2 studies on
human blood cells.
Most of the studies utilized RFR exposure in MW range,
including a use of commercial or trial cell phones as sources
of radiation. The power densities of RFR applied in positive
studies varied from 0.1
mW/cm
2
(Oksay et al., 2014) to
680
mW/cm
2
(Jelodar et al., 2013) and SAR values varied
from 3
mW/kg
(Burlaka et al., 2013) to the ICNIRP recom-
mended limit of 2 W/kg (Naziroglu et al., 2012a; Xu et al.,
2010). Exposure times in positive studies varied from 5 min
(Friedman et al., 2007) to 12.5 years, 29.6 h/month (Hamzany
et al., 2013).
The most often used indexes of oxidative stress analyzed in
the studies were ROS production, levels of lipid peroxidation
(LPO)/malondialdehyde (MDA), protein oxidation (PO),
nitric oxides (NO
x
), glutathione (GSH), activity of antioxidant
enzymes (superoxide dismutase (SOD), catalase (CAT),
glutathione peroxidase (GSH-Px)). It is important that some
studies directly pointed to induction of free radicals (super-
oxide radical, NO) as a primary reaction of living cells to
RFR exposure (Burlaka et al., 2013; Friedman et al., 2007).
As we pointed out earlier, direct activation of NADH oxidase
(Friedman et al., 2007) and the mitochondrial pathway of
superoxide overproduction (Burlaka et al., 2013; De Iuliis
et al., 2009) have been experimentally proven. Besides, a
significant overproduction of nitrogen oxide was revealed in
some studies (Avci et al., 2012; Bilgici et al., 2013; Burlaka
et al., 2013), although it is unclear whether an induction of
expression of NO-synthases or direct activation of the enzyme
took place. It is however clear that significantly increased
levels of these free radical species (superoxide and nitrogen
oxide) in cells due to RFR exposure result in an activation of
peroxidation and repression of activities of key antioxidant
enzymes. It is indicative that many studies demonstrated
effectiveness of different antioxidants to override oxidative
stress caused by RFR exposure. Such effects have been
reported for melatonin (Ayata et al., 2004; Lai and Singh,
1997; Oktem et al., 2005; Ozguner et al., 2006; Sokolovic
et al., 2008), vitamin E and C (Jelodar et al., 2013; Oral et al.,
2006), caffeic acid phenethyl ester (Ozguner et al., 2006),
selenium,
L
-carnitine (Turker et al., 2011) and garlic (Avci
et al., 2012; Bilgici et al., 2013).
It is worthwhile to emphasize a strict non-thermal
character of ROS overproduction under RFR exposure
described in the cited reports. As low as 0.1
mW/cm
2
intensity
of RFR and absorbed energy (specific absorption rate, SAR)
of 0.3
mW/kg
were demonstrated to be effective in inducing
significant oxidative stress in living cells (Burlaka et al.,
2013; Oksay et al., 2014). This observation is particularly
important as the modern international safety limits on RFR
exposure are based solely on the thermal effects of radiation
and only restrict RFR intensity to 450–1000
mW/cm
2
and
SAR to 2 W/kg (ICNIRP, 1998). Moreover, studies where
high (thermal) intensities of RFR have been used could not
reveal oxidative effects (Hong et al., 2012; Kang et al., 2013;
Luukkonen et al., 2009), which might point to the variety of
molecular mechanisms for different radiation intensities.
Taken together, the analysis of the contemporary scientific
literature on the biological effects of RFR persuasively proves
that the exposure to low-intensity RFR in living cells leads to
generation of significant levels of ROS and results in a
significant oxidative stress.
Oxidative damage of DNA under RFR exposure
To date more than hundred papers have been published on
mutagenic effects of RFR and most of them revealed signifi-
cant effects (Ruediger, 2009). There is a substantial number of
studies which demonstrated the formation of micronuclei
(Garaj-Vrhovac et al., 1992; Tice et al., 2002; Zotti-Martelli
et al., 2005) or structural anomalies of metaphase chromo-
somes (Garson et al., 1991; Kerbacher et al., 1990; Maes et al.,
2000) in living cells due to low-intensity RFR exposure.
However, majority of the studies on the mutagenic effects of
RFR successfully used a comet assay approach (Baohong et al.,
2005; Belyaev et al., 2006; Diem et al., 2005; Kim et al., 2008;
Lai and Singh, 1996; Liu et al., 2013a). Particular studies
identified specific marker of oxidative damage of DNA, 8-
hydroxy-2’-deoxyguanosine (8-OH-dG) (Burlaka et al., 2013;
De Iuliis et al., 2009; Guler et al., 2012; Khalil et al., 2012; Xu
et al., 2010). Thus, the level of 8-OH-dG in human
spermatozoa was shown to be significantly increased after
in vitro
exposure to low-intensity RFR (De Iuliis et al., 2009).
Likewise, we demonstrated that the exposure of quail embryos
in ovo
to GSM 900 MHz of 0.25
mW/cm
2
during a few days was
sufficient for a significant, two-threefold, increase of 8-OH-dG
level in embryonic cells (Burlaka et al., 2013).
It would be logical to assume that most mutagenic effects
due to the RFR exposure are caused by oxidative damage to
DNA, as the overproduction of ROS in living cells due to
RFR exposure was reliably documented. It is known that
superoxide itself does not affect DNA. The most aggressive
form of ROS, which is able to affect the DNA molecule
directly, is hydroxyl radical (Halliwell, 2007). The hydroxyl
radicals are generated in cell in the Fenton reaction (Fe
2+
+
H
2
O
2
-4 Fe
3+
+ OH

+ OH
À
) and in the Haber–Weiss
reaction (O
2
À
+ H
2
O
2
-4 O
2
+ OH

+ OH
À
) (Valko et al.,
2006). On the other hand, increased concentration of NO in
addition to superoxide in the RFR-exposed cells can lead to
the formation of other aggressive form of ROS, peroxynitrite
(ONOO
À
), which can also cause DNA damage (Valko et al.,
2006).
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Free radicals induced under the RFR exposure can
perturb cellular signaling
Taking into account the abovementioned data, we can state
that the exposure to RFR leads to overproduction of free
radicals/ROS in living cell. Certainly, free radicals can induce
harmful effects via direct damage due to oxidation of
biological macromolecules. To that, it becomes clear now-
adays that free radicals/ROS are an intrinsic part of the
cellular signaling cascades (Forman et al., 2014). Thus,
hydrogen peroxide appears as a second messenger both in
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RFR as a powerful oxidative agent
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Table 1. Publications which reported positive findings on oxidative stress caused by RFR exposure of cells
in vitro.
Biological system
exposed
Human spermatozoa
Rat astroglial cells
Human spermatozoa
HeLa membranes
Mouse embryonic
fibroblasts (NIH/3T3)
Cancer cell cultures
Human blood cells
Statistically significant effects
reported*
Increase in reactive oxygen species
(ROS) level, decrease in sperm
motility and viability.
Increase in ROS levels and DNA
fragmentation after exposure to
modulated RFR for 20 min.
Increased amounts of ROS.
Increased NADH oxidase activity.
Increased intracellular ROS levels.
Reference
(Agarwal et al., 2009)
(Campisi et al., 2010)
(De Iuliis et al., 2009)
(Friedman et al., 2007)
(Hou et al., 2014)
RFR exposure
Cell phone RFR, in talk mode,
for 1 h
900 MHz (continuous or modu-
lated), electric field 10 V/m,
for5; 10; 20 min
1.8 GHz, SAR
¼
0.4–27.5 W/kg
875 MHz, 200
mW/cm
2
, for 5 and
10 min
1800-MHz GSM-talk mode RFR,
SAR
¼
2 W/kg, intermittent
exposure (5 min on/10 min off)
for 0.5–8 h
900 MHz RFR, SAR
¼
0.36 W/kg,
for 1 h
Continuous wave or GSM
signal,SAR
¼
2 W/kg, for 30 or
45 min of continuous or 5 min
ON, 5 min OFF
Continuous wave, GSM speaking
only, GSM hearing only, GSM
talk, SARs of 0.5, 1.0, 1.5 and
2.0 W/kg.
1800 MHz, SAR
¼
1; 2 W/kg,5 min
ON, 10 min OFF for 24 h
900 MHz, SAR
¼
0.4 W/kg, for
1–8 h
1800 MHz, SAR
¼
1.6 W/kg, for
10, 30 and 60 min
(Kahya et al., 2014)
(Lantow et al., 2006a)
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(Lantow et al., 2006b)
Human Mono Mac 6
and K562 cells
GC-2 cells
Human blood mononuclear cells
Induced apoptosis effects through
oxidative stress, selenium counter-
acted the effects of RFR exposure.
After continuous or intermittent
GSMsignal a different ROS pro-
duction was detected in human
monocytes compared to sham.
The GSM-DTX signal at 2 W/kg
produced difference in free radical
production compared to sham.
In the 2 W/kg exposed cultures, the
level of ROS was increased.
The increased level of apoptosis
induced through the mitochondrial
pathway and mediated by activating
ROS and caspase-3.
ROS level increased after 10 min of
exposure. Decrease in ROS level
after 30-min treatment indicating
antioxidant defense mechanism
activation.
Lipid peroxide (LPO) levels were
increased at all exposure times.
The ROS and malondialdehyde
(MDA) levels were increased.
Increased level of nitric oxide (NO).
(Liu et al., 2013b)
(Lu et al., 2012)
(Marjanovic et al., 2014)
V79 cells
(Naziroglu et al., 2012b)
(Ni et al., 2013)
(Pilla, 2012)
HL-60 cells
Human lens epithelial cells
Neuronal cells and
human fibroblasts
HEK293T cells
2450 MHz, pulsed, SAR
¼
0.1–
2.5 W/kg,for 1; 2; 12 or 24 h
1800 MHz, SAR
¼
2; 3; 4 W/kg
27.12 MHz, pulsed, electric field
41 V/m, 2 min prior to lipo-
polysaccharide administration
or for 15 min
940 MHz, SAR
¼
0.09 W/kg, for
15, 30, 45, 60 and 90 min
(Sefidbakht et al., 2014)
(Xu et al., 2010)
´
(Zmyslony et al., 2004)
Primary cultured neurons
Rat lymphocytes
1800 MHz, pulsed, SAR
¼
2 W/kg,
for 24 h
930 MHz, PD of 500
mW/cm
2
,
SAR
¼
1.5 W/kg, for 5 and
15 min
ROS generation increased in the
30 min exposed cells. A sharp rise
in catalase (CAT) and superoxide
dismutase (SOD) activity and ele-
vation of glutathione (GSH) during
the 45 min exposure.
An increase in the levels of8-hydroxy-
2’-deoxyguanosine (8-OH-dG).
Intracellular ROS level increased in
exposed FeCl
2
treated cells com-
pared with unexposed FeCl
2
treated
cells.
*All effects were statistically significant (at least
p50.05)
as compared to control or sham exposed groups.
insulin signaling and in growth factor-induced signalling
cascades (Sies, 2014). These species are also implicated in
biochemical mechanism of oxidation of ethanol and in other
metabolic processes (Oshino et al., 1975) and is also required
for initiation of wound repair (Enyedi and Niethammer,
2013). In addition, ROS at relatively low concentrations can
modulate inflammation via activation of NF-kB pathway
(Hayden and Ghosh, 2011). Therefore, even subtle exposures
to RFR with generation of hardly detectable quantities of free
radicals can have their meaningful biological consequences.
We could ascertain the signaling effects of moderate
levels of free radicals from our experiments in quail
embryos irradiated with the commercial cell phone. Thus,
we were able to show that the prolonged exposures of
embryos
in ovo
led to robust repression of their development
(Tsybulin et al., 2013), which was concomitant with
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
2259378_0242.png
6
I. Yakymenko et al.
Electromagn Biol Med, Early Online: 1–16
Table 2. Publications which reported positive findings on oxidative stress caused by RFR exposure of animals and plants.
Statistically significant effects
reported*
Glutathione peroxidase (GSH-Px),
SOD, and CAT activity
decreased and level of MDA
increased. Vitamin C reduced
the effect.
Levels of conjugated dienes, LPO
and CAT activities in serum and
testicular tissue increased, the
total serum and testicular tissue
GSH and GSH-Px levels
decreased.
An increased level of protein oxi-
dation (PO) in brain tissue and
an increase in serum NO. Garlic
administration reduced protein
oxidation in brain tissue.
MDA and hydroxyproline levels
and activities of CAT and GSH-
Px were increased, andsuperox-
ide dismutase (SOD) activity
was decreased in skin.
Melatonin treatment reversed
effect.
LPO was increased, an adminis-
tration of melatonin prevented
this effect.
In corneal tissue, MDA level and
CAT activity increased,
whereas SOD activity was
decreased. In the lens tissues,
the MDA level was increased.
The serum NO levels and levels of
MDA and the PO in brain were
increased. An administration of
garlic extract diminished these
effects.
Reduced antioxidant capacity both
in healthy animals and in those
with paw inflammation.
Overproduction of superoxide and
NO, increased levels of thio-
barbituric acid reactive sub-
stances (TBARS) and 8-OH-
dG, decreased SOD and CAT
activities.
Increased rates of superoxide pro-
duction, formation of the iron-
nitrosyl complexes and
decreased activity of NADH-
ubiquinone oxidoreductase
complex in liver, cardiac and
aorta tissues 28 days after the
exposure.
Difference in guinea pigs subjected
to 900 and 1800 MHz for
plasma oxidant status levels.
NO level changed in 900 MHz
subjected guinea pigs, as com-
pared to the control.
Brain and liver GSH-Px activities,
selenium concentrations in the
brain and liver vitamin A and
b-carotene
concentrations
decreased in offspring.
The total antioxidant capacity and
CATactivity in brains were
higher than that in the sham
group.
(continued )
Reference
(Akbari et al., 2014)
Biological system exposed
Rat whole body
RFR exposure
RFR from base transceiver station
(Al-Damegh, 2012)
Rat whole body
Cell phone RFR, 15, 30, or 60 min/day
for 2 weeks
(Avci et al., 2012)
Rat whole body
1800 MHz, SAR
¼
0.4 W/kg, 1 h/day
for 3 weeks
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(Ayata et al., 2004)
Rat whole body
900 MHz, 30 min/day for 10 days
(Aynali et al., 2013)
(Balci et al., 2007)
Rat whole body
Rat whole body
2450 MHz, pulsed, SAR
¼
0.143 W/
kg,60 min/day for 30 days
‘‘Standardized daily dose’’ of cell
phoneRFR for 4 weeks
(Bilgici et al., 2013)
Rat whole body
850–950 MHz,SAR
¼
1.08 W/kg,1 h/
day for 3 weeks
(Bodera et al., 2013)
(Burlaka et al., 2013)
Rat whole body
Quail embryo
in ovo
1800 MHz, GSM, for 15 min
GSM 900 MHz, power density (PD) of
0.25
mW/cm
2
, SAR
¼
3
mW/kg,
48 sec ON - 12 sec OFF, for 158–
360 h
Pulsed and continuous MWin the
doses equivalent to the maximal
permitted energy load for the staffs
of the radar stations
(Burlaka et al., 2014)
Male rat whole body
(Cenesiz et al., 2011)
Guinea pig whole body
900; 1800 MHz RFR from base station
antennas, 4 h/day for 20 days
(Cetin et al., 2014)
Pregnant rats and offspring
900; 1800 MHz RFR, 1 h/day during
pregnancy and neonatal
development
900 MHz, 2 h/day for 10 months
(Dasdag et al., 2009)
Head of rats
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2259378_0243.png
DOI: 10.3109/15368378.2015.1043557
RFR as a powerful oxidative agent
Table 2. Continued
7
Reference
(Dasdag et al., 2012)
(Dasdag et al., 2008)
(Deshmukh et al., 2013)
(Esmekaya et al., 2011)
Biological system exposed
Head of rats
Rat whole body
Rat whole body
Rat whole body
RFR exposure
900 MHz, cell-phones-like, 2 h/day for
10 months
900 MHz, PD of 78
mW/cm
2
, 2 h/days
for10 months.
900 MHz, 2 h/day, 5 days a week for
30 days
900 MHz, pulsed, modulated,
SAR
¼
1.2 W/kg, 20 min/day for
3 weeks
950 MHz, SAR
¼
0.01–0.88 W/
kg,30 min/day for 21 days during
pregnancy (or additionally 6 or
15 days of postnatal period)
GSM 1800 MHz, 15 min/day for 7
days (females) or 14 days (males)
900 MHz, 30 min/day for 30 days
Statistically significant effects
reported*
Protein carbonyl level was higher
in the brain of exposedrats.
Increased levels of MDA and total
oxidative status in liver tissue.
The levels of LPO and PO were
increased.
The increased level of MDA and
NOx, and decreased levels of
GSH in liver, lung, testis and
heart tissues.
Neonatal rats exposed in utero had
decreased levels of CAT and
lower LPO, and genotoxic
effect.
LPO levels in the liver tissues of
females and males increased,li-
ver 8-OH-dG levels of females
were increased.
Endometrial levels of NO and
MDA increased,endometrial
SOD, CAT and GSH-Px activ-
ities were decreased.Vitamin E
and C treatment prevented these
effects.
Increased 8-OH-dG level in both
plasma and brain tissue whereas
it increased PO level only in
plasma. Garlic prevented the
increase of 8-OH-dG level in
brain tissue and plasma PO
levels.
Increase in MDA, NO levels,
andxanthine oxidase (XO)
activity, decrease in SOD and
GSH-Px activities in brain.
These effects were prevented by
Ginkgo bilobaextract treatment.
The concentration of MDA was
increased and activities of SOD,
GSH-Px and CAT were
decreased in rat eyes. An
administration of vitamin C
prevented these effects.
Increased level of MDA and
decreased antioxidant enzymes
activity in rat testis.
After 30 and 60 min the level of
MDA was increased, the activ-
ities of SOD and GSH-Pxwere
decreased.
Tissue MDA levels were
increased, SOD, CAT and GSH-
Pxactivities were reduced.
Melatonin treatment reversed
these effects.
Reduction in protein kinase activ-
ity, decrease in sperm count and
increase in apoptosis.
Increase in the level of ROS,
decrease in the activities of
SOD and GSH-Px,and in the
level of pineal melatonin.
The level of ROS, DNA damage
and theapoptosis rate were
increased.
Elevations in the levels of 8-OH-
dG in urine.
(continued )
(Furtado-Filho et al., 2014)
Rat whole body
(Guler et al., 2012)
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Rabbit infant whole body
(Guney et al., 2007)
Rat whole body
¨
(Gurler et al., 2014)
Rat whole body
2450 MHz, 3.68 V/m, 1 h/day for
30 days
(Ilhan et al., 2004)
Rat whole body
900 MHz, from cell phone,1 h/day for
7 days
(Jelodar, et al., 2013)
Rat whole body
900 MHz, PD of 680
mW/cm
2
, 4 h/day
for 45 days,
(Jelodar et al., 2013)
(Jing et al., 2012)
Rat whole body
Rat whole body
900 MHz, daily for 45 days
Cell phone RFR, SAR
¼
0.9 W/kg,3 x
10; 30 or 60 min for 20 days during
gestation
900 MHz, 30 min/day for 10 days
(Kerman & Senol, 2012)
Rat whole body
(Kesari et al., 2010)
(Kesari et al., 2011)
Male rat whole body
Rat whole body
Cell phone RFR, SAR
¼
0.9 W/kg,2 h/
day for 35 days
900 MHz, pulsed, SAR
¼
0.9 W/
kg,2 h/day for 45 days
2115 MHz, SAR
¼
0.26 W/kg,2 h/day
for 60 days
1800 MHz, electric field 15–20 V/m,
for2 h
(Kesari et al., 2013)
(Khalil et al., 2012)
Rat whole body
Rat whole body
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2259378_0244.png
8
I. Yakymenko et al.
Table 2. Continued
Electromagn Biol Med, Early Online: 1–16
Reference
(Kismali et al., 2012)
(Koc et al., 2013)
(Koylu et al., 2006)
Biological system exposed
Rabbit whole body (non-
pregnant and pregnant)
Male rat whole body
Rat whole body
RFR exposure
1800 MHz, GSM modulation,
15 min/day for 7 days
Cell phone RFR at calling or stand-by
900 MHz
Statistically significant effects
reported*
Creatine kinases levels’ changes.
Oxidative stress detected at both
calling and stand-by exposures.
The levels of LPO in the brain
cortex and hippocampus
increased.These levels in the
hippocampus were decreased by
melatonin administration.
The activities of XO, CAT and
level of LPO increased in
liver.XO, CAT activities and
LPO levels were decreased by
caffeic acid phenethyl ester
(CAPE) administration.
Increase in LPO, damage in sperm
cells and DNA damage.
Melatonin or spin-trap compound
blocked DNA strand breaks
induced by RFR exposure in rat
brain cells.
Contents of liver MDA and Nrf2
protein increased, contents of
liver SOD and GSH decreased.
Increase in LPO and decreased
GSH content in the testis and
epididymis.
Increase in ROS levels in male and
female bodies, a quick response
in ROS increase in ovaries.
SOD and CAT activities were
reduced in blood, sesame oil
reversed the effect
Increased level of MDA and ROS
in testis. Melatonin prevented
oxidative stress.
The levels of the LPO and PO were
increased; the level of GSH was
decreased.
MDA level increased, GSH level
and CAT activity werede-
creased in the brain. MDA,
vitamins A, D
3
and E levels and
CAT enzyme activity increased,
and GSH level was decreased in
the blood.
Increments in conjugated dienes,
protein carbonyls, total oxidant
status and oxidative stress index
along with a reduction of total
antioxidant capacity levels.
Decrease of the cortex brain vita-
min A, vitamin C and vitamin E
levels.
LPO, cell viability and cytosolic
Ca
2+
values in dorsal root gan-
glion neurons were increased.
LPO was higher in exposed ani-
mals. Melatonin treatment
reversed the effect.
Renal tissue MDA level increased,
SOD, CAT and GSH-Px activ-
ities were reduced. Melatonin
treatment reversed these effects.
Increased MDA levels and apop-
tosis in endometrial
tissue.Treatment with vitamins
E and C diminished these
changes.
(continued )
(Koyu et al., 2009)
Rat whole body
900 MHz
(Kumar et al., 2014)
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Rat whole body
Rat whole body
(Lai & Singh, 1997)
Cell phone 1910.5 MHz RFR, 2 h/day
for 60 days day (6 days a week).
2450 MHz, pulsed, PD
¼
2 mW/cm
2
,
SAR
¼
1.2 W/kg
900 MHz imitated cell phone RFR,
4 h/day for 12 days
900/1800 MHz,GSM,1 h/day for 28
days
1880–1900 MHz, DECT modulation,
SAR
¼
0.009 W/kg, for 0.5–96 h
900 MHz from cellular tower, 24 h/day
for 8 weeks
2450 MHz, PDof 210
mW/cm
2
,
SAR
¼
0.14 W/kg, 2 h/day for
45 days
900; 1800 MHz, PD of 170
mW/cm
2
,
SAR
¼
0.6 mW/kg, 2 h/day, 5 days/
week for 30 days
890–915 MHz,from cell phone,
SAR
¼
0.95 w/kg, 12 h/day for
30 days (11 h 45 min stand-by and
15 min spiking mode)
(Luo et al., 2014)
(Mailankot et al., 2009)
(Manta et al., 2013)
(Marzook et al., 2014)
(Meena et al., 2013)
(Megha et al., 2012)
(Meral et al., 2007)
Rat whole body
Rat whole body
Drosophila whole body
Rat whole body
Rat whole body
Rat whole body
Guinea pig whole body
(Motawi et al., 2014)
Rat whole body
Test cellphone RFR, SAR
¼
1.13
W/kg, 2 h/day for 60 days
(Naziroglu & Gumral, 2009)
(Naziroglu et al., 2012a)
(Oksay et al., 2014)
(Oktem et al., 2005)
Rat whole body
Rat whole body
Rat whole body
Rat whole body
2450 MHz,60 min/day for 28 days
2450 MHz, 60 min/day for 30 days
2450 MHz, pulsed, PD of0.1
mW/cm
2
,
SAR
¼
0.1 W/kg, 1 h/day for 30
days
900 MHz, 30 min/day for 10 days
(Oral et al., 2006)
Rat whole body
900 MHz, 30 min/day for 30 days
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2259378_0245.png
DOI: 10.3109/15368378.2015.1043557
RFR as a powerful oxidative agent
Table 2. Continued
9
Reference
(Ozguner et al., 2005a)
Biological system exposed
Rat whole body
RFR exposure
900 MHz, 30 min/day for 10 days
Statistically significant effects
reported*
Heart tissue MDA and NO levels
increased, SOD, CAT and GSH-
Px activities were reduced.
CAPE treatment reversed these
effects.
Retinal levels of NO and MDA
increased, SOD, GSH-Px and
CAT activities were
decreased.Melatonin and CAPE
treatment prevented effects.
Renal tissue MDA and NO levels
increased, the activities of SOD,
CAT and GSH-Px were
reduced. CAPE treatment
reversed these effects.
Increases in MDA and total NO(x)
levels and decreases in activ-
ities of SOD, myeloperoxidase
and GSH-Px in liver. Extent of
oxidative damage was propor-
tional to the duration of
exposure.
The amount of LPO was increased
in the prenatal exposure group.
At the age of six weeks, an
increased LPO in the kidney
and testis, and decreased level
of GSH and total antioxidant
status.
Decreased activities of CAT and
GSH-Px and increasedlevel of
MDA in cerebrum. Nano-sel-
enium decreased MDA level,
and increased GSH-Px and CAT
activities.
Increase in MDA levels and
decrease total antioxidant cap-
acity levels in brain, liver and
kidneys tissues. These alter-
ations were corrected by with-
drawal of RFR exposure during
30 days.
A significant change in level of
antioxidant enzymes and non-
enzymatic antioxidants, and an
increase in LPO.
An increase in ROS, decrease in
NO and antioxidant enzymes
activities.
Increased level of MDA,H
2
O
2
accumulation and root oxidiz-
ability, upregulation in the
activities of SOD, CAT, ascor-
bate peroxidases, guaiacol per-
oxidases and GSHreductases in
roots.
The increased level of MDA,
hydrogen peroxide and proline
content in hypocotyls.
An increase in the brain tissue
MDA and carbonyl group con-
centration. Decreased activity
of CAT and increased activity
of xanthine oxidase (XO).
Melatonin treatment prevented
the effects.
(continued )
(Ozguner et al., 2006)
Rat whole body
900 MHz, from cell phone
(Ozguner et al., 2005b)
Rat whole body
900 MHz
(Ozgur et al., 2010)
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Guinea pig whole body
1800 MHz,GSM, SAR
¼
0.38 W/kg,
10 or 20 min/day for 7 days
(Ozgur et al., 2013)
¨
(Ozorak et al., 2013)
Rabbit whole body
Rat whole body
1800 MHz, pulsed, 15 min/day for
7 days in pregnant animals, for 7 or
15 days in infants
900; 1800; 2450 MHz, pulsed, PD of
12
mW/cm
2
.SAR
¼
0.18; 1.2 W/kg,
60 min/day during gestation and
6 weeks following delivery
1800 MHz, 208
mW/cm
2
, 30 or
120 min/d for 30 days
(Qin et al., 2014)
Male mouse whole body
(Ragy, 2014)
Rat whole body
Cell phone 900 MHz RFR, 1 h/d for
60 days
(Saikhedkar et al., 2014)
Rat whole body
Cell phone 900 MHz RFR, 4 h/d for
15 days
2450 MHz, PD of 33.5
mW/cm
2
,
SAR
¼
23 mW/kg, 2 h/day for
45 days
900 MHz, from cell phone, PD of
8.55
mW/cm
2
; for 0.5; 1; 2, and 4 h
(Shahin et al., 2013)
(Sharma et al., 2009)
Mouse whole body
Plant(mung bean) whole
body
(Singh et al., 2012)
(Sokolovic et al., 2008)
Plant (mung bean)
whole body
Rat whole body
900 MHz,from cell phone
RFR from cell phone, SAR
¼
0.043–
0.135 W/kg, for 20, 40 and 60 days
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2259378_0246.png
10
I. Yakymenko et al.
Table 2. Continued
Electromagn Biol Med, Early Online: 1–16
Reference
(Sokolovic et al., 2013)
Biological system exposed
Rat whole body
RFR exposure
900 MHz, SAR
¼
0,043–0.135 W/
kg,4 h/day for 29; 40 or 60 days,
Statistically significant effects
reported*
The level of LPO and PO, activ-
ities of CAT, XO, number of
apoptotic cells were increased
in thymus tissue. An adminis-
tration of melatonin prevented
these effects.
MDA concentration was increased
in brains.
LPO and H
2
O
2
content increased:
CAT activity increased, pyro-
gallol peroxidase decreased.
The protein carbonyl content was
increased in all exposures above
30
mWc/m
2
. The level of MDA
was increased at 140mW/cm
2
.
Decreased GSH-Px activity. GSH-
Px activity and GSH values
increased after melatonin
treatment.
Increase of MDA and ferrous oxi-
dation in xylenol orange levels.
Increased level of TBARS in
brains and livers of hatchlings.
The increased level of LPO, the
decreased concentrations of
vitamin A, vitamin C and vita-
min E. There was a protective
effect of selenium and L-
carnitine.
MDA, SOD and CAT values
increased, GSH values
decreased in exposed pups.
MDA level and SOD activity
increased, GSH concentration
was decreased.
(Suleyman et al., 2004)
(Tkalec et al., 2007)
(Tkalec et al., 2013)
Rat whole body
Plant Lemna minor
(duckweed)
Earthworm whole body
Cell phoneRFR,SAR
¼
0.52 W/
kg,20 min/day for 1 month
400 and 900 MHz, 10, 23, 41 and
120 V/m, for 2 or 4 h
900 MHz, PD of 30–3800
mW/cm
2
,
SAR
¼
0.13–9.33 mW/kg, for 2 h
2450 MHz, Wi-Fi RFR, 60 min/day for
30 days
1800 MHz, GSM-like signal,
15 min/day for a week
900 MHz, fromcell phone, GSM, PD
of 0.024–0.21
mW/cm
2
, intermittent
for 14 days
2450 MHz, pulsed,
SAR
¼
0.1 W/kg,1 h/day for 28
days
¨
(Tok et al., 2014)
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Rat whole body
(Tomruk et al., 2010)
(Tsybulin et al., 2012)
(Turker et al., 2011)
Rabbit whole body
Quail embryo
in ovo
Rat partial body
¨
(Turedi et al., 2014)
(Yurekli et al., 2006)
Pregnant rat whole body
Rat whole body
900 MHz, 13.7 V/m, 50
mW/cm
2
,
1 h/day for 13–21 days of
pregnancy
945 MHz, GSM, PD of 367
mW/cm
2
,
SAR
¼
11.3 mW/kg
*All effects were statistically significant (at least
p50.05)
as compared to control or sham exposed groups.
Table 3. Publications which reported positive findings on oxidative stress caused byRFR exposure of humans.
Statistically significant effects
reported*
SOD activity in saliva increased.
Increased level of MDA, decreased
level of GSH.
Increase in all salivary oxidative
stress indices.
Plasma level of LPO was
increased, activities of SOD and
GSH-Px in erythrocytes decreased.
Reference
(Abu Khadra et al., 2014)
(Garaj-Vrhovac et al., 2011)
(Hamzany et al., 2013)
(Moustafa et al., 2001)
Biological system exposed
Human male head
Human whole body
Human head/whole body
Human male body
RFR exposure
GSM 1800 MHz from cell phone,
SAR
¼
1.09 W/kg, for 15 and
30 min
3; 5.5; 9.4 GHz, pulsed, from radars
RFR from cell phone a mean time
of 29.6 h/month for 12.5 years
Cell phone in a pocket in standby
position, for 1; 2 or 4 h
*All effects were statistically significant (at least
p50.05)
as compared to control or sham-exposed groups.
significant overproduction of superoxide radical and NO
radical, increased rates of lipid peroxidation and oxidative
damage of DNA (Burlaka et al., 2013; Tsybulin et al.,
2012). Notably, shorter exposures instead led to enhance-
ment in embryonic development (Tsybulin et al., 2012,
2013). We demonstrated the favorable effects of shorter
exposures also on the molecular level. Thus, after the short-
time RFR exposure the DNA comets in embryonic cells
were significantly shorter than in the control non-irradiated
embryos, pointing to activation of mechanisms maintaining
the integrity of DNA. The ‘‘beneficial’’ consequences of the
irradiation could be explained by hormesis effect (Calabrese,
2008). However, one could hypothesize that the ‘‘benefi-
cial’’ effects of the irradiation could be explained by the
signaling action of free radicals induced at levels below the
damaging concentrations. Obviously, any seemingly benefi-
cial effect of external environmental impact should be
treated with caution and possibly minimized before careful
evaluation of the long-term consequences. Altogether,
this gives a clear warning of the adverse health effects of
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2259378_0247.png
DOI: 10.3109/15368378.2015.1043557
RFR as a powerful oxidative agent
11
Table 4. Publications which reported no significant oxidative effectsafter RFR exposure.
Reference
(Hook et al., 2004)
Biological system exposed
Mammalian cells
in vitro
RFR exposure
835.62 MHz (frequency-modulated
continuous-wave, FMCW) and
847.74 MHz (code division
multiple access, CDMA),
SAR
¼
0.8 W/kg, for 20–22 h
800–1800 MHz, from cell phone
Effects reported
FMCW- and CDMA-modulated RFR
did not alter parameters indicative of
oxidative stress.
No changes in lipid and protein
damage, and in non-enzymatic anti-
oxidant defense in frontal cortex or
hippocampus.
No differences in oxidative parameter
of offspring blood and liver, but
increase in erythrocytes micronuclei
incidence in offspring.
No alteration in MDA concentration.
No difference in GSH-Px and CAT
activity in eye tissues, in MDA and
GSH levels in blood.
No relationship between exposure and
changes in the salivary oxidant/anti-
oxidant profile.
No difference in the saliva from the
parotid gland exposed to cell phone
RFR to the saliva from the opposite
gland of each individual.
(Ferreira et al., 2006a)
Rat whole body
(Ferreira et al., 2006b)
Pregnant rat whole body
RFR from cell phone
(Dasdag et al., 2003)
(Demirel et al., 2012)
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Rat whole body
Rat whole body
Human head/whole body
Human head/whole body
Cell phone RFR, SAR
¼
0.52 W/kg,
20 min/day for 1 month
3G cell phone RFR, ‘‘standardized
daily dose’’ for 20 days
Cell phone RFR (talking mode) for
15 or 30 min
Cell phone RFR
(Khalil et al., 2014)
(de Souza et al., 2014)
low-intensity RFR, which could be evoked both by the direct
oxidative damage and by disturbed cellular signaling.
Oxidative effects and non-cancer health effects
of RFR
A new medical condition, so-called electrohypersensitivity
(EHS), in which people suffer due to RFR exposure, has been
described (Johansson, 2006). Typically, these persons suffer
from skin- and mucosa-related symptoms (itching, smarting,
pain, heat sensation), or heart and nervous system disorders
after exposure to computer monitors, cell phones and other
electromagnetic devices. This disorder is growing continu-
ously: starting from 0.06% of the total population in 1985, this
category now includes as much as 9–11% of the European
population (Hallberg and Oberfeld, 2006). In Sweden, for
example, EHS has become an officially recognized health
impairment.
To that, a high percentage, up to 18–43% of young people,
has recently been described to be suffering from headache/
earache during or after cell phone conversations (Chu et al.,
2011; Yakymenko et al., 2011). Likewise, a number of
psychophysical and preclinical disorders including fatigue,
irritation, headache, sleep disorders, hormonal imbalances
were detected in high percent of people living nearby cell
phone base transceiver stations (Buchner and Eger, 2011;
Santini et al., 2002).
An allergy reaction to RFR in humans has been confirmed
by a significant increase in the level of mast cells in skin of
persons under exposure to electromagnetic devices
(Johansson et al., 2001). Likewise, higher level of degranu-
lated mast cells in dermis of EHS persons has been detected
(Johansson, 2006). In turn, the activated mast cells can release
histamine and other mediators of such reactions which
include allergic hypersensitivity, itching, dermatoses, etc.
Importantly, an implication of ROS in allergic reactions is
rather clear nowadays. For example, in case of airway allergic
inflammation, the lung cells generate superoxide in nanomo-
lar concentrations following antigen challenges (Nagata,
2005). Then, mast cells generate ROS following aggregation
of Fc"RI, a high-affinity IgE receptor (Okayama, 2005). In
addition, pollen NADPH oxidases rapidly increase the level of
ROS in lung epithelium (Boldogh et al., 2005); and removal
of pollen NADPH oxidases from the challenge material
reduced antigen-induced allergic airway inflammation. Thus,
it seems plausible that EHS-like conditions can be attributed
at least partially to ROS overproduction in cells due to RFR
exposures.
Oxidative effects and potential carcinogenicity
of RFR
During recent years, a number of epidemiological studies
indicated a significant increase in incidence of various types
of tumors among long-term or ‘‘heavy’’ users of cellular
phones (Yakymenko et al., 2011). Briefly, reports pointed to
the increased risk in brain tumors (Cardis et al., 2010; Hardell
and Carlberg, 2009; Hardell et al., 2007), acoustic neuroma
(Hardell et al., 2005; Sato et al., 2011), tumors of parotid
glands (Sadetzki et al., 2008), seminomas (Hardell et al.,
2007), melanomas (Hardell et al., 2011) and lymphomas
(Hardell et al., 2005) in these cohorts of people. To that, a
significant increase in tumor incidence among people living
nearby cellular base transceiver stations was also reported
(Eger et al., 2004; Wolf and Wolf, 2007). Similarly, experi-
mental evidences of cancer expansion in rodents caused by
long-term low-intensity RFR exposure were published (Chou
et al., 1992; Repacholi et al., 1997; Szmigielski et al., 1982;
Toler et al., 1997). To that, activation of ODC was detected in
RFR-exposed cells (Hoyto et al., 2007). ODC is involved in
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Electromagn Biol Med Downloaded from informahealthcare.com by 178.54.177.229 on 07/07/15
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processes of cell growth and differentiation, and its activity is
increased in tumor cells. Although overexpression of ODC is
not sufficient for tumorigenic transformation, an increased
activity of this enzyme was shown to promote the develop-
ment of tumors from pre-tumor cells (Clifford et al., 1995).
Significant overproduction of ROS leads to oxidative stress
in living cells, induces oxidative damage of DNA and can
cause malignant transformation (Halliwell and Whiteman,
2004; Valko et al., 2007). It is known that in addition to
mutagenic effects, ROS play a role as a second messenger for
intracellular signaling cascades which can also induce
oncogenic transformation (Valko et al., 2006). Earlier we
hypothesized (Burlaka et al., 2013) that low-intensity RFR
exposure leads to dysfunctions of mitochondria, which result
in overproduction of superoxide and NO, and subsequently to
ROS-mediated mutagenesis. To that, it is well established that
oxidative stress is associated with carcinogenesis; for
instance, the oxidative stress elicited by Membrane-Type 1
Matrix Metalloproteinase is implicated in both the pathogen-
esis and progression of prostate cancer (Nguyen et al., 2011).
Similarly, a progressive elevation in mitochondrial ROS
production (chronic ROS) under both hypoxia and/or low
glucose, which leads to stabilization of cells via increased
HIF-2alpha expression, can eventually result in malignant
transformation (Ralph et al., 2010). These data, together with
the strong experimental evidences on activation of NADH
oxidase under RFR exposure (Friedman et al., 2007) suggest
that low-intensity RFR is a multifactorial stress factor for
living cell, significant feature of which is oxidative effects and
potential carcinogenicity as a result.
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The analysis of modern data on biological effects of low-
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agent is a powerful oxidative stressor for living cell. The
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activities of key ROS-generating systems, including mito-
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Acknowledgments
The authors are grateful to the unknown referees
for the valuable comments on the first version of the
manuscript.
Declaration of interest
The authors declare no conflicts of interest. This study was
supported by National Academy of Sciences of Ukraine (I.Y.,
E.S.) and by University of Campinas via PPVE (Programa
Professor Visitante do Exterior), Brazil (S.K.).
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DOI: 10.3109/15368378.2015.1043557
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BRIEFING
Effects of 5G wireless communication
on human health
SUMMARY
The fifth generation of telecommunications technologies, 5G, is fundamental to achieving a
European gigabit society by 2025.
The aim to cover all urban areas, railways and major roads with uninterrupted fifth generation
wireless communication can only be achieved by creating a very dense network of antennas and
transmitters. In other words, the number of higher frequency base stations and other devices will
increase significantly.
This raises the question as to whether there is a negative impact on human health and environment
from higher frequencies and billions of additional connections, which, according to research, will
mean constant exposure for the whole population, including children. Whereas researchers
generally consider such radio waves not to constitute a threat to the population, research to date
has not addressed the constant exposure that 5G would introduce. Accordingly, a section of the
scientific community considers that more research on the potential negative biological effects of
electromagnetic fields (EMF) and 5G is needed, notably on the incidence of some serious human
diseases. A further consideration is the need to bring together researchers from different disciplines,
in particular medicine and physics or engineering, to conduct further research into the effects of 5G.
The EU’s current provisions on exposure to wireless signals, the Council Recommendation on the
limitation of exposure of the general public to electromagnetic fields (0 Hz to 300 GHz), is now
20 years old, and thus does not take the specific technical characteristics of 5G into account.
In this Briefing
Difference between 5G and current
technology
Regulation of electromagnetic fields and
5G exposure
European Parliament
Research on EMF and 5G effects on
human health
Stakeholders' views
The road ahead for 5G
EPRS | European Parliamentary Research Service
Author: Miroslava Karaboytcheva
Members' Research Service
PE 646.172 – February 2020
EN
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EPRS | European Parliamentary Research Service
Background
Under the EU
digital single market strategy,
the European Commission presented new policy
measures in its 2016 communication on
Connectivity for a Competitive Digital Single Market –
Towards a European Gigabit Society.
The Commission's aim is to advance the digitalisation of the
EU and to increase its competitiveness by launching networks with much higher capacities, with
5G
as a building block to achieve a 'gigabit society' by 2025. Its main characteristics would enable the
internet of things,
which means that billions of connections between devices share information.
1
The Commission has established the following connectivity targets for 2025:
schools, universities, research centres, hospitals, main providers of public services and
digitally intensive enterprises should have access to internet download/upload speeds
of one gigabit of data per second;
urban and rural households should have access to connectivity of download speed of
at least 100 megabits per second;
urban areas, major roads and railways should have uninterrupted 5G coverage.
The '5G
for Europe: An action plan'
presents measures for timely and coordinated deployment of 5G
networks in Europe through a partnership between the Commission, Member States, and industry.
This initiative concerns all private and public stakeholders, in all EU Member States.
The connectivity objective has been regulated by the adoption of the
European Electronic
Communication Code
(EECC) at the end of 2018, under which EU Member States have to authorise
the use of the new 5G frequency bands at
700 MHz, 3.5 GHz and 26 GHz
2
and reorganise them by
the
end of 2020,
3
in line with the EECC. This decision enables the take-up of 5G services in the Union.
According to the
European 5G observatory,
supported by the European Commission, at the end of
September 2019, 165 trials had been carried out in the European Union and 11 Member States had
already published their
national 5G action plans.
Challenges and opportunities of 5G
Advantages
Allowing much larger volumes of data to be transported more quickly, and reducing response time,
5G will enable instantaneous connectivity to billions of devices, the internet of things and a truly
connected EU population. Furthermore,
millions of jobs and billions of euros
could be expected to
be gained from the digital economy.
The possibilities that the fifth generation of wireless communication offers, such as downloading or
uploading one gigabit of data per second, may provide advantages, for instance, for the military and
medical research, which could benefit from having access to such extremely high gigabit
connectivity. However, the military, hospitals, the police and banks continue to use wired
connections, at least for their most essential communications, mainly for security reasons. Wired
networks generally offer a faster internet speed and are considered to be more secure. This is due
to the fact that a wired network is only accessible through a physical cable connection, whereas with
wireless networks, the signal may be broadcast outside the physical premises. Wired connection
offers more control than radio or wifi, because such organisations already provide protection for
servers and internal IT facilities within their physical locations, taking advantage of almost 100 % of
the bandwidth, which also reduces response times. That also contributes to increased security.
Disadvantages
Because it is more complex and requires a denser coverage of base stations
4
to provide the expected
capacity, 5G will
cost much more to deploy
than previous mobile technologies. According to
European Commission
estimates, to reach the target, including 5G coverage in all urban areas, this
cost is estimated at around
€500
billion by 2025.
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Effects of 5G wireless communication on human health
Questions remain unanswered as to what 5G actually is, what it is for, whether it has impacts on
human health and environment, whether it is secure, whether it offers good value for money or
whether anyone will be prepared to pay for it.
5
As an alternative, according to some experts,
6
fibre
optics would be more secure, safe and offer higher speed than 5G. However, fibre optics are not
wireless.
Difference between 5G and current technology
Employing millimetre waves and higher frequencies than previous technologies, 5G needs a much
more extensive network of antennas and other transmitting devices. Electromagnetic fields (EMF)
are invisible areas of energy,
7
measured in hertz (Hz). Longer wavelengths with lower frequency are
less powerful in terms of energy, while shorter wavelengths at higher frequencies are more
powerful. Depending on the frequency, there are two categories of EMF: ionising and non-ionising
radiation (see Figure 1).
Figure 1 – Electromagnetic spectrum
Source: Polina Kudelkina / Shutterstock.com.
Ionising radiation (mid to high-frequency) includes ultraviolet rays, x-rays and gamma rays. The
energy from ionising radiation can
damage human cells and cause cancer.
Non-ionising radiation
has lower frequencies and bigger wavelengths. Many experts are of the opinion that non-ionising
radiation produces only thermal effects, or
tissue heating,
and that at high exposure levels,
temperature-sensitive biological structures, including humans, and processes can become
damaged.
Microwave and millimetre wavelength radiation is non-ionising. Millimetre wave ranges from
around 10 to 1 millimetre. This is a very effective spectrum with large bandwidth, but it is also very
sensitive to external variables and can be subject to interference from walls, trees or even rain.
For the first time, 5G will use millimetre waves in addition to the microwaves that have been used
to date in 2G, 3G and 4G technology. Due to the limited coverage, to implement 5G, cell antennas
will have to be installed very close to one another, which will result in constant exposure of the
population to millimetre wave radiation. Use of 5G will also require new technologies to be
employed, such as active antennas capable of
beam-forming,
massive inputs and outputs.
8
With
higher frequencies and shortened ranges, base stations will be more closely packed into an area, to
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provide complete coverage and avoid 'not-spots'. This could mean possible ranges of 20-150 metres
with smaller coverage areas per 'small cell.
9
A cell radius of 20 metres would imply about 800 base
stations per square kilometre (or 'small area wireless access points' (SAWAPs), the term used in the
EECC). This contrasts with 3G and 4G technologies, which use large or 'macro' cells, offering ranges
of 2-15 kilometres or more, and therefore covering a larger area but allowing fewer simultaneous
users since they have fewer individual channels.
10
Furthermore, 5G will employ higher frequencies
11
than previous 'G' networks and greater
bandwidth which will enable users to transfer wireless data faster.
Regulation of electromagnetic fields and 5G exposure
European Union
Primary responsibility for protecting the population from the potential harmful effects of EMF falls
to the governments of EU Member States under
Article 168 of the Treaty on the Functioning of the
European Union.
In 1996, the World Health Organization (WHO) established
the International EMF
Project
to evaluate the scientific evidence of possible health effects of EMF in the frequency range
from 0 to 300 GHz. It has elaborated 'model legislation' to offer a legal framework for implementing
protection programmes against non-ionising radiation.
The International Commission on Non-Ionising Radiation Protection (ICNIRP), a non-governmental
organisation formally recognised by WHO, issues
guidelines
for limiting exposure to electric,
magnetic and electromagnetic fields (EMF), which are revised periodically. In the EU,
Council
Recommendation
1999/519/EC,
of 12 July 1999, on the limitation of exposure of the general public
to EMF (0 Hz to 300 GHz), follows these guidelines.
As the Council Recommendation is the common protective framework guiding EU Member States
and setting basic restrictions and reference levels, depending on frequency, the following physical
quantities specify basic restrictions on electromagnetic fields:
between 0 and 1 Hz, basic restrictions are provided for magnetic flux density for static
magnetic fields (0 Hz) and current density for time-varying fields12 up to 1 Hz, to
prevent effects on the cardiovascular and central nervous system;
between 1 Hz and 10 MHz, basic restrictions are provided for current density13 to
prevent effects on nervous system functions;
between 100 kHz and 10 GHz, basic restrictions on the specific absorption rate (SAR) are
provided to prevent whole-body heat stress and excessive localised tissue heating. In
the 100 kHz to 10 MHz range, restrictions on both current density and SAR are provided;
between 10 GHz and 300 GHz, basic restrictions on power density are provided to
prevent tissue heating on or near the surface of the human body.
While these exposure limits are non-binding on EU Member States, some Member States have
nevertheless adopted stricter limits than those recommended above.
The recommendation encourages Member States to establish a common protective framework and
inform the public of the health impact of electromagnetic fields, as well as to harmonise national
approaches for measurement. The Council suggests that the European Commission keep possible
health effects under review.
The
European Environment Agency
(EEA) has long advocated
precaution
concerning EMF
exposure, pointing out that there were cases of failure to use the precautionary principle in the past,
which have resulted in often irreversible damage to human health and environments. Appropriate,
precautionary and proportionate actions taken now to avoid plausible and potentially serious
threats to health from EMF are likely to be seen as prudent and wise from future perspectives. The
EEA requests that EU Member States do more to inform citizens about the risks of EMF exposure,
especially to children.
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Effects of 5G wireless communication on human health
In its
2 April 2009 resolution,
the European Parliament urged the Commission to review the scientific
basis and adequacy of the EMF limits in Recommendation 1999/519/EC and to report back.
Parliament also requested that the Scientific Committee on Emerging and Newly Identified Health
Risks carry out a review of the EMF limits. Parliament requested consideration of the biological
effects, acknowledging the results of studies that reveal harmful effects at lowest levels of
electromagnetic radiation, as well as calling for active further research and consequently
development of solutions to negate or reduce pulsations used for transmission. It suggested that
the Commission elaborate a guide to available technology options for reducing exposure to EMF in
coordination with experts from Member States and the industries concerned.
The European Commission
Scientific Committee on Emerging and Newly Identified Health
Risks
(SCENIHR) has a mandate to evaluate the
risks of electromagnetic fields
and periodically
reviews the scientific evidence available to assess whether it still supports the exposure limits
proposed in Council Recommendation 1999/519/EC. In its latest
opinion
of January 2015, SCENIHR
suggested that there is a lack of evidence that EMF radiation affects cognitive functions in humans
or contributes to an increase of the cases of cancer in adults and children. However, the
International
EMF Alliance
(IEMFA) suggested that many members of SCENIHR could have a conflict of interests,
as they had professional relationships with or received funding from various
telecom companies.
Consequently, the Scientific Committee on Health, Environmental and Emerging Risks (SCHEER),
replacing the former Scientific Committee on Emerging and Newly Identified Health Risks
(SCENIHR), indicated a preliminary estimate of the importance of 5G as high, in a
statement
in
December 2018. Furthermore, it evaluates the scale, urgency and interactions (with ecosystems and
species) of possible hazard as high. It suggested that there could be biological consequences from
a 5G environment, due to the fact that there is a lack of 'evidence to inform the development of
exposure guidelines to 5G technology'.
Council of Europe
Council of Europe
Resolution 1815 (2011)
points to the potential health effects of the very low
frequency of electromagnetic fields surrounding power lines and electrical devices, which are the
subject of ongoing research and public debate. It also states that some non-ionising frequencies
appear to have more or less potentially harmful, non-thermal, biological effects on humans, other
animals and plants, even when exposed to levels that are below the official threshold values. The
resolution identifies young people and children as particularly vulnerable groups and suggests that
there could be extremely high human and economic costs if early warnings are neglected. The issue
of possible environmental and health effects of electromagnetic fields is considered to have clear
parallels with other current issues: the licensing of medication, chemicals, pesticides, heavy metals
or genetically modified organisms. The resolution highlights that the independence and credibility
of the scientific expertise employed is crucial for a transparent and balanced assessment of possible
negative effects on human health and environment. The resolution recommends:
taking all reasonable measures to reduce exposure to EMF (especially from mobile
phones) and particularly to protect children and young people who seem to be most at
risk of developing head tumours;
reconsidering the scientific basis for the present standards on exposure to
electromagnetic fields set by the International Commission on Non-Ionising Radiation
Protection, which have serious limitations;
distributing information and awareness-raising campaigns on the risks of potentially
harmful long-term biological effects on the environment and on human health,
especially targeting children, teenagers and young people of reproductive age;
giving preference to wired internet connections (for children in general and particularly
in schools), and strictly regulating the use of mobile phones by schoolchildren on school
premises;
increasing public funding of independent research to evaluate health risks.
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European Parliament
A
resolution
of 2 April 2009 on health concerns associated with electromagnetic fields urged the
European Commission to review the scientific basis and adequacy of the EMF limits in
Recommendation 1999/519/EC and to report back. It also requested that the Scientific Committee
on Emerging and Newly Identified Health Risks carries out a review of the EMF limits.
Research on EMF and 5G effects on human health
The academic literature on EMF exposure effects and 5G in particular is growing rapidly. Some
research papers support possible health risks, while others do not.
The WHO
14
/International Agency for Research on Cancer (IARC) classified radiofrequency EMF as
possibly carcinogenic to humans
in 2011. The IARC has recently prioritised EMF radiation for review
in the next five years (2020-2024).
A section of the scientific community – mainly doctors and researchers in medical sciences – argues
that there are negative impacts from EMF exposure and that these will increase with the
implementation of 5G. A
5G appeal
was presented to the
United Nations
in 2015, and to the
European Union
from 2017, with an increasing
number of scientists' signing (268 scientists and
Ethics in research
medical doctors as of 18 December 2019). The
The
European Code of Conduct for Research
signatories state that with the increasingly
Integrity
(last revised in
2017)
sets out principles of
extensive use of wireless technology, especially
research integrity, criteria for good research
when 5G is deployed, nobody could avoid
practice, and describes how to prevent violations
exposure to constant EMF radiation because of
of research integrity.
the huge number of 5G transmitters with an
The principles it states are the following:
estimated 10 to 20 billion connections (to self-
•
Reliability
in ensuring the quality of research,
driving cars, buses, surveillance cameras,
reflected in the design, the methodology, the
domestic appliances, etc.). In addition, the
analysis and the use of resources.
appeal states that a large number of scientific
publications illustrate EMF exposure effects
•
Honesty
in developing, undertaking, reviewing,
such as an elevated risk of cancer, genetic
reporting and communicating research in a
transparent, fair, full and unbiased way.
damage, learning and memory deficits,
neurological disorders, etc. The appeal points
•
Respect
for colleagues, research participants,
out not only harm to humans, but also to the
society, ecosystems, cultural heritage and the
environment.
environment.
The appeal recommends a moratorium on the
deployment of 5G for telecommunications until
potential hazards for human health and the
environment have been fully investigated by
scientists independent of industry. They urge
the EU to follow Resolution 1815 of the Council
of Europe, and demand that a new assessment is carried out by an independent task force.
•
Accountability
for the research from idea to
publication, for its management and organisation,
for training, supervision and mentoring, and for its
wider impacts.
In this regard, some scientists consider it necessary to establish new exposure limits that take
account of the new characteristics of exposure. Such limits should be based on the
biological effects
of EMF radiation,
rather than on the energy-based specific absorption rate.
Non-ionising radiation, which includes radiation from mobile phones and 5G, is perceived as
harmless in general, due to its lack of potency. However, some of the above-mentioned scientists
point out that, in the particular case of 5G, the issue is not the potency, but the pulse,
15
the frequency
to which the whole population will be exposed due to the dense network of antennas and the
estimated billions of simultaneous connections. As 5G employs a very high level of pulsations, the
idea behind 5G is to use higher frequencies, which allows such high levels of pulsation, in order to
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Effects of 5G wireless communication on human health
carry very large amounts of information per second. Studies show that pulsed EMF are in most cases
more biologically active and therefore more dangerous than non-pulsed EMF. Every single wireless
communication device communicates at least partially via pulsations, and the smarter the device,
the more pulsations. Consequently, even though 5G can be weak in terms of power, its constant
abnormal pulse radiation can have an effect. Along with the mode and duration of exposures,
characteristics of the 5G signal such as pulsing seem to
increase the biologic and health impacts of
exposure,
including DNA damage, which is considered to be a cause of cancer. DNA damage is also
linked to reproductive decline and neurodegenerative diseases.
A 2018
review
of more recently published peer-reviewed articles on the biological and health effects
of radio frequency EMF, including 5G, also verifies the available evidence on the effects of millimetre
waves. The review concludes that evidence of the biological properties of radiofrequency EMF are
accumulating progressively and even though they are, in some cases, still preliminary or
controversial, point to the existence of multi-level interactions between high-frequency EMF and
biological systems, and to the possibility of oncological and non-oncological (mainly reproductive,
metabolic, neurological, microbiological) effects. Moreover, it points out that the wide and
increasing density of wireless devices and antennas raises particular concerns. Taking this into
account, '... although the biological effects of 5G communication systems are very scarcely
investigated, an international action plan for the development of 5G networks has started, with a
forthcoming increase in devices and density of small cells, and with the future use of millimetre
waves'. However, there are indications that millimetre waves can increase skin temperature,
promote cellular proliferation, and inflammatory and metabolic processes. According to the review,
further studies are necessary to improve independent exploration of the health effects of radio
frequency EMF in general and of millimetre waves in particular.
16
Far less research exists to determine the effects of 5G technologies on humans and the environment,
according to another
review of studies
published in 2018. Considering the already existing complex
mix of lower frequencies, it argues that in addition to those, the expected higher frequency 5G
radiation would cause negative impacts on physical and mental public health. Concretely in the case
of millimetre waves, it analyses the results of studies which find effects on the skin, eyes, and
immune system, and bacterial antibiotic resistance. The review suggests that the effects of
radiofrequency EMF will be problematic to sort out epidemiologically, as no unexposed control
group will remain. The study consequently calls for precaution in the deployment of this new
technology. The author argues that while physicists and engineers give assurances that the only
measure to harm health is heat, medical scientists indicate that there are other mechanisms
whereby cellular functioning can be disrupted by non-thermal exposures to radiofrequency.
A 2016
review of scientific articles,
covering experimental data on the oxidative effects of low-
intensity radiofrequency radiation in living cells, finds that, among 100 currently available peer-
reviewed studies (18
in vitro
studies, 73 studies in animals, 3 studies in plants and 6 studies in
humans),
'...
dealing with oxidative effects of low-intensity radiofrequency radiation, in general,
93 confirmed that radiofrequency radiation induces oxidative effects in biological systems'. More
precisely, in 58 studies of laboratory rats, 54 show positive results, and 4 of 6 studies in humans were
positive. In addition, 17 of the 18 of the
in vitro
studies were positive, including two on human
spermatozoa and two on human blood cells. According to the authors, 'The analysis of modern data
on biological effects of low-intensity radiofrequency radiation (RFR) leads to a firm conclusion that
this physical agent is a powerful oxidative stressor for living cells'.
A 2018
study
carried out on animals, showed that electromagnetic radiation emitted by wifi
networks can lead to hyperglycaemia, increased oxidative stress and impaired insulin secretion in
rat pancreatic islets. A method of creating diabetes (which can lead to kidney deficiency in the long
term) in laboratory rats is to expose them, even briefly, to 2.4 Ghz.
A 2019 report of the
Swedish Radiation Safety Authority's Scientific Council on Electromagnetic
Fields
considers two large animal studies:
the US National Toxicology Program (NTP) study
and the
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Italian
Falcioni et al.
study, which analyse the relationship between radio wave exposure and
schwannoma
of the heart in male rats.
17
The report concludes that there is some inconsistency in
the results between the two studies and that no new causal relationship between EMF exposure
and health risks was established. It recommends that further research is important, particularly
regarding long-term effects and especially since the entire population will be exposed. It points out
that a possible relationship between radio wave exposure and oxidative stress should be a subject
of further research, as well as the association between weak low-frequency magnetic fields and
childhood leukaemia, as observed in epidemiological studies.
The scientific community reaction in response to this report, is illustrated in the recent 'Commentary
on the utility of the National Toxicology Program study on cell phone radiofrequency radiation data
for assessing human health risks despite unfounded criticisms aimed at minimizing the findings of
adverse health effects.' The author states that the NTP study was designed to test the hypothesis
that, at non-thermal exposure intensities, mobile phone radiation could not lead to adverse health
effects, and to provide data for assessment of health risks caused by any detected toxic or
carcinogenic effects, as little was known about long-term exposure to mobile phone radiation
health effects. Regarding the NTP study results, among others, the author defends the use of animal
studies that can eliminate the need to wait until enough human cancer data are available before
implementing strategies to protect public health. According to the author, the intensity of exposure
in the brains of rats in the NTP study were similar to potential human mobile phone exposures.
In turn, a 2019
review
of 94 articles, funded by Deutsche Telekom, states that the '... available studies
do not provide adequate and sufficient information for a meaningful safety assessment, or for the
question about non-thermal effects. There is a need for research regarding local heat developments
on small surfaces, e.g., skin or the eye, and on any environmental impact. There was no consistent
relationship between power density, exposure duration, or frequency, and exposure effects'.
There is no noticeable increase in everyday EMF exposure since 2012, despite the increasing use of
wireless communication devices, according to another
review of studies from 2019.
Nevertheless, it
remains unclear how well these studies of everyday exposure represent the population's absorbed
radiofrequency EMF dose. This study maintains the urgent need for better quantification of the
population's absorbed radiofrequency EMF dose from their own communication devices.
Stakeholders' views
Considering the huge estimated investment, the mobile telecommunications industry needs to
convince governments of 5G's economic and social benefits and perform widespread marketing
campaigns. 'It suits the industry if policy-makers believe that there is a race between nations to be
the first to launch 5G services'.
18
The EU telecommunications industry continues to state that the weight of evidence regarding harm
from EMF exposures is inconclusive. The 5G Infrastructure Public Private Partnership (5G
PPP),
a joint
initiative between the European Commission and European information and telecommunications
(ICT) industry (ICT manufacturers, telecommunications operators, service providers, SMEs and
research institutions), supports research and innovation to develop 5G networks that comply with
international standards and regulations and develops systems designed to operate below the safe
health limits of electromagnetic emissions.
19
However, it does not refer to the biological impacts of
5G radiation.
Nevertheless, according to the
IEMFA,
a need to measure real potential exposure to 5G and update
the safety limits of such exposure does exist. The alliance calls for more research and scientific
consent along these lines. It maintains that scientists with experience of long research into EMF
health effects should be included in the SCENIHR, following the demands of the 2015
IEMFA
complaint.
20
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Effects of 5G wireless communication on human health
The road ahead for 5G
There is an urgent need for economic recovery and leadership in implementing digital technologies;
and for long-lasting economic growth in Europe. However, it is necessary to consider any possible
collateral negative impacts. Taking the economic aspects of 5G into account, there are many
challenges ahead on the path to achieving a 'gigabit society', such as for instance industry concerns
whether the plans for commercial launch of 5G in 2020 will be fulfilled, considering the technical
complexity and the necessary investment.
Other concerns relate to the creation of sufficient demand for 5G, security and health, safety and
environmental issues.
21
These need wider public awareness and consent, however this is doubly
salient regarding the possible negative health impacts due to the inescapability of constant
exposure of citizens in a 5G environment. The recent academic literature illustrates that continuous
wireless radiation seems to have biological effects especially considering the particular
characteristics of 5G: the combination of millimetre waves, a higher frequency, the quantity of
transmitters and the quantity of connections. Various studies suggest that 5G would affect the
health of humans, plants, animals, insects, and microbes – and as 5G is an untested technology, a
cautious approach would be prudent. The
UN Universal Declaration of Human Rights,
the
Helsinki
Accords
and other international treaties recognise that informed consent prior to interventions that
might affect human health is an essential, fundamental human right, which becomes even more
controversial when considering children's and young people's exposure.
A certain divergence exists among scientists on the potential negative effects of EMF exposure and
5G. Experts rarely possess complementary backgrounds in both physics or engineering and
medicine, therefore more complete scientific expertise could be achieved by combining research
teams experienced in all relevant disciplines. Optical fibre technology has been suggested by some
experts as a secure alternative to 5G, because the signal is confined within the fibre. Its potential is
much higher than that of 5G and there is no comparison between optical fibre and wireless.
Investment in optical fibre can be upgraded to superior speeds in the future, whereas it is necessary
to change the whole system for wireless technologies.
According to the 2019
study
'5G deployment: State of Play in Europe, USA and Asia' prepared for the
European Parliament, long-term technology research is essential. 'One key problem is the unusual
propagation phenomena, especially controlling and measuring radio frequency EMF exposure with
Multiple Input Multiple Output (MIMO) at millimetre wave frequencies for the handset and the base
station. The technology presents challenges to the current level of expertise (based on previous
generations of mobile cellular radio engineering) both for suppliers and standards organisations
who must incorporate the specifications in future 5G standards'. The study states that the main
problem seems to be that it is not currently possible to accurately simulate or measure 5G emissions
in the real world.
To understand potential mechanisms underlying possible health effects of EMF better and to
characterise population levels of exposure, the
Generalised EMF Research using Novel Methods
(GERoNiMO) project was launched in 2014, funded under the EU’s Seventh Framework Programme
for Research and Technological Development to address pertinent questions on EMF and health. It
proposes an integrated approach using epidemiological studies, exposure assessment techniques,
mechanistic and animal models, and expert networks applying novel methods when possible. The
project ended in 2018.
The European Commission has not yet conducted studies on the potential health risks of the
5G technology.
22
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MAIN REFERENCES
5G Deployment: State of Play in Europe, USA and Asia,
Policy Department for Economic, Scientific and
Quality of Life Policies, Directorate-General for Internal Policies, European Parliament, June 2019.
Di Ciaula A.,
Towards 5G communication systems: Are there health implications?,
International Journal of
Hygiene and Environmental Health, Volume 221, Issue 3,
pp. 367-375, April 2018.
Negreiro M.,
Towards a European gigabit society Connectivity targets and 5G,
EPRS, European
Parliament, June 2017.
Russel C.,
5 G wireless telecommunications expansion: Public health and environmental implications,
Environmental Research, Volume 165,
pp. 484-495, 2018.
Simko M. and Mattsson M.-O.,
5G Wireless Communication and Health Effects – A Pragmatic Review
Based on Available Studies Regarding 6 to 100 GHz,
International Journal of Environmental Research and
Public Health,
16(18), September 2019.
Scholz N.,
Mobile phones and health: Where do we stand?,
EPRS, European Parliament, March 2019.
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ENDNOTES
1
Industry estimates that 5G capacity will be 40 times that offered by current 4G technology. See M. Negreiro,
Towards
a European gigabit society Connectivity targets and 5G,
EPRS, June 2017.
A Megahertz (MHz) is a million cycles per second and a Gigahertz (GHz) pulses at a billion cycles per second. In order
to carry data at faster speeds, each new generation of telecommunications uses higher frequency radio waves.
See
5G deployment agenda.
In addition to spectrum licensing costs, a large share of the cost will be due to the much denser network needed,
rolling out the
small cells
necessary to transmit signals in much higher frequency bands.
See '5G
Deployment: State of Play in Europe, USA and Asia',
European Parliament, June 2019.
'Fiber
is safer, faster, more reliable, and far more cyber secure and energy efficient than wireless.'
R. M. Powell. See also
similar opinions from experts such as
T. Schoechle
and
P. Héroux.
Also known as waves or radiation.
Which would make measuring radiation exposures even more difficult.
Usually, the longer the wavelength the further it travels. The higher frequency millimetre wavelengths of 5G travel
only a few hundred metres.
See '5G
Deployment: State of Play in Europe, USA and Asia',
European Parliament, June 2019.
Radio frequency includes a continuum of the electromagnetic spectrum wavelengths from around 3 kHz to 300 GHz.
The wavelengths in the radio frequency vary from hundreds of metres to fractions of a centimetre. The frequencies
used in current digital communications have shorter wavelengths and faster data transfer. This enables the transfer of
more data simultaneously.
Time-varying means that as time (t) increases, the magnetic field changes.
The amount of charge per unit of time that flows through a unit area of a chosen cross section.
According to the WHO, EMFs of all frequencies represent one of the most common and fastest growing environmental
influences. Exposure of the whole population to EMFs will continue to increase along with technological advance.
An electromagnetic pulse is a short blowout of electromagnetic energy. Its origin can be manmade and can occur as
a radiated, electric, or magnetic field or a conducted electric current.
Millimetre waves, which will be employed by 5G, are mostly absorbed within a few millimetres of human skin and in
the surface layers of the cornea. Short-term exposure
can have adverse physiological effects in the peripheral nervous
system,
the immune system and the cardiovascular system.
For more information on the two studies, see also the EPRS briefing on
Mobile phones and health,
March 2019.
See '5G
Deployment: State of Play in Europe, USA and Asia',
European Parliament, June 2019
According to the limits established by Council Recommendation 1999/519/EC.
In an
open letter
from 2011 to the Health and Consumer Policy Commissioner, public interest stakeholders expressed
their concerns over the lack of transparency and pluralism
in the evaluation of evidence by SCENIHR,
and other EU risk
assessment committees, of the health risks of non-ionising EMF radiation (see
EPRS Briefing,
March 2019).
See EPRS briefing 'Towards
a European gigabit society: Connectivity targets and 5G',
June 2017.
See answer given by the European Commission to parliamentary question
E-005128/2018(ASW).
See also 'MEP:
Commission ‘irresponsible’ on 5G health risks',
Euractiv, 12 December 2019.
2
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DISCLAIMER AND COPYRIGHT
This document is prepared for, and addressed to, the Members and staff of the European Parliament as
background material to assist them in their parliamentary work. The content of the document is the sole
responsibility of its author(s) and any opinions expressed herein should not be taken to represent an official
position of the Parliament.
Reproduction and translation for non-commercial purposes are authorised, provided the source is
acknowledged and the European Parliament is given prior notice and sent a copy.
© European Union, 2020.
Photo credits: © PopTika / Shutterstock.com.
[email protected]
(contact)
www.eprs.ep.parl.union.eu
(intranet)
www.europarl.europa.eu/thinktank
(internet)
http://epthinktank.eu
(blog)
11
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Bilag til habilitetserklæring til Sundhedsstyrelsen
Christoffer Johansen
Pr. januar 2010
København
Christoffer Johansens habilitetserklæring vedrørende finansiering og data fra industri, der er
involveret i produktion, transmission og distribution af elektricitet samt mobiltelefonoperatø-
rer og lignende industri, der producerer, forhandler eller anvender genstande som skaber
elektromagnetiske felter i hele frekvensområdet.
Finansiering
Jeg har i perioden 1994 til 2004 modtaget midler fra Dansk Energi for at undersøge risiko for
en række sygdomme blandt danskere med ansættelse ved danske el-selskaber, samt midler til
at undersøge risiko for kræft blandt børn med bopæl tæt på elektriske højspændingsinstallati-
oner.
Jeg har i 2006 fået en fornyet bevilling fra Energinet.dk for perioden 2006 til 2008 med hen-
blik på at opdatere de allerede gennemførte undersøgelser.
Jeg har i 1994/95 modtaget fondsmidler fra det daværende Tele Danmark Mobil og Sonofon
med henblik på at gennemføre en undersøgelse af kræftrisiko blandt brugere af mobiltelefo-
ner.
Jeg har fire gang siden 1994 modtaget et personligt honorar for at udfærdige et notat, der i
form af en VVM rapport, gennemgår den videnskabelige litteratur inden for forskningsområ-
det elektromagnetiske felter og helbredseffekter hos mennesker, sidste gang i 2010. Notatet er
udarbejdet som en del af en såkaldt VVM rapport i forbindelse med forskellige udbygninger
af højspændingsnettet i Danmark.
Data
Jeg har i perioden 1994 - 1996 modtaget information om samtlige ansatte ved de 104 danske
elselskaber med oplysning om navn, CPR nummer, arbejdsfunktion, stillingsbetegnelse og
ansættelses periode(r).
Jeg har i 1996 modtaget data fra det daværende TeleDanmarkMobil og Sonofon vedrørende
samtlige abonnenters navne, adresse, mobiltelefon type og abonnements periode(r).
I 2007/2008 vil vi her på instituttet, fra de største mobiltelefon operatører få oplysninger om
mobiltelefon forbrug blandt en større gruppe danskere der indgår i en international forløbsun-
dersøgelse.
Vi vil desuden fra de samme mobiltelefon operatører modtage de samme informationer om
børn med hjerne svulster og raske kontrolbørn, der indgår i en nordisk undersøgelse af risiko
for hjernetumorer blandt børn og unge.
Jeg er medarbejder i disse to projektgrupper, mens det videnskabelige og økonomiske ansvar
ligger hos Dr Joachim Schuez.
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IARC Monographs on the Identification of
Carcinogenic Hazards to Humans
Report of the Advisory
Group to Recommend
Priorities for the
IARC Monographs
during
2020–2024
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Report of the Advisory Group to Recommend Priorities
for the
IARC Monographs
during 2020–2024
Non-ionizing radiation (radiofrequency) and extremely low-frequency magnetic fields
Radiofrequency electromagnetic fields (RF-EMF) were evaluated by the
IARC Monographs
as
possibly
carcinogenic to humans
(Group 2B) (IARC, 2013e), on the basis of limited evidence of an increased risk of
glioma. Extremely low-frequency magnetic fields (ELF-MF) were evaluated as
possibly carcinogenic to
humans
(Group 2B) (IARC, 2002), on the basis of
limited evidence
of an increased risk of childhood
leukaemia.
Exposure Data
Human exposures to RF-EMF can occur from use of personal devices (e.g. cell phones, cordless
phones, and Bluetooth) and from environmental sources such as cell phone base stations, broadcast
antennas, and medical applications. More than 5 billion people now have access to cell phone devices, and
the technology is constantly evolving. Use has also expanded rapidly in low- and middle-income countries,
where more than 75% of adults now report owning a cell phone; in high-income countries, the proportion is
96% (Pew Research Center, 2018).
Cancer in Humans
Since the previous
IARC Monographs
evaluation, several new epidemiological studies have been
published on the association between RF-EMF and cancer, although the evidence remains mixed. In the
Million Women Study cohort, there was no evidence of increased risk of glioma or meningioma, even
among long-term users. There was an increased risk of acoustic neuromas with long-term use and a
significant dose–response relationship (Benson et al., 2013). Updated follow-up in the Danish nationwide
subscribers study did not find increased risks of glioma, meningioma, or vestibular schwannoma, even
among those with subscriptions of 10 years or longer (Frei et al., 2011; Schüz et al., 2011). New reports
from case–control studies that assessed long-term use also found mixed results; for example, increased risks
of glioma and acoustic neuroma were reported by Hardell & Carlberg (2015) and Hardell et al. (2013), but
no evidence of increased risks for these tumours were reported by Yoon et al. (2015) and Pettersson et al.
(2014). Röösli et al. (2019) recently reviewed these new data. Several large-scale studies are still in progress
and should report results within the next few years. Mobi-Kids is a multicentre case–control study of brain
tumours in those aged 10–24 years. Cohort Study of Mobile Phone Use and Health
(COSMOS)
is a new
European cohort of adult cell phone users. There will also be updated results from the Million Women
Study.
Cancer in Experimental Animals
New data in experimental animals for exposure to RF-EMF have been published since the previous
IARC Monographs
evaluation. The large study by the United States National Toxicology Program found an
increased risk of malignant schwannomas of the heart in male rats with high exposure to radiofrequency
radiation at frequencies used by cell phones, as well as possible increased risks of certain types of tumours in
148
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Report of the Advisory Group to Recommend Priorities
for the
IARC Monographs
during 2020–2024
the brain and adrenal glands, but no increased risks in mice or female rats (NTP, 2018a, b). Another study in
experimental animals also found an increase in schwannomas of the heart in highly exposed male rats and a
possible increase in gliomas in female rats (Falcioni et al., 2018).
Mechanistic Evidence
The previous IARC evaluation concluded that there was weak evidence that radiofrequency radiation
was genotoxic but that there was no evidence for mutagenicity (IARC, 2013e). Although there have been
many new publications from a wide variety of experiments, uncertainty remains about the mechanisms, and
there are few systematic reviews of the new data (Kocaman et al., 2018).
Although a future evaluation could be broadened to consider exposure to all non-ionizing radiation
(including ELF-MF), ELF-MF were evaluated by IARC as
possibly carcinogenic to humans
(Group 2B),
and the Advisory Group did not recommend an update, because of a lack of new informative
epidemiological findings, no toxicological evidence, and little supporting mechanistic evidence.
Key References
The following key references were also identified: Coureau et al. (2014); Carlberg & Hardell (2015);
Pedersen et al. (2017).
Recommendation for non-ionizing radiation (radiofrequency):
High priority (and ready for
evaluation within 5 years)
Recommendation for extremely low-frequency magnetic fields:
No evaluation
Nuclear industry work
Different types of ionizing radiation have been evaluated repeatedly by the
IARC Monographs
programme (IARC, 2000b, 2012f), and all types have been classified as
carcinogenic to humans
(Group 1);
overall evaluations are based on different evidence streams, often including
sufficient evidence
in humans
for several cancer sites. New research in recent years has confirmed increased risks per unit of exposure to
ionizing radiation for cancer sites and groups of cancer sites that have already been linked with ionizing
radiation. No specific evaluation has been made in respect of work in the nuclear industry, which represents
a specific exposure condition for agents already classified as
carcinogenic to humans
(Group 1).
Key References
The following key references were identified: Lee et al. (2015c); Leuraud et al. (2015); Richardson et al.
(2015); Schubauer-Berigan et al. (2015); Grellier et al. (2017).
Recommendation:
No evaluation
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Corte di Cassazione n. 17438/2012 - l'uso massiccio
del cellulare può avere "un ruolo almeno
concausale" nella genesi di alcuni tumori –
12.10.2012. - - Giudice di Pace
claps carlo
Con la sentenza n. 17438/2012, la Corte di Cassazione ha stabilito che l'uso massiccio del
cellulare, per parecchie ore al giorno, e per un lungo periodo di anni, possa avere "un ruolo almeno
concausale" nella genesi di alcuni tumori dei nervi cranici. Gli Ermellini hanno precisato che gli studi
indipendenti condotti tra il 2005 e il 2009, che hanno evidenziato un maggiore rischio di insorgenza di
neoplasie negli utilizzatori 'forti' di telefonia mobile, sono, correttamente, stati considerati di "maggiore
attendibilità" per non essere stati cofinanziati, a differenza di altri, anche dalle stesse ditte produttrici di
cellulari".
CORTE DI CASSAZIONE
SEZIONE LAVORO
SENTENZA n. 17438 DEL 12 ottobre 2012
SVOLGIMENTO DEL PROCESSO
Con sentenza del 10 - 22.12.2009 la Corte d'appello di Brescia, in riforma della pronuncia di prime cure,
condannò l'Inail a corrispondere a M. I. la rendita per malattia professionale prevista per l'invalidità all'80%.
Il M. aveva agito in giudizio deducendo che, in conseguenza dell'uso lavorativo protratto, per dodici anni e
per 5-6 ore al giorno, di telefoni cordless e cellulari all'orecchio sinistro aveva contratto una grave patologia
tumorale; le prove acquisite e le indagini medico legali avevano permesso di accertare, nel corso del giudizio,
la sussistenza dei presupposti fattuali dedotti, in ordine sia all'uso nei termini indicati dei telefoni ne! corso
dell'attività lavorativa, sia all'effettiva insorgenza di un "neurinoma del Ganglio di Gasser" (tumore che
colpisce i nervi cranici, in particolare il nervo acustico e, più raramente, come nel caso di specie, il nervo
cranico trigemino), con esiti assolutamente severi nonostante le terapie, anche di natura chirurgica, praticate;
sulla ricorrenza di tali elementi fattuali, come evidenziato nella sentenza impugnata, non erano state
svolte contestazioni in sede di appello, incentrandosi la questione devoluta al Giudice del gravame sul nesso
causale tra l'uso dei telefoni e l'insorgenza della patologia.
La Corte territoriale, rinnovata la consulenza medico legale, ritenne dì dover seguire le conclusioni a cui era
pervenuto il CTU nominato in grado d'appello, osservando in particolare quanto segue:
- i telefoni mobili (cordless) e i telefoni cellulari funzionano attraverso onde elettromagnetiche e, secondo il
CTU, "In letteratura gli studi sui tumori cerebrali per quanto riguarda il neurinoma considerano il tumore con
localizzazione al nervo acustico che è il più frequente. Trattandosi del medesimo istotipo è del tutto logico
assimilare i dati al neurinoma del trigemino"; in particolare era stato osservato che i due neurinomi
appartengono al medesimo distretto corporeo, in quanto entrambi i nervi interessati si trovano nell'angolo
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ponto-cerebellare, che è una porzione ben definita e ristretta dello spazio endocranico, certamente compresa
nel campo magnetico che si genera dall'utilizzo dei telefoni cellulari e cordless;
nella CTU erano stati riassunti con una tabella alcuni studi effettuati dal 2005 al 2009 ed in tre, effettuati
dall'Hardell group, era stato evidenziato un aumento significativo de! rischio relativo di neurinoma
(intendendosi per rischio relativo la misura di associazione fra l'esposizione ad un particolare fattore di rischio
e l'insorgenza di una definita malattia, calcolata come il rapporto fra i tassi di incidenza negli esposti
[numeratore] e nei non esposti [denominatore]);
- un lavoro del 2009 del medesimo gruppo aveva considerato anche altri elementi quali età dell'esposizione,
l'ipsilateralità e il tempo di esposizione, indicando, per quanto riguarda il neurinoma dell'acustico, un Odd
ratio per l'uso dei cordless di 1,5 e per il telefono cellulare di 1,7;
considerando l'uso maggiore di 10 anni, gli Odd ratio erano rispettivamente di 1,3 e di 1,9, intendendosi per
Odd ratio il rapporto tra la frequenza con la quale un evento si verifica in un gruppo di pazienti e la frequenza
con la quale lo stesso evento si verifica in un gruppo di pazienti di controllo, onde se il valore dell'Odd ratio è
superiore a 1 significa che la probabilità che si verifichi l'evento considerato (per esempio una malattia) in un
gruppo (per esempio tra gli esposti) è superiore rispetto a quella di un altro gruppo (per esempio tra i non
esposti), mentre significato opposto ha un valor inferiore a 1;
- una recente review della The International Commission on Non- lonizing Radiation Protection aveva
evidenziato i limiti degli studi epidemiologici fino ad allora attuati, concludendo che, allo stato attuale, non vi
era una convincente evidenza del ruolo delle radiofrequenze nella genesi dei tumori, ma aggiungendo che gli
studi non ne avevano escluso l'associazione;
- un'ulteriore autorevole review (Kundi nel 2009) aveva confermato i dubbi che gli studi epidemiologici
inducono per quanto riguarda il tempo di esposizione e concluso per un rischio individuale basso, ma
presente; l'esposizione poteva incidere sulla storia naturale della neoplasia in vari modi: interagendo nella fase
iniziale di induzione, intervenendo sul tempo di sviluppo dei tumori a lenta crescita, come i neurinomi,
accelerandola ed evitando la possibile naturale involuzione;
- l'analisi della letteratura non portava quindi ad un giudizio esaustivo, ma, con tutti i limiti insiti nella
tipologia degli studi, un rischio aggiuntivo per i tumori cerebrali, ed in particolare per il neurinoma, era
documentato dopo un'esposizione per più di 10 anni a radiofrequenze emesse da telefoni portatili e cellulari;
- tale tempo di esposizione era un elemento valutativo molto rilevante, poiché, nello studio del 2006,
l'esposizione per più di 10 anni comportava un rischio relativo calcolato di 2,9 sicuramente significativo;
- si trattava quindi di una situazione "individuale" che gli esperti riconducevano al "modello probabilistico-
induttivo" ed alla "causalità debole", avente comunque valenza in sede previdenziale;
- doveva dunque riconoscersi, secondo il CTU, un ruolo almeno concausale delle radiofrequenze nella genesi
della neoplasia subita dall'assicurato, configurante probabilità qualificata:
- la censura dell'lnail relativa agli studi utilizzati dal CTU non coglieva nel segno, poiché lo studio del 2000
dell'OMS, che aveva escluso effetti negativi per la salute, si era basato su dati ancor più risalenti, non tenendo
quindi conto dell'uso più recente, ben più massiccio e diffuso, di tali apparecchi e del fatto che si tratta di
tumori a lenta insorgenza, risultando quindi più attendibili gli studi svolti nel 2009;
- inoltre, come osservato dal CT di parte M., gli studi del 2009 non erano stati condotti su un basso numero di
casi, ma, al contrario, sul numero totale dei casi (679) che si erano verificati in un anno in Italia; inoltre, a
differenza dello studio della IARC, co-finanziato dalla ditte produttrici di telefonicellulari, gli studi citati dal
CTU erano indipendenti;
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- ancora, secondo quanto osservato dal CT di parte M., confrontando il dato di rischio individuale calcolato
dal CTU (2,9) con quello rilevato per il fattore di rischio, universalmente riconosciuto, dell'esposizione alle
radiazioni ionizzanti, doveva considerarsi come per i sopravvissuti alle esplosioni atomiche giapponesi di
Hiroshima e Nagasaki fosse stato accertato un rischio relativo di tipo oncologico di 1,39 per "tutti i tumori"
con un minimo di 1,22 per i tumori di "utero e cervice" ed un massimo di 4,92 per la "leucemia", il che stava a
significare che il rischio oncogeno medio delle radiazioni ionizzanti era inferiore a quello che si aveva per
l'esposizione alle radio frequenze in riferimento ai neurinomi endocranici, ciò che rendeva ancora più evidente
la reale portata di quanto affermato dal CTU;
- secondo l'insegnamento della giurisprudenza di legittimità, nel caso di malattia professionale non tabellata,
come anche in quello di malattia ad eziologia multifattoriale, la prova della causa di lavoro, che grava sul
lavoratore, deve essere valutata in termini di ragionevole certezza, nel senso che, esclusa la rilevanza della
mera possibilità dell'origine professionale, questa può essere invece ravvisata in presenza di un rilevante
grado di probabilità; e, a tale riguardo, il giudice deve non solo consentire all'assicurato di esperire i mezzi di
prova ammissibili e ritualmente dedotti, ma deve altresì valutare le conclusioni probabilistiche del consulente
tecnico in tema di nesso causale, considerando che la natura professionale della malattia può essere desunta
con elevato grado di probabilità dalla tipologia delle lavorazioni svolte, dalla natura dei macchinari
presenti nell'ambiente di lavoro, dalla durata della prestazione lavorativa e dall'assenza di altri
fattori extralavorativi, alternativi o concorrenti che possano costituire causa della malattia;
- doveva quindi ritenersi la sussistenza del requisito di elevata probabilità che integra il nesso causale richiesto
dalla normativa. Avverso la suddetta sentenza della Corte territoriale rinati ha proposto ricorso fondato su due
motivi e illustrato con memoria L'intimato M. I. ha resistito con controricorso, illustrato con memoria.
Motivi della decisione1. Con il primo motivo l'Istituto ricorrente denuncia violazione dell'art. 3 dpr n.
1124/65, rilevando che, secondo i principi di diritto elaborati in materia dalla giurisprudenza di legittimità, la
corretta applicazione della norma suddetta richiede, in particolare, l'accertamento sulla base di dati
epidemiologici e di letteratura ritenuti affidabili dalla comunità scientifica, che l'agente dedotto in giudizio sia
dotato di efficienza patogenetica, quanto meno probabile, per la specifica malattia allegata e diagnosticata; la
suddetta relazione causale non poteva dunque essere suffragata "dalla personale valutazione dell'ausiliario del
giudice, fondata sulla preferenza per taluni dati epidemiologici rispetto ad altri, ma deve essere supportata da
un giudizio di affidabilità dei dati stessi espresso dalla comunità scientifica"; nel caso di specie il CTU si era
soffermato esclusivamente sui risultati del gruppo Hardell, in contrasto con quelli della comunità scientifica;
inoltre il CTU aveva del tutto arbitrariamente utilizzato la contabilità tra esposizioni a radiofrequenze e
neurinoma del nervo acustico, ipotizzata dal gruppo Hardeil, per affermare la relazione causale, addirittura
con giudizio di probabilità qualificata, tra tali radiofrequenze e il neurinoma del trigemino; doveva al riguardo
rilevarsi che la Commissione scientifica per l'elaborazione e la revisione periodica delle malattie di cui è
obbligatoria la segnalazione ai sensi dell'art. 139 dpr n. 1124/65, in occasione dell'aggiornamento dell'elenco
approvato con decreto ministeriale 11.12.2009, non aveva ritenuto di dover includere i tumori dei nervi
cranici, indotti da esposizione alle radiofrequenze, tra le malattie di possibile origine professionale.
1.2Secondo la
giurisprudenza di questa Corte, nel caso di malattia professionale non tabellata, come anche in quello di
malattia ad eziologia multifattoriale, la prova della causa di lavoro, che grava sul lavoratore, deve essere
valutata in termini di ragionevole certezza, nel senso che, esclusa la rilevanza della mera possibilità
dell'origine professionale, questa può essere invece ravvisata in presenza di un rilevante grado di probabilità;
a tale riguardo, il giudice deve non solo consentire all'assicurato di esperire i mezzi di prova ammissibili e
ritualmente dedotti, ma deve altresì valutare le conclusioni probabilistiche del consulente tecnico in tema di
nesso causale, facendo ricorso ad ogni iniziativa ex officio diretta ad acquisire ulteriori elementi in relazione
all'entità ed
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all'esposizione del lavoratore ai fattori di rischio ed anche considerando che la natura professionale della
malattia può essere desunta con elevato grado di probabilità dalla tipologia delle lavorazioni svolte, dalia
natura dei macchinari presenti nell'ambiente di lavoro, dalla durata della prestazione lavorativa e dall'assenza
di altri fattori extralavorativi, alternativi o concorrenti, che possano costituire causa della malattia (cfr, ex
plurimis, Cass., nn. 6434/1994; 5352/2002; 11128/2004;15080/2009).
La sentenza impugnata ha fatto applicazione di tali principi, ravvisando, in base alle
considerazioni diffusamente esposte nello storico di lite, la sussistenza del requisito di elevata probabilità
che integra il nesso causale.
Non è quindi ravvisabile il denunciato vizio di violazione di legge, che si fonda infatti su una
pretesa erronea valutazione (da parte del CTU e della Corte territoriale) della affidabilità dei dati
presi in considerazione al fine di suffragare tale requisito e, pertanto, sostanzialmente su un vizio di
motivazione (in effetti dedotto con il secondo motivo di ricorso).
Il motivo all'esame va pertanto disatteso.
2. Con il secondo motivo l'Istituto ricorrente denuncia appunto vizio di motivazione, assumendo
che:
- il CTU di secondo grado, dopo avere evidenziato che la review della The International
Commission on Non-lonizing Radiation Protection aveva concluso che, allo stato attuale, non vi era
una convincente evidenza del ruolo delle radiofrequenze nella genesi dei tumori, pur non
escludendosene l'associazione, senza consequenzialità logica e senza motivazione aveva tratto la
conclusione della probabilità qualificata di un ruolo almeno concausale delle radiofrequenze nella
genesi della neoplasia per cui è causa;
- doveva ritenersi priva dì qualsivoglia fondamento scientifico la ritenuta assimilabilità, sul piano
eziopatogenetico, del neurinoma del nervo acustico e di quello del trigemino, essendo "nozione
comune" della scienza medica che tumori dello stesso istotipo, ma con localizzazione diversa, anche se
nell'ambito dello stesso distretto anatomico, riconoscono cause diverse e che qualsiasi potenziale
agente cancerogeno che venga in contatto con il corpo umano modifica la sua azione a seconda dei
tessuti che attraversa o con cui viene in contatto; e, in effetti, il nervo acustico e il nervo trigemino,
in particolare il ganglio di Gasser, hanno una diversa collocazione nella teca cranica e diverse sono
le strutture anatomiche che li separano dall'esterno e fra loro;
la Corte territoriale non aveva risposto alle osservazioni svolte dall'Istituto, anche con riferimento
alla circostanza che era "in corso" uno studio epidemiologico internazionale "interphone",
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coordinato dalla IARC e che l'OMS, in base al principio di precauzione, aveva suggerito "una
politica di gestione del rischio che viene applicata in una situazione di "incertezza scientifica"":
- doveva ritenersi inconferente sul piano scientifico l'affermazione della Corte territoriale circa
l'attendibilità, perché indipendente, dello studio del gruppo Hardell, a fronte del cofinanziamento
della ricerca "interphone" da parte dei produttori di telefoni cellulari, trascurando che tale ricerca è
finanziata dalla Unione Europea e diretta e coordinata dalla IARC (Agenzia internazionale ricerca
sul cancro dell'OMS);
- neppure la Corte territoriale aveva ritenuto di chiamare il CTU a chiarimenti a fronte delle
ricordate osservazioni critiche. 2.1 La giurisprudenza di legittimità ha reiteratamente affermato che
nei giudizi in cui sia stata esperita CTU di tipo medico-legale, nei caso in cui il giudice del merito si
basi sulle conclusioni dell'ausiliario giudiziario, affinché i lamentati errori e lacune della consulenza
tecnica determinino un vizio di motivazione della sentenza denunciabile in cassazione, è necessario
che i relativi vizi logico -formali si concretino in una palese devianza dalle nozioni della scienza
medica o si sostanzino in affermazioni illogiche o scientificamente errate, con il relativo onere, a
carico della parte interessata, di indicare le relative fonti, senza potersi la stessa limitare a mere
considerazioni sulle prospettazioni operate dalla controparte, che si traducono in una inammissibile
critica del convincimento del giudice di merito che si sia fondato, per l'appunto, sulla consulenza
tecnica (cfr, ex plurimis, Cass., nn. 16392/2004; 17324/2005; 7049/2007; 18906/2007).
Nel caso all'esame l'Istituto ricorrente, nel contestare la ritenuta assimilabilità, sul piano
eziopatogenetico, del neurinoma del nervo acustico e di quello del trigemino, non specifica -
rifugiandosi nel concetto di "nozione comune" - le fonti scientifiche, ritualmente dedotte ed
acquisite al giudizio, in base alle quali avrebbero dovuto ritenersi scientificamente errate le
affermazioni rese al riguardo dal CTU e seguite dalla sentenza impugnata, finendo per richiedere al
riguardo a questa Corte una valutazione di merito inammissibile in sede di legittimità.
Neppure è dato rilevare il preteso e denunciato vizio di mancanza di consequenzialità logica e di
motivazione in ordine alle conclusioni della probabilità qualificata di un ruolo almeno concausale
delle radiofrequenze nella genesi della neoplasia per cui è causa, posto che tale giudizio, come
diffusamente esposto nello storico di lite, non discende dalla mera indicazione delle conclusioni
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(evidentemente difformi) a cui era pervenuta la ricordata review della The International
Commission on Non-lonizing Radiation Protection, ma, piuttosto, dai riscontri di altri studi a
carattere epidemiologico svolti al riguardo.
Inoltre, e significativamente, la sentenza impugnata, seguendo le osservazioni del CTU, ha ritenuto
di dover ritenere di particolare rilievo quegli studi che avevano preso in considerazione anche altri
elementi, quali l'età dell'esposizione, l’ipsilateralità e il tempo di esposizione, atteso che, nella
specie, doveva valutarsi la sussistenza del nesso causale in relazione ad una situazione fattuale dei
tutto particolare, caratterizzata da un'esposizione alle radiofrequenze per un lasso temporale
continuativo molto lungo (circa 12 anni), per una media giornaliera di 5 - 6 ore e concentrata
principalmente sull'orecchio sinistro dell'assicurato (che, com'è di piana evidenza, concretizza una
situazione affatto diversa da un normale uso non professionale del telefono cellulare).
L'ulteriore rilievo circa la maggiore attendibilità proprio di tali studi, stante la loro posizione di
indipendenza, ossia per non essere stati cofinanziati, a differenza di altri, anche dalle stesse ditte
produttrici di cellulari, costituisce ulteriore e non illogico fondamento delle conclusioni accolte.Né è stato
dedotto - e tanto meno, dimostrato - che le indagini epidemiologiche Se cui conclusioni
sono state prese in particolare considerazione provengano da gruppi di lavoro privi di serietà ed
autorevolezza e, come tali, sostanzialmente estranei alla comunità scientifica.
L'asserita prevalenza che, secondo il ricorrente, dovrebbe essere attribuita alle conclusioni di altri
gruppi di ricerca (le cui indagini, peraltro, secondo quanto dedotto, almeno all'epoca del giudizio di
merito erano ancora "in corso"), si risolvono anch'essi nella richiesta di un riesame del merito, non
consentito in sede di legittimità. Avendo inoltre la Corte territoriale riscontrato nelle considerazioni
già svolte dal CTU e dal CT di parte M. elementi ritenuti sufficienti a confutare le osservazioni
critiche dell'Istituto, non sussisteva la necessità di investire ulteriormente il CTU di una richiesta a
chiarimenti.
Anche il secondo motivo di ricorso va quindi disatteso.
3. In definitiva il ricorso va rigettato
L'esito fra loro difforme dei giudizi di merito e la novità, sotto il profilo della peculiarità fattuale,
della vicenda dedotta in causa, consigliano la compensazione delle spese.
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P.Q.M.
Rigetta il ricorso; spese compensate.
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Comment
Planetary electromagnetic pollution: it is time to assess its
impact
As the Planetary Health Alliance moves forward after a
productive second annual meeting, a discussion on the
rapid global proliferation of artificial electromagnetic
fields would now be apt. The most notable is the
blanket of radiofrequency electromagnetic radiation,
largely microwave radiation generated for wireless
communication and surveillance technologies, as
mounting scientific evidence suggests that prolonged
exposure to radiofrequency electromagnetic radiation
has serious biological and health effects. However,
public exposure regulations in most countries con-
tinue to be based on the guidelines of the International
Commission on Non-Ionizing Radiation Protection
1
and
Institute of Electrical and Electronics Engineers,
2
which
were established in the 1990s on the belief that only
acute thermal effects are hazardous. Prevention of tissue
heating by radiofrequency electromagnetic radiation is
now proven to be ineffective in preventing biochemical
and physiological interference. For example, acute
non-thermal exposure has been shown to alter human
brain metabolism by NIH scientists,
3
electrical activity
in the brain,
4
and systemic immune responses.
5
Chronic
exposure has been associated with increased oxidative
stress and DNA damage
6,7
and cancer risk.
8
Laboratory
studies, including large rodent studies by the US National
Toxicology Program
9
and Ramazzini Institute of Italy,
10
confirm these biological and health effects in vivo. As we
address the threats to human health from the changing
environmental conditions due to human activity,
11
the increasing exposure to artificial electromagnetic
radiation needs to be included in this discussion.
Due to the exponential increase in the use of wireless
personal communication devices (eg, mobile or cordless
phones and WiFi or Bluetooth-enabled devices) and
the infrastructure facilitating them, levels of exposure
to radiofrequency electromagnetic radiation around
the 1 GHz frequency band, which is mostly used for
modern wireless communications, have increased from
extremely low natural levels by about 10¹⁸ times (figure).
Radiofrequency electromagnetic radiation is also used
for radar, security scanners, smart meters, and medical
equipment (MRI, diathermy, and radiofrequency
ablation). It is plausibly the most rapidly increasing
www.thelancet.com/planetary-health
Vol 2 December 2018
anthropogenic environmental exposure since the mid-
20th century, and levels will surge considerably again,
as technologies like the Internet of Things and 5G add
millions more radiofrequency transmitters around us.
Unprecedented human exposure to radiofrequency
electromagnetic radiation from conception until death
has been occurring in the past two decades. Evidence
of its effects on the CNS, including altered neuro-
development
14
and increased risk of some neuro-
degenerative diseases,
15
is a major concern considering
the steady increase in their incidence. Evidence exists
for an association between neurodevelopmental or
10
9
ICNIRP (occupational peak)
ICNIRP (occupational)
ICNIRP (public peak)
ICNIRP (public)
2010s, typical
1980s, typical
1950s, typical
Natural background
300 GHz end of ICNIRP radiofrequency guidance
2010s
10
–12
Medium-wave broadcasting
Short-wave broadcasting
Mobile phones, WiFi, etc
1980s
Mobile phones
FM VHF radio
0
10
6
1 MHz
Television
1950s
10
9
1 GHz
Frequency (Hz)
10
12
1 THz
10
6
10
3
1
Power flux density (W/m
2
)
10
–3
10
–6
10
–9
10
–15
10
–18
Figure:
Typical maximum daily exposure to radiofrequency electromagnetic radiation from man-made and
natural power flux densities in comparison with International Commission on Non-Ionizing Radiation
Protection safety guidelines
1
Anthropogenic radiofrequency electromagnetic radiation levels are illustrated for different periods in the
evolution of wireless communication technologies. These exposure levels are frequently experienced daily by
people using various wireless devices. The levels are instantaneous and not time-averaged over 6 minutes as
specified by International Commission on Non-Ionizing Radiation Protection for thermal reasons. Figure modified
from Philips and Lamburn
12
with permission. Natural levels of radiofrequency electromagnetic radiation were
based on the NASA review report CR-166661.
13
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Comment
For the
Oceania Radiofrequency
Scientific Advisory Association
see www.orsaa.org
For the
International EMF
Scientist Appeal
see www.
emfscientist.org
behavioural disorders in children and exposure to
wireless devices,
14
and experimental evidence, such as
the Yale finding, shows that prenatal exposure could
cause structural and functional changes in the brain
associated with ADHD-like behaviour.
16
These findings
deserve urgent attention.
At the Oceania Radiofrequency Scientific Advisory
Association, an independent scientific organisation,
volunteering scientists have constructed the world’s
largest categorised online database of peer-reviewed
studies on radiofrequency electromagnetic radiation
and other man-made electromagnetic fields of lower
frequencies. A recent evaluation of 2266 studies
(including in-vitro and in-vivo studies in human,
animal, and plant experimental systems and population
studies) found that most studies (n=1546, 68·2%)
have demonstrated significant biological or health
effects associated with exposure to anthropogenic
electromagnetic fields. We have published our
preliminary data on radiofrequency electromagnetic
radiation, which shows that 89% (216 of 242) of
experimental studies that investigated oxidative stress
endpoints showed significant effects.
7
This weight of
scientific evidence refutes the prominent claim that
the deployment of wireless technologies poses no
health risks at the currently permitted non-thermal
radiofrequency exposure levels. Instead, the evidence
supports the International EMF Scientist Appeal by
244 scientists from 41 countries who have published on
the subject in peer-reviewed literature and collectively
petitioned the WHO and the UN for immediate
measures to reduce public exposure to artificial
electromagnetic fields and radiation.
Evidence also exists of the effects of radiofrequency
electromagnetic radiation on flora and fauna. For
example, the reported global reduction in bees and
other insects is plausibly linked to the increased
radiofrequency electromagnetic radiation in the
environment.
17
Honeybees are among the species
that use magnetoreception, which is sensitive to
anthropogenic electromagnetic fields, for navigation.
Man-made electromagnetic fields range from
extremely low frequency (associated with electricity
supplies and electrical appliances) to low, medium,
high, and extremely high frequency (mostly associated
with wireless communication). The potential effects
of these anthropogenic electromagnetic fields on
natural electromagnetic fields, such as the Schumann
Resonance that controls the weather and climate,
have not been properly studied. Similarly, we do not
adequately understand the effects of anthropogenic
radiofrequency electromagnetic radiation on other
natural and man-made atmospheric components
or the ionosphere. It has been widely claimed that
radiofrequency electromagnetic radiation, being non-
ionising radiation, does not possess enough photon
energy to cause DNA damage. This has now been
proven wrong experimentally.
18,19
Radiofrequency
electromagnetic radiation causes DNA damage
apparently through oxidative stress,
7
similar to near-UV
radiation, which was also long thought to be harmless.
At a time when environmental health scientists
tackle serious global issues such as climate change and
chemical toxicants in public health, there is an urgent
need to address so-called electrosmog. A genuine
evidence-based approach to the risk assessment and
regulation of anthropogenic electromagnetic fields
will help the health of us all, as well as that of our
planetary home. Some government health authorities
have recently taken steps to reduce public exposure to
radiofrequency electromagnetic radiation by regulating
use of wireless devices by children and recommending
preferential use of wired communication devices in
general, but this ought to be a coordinated international
effort.
*Priyanka Bandara, David O Carpenter
Oceania Radiofrequency Scientific Advisory Association,
Scarborough, QLD 4020, Australia (PB); and Institute for Health
and the Environment, University at Albany, Rensselaer, NY, USA
(DOC)
[email protected]
We declare no competing interests. We thank Alasdair Philips for assistance with
the figure and Victor Leach and Steve Weller for assistance with the ORSAA
Database, which has enabled our overview of the scientific evidence in this area
of research.
Copyright © The Author(s). Published by Elsevier Ltd. This is an Open Access
article under the CC BY-NC-ND 4.0 license.
1
International Commission on Non-Ionizing Radiation Protection. ICNIRP
guidelines for limiting exposure to time-varying electric, magnetic, and
electromagnetic fields (up to 300 GHz).
Health Phys
1998;
74:
494–522.
Institute of Electrical and Electronics Engineers. IEEE C95.7-2014—IEEE
recommended practice for radio frequency safety programs, 3 kHz to
300 GHz. IEEE Standards Association, 2014. https://standards.ieee.org/
standard/C95_7-2014.html (accessed Nov 6, 2018).
Volkow ND, Tomasi D, Wang GJ, et al. Effects of cell phone radiofrequency
signal exposure on brain glucose metabolism.
JAMA
2011;
305:
808–13.
Schmid MR, Loughran SP, Regel SJ, et al. Sleep EEG alterations: effects of
different pulse-modulated radio frequency electromagnetic
fields.
J Sleep Res
2012;
21:
50–58.
2
3
4
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Comment
5
6
7
8
9
10
11
12
Kimata H. Microwave radiation from cellular phones increases
allergen-specific IgE production.
Allergy
2005;
60:
838–39.
Zothansiama, Zosangzuali M, Lalramdinpuii M, Jagetia GC. Impact of
radiofrequency radiation on DNA damage and antioxidants in peripheral
blood lymphocytes of humans residing in the vicinity of mobile phone base
stations.
Electromagn Biol Med
2017;36: 295–305.
Bandara P, Weller S. Biological effects of low-intensity radiofrequency
electromagnetic radiation—time for a paradigm shift in regulation of
public exposure.
Radiat Protect Australas
2017;
34:
2–6.
Carlberg M, Hardell L. Evaluation of mobile phone and cordless phone use
and glioma risk using the bradford hill viewpoints from 1965 on
association or causation.
Biomed Res Int
2017;
2017:
9218486.
Cell phone radio frequency radiation. National Toxicology Program,
US Department of Health and Human Services, 2018. https://ntp.niehs.nih.
gov/results/areas/cellphones/index.html (accessed Nov 8, 2018).
Falcioni L, Bua L, Tibaldi E, et al. Report of final results regarding brain and
heart tumors in Sprague-Dawley rats exposed from prenatal life until
natural death to mobile phone radiofrequency field representative of a
1.8GHz GSM base station environmental emission.
Environ Res
2018;
165:
496–503.
Myers SS. Planetary health: protecting human health on a rapidly changing
planet.
Lancet
2018;
390:
2860–68.
Philips A, Lamburn G. Natural and human-activity-generated
electromagnetic fields on Earth. Childhood Cancer 2012; London;
April 24–26, 2012.
13
14
15
16
17
18
19
Raines JK. NASA-CR-166661. Electromagnetic field interactions with the
human body: observed effects and theories. NASA Technical Reports
Server, 1981. https://ntrs.nasa.gov/archive/nasa/casi.ntrs.nasa.
gov/19810017132.pdf (accessed Oct 10, 2018).
Divan HA, Kheifets L, Obel C, Olsen J. Prenatal and postnatal exposure to
cell phone use and behavioral problems in children.
Epidemiology
2008;
19:
523–29.
Zhang X, Huang WJ, Chen WW. Microwaves and Alzheimer’s disease.
Exp Ther Med
2016;
12:
1969–72.
Aldad TS, Gan G, Gao XB, Taylor HS. Fetal radiofrequency radiation
exposure from 800–1900 mhz-rated cellular telephones affects
neurodevelopment and behavior in mice.
Sci Rep
2012;
2:
312.
Taye RR, Deka MK, Rahman A, Bathari M. Effect of electromagnetic
radiation of cell phone tower on foraging behaviour of Asiatic honey bee,
Apis cerana
F. (Hymenoptera: Apidae).
J Entomol Zool Stud
2017;
5:
1527–29.
Smith-Roe SL, Wyde ME, Stout MD, et al. Evaluation of the genotoxicity of
cell phone radiofrequency radiation in male and female rats and mice
following subchronic exposure. Environmental Mutagenesis and Genomics
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Largest Unethical Medical Experiment in Human History
Copyright 2020
RN Kostoff
THE LARGEST UNETHICAL MEDICAL EXPERIMENT IN HUMAN HISTORY
Ronald N. Kostoff, Ph.D.
Research Affiliate, School of Public Policy, Georgia Institute of Technology
KEYWORDS
Unethical Research; Electromagnetic Fields; Wireless Radiation; Radiofrequency Radiation; RF;
Non-Ionizing Radiation; Mobile Networking Technology; 5G; Adverse Health Effects
ABSTRACT
This monograph describes the largest unethical medical experiment in human history: the
implementation and operation of non-ionizing non-visible EMF radiation (hereafter called
wireless radiation) infrastructure for communications, surveillance, weaponry, and other
applications. It is unethical because it violates the key ethical medical experiment requirement
for
“informed
consent” by the overwhelming majority of the participants.
The monograph provides background on unethical medical research/experimentation, and
frames the implementation of wireless radiation within that context. The monograph then
identifies a wide spectrum of adverse effects of wireless radiation as reported in the premier
biomedical literature for over seven decades. Even though many of these reported adverse
effects are extremely severe, the
true extent of their severity has been grossly underestimated.
Most of the reported laboratory experiments that produced these effects are not reflective
of the real-life environment in which wireless radiation operates. Many experiments do not
include pulsing and modulation of the carrier signal, and most do not account for synergistic
effects of other toxic stimuli acting in concert with the wireless radiation. These two additions
greatly exacerbate the severity of the adverse effects from wireless radiation,
and their neglect
in current (and past) experimentation results in substantial under-estimation of the breadth and
severity of adverse effects to be expected in a real-life situation. This lack of credible safety
testing, combined with depriving the public of the opportunity to provide informed consent,
contextualizes the wireless radiation infrastructure operation as an unethical medical experiment.
Addition of the nascent fifth generation of mobile networking technology (5G) globally to the
existing mobile technology network will contribute further to the largest unethical medical
experiment in human history!
This monograph consists of four chapters and eight appendices. Chapter 1 focuses on
unethical research, showing how wireless radiation infrastructure implementation fits into the
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Largest Unethical Medical Experiment in Human History
Copyright 2020
RN Kostoff
framework of unethical medical experimentation, and providing many examples of other types of
unethical medical experimentation.
Chapter 2 is the main technical chapter, focusing on adverse health effects of wireless
radiation. It describes:
•
•
•
adverse effects from past research, and what additional adverse effects can be expected
when 5G is implemented fully
lack of full consensus among key stakeholders on adverse effects from wireless radiation,
and the role played by conflicts-of-interest in this lack of consensus
the main reason that this unethical medical experiment was allowed to take place:
The Federal government that
promotes
accelerated implementation of wireless radiation
technology also 1)
sponsors
research examining the technology’s potential adverse effects
and 2)
regulates
the technology’s potentially adverse impacts on the
public. This unethical
promotion-sponsorship-regulation conflict-of-interest lays the groundwork for unethical
medical experimentation!
Chapter 3 contains the references for the main text, and Chapter 4 contains the eight
appendices.
Appendix 1 presents more details about unethical medical experiments, including
examples and many references for further study.
Appendix 2 contains a manual taxonomy of a representative adverse EMF effects
database; Appendix 3 contains a factor analysis taxonomy of the same database; and, Appendix 4
contains a text clustering taxonomy of the same database. All three taxonomies contain links
between the categories in the summary tables and the titles of papers associated with each
category.
Appendix 5 shows the
potential contribution of wireless radiation to the opioid crisis
and
potential contribution of wireless radiation to exacerbation of the coronavirus pandemic.
Appendix 6 shows the
link between funding source and research outcomes,
and
presents many references on the topic of funding source-driven bias.
Appendix 7 describes the under-recognized adverse effects of wireless radiation related
to
medical implants
(pacemakers, defibrillators, cochlear implants, dental implants, bone pins,
etc) and metal appendages (metal jewelry, etc), and potential
micro/nano-implant
analogues.
Appendix 8 shows
adverse effects of wireless radiation on automotive vehicle
occupants
(and bystanders), and the under-advertised on-board and external sources of this
radiation.
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Largest Unethical Medical Experiment in Human History
Copyright 2020
RN Kostoff
CITATION TO MONOGRAPH
Kostoff RN. The largest unethical medical experiment in human history. 2020. PDF.
http://hdl.handle.net/1853/62452
COPYRIGHT AND CREATIVE COMMONS LICENSE
COPYRIGHT
Copyright © 2020 by Ronald N. Kostoff
Printed in the United States of America; First Printing, 2020
CREATIVE COMMONS LICENSE
This work can be copied and redistributed in any medium or format provided that credit is
given to the original author. For more details on the CC BY license, see:
http://creativecommons.org/licenses/by/4.0/
This work is licensed under a Creative Commons Attribution 4.0 International
License<http://creativecommons.org/licenses/by/4.0/>.
DISCLAIMERS
The views in this monograph are solely those of the author, and do not represent the views of
the Georgia Institute of Technology.
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Largest Unethical Medical Experiment in Human History
Copyright 2020
RN Kostoff
PREFACE
Humanity is racing along two parallel paths to self-destruction: 1) accelerating
irreversible climate change, and 2) rapidly increasing exposure to health and life-threatening
mixtures of toxic stimuli. The most ubiquitous constituent of these toxic mixtures is wireless
radiation, which is proceeding to blanket humanity and its ecological life support chain.
A small fraction of the population has given informed consent to wireless radiation
exposure, gambling (like users of cigarettes, cocaine, fentanyl) that they can escape the severe
adverse consequences of exposure. Another small fraction of the population has not given
informed consent, but receives harmful second-hand exposure because of the broad-scale
transmission of wireless radiation from terrestrial and satellite sources. The vast majority of the
population has given
Mis-informed
Consent to this exposure. This
mis-information
is supplied
by the telecommunications industry, its lobbyists, its government partners, its political enablers,
its marketing arm (the mainstream media), and even some academic enablers.
While research over the past seventy+ years has shown hard evidence of severe adverse
effects from wireless radiation, the full extent of the damage from existing wireless radiation
infrastructure is not known, much less the damage expected from 4G/5G infrastructure being
implemented rapidly today. Attempting to identify the full extent of these adverse effects is the
global medical experiment being conducted today. The fact that this experiment is being
conducted with
mis-informed
consent makes it an unethical medical experiment. Because of the
magnitude of this experiment, it is the
largest unethical medical experiment in human history!
Chapter 1 of this monograph presents the case for wireless radiation infrastructure
implementation without credible safety testing being not only an unethical medical experiment,
but the largest in human history. It presents wireless radiation infrastructure implementation in
the context of other recent examples of unethical medical experiments, and shows how these
others pale in comparison to the projected suffering and lethality from wireless radiation
exposure based on even the incomplete biomedical data gathered to date.
Chapter 2 is the main technical chapter in this monograph. It covers a broad scope of
adverse health and life-supporting ecological effects from wireless radiation, mainly at
communications frequencies. Some of these adverse effects are not well-known to the general
public, but they are important nevertheless. While the majority of the chapter is technical, its
initial section provides the context for evaluating the biomedical literature results. In particular,
it emphasizes the conflicts-of-interest operable in all aspects of the wireless radiation biomedical
research process, ranging from the initial health-effects research sponsorship to the final research
results dissemination in the premier technical literature and other forums. As Chapter 2 shows,
we have known about the adverse health and ecological effects of wireless radiation exposure for
seventy+ years, but decision-makers of all stripes have nevertheless chosen to impose this health
and life-threatening toxic stimulus on an unsuspecting global populace.
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Additionally, there are eight appendices. The copious material contained in the
appendices supports the statements made in the main text (Chapters 1 and 2). Three sub-
appendices, while grounded in hard evidence, are somewhat more hypothetical than the rest.
They include 1) linkages between wireless radiation exposure and exacerbation of the opioid
crisis and the coronavirus pandemic, and 2) potentially enhanced heating and temperature
increases to thermally-damaging levels from short RF pulses and tissue-imbedded nanoparticles.
My purpose in presenting these three more hypothetical sub-appendices is to stimulate more
discussion, and especially more research, on the nature and validity of these linkages.
Finally, it is my hope that this monograph receives the widest distribution, especially
among those who have 1) been the targets of this decades-long mis-information campaign and 2)
given their consent to wireless radiation exposure based upon mis-information. It is this segment
of the public whose informed actions could reverse the increasing implementation of wireless
radiation infrastructure, and prevent the infliction of even more damage, since the other
stakeholders involved in the promotion of wireless radiation infrastructure have shown little
desire to protect the public against the known and projected ravages of wireless radiation.
Ronald N. Kostoff, Gainesville, VA, 15 February 2020
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TABLE OF CONTENTS
TITLE
KEYWORDS
ABSTRACT
CITATION TO MONOGRAPH
COPYRIGHT
CREATIVE COMMONS LICENSE
DISCLAIMERS
PREFACE
TABLE OF CONTENTS
EXECUTIVE SUMMARY
Chapter 1
–
Unethical Research
1A. Monograph Overview
1B. Unethical Research
1B1. Broad Definition
1B2. Informed Consent
1B3. Examples of Unethical Medical Experimentation
Chapter 2
–
Adverse Impacts of Wireless Radiation
2A. Overview
2A1. The Context of Wireless Radiation Health and Safety Research
2B. Wireless Radiation/Electromagnetic Spectrum
2C. Modern Non-Ionizing EMF Radiation Exposures
2D. Demonstrated Biological and Health Effects from Prior Generations of Wireless Networking
Technology
2D1. Limitations of Previous Wireless Radiation Health Effects Studies
2D2. Adverse Health Effects Identified in Major Review Studies
2D3. Adverse Health Effects from Open Literature Analysis
2D4. Adverse Wireless Radiation Health Effects from Former USSR Literature Analysis
2E. Potential Adverse Health Effects Expected from 5G Mobile Networking Technology
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2F. Why is there not Full Consensus on Adverse Effects from Wireless Radiation?
2F1. Reasons for Lack of Full Consensus
2F2. The Role of Conflicts-of-Interest in Lack of Full Consensus
2F3. Interpreting Wireless Radiation Health Study Findings
2G. Conclusions
Chapter 3 - References
Chapter 4
–
Appendices
Appendix 1
–
Unethical Medical Experiments
A1-A. Overview
Appendix 1A
–
Unethical Medical Experiments - Examples
Appendix 1B
–
Ethics of Medical Experiments
–
References
Appendix 2
–
Manual Taxonomy of Adverse EMF Effects Database
A2-A. Category Themes
Table A2-1
–
Manual Taxonomy
A2-B. Category Record Titles
Appendix 3
–
Factor Analysis of Adverse EMF Effects Database
A3-A. Factor Themes
Table A3-1 - Factor Analysis Taxonomy
A3-B. Factor Record Titles
Appendix 4
–
Hierarchical Text Clustering Taxonomy of Adverse EMF Effects Database
A4-A. Cluster Themes
Table A4-1 - CLUTO-Based Text Clustering Taxonomy
–
Top Levels
Table A4-2 - CLUTO-Based Text Clustering Taxonomy - Bottom Levels
A4-B. Cluster Record Titles
Appendix 5 - Wireless Radiation Impact on the Opioid Crisis and Coronavirus Pandemic
Appendix 6
–
Funding Source Bias on Research Outcomes
Appendix 7
–
Adverse Effects of Wireless Radiation Related to Implants and Appendages
A7-A. Overview
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A7-B. Specific Impacts from Passive Implants
A7-B1. Overview
A7-B2. Impacts from Passive Metallic Medical Implants
A7-B3. Impacts from Passive Macro/Nano Implant Analogues
Table A7-1
–
Implant Taxonomy
Appendix 8
–
Adverse Effects of Automotive-Based Wireless Radiation
A8-A. Overview
A8-B. Specific Automotive Wireless Radiation Sources
Table A8-1
–
Appendix 8 References
AUTHOR BIO
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EXECUTIVE SUMMARY
ES-1. Overview
We are in the midst of the largest unethical medical experiment in human history. This
experiment is the implementation and operation of a global wireless network for
communications, surveillance, and other purposes. It is a
medical experiment
because we do not
know the full extent of the adverse health effects that will result from this wireless network
implementation and operation. It is an
unethical
medical experiment because it violates the key
ethical medical experiment requirement of
‘informed consent’
from the participants.
Even though the adverse health effects of wireless radiation reported over the past
seventy+ years span the range of severity from discomfort to lethality, we do not know the full
extent of adverse health effects from this technology because:
Most laboratory experiments aimed at identifying wireless radiation health effects bear
no relation to real-life exposures, and are performed under the most benign conditions of
•
•
•
single stressors (wireless radiation only)
no pulsing and modulation of the carrier signal
no synergistic effects of other toxic stimuli acting in concert with the wireless radiation
These experimental deficiencies are compounded by
•
•
lack of access to the global classified literature on adverse health effects from wireless
radiation
lack of knowledge of proprietary basic and advanced studies on adverse health effects
from wireless radiation.
The adverse wireless radiation health effects that have been identified already from the
incomplete literature openly available are massive in scope and magnitude. They support the
conclusion that
wireless radiation as already implemented is extremely dangerous to human
health.
It acts as both a
promoter/accelerator
and
initiator
of adverse health effects. Addition
of the missing elements described above and more wireless radiation infrastructure will
exacerbate further the adverse effects from wireless radiation on
•
•
human health directly through contribution to chronic disease and
human health indirectly through degradation of the food chain ecosystem.
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ES-2. Adverse Impacts of Wireless Radiation on the Most Vulnerable Members of Society
In the spirit of the ‘unethical’ medical experiments described in this monograph,
it is the poor and dispossessed who will suffer the most from wireless radiation exposure.
This is because wireless radiation plays a dual role of
initiator
and
promoter/accelerator
of serious disease. In its
promoter/accelerator
role, it can accelerate the progression of existing
serious diseases such as cancer, and/or, through synergy, can produce serious adverse health
effects when combined with other toxic stimuli that neither constituent of the combination could
produce in isolation.
Many toxic stimuli, such as harsh chemicals, biotoxins, ionizing radiation sources,
vibrating machinery, prolonged sitting doing repetitive tasks, high air pollution, etc, are
used/experienced by the poorest members of society in their occupations, and many toxic
stimuli, such as air pollutants, toxic wastes, etc, are very prevalent in their residential
environments. Thus, people who spray pesticides in farm labor or household applications,
people who do cleaning with harsh chemicals, people who dispose of hazardous materials,
basically,
people who do the dirty work in our society and live in dirty environments,
are
already leading candidates for higher risk of serious diseases. Adding a wireless radiation
promoter/accelerator
to their residential and occupational environments will radically increase
their chances for developing serious diseases. Closing the ‘digital divide’ for them will translate
to increased suffering and reduced longevity!
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ES-3. Role of Conflicts-of-Interest in the Sponsorship, Conduct, and Dissemination of Wireless
Radiation Research
The results shown in the literature cannot be separated from the context in which this
research has been sponsored, conducted, and disseminated!
In the USA (and in most, if not all, countries), the two major sponsors of wireless
radiation health and safety research are the Federal government and the wireless radiation
industry, in that order. Both of these organizations have a strong intrinsic conflict-of-interest
with respect to wireless radiation.
The Federal government is a strong promoter of wireless radiation infrastructure
development and rapid expansion, most recently supporting accelerated implementation of 5G
infrastructure.
The Federal government that
promotes
accelerated implementation of wireless radiation
technology also 1)
sponsors
research examining
the technology’s
potential adverse effects
and 2)
regulates
the technology’s potentially adverse impacts on the public. The fact that
these development, regulation, and safety functions may be assigned to different Executive
Agencies within the Federal government is irrelevant from an independence perspective.
The separate Executive Agencies in the Federal government are like the tentacles of an
Octopus; they operate synchronously under one central command.
The wireless
promoters’ main objectives of developing and implementing the technology
rapidly are enabled by suppressing knowledge (to the public) of potential adverse effects from
the technology’s operation.
These fundamental conflicts impact the objectivity of the health
and safety R&D sponsors and performers. Any
Federal research sponsor
of wireless
radiation technology safety would be highly conflicted between 1) a desire to satisfy
Executive and Legislative objectives of accelerating expansion of wireless radiation
technology and implementation and 2) sponsoring objective research focused on identifying
and reporting adverse effects of wireless radiation expected under real-life conditions.
Likewise, any
sponsored research performer
addressing wireless radiation technology safety
would be highly conflicted between 1) reporting the actual adverse effects expected under
real-life conditions and 2) the desire to satisfy wireless radiation promotional objectives of the
research sponsors in order to maintain long-range funding.
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ES-4. Adverse Health Effects from Wireless Radiation Exposure.
In aggregate, for the high frequency (radiofrequency-RF) part of the spectrum, expert
reviews show that RF radiation below the FCC (Federal Communications Commission) exposure
guidelines can result in:
-carcinogenicity (brain tumors/glioma, breast cancer, acoustic neuromas, leukemia,
parotid gland tumors),
-genotoxicity (DNA damage, DNA repair inhibition, chromatin structure),
-mutagenicity, teratogenicity,
-neurodegenerative
diseases (Alzheimer’s Disease, Amyotrophic Lateral Sclerosis),
-neurobehavioral problems, autism,
-reproductive problems, pregnancy outcomes,
-oxidative stress, inflammation, apoptosis, blood-brain barrier disruption,
-pineal gland/melatonin production, sleep disturbance, headache,
-irritability, fatigue, concentration difficulties, depression, dizziness, tinnitus,
-burning and flushed skin, digestive disturbance, tremor, cardiac irregularities, and can
-adversely impact the neural, circulatory, immune, endocrine, and skeletal systems.
The effects range from myriad feelings of discomfort to life-threatening diseases. From
this perspective, RF exposure is a highly pervasive cause of disease!
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ES-5. Adverse Impacts of Wireless Radiation on the Food Chain
The struggle for survival of human life on Earth is dependent on the logistical food
supply chain. At the foundation of this supply chain (before the farmers become involved in
harvesting its bounty) are the insects, seeds, flora, trees, etc, that enable the bountiful growth of
the myriad potential foods. If the integrity of this foundational logistical supply chain is
threatened in any way, then both the animals and plant products we consume become
unavailable.
There is a substantial literature on the adverse impacts of wireless radiation on this
foundational logistical supply chain. These adverse effects are from the pre-5G wireless
radiation exposures, and would include enhanced coupling from the higher frequency harmonics
of the RF signal. Many of these supply chain elements (e.g., insects, seeds, larvae, etc) are very
small, and we could expect enhanced resonance/energy coupling with the shorter-wavelength 5G
radiation when implemented. This indirect impact of wireless radiation may turn out to be at
least as (if not more) important as the direct impact of wireless radiation on human survival!
From a broader perspective, most of the laboratory experiment component of the wireless
radiation adverse effects literature can be viewed as related to the foundational food supply
chain. Much of this research is focused on mice, rats, insects, small birds, small fish, etc. These
species tend to be prey of larger animals/fowl/fish, and eventually make their way to the human
food table. Any environmental factor that affects the health of these species adversely will
eventually impact the humans who are at the end of that chain. In reality, we have accumulated a
massive literature describing the adverse impacts of wireless radiation on myriad contributing
components to our food supply, and the results do not bode well for our future ability to feed the
growing world’s population!
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ES-6. Adverse Impacts of Wireless Radiation on Medical and Non-Medical Implants
There were two major types of medical implants covered by the database articles
showing adverse effects: active implants that produced electrical signals mainly for controlling
heart irregularities (e.g., pacemakers, defibrillators) and hearing deficiencies (e.g., cochlear
implants), and passive metallic implants for structural support (e.g., dental implants, bone pins,
plates, etc). Additionally, there are articles addressing adverse effects from wireless radiation in
the vicinity of metallic appendages (e.g., metallic eyeglasses, metallic jewelry, etc).
The external EMF (electromagnetic fields) from microwaves (and other sources) could 1)
impact the electrical operation of the active medical implants adversely, 2) increase the Specific
Absorption Rate (SAR) values of tissue in the vicinity of the passive implants substantially
because of resonance effects, and 3) increase the flow and acidity of saliva in the vicinity of
dental structures. While the EMF effects on the cochlear implants could adversely affect
auditory capability, EMF effects on the heart-related implants could potentially be life-
threatening. The increased SAR values around the passive metal implants could result in
increased tissue temperatures, and could adversely impact integration and longevity of the
passive metallic implants.
In the mouth, the combination of 1) increased tissue temperatures in proximity to the
implant or other orthodontic structures and 2) increased flow rate and acidity of saliva could lead
to 3) increased leaching of heavy metals (a known contributor to serious diseases). This also
raises the question: what other adverse health effects from the exposure of both the active and
passive implants to increasing levels of wireless radiation have not been identified or addressed?
There is a third class of structures whose interaction physics with RF are related to those
of the passive implants. These are termed implant analogues, and include myriad exogenous
particles (mainly nanoparticles) that penetrate, and imbed in, the skin. The resultant
nanoparticle-imbedded tissues have the potential for increased energy absorption from the
incoming RF signal, thereby resulting in potentially increased thermal damage over and above
the thermal damage resulting from the pulsed high-peak-to-average power of the RF signal.
Additionally, more research needs to be done to ascertain the magnitudes of these thermal
transients and associated stresses, in order to estimate the levels of enhanced potential damage
from RF radiation.
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ES-7. Studies in the USSR on Wireless Radiation Health Effects
Much research examining potential adverse effects from wireless radiation, especially in
the athermal parameter range, was performed in the USSR as far back as seventy+ years ago.
Their results confirm the wide scope of adverse effects reported in recent years and summarized
in the present monograph. Unfortunately, their results appear to have had little effect in
influencing wireless radiation safety standards in the USA and many other countries.
ES-8. Adverse Effects Expected from Addition of 5G to Existing Communications Networks
The potential 5G adverse health effects derive from the intrinsic nature of the radiation,
and how this radiation interacts with tissue and other target structures. 4G networking
technology was associated mainly with carrier frequencies in the range of ~1-2.5 GHz (cell
phones, WiFi). The wavelength of 1 GHz radiation is 30 cm, and the penetration depth in human
tissue is a few centimeters. The highest performance 5G networking technology (millimeter
wave) is mainly associated with carrier frequencies at least an order of magnitude above the 4G
frequencies, although, as stated in Chapter 2,
“ELFs (0–3000Hz)
are always present in all
telecommunication EMFs in the form of pulsing and modulation”. Penetration depths for the
high-performance carrier frequency component of 5G radiation (aka high-band) will be on the
order of a few millimeters.
For much of the early implementation of 5G, and perhaps later, 5G will be integrated
with 4G. Some vendors will start out/have started out with ‘low-band’ 5G (~600-900
MHz);
some will start out with
‘mid-band’ 5G (~2.5 GHz-4.2 GHz); and some will start out with ‘high
band’ 5G (~24-47
GHz). All these modes are associated with potentially severe adverse health
effects, and none have been tested for safety in any credible manner.
At the millimeter carrier wavelengths characteristic of high-band high-performance 5G,
one can expect resonance phenomena with small-scale human structures, as well as resonances
with insects/insect components, seeds, etc.
The common ‘wisdom’ being presented in the literature and the
broader media is that, if
there are adverse impacts resulting from millimeter-wave 5G, the main impacts will be focused
on near-surface phenomena, such as skin cancer, cataracts, and other skin conditions, because of
shallow RF penetration depths. However, there is evidence that biological responses to
millimeter-wave irradiation can be initiated within the skin, and the subsequent systemic
signaling in the skin can result in physiological effects on the nervous system, heart, and immune
system. There is additional evidence that adverse effects from millimeter-wave radiation can
occur in organs and tissue well below the skin surface. This should not be surprising, since there
are myriad signaling conduits connecting the skin to deeper structures in the body.
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ES-9. Lack of Full Consensus on Wireless Radiation Adverse Effects
Not all studies of wireless radiation have shown adverse effects on health. There are
many possibilities to explain this.
1) There could
be ‘windows’ in parameter space where adverse effects occur,
and the
studies/experiments were conducted outside these ‘windows’. Operation
outside these
windows could show
•
no effects or
•
hormetic effects or
•
therapeutic effects.
The single stressor studies that constitute most of wireless radiation laboratory health
research, and indeed constitute most of the laboratory medical research literature, essentially
yield very narrow windows. Adverse effects are identified over very limited parameter
ranges, and adverse effects shown by many combinations of stressors are not revealed when
these stressors are tested in isolation over the same parametric ranges.
One could conclude that, whether by design or accident,
the real-world impact of single
stressor studies is to conceal, rather than reveal, many of the more serious adverse health
effects of wireless radiation.
The stressor variables to be used for health studies should not be limited to single
stressors in isolation, but should include to the extent possible combinations of toxic stimuli
stressors, since these combinations reflect more accurately real-life exposures.
2)
3)
Research quality could be poor, and adverse effects were overlooked.
Or, the research team could have had a preconceived agenda
where finding no adverse effects from wireless radiation was the main objective of the
research!
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ES-10. Potential Links of Wireless Radiation to Enhancement of Opioid Crisis
The previous findings reported in this Executive Summary are based on hard evidence
and have been validated in numerous studies. The present section is based on hard evidence as
well, but the link of wireless radiation to the opioid crisis is not as far along in the validation
process. It should be viewed as a hypothesis at this point, and serve as a basis for discussion and
further research.
It has been shown many times that one impact of wireless radiation (at myriad
frequencies) is release of endogenous opioids. This release of endogenous opioids can enable
analgesic effects by itself, or can enhance the analgesic effects of exogenous analgesics. This
has been demonstrated at pulsed millimeter-wave frequencies, WiFi frequencies, mobile phone
frequencies, radiofrequencies, and extremely low frequencies. Additionally, as has been
demonstrated by the results of the current monograph, wireless radiation at all the above
frequencies has resulted in serious mid-term and especially long-term adverse health effects.
Therefore, wireless radiation exposure, especially at cell phone, WiFi, and millimeter-
wave pulsed and modulated frequencies, generates
1) analgesic and pleasurable short-term
effects and 2) serious adverse mid- and long-term effects.
There would be some exceptions for
the short-term, such as electrohypersensitivity (EHS) sufferers, who are immediately affected
adversely and strongly by wireless radiation exposure.
For most people, the enhanced analgesic short-term effects of the wireless radiation would
in effect mask the long-term damage from this radiation.
As time proceeds, the increasing discomfort from the adverse mid-and long-term effects
of wireless radiation requires increasingly stronger analgesics to suppress, and the increasing use
of exogenous analgesics becomes necessary. This potentially enhanced use of exogenous
analgesics could lead to opioid and/or other analgesic addictions.
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ES-11. Potential Links of Wireless Radiation to Current Coronavirus Pandemic
The previous findings reported in this Executive Summary are based on hard evidence
and have been validated in numerous studies. The present section is based on hard evidence as
well, but the link of wireless radiation to the coronavirus pandemic is not as far along in the
validation process. It should be viewed as a hypothesis at this point, and serve as a basis for
discussion and further research.
There are on the order of 300,000 viruses, many/most of which have zoonotic potential.
To develop vaccines for all of these viruses (before an epidemic or pandemic strikes) is
unreasonable (based on present technology) because of the sheer numbers involved. To develop
vaccines for any specific virus during an epidemic or pandemic (which was the mainstream
approach taken for the coronavirus during the SARS pandemic of 2002-2003) is completely
unrealistic, because of the lead times required for vaccine development, efficacy testing, credible
mid-and long-term safety testing, and implementation.
Those who succumbed during the SARS pandemic had 1) myriad co-morbidities and 2)
weakened immune systems unable to neutralize the SARS coronavirus.
Having a strong
immune system that allowed a smooth transition from innate immune system operation to
adaptive immune system operation was the one intrinsic defense that worked!
The SARS
experience showed that the best and most realistic approach for defense against any potential
viral attack is
reversing immune-degrading lifestyles
well before any pandemic or epidemic
outbreaks. In that case, the immune system would be sufficiently strong to be able to handle
viral exposure on its own without the emergence of serious symptoms, as was the case with those
exposed to the SARS coronavirus (with coronavirus antibodies in their serum) who exhibited no
(or minimal) symptoms.
This gets to the link between wireless radiation exposure and the latest coronavirus
pandemic. To the degree that non-ionizing radiation exposure, superimposed on the myriad
toxic stimuli to which many people are exposed by choice or imposition, degrades the operation
of the innate and adaptive immune systems, it would increase the likelihood that the immune
system could not counteract the exposure to the coronavirus (or any virus) as nature intended.
Thus,
it would contribute to the exacerbation of adverse effects from coronavirus exposure.
The bottom line is that exposures to essentially ALL the exogenous immune-damaging toxic
stimuli (including, but not limited to, wireless radiation) need to be removed before resistance to
viral exposures of any type can be improved substantially.
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ES-12. Adverse Effects of Wireless Radiation in Automotive Sector
The modern automobile is a powerful source of wireless radiation at myriad frequencies,
and is subject to external wireless radiation at myriad frequencies as well. The trend has not
been to reduce these sources, but rather to add equipment both to the vehicle and to the external
environment that will substantially increase the wireless radiation flux associated with the
vehicle. The numbers and types of sources are not well-known, even among those experts and
laymen concerned about adverse effects from wireless radiation.
An interesting diagram (and narrative) showing radars and other wireless sensors in
modern cars can be found at the following link: (
http://www.radiationdangers.com/automotive-
radiation/automotive-radiation/
). I would recommend the reader study that diagram in detail, to
better appreciate how ubiquitous are these sources of wireless radiation. Not all the wireless
radiation enters the cabin, since some/much is outward-directed, but some/much of it will enter
the cabins of other cars on the road.
However, that diagram tells only part of the story. Assume there is a car pool commuting
to work from the suburbs of a major city. It is not uncommon (in today’s world) for a one-way
trip to take from one-two hours, or more. Even in a regular car, or mid-size SUV, there might be
four or so passengers. They may be using cell phones, WiFi, or both, thereby adding to the
radiation from the automotive-based sensors/transmitters.
There will be cell towers lining the sides of a major highway, thereby increasing the
radiation to the occupants substantially. Depending on conditions, there may be substantial air
pollution to which the occupants are exposed. Additionally, the prolonged sitting is very
dangerous, and is a contributing factor to many serious diseases. If the vehicle is new, there may
be substantial out-gassing of toxic chemicals from the interior materials. Combined exposure to
the wireless radiation, air pollution and other toxic substances, coupled with prolonged sitting
and continual impacts
from the car’s motions, produces a synergistic effect that
substantially
exacerbates adverse impacts from any of the constituent components.
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Chapter 1
–
Unethical Research
1A. Monograph Overview
We are in the midst of the largest unethical medical experiment in human history. This
experiment is the implementation and operation of a global wireless network for
communications, surveillance, and other purposes. It is a
medical experiment
because we do not
know the full extent of the adverse health effects that will result from this wireless network
implementation and operation. It is an
unethical
medical experiment because it violates the key
ethical medical experiment requirement of
‘informed
consent’
from the participants.
The current chapter provides 1) some background on the requirements for ethical medical
research/experimentation and 2) examples of how those requirements have been violated in the
past century. It places wireless radiation implementation and operation in the context of these
other examples of unethical medical experiments.
Chapter 2
presents a detailed description of some of the adverse health effects of wireless
radiation as reported in the unclassified open literature. Even though the adverse health effects
of wireless radiation reported over the past seventy+ years span the range of severity from
discomfort to lethality, we do not know the full extent of adverse health effects from this
technology because:
Most laboratory experiments aimed at identifying wireless radiation health effects bear
no relation to real-life exposures, and are performed under the most benign conditions of
•
•
•
single stressors (wireless radiation only)
no pulsing and modulation of the carrier signal
no synergistic effects of other toxic stimuli acting in concert with the wireless radiation
These experimental deficiencies are compounded by
•
•
lack of access to the global classified literature on adverse health effects from wireless
radiation
lack of knowledge of proprietary basic and advanced studies on adverse health effects
from wireless radiation.
As
Chapter 2
shows, the adverse wireless radiation health effects that have been
identified already from the incomplete literature openly available are massive in scope and
magnitude. They support the conclusion that
wireless radiation as already implemented is
extremely dangerous to human health.
It acts as both a
promoter/accelerator
and
initiator
of
adverse health effects. Addition of the missing elements described above and more wireless
radiation infrastructure will exacerbate further the adverse effects from wireless radiation on
•
•
human health directly through contribution to chronic disease and
human health indirectly through degradation of the food chain ecosystem.
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Chapter 3
contains the references for the main text.
Chapter 4
contains eight Appendices:
•
•
Appendix 1
contains examples of unethical medical experiments conducted in the last
century, mainly (not entirely) in the USA or under USA auspices;
Appendix 2
contains a manual taxonomy of the adverse health and biomedical effects
component of a representative wireless radiation literature, and is derived in part from the
taxonomies in Appendices 3 and 4;
Appendix 3
contains a taxonomy based on factor analysis of the same representative
wireless radiation literature;
Appendix 4
contains a taxonomy based on text clustering of the same representative
wireless radiation literature;
Appendix 5
shows
potential links between wireless radiation exposure and 1)
expansion of the opioid crisis
and
2) exacerbation of coronavirus pandemic;
Appendix 6
lists references showing
effects of industry funding on research outcomes
for myriad (mainly biomedical) research disciplines;
Appendix 7
overviews the oft-neglected topics of wireless radiation adverse effects on
regions containing
medical implants
(e.g., pacemakers, defibrillators, cochlear implants,
dental implants, bone pins, plates, etc) and appendages (e.g., metal eyeglasses, earrings,
metal jewelry, etc), as well as other
micro/nano
exogenous implant analogues;
Appendix 8
describes
adverse effects of automotive-based wireless radiation.
•
•
•
•
•
•
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1B. Unethical Research
1B1. Broad Definition
There are myriad definitions for 'unethical' research (e.g.,
http://icahn.mssm.edu/about-
us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook/research-
environment/research-integrity;
https://oprs.usc.edu/training/booklets/;
https://history.nih.gov/about/timelines_laws_human.html
).
These definitions of 'unethical' research encompass a broad spectrum of actions. Much
reporting of 'unethical' medical research in myriad media tends to focus on one aspect only:
biomedical experiments performed on subjects who did not give 'informed consent'. The classic
example reflects the experiments performed on concentration camp inmates by the Nazi-regime
doctors during WWII, and the lesser-known experiments performed by their Japanese
counterparts during WWII. These experiments were certainly horrific, but not unique. The test
subjects in these experiments were neither
informed
about the nature and consequences of these
experiments, nor did they give
consent.
1B2. Informed Consent
A comprehensive discussion of the importance of ‘informed consent’
in medical
experimentation was presented in a journal Special Issue [Goodwin, 2016]. An excellent
overview and rationale for informed consent in human experiments is shown in the following
box (obtained from a booklet titled Informed Consent in Human Subjects Research), prepared by
the Office for Protection of Research Subjects, University of Southern California
(
https://oprs.usc.edu/training/booklets/
).
Informed Consent is a voluntary agreement to participate in research. It is not merely a form
that is signed but is a process, in which the subject has an understanding of the research and
its risks. Informed consent is essential before enrolling a participant and ongoing once
enrolled. Informed Consent must be obtained for all types of human subjects’ research
including; diagnostic, therapeutic, interventional, social and behavioral studies, and for
research conducted domestically or abroad. Obtaining consent involves informing the
subject about his or her rights, the purpose of the study, the procedures to be undergone, and
the potential risks and benefits of participation. Subjects in the study must participate
willingly. Vulnerable populations (i.e. prisoners, children, pregnant women, etc.) must
receive extra protections. The legal rights of subjects may not be waived and subjects may
not be asked to release or appear to release the investigator, the sponsor, the institution or its
agents from liability for negligence.
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There are three important concepts in this definition: research, informed, and consent.
Research
What is a research experiment? According to myriad Web sources, an experiment is a set
of actions undertaken to
•
•
•
make a discovery or
test a hypothesis or
demonstrate a known fact.
The first two of these can be classified as
research
experiments, and the third is a
demonstration
experiment. A further breakdown would be informative. There are
proactive
experiments, where established rules and procedures (the scientific approach) are used to plan,
conduct, and report the experiment. There are
reactive
experiments, where the experiment is
secondary to higher priority actions, and consequently is conducted and reported under more
constrained conditions. The proactive experiments can be viewed generally as explicit or
‘a
priori’, and the reactive experiments can be viewed generally as implicit or
‘a
posteriori’.
Where does wireless technology implementation and operation fit in this research
experiment categorization? Wireless technology implementation has two major characteristics:
development and operation of a technology to achieve targeted technical goals (explicit), and
conduct of an experiment that may result in serious adverse health impacts (implicit). Of interest
in the current document is the experiment (implicit) component.
Identification of wireless radiation health effects will result from both proactive and
reactive experiments. The proactive experiments are (mainly) the thousands of laboratory-based
studies (performed to estimate wireless radiation health impacts) that have been reported in the
biomedical literature. The reactive experiments are (mainly) those studies that have been done
after the previous generations of mobile networking technologies have been implemented
(usually epidemiology), and those studies that will be done after 5G is implemented.
Thus, 5G implementation can be viewed mainly as an implicit reactive
research
experiment with respect to identifying myriad adverse health effects on the exposed population.
It will also have a
demonstration
component, confirming thousands of pre-5G research studies
that have shown adverse health effects from wireless radiation in 5G and non-5G frequency
ranges. Because these studies tend to under-estimate real-life effects of wireless radiation, the
full scope of adverse health effects from 5G operation under real-life conditions are currently
unknown. Ascertainment of these adverse health effects will require
‘a
posteriori’ reactive
research experiments after 5G implementation, under
today’s 5G implementation scenario.
A
major concern, especially in the current environment of accelerating 5G implementation, is that
serious longer-term latent health effects will be discovered
only after 5G has been fully
implemented.
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Informed
There is much information available in the open literature detailing the adverse health
effects of wireless radiation. These adverse effects reflect the role of wireless radiation both as a
promotor/accelerator and/or initiator
of myriad biomedical abnormalities and serious diseases.
However, the vast public is not informed (or is misinformed) of these adverse health effects by
the:
•
•
•
•
•
developers of wireless radiation systems,
vendors of these systems,
mainstream media
government regulators of these systems, and
Federal, State, and Local politicians who pass laws that accelerate implementation of
these systems.
These stakeholders 1)
do not inform
the public of the demonstrated adverse effects of wireless
radiation and, in many cases, 2)
misinform
the public that wireless radiation is safe from a
health perspective.
Consent
Many segments of the public
do provide
consent to be exposed to wireless radiation,
because of its perceived benefits to them. A small amount of this consent may be informed, and
the providers of this consent may be gambling that they can escape the adverse health effects.
Most of the consent is probably not informed, since most people will not do the independent
research required to gather in the relevant information on adverse health effects, but will rely on
the government’s and mainstream media’s
misleading assurances that wireless radiation is safe.
However, other segments of the public
do not provide
consent to be exposed to wireless
radiation from these implemented technologies. Unlike other forms of toxic stimuli (e.g.,
cigarettes, cocaine, alcohol, etc), where exposures may be individual or very local, wireless
radiation exposure is very large in extent. With the advent of the latest generation of wireless
radiation (5G), there may be 1) small cell towers erected outside of every few houses, with the
consequent radiation blanketing the environment, and 2) thousands of satellites blanketing the
Earth’s surface with wireless radiation.
There are Federal laws that essentially prevent
opposition to construction and operation of these small cell towers, and prevent opposition to the
launching and operation of these satellites. Forcing exposure to this harmful wireless radiation
on members of the public who do not provide consent is the cornerstone of wireless radiation
implementation and operation being labeled unethical medical experimentation.
Its context differs from some other technologies with serious adverse effects, such as
automotive technology and cigarette smoking. For the most part, users of these other
technologies have been informed about potential serious consequences, and non-users are
impacted minimally (at least today). Those users are able to make a more informed choice.
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1B3. Examples of Unethical Medical Experimentation
Many books and articles have been written concerning horrific medical experiments (that
were performed in the USA over the past century)
without obtaining ‘informed consent’ from the
test subjects. These books describe a wide spectrum of experiments. Individual readers could
have different opinions on whether any of the individual experiments reported are more or less
'unethical' than those in the Nazi concentration camps, or whether they are 'unethical' at all.
Appendix 1
contains references to books and journal articles that describe some of these
experiments (mainly, but not entirely, conducted in the USA or under USA auspices), based on
Medline searches and Web sources. Like most research of this type, the conduct of the
experiments and the experimental results are not advertised widely. I was not aware of most of
these experiments prior to conducting the analysis on under-reporting of adverse events in my
2015 eBook
“Pervasive
Causes of Disease” [Kostoff, 2015].
The experiments reported in
Appendix 1
cover the full spectrum of toxic stimuli, including
biological, chemical, and nuclear. These are the three types of toxic stimuli that constitute the
core of Weapons of Mass Destruction (WMD).
Interestingly, with all of the USA’s concern
about potential WMD attacks from Russia, China, Iran, and North Korea, we have completely
overlooked the ongoing and exponentially increasing WMD attack on the Homeland that has
been occurring for at least two decades: 24/7 spewing of harmful wireless radiation in almost
every corner of the USA, with far more to come if 5G is implemented!
The copious references identified in
Appendix 1
are not the result of an exhaustive
search; they were obtained after a very brief survey. There are undoubtedly many other
examples (of 'unethical' medical experiments) published already that were missed by the survey.
Given the odious nature of these experiments, there are probably far more experiments whose
disclosure has not yet seen the light of day. As shown in the tobacco and asbestos examples in
section 9C of Kostoff [2015], most of this information comes to light either from 1)
whistleblowers or 2) 'discovery' resulting from lawsuits. In addition, some investigators may
stumble across evidence of this type of 'unethical' research while doing relatively unrelated types
of investigations.
Documentation of many types of 'unethical' medical experiments may:
•
•
•
not have been done, or
have been done and destroyed, or
have been done but distorted to protect the miscreants.
This is why retrospective analysis of this type of 'research', which in many cases relies heavily on
the printed word as 'proof', may be highly under-reflective of the full spectrum of what was
actually done in these experiments
(e.g., Stephen Kinzer’s description of the records destroyed
by the Head of the CIA’s MK-Ultra
program
https://www.c-span.org/video/?464648-1/poisoner-
chief
).
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While there are many stages of the medical research process that could be subjected to
'unethical' practices (e.g., those outlined in Chapter 9 of Kostoff [2015], including selection of
the most important research problems for funding, conducting the research, disseminating the
results of the research, etc), conducting the medical research experiments 'unethically' has
received the most attention by far. The references in
Appendix 1,
and additional books and
journal and magazine articles on unethical medical research experiments, are testimony to this
imbalance.
Books and articles only tell part of the larger story. A more representative reporting on
the damage from any type of 'unethical' medical research would reflect the pain, suffering, and
premature mortality resulting from the medical research experimentation. A simple estimate of
the experiment’s damage
could be obtained by integrating the number of people affected by the
'unethical' medical experimentation and the degree of damage experienced by each person. This
could be viewed as a ‘weighted’ impact of the adverse effects of the unethical
medical
experimentation.
In the most widely reported examples of 'unethical' medical research (the medical
experiments performed in the Nazi concentration camps during WWII), perhaps a few thousand
prisoners were involved; it is difficult to find accurate information for actual numbers of
prisoners involved. Further, it is difficult to separate out the 1) many thousands of German
citizens subjected to forced sterilization procedures starting in 1933 and 2) many deliberately
exterminated in the concentration camps, from 3) those who suffered from the medical
experiments in the camps and died as a result of the experiments alone.
In the references in
Appendix 1
•
•
•
some of the ‘unethical’ medical experiments described involved under
a hundred
test subjects,
many of the 'unethical' medical experiments described tended to involve on the
order of hundreds of test subjects (who did not provide 'informed consent'), and
in some rarer cases, perhaps thousands of test subjects were involved.
Many of these experiments, in parallel with the spirit of the Nazi concentration camp
experiments, involved people confined in large institutions who were (usually) not told the full
story of the nature of the experiments, or, if they were told, either did not 1) understand it or 2)
give 'informed consent'. These people were confined in prisons, the military service, mental
institutions, children's institutions, etc.
How do the above odious procedures in these references differ conceptually from the recent
trend toward government effectively promoting/mandating implementation of wireless
radiation infrastructure whose safety has not been demonstrated, but (a fraction of) whose
adverse health effects have been widely demonstrated?
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Based on what has been reported in the experiments referenced in
Appendix 1
(which
could in fact be the tip of a much larger unreported iceberg), perhaps on the order of 10,000-
30,000 people may have been subjected to
‘unethical’
medical experiments in the past century
(excluding those who unwittingly participated in clinical trials that were “off-shored” to
(typically) developing countries with knowingly less stringent test subject protections [Kostoff,
2015, section 9D3]). A few thousand of these test subjects would have died prematurely, and
most would have suffered unnecessarily. These, of course, are horrific numbers. Unfortunately,
they pale in comparison to what can be expected if wireless radiation infrastructure is expanded
domestically and globally to satisfy the requirements of 5G. The following box shows one
estimate of potential adverse effects from wireless radiation.
One of the many adverse health effects of wireless radiation is cancer of the brain, especially
gliomas. What approximate increases in glioma incidence can be expected from widespread
expansion of wireless radiation?
There are different estimates of glioma incidence and trends in glioma incidence. For an
approximate estimate, Rasmussen et al [2017] estimates the glioma incidence in the Danish
population at about 7/100,000, a figure in line with other national and global estimates.
Additionally, Phillips et al [2018] presents evidence of a 100% increase in Glioblastoma
Multiforme from 1995-2015, a major component of glioma. Some of this increase may have
been due to wireless radiation exposure, since that time period was associated with a major
expansion of cell phone and other wireless device use. For approximate estimation purposes,
assume the wireless-free glioma incidence to be about 5/100,000.
Hardell et al [2011] showed, in a case-controlled study, that glioma incidence doubled for
those who starting using cell phones as adults (>20 years old),
were ‘heavy’ users (>30
minutes per day), and used cell phones for more than ten years. Hardell also showed glioma
incidence quadrupled for those who started using cell phones younger than twenty years old,
were heavy users, and used cell phones for more than ten years.
If we apply Hardell’s conservative doubling estimate to all potential users,
then we can expect
an increased glioma incidence per year of about 5/100,000. By the time 5G is rolled out, the
global population will be at least eight billion. If we assume
¾
of the global population will
be cell phone users and/or exposed to cell towers and other sources of wireless radiation, then
about six billion people would be the pool for potential glioma victims from wireless
radiation. Multiplying 5/100,000 by 6,000,000,000 yields 300,000 new cases of glioma/year.
In one year, the deaths from glioma alone attributed to wireless radiation
will swamp all the deaths from all the horrific unethical medical
experiments of the twentieth century referenced in Appendix 1!
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This number was obtained using the most conservative estimates of Hardell and the incidence
data, and it didn’t take into account the increase in glioma incidence that would be expected as
latency times increase. For smoking, the average latency period between initiation of
smoking and lung cancer is between twenty and thirty years, depending on which database
was examined. The fact that glioma incidence shows measurable increases after only a ten-
year latency period should be most disturbing, and does not bode well for glioma incidences
after a twenty, thirty, or forty-year latency!
Again, glioma is but one of the large numbers of adverse health effects potentially resulting
from exposure to wireless radiation. Integrating over all the adverse health effects potentially
resulting from the wireless radiation experiment would yield numbers of
experiment-based
premature deaths and enhanced suffering unparalleled in human history!
Given the magnitude of 5G projected global implementation, the numbers of people that
will be exposed to this radiation, the numbers of people expected to suffer myriad adverse effects
from this technology, and the lack of credible ‘informed consent’ from the vast majority of these
people, we are well justified in calling global implementation of mobile networking technology
The Largest Unethical Medical Experiment in Human History!
Finally, in the spirit of the ‘unethical’ medical experiments referenced in
Appendix 1,
it is the poor and dispossessed who will suffer the most from wireless radiation exposure.
This is because wireless radiation plays a dual role of
initiator
and
promoter/accelerator
of serious disease, as will be shown in the next chapter. In its
promoter/accelerator
role, it can
accelerate the progression of existing serious diseases such as cancer, and/or, through synergy,
can produce serious adverse health effects when combined with other toxic stimuli that neither
constituent of the combination could produce in isolation.
Many toxic stimuli, such as harsh chemicals, biotoxins, ionizing radiation sources,
vibrating machinery, prolonged sitting doing repetitive tasks, high air pollution, etc, are
used/experienced by the poorest members of society in their occupations, and many toxic
stimuli, such as air pollutants, toxic wastes, etc, are very prevalent in their residential
environments. Thus, people who spray pesticides in farm labor or household applications,
people who do cleaning with harsh chemicals, people who dispose of hazardous materials,
basically,
people who do the dirty work in our society and live in dirty environments,
are
already leading candidates for higher risk of serious diseases. Adding a wireless radiation
promoter/accelerator
to their residential and occupational environments will radically increase
their chances for developing serious diseases. Closing the ‘digital divide’ for them will translate
to increased suffering and reduced longevity!
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Chapter 2
–
Adverse Impacts of Wireless Radiation
2A.
Overview
Wireless communications have been expanding globally at an exponential rate. The
latest imbedded version of mobile networking technology is called 4G (fourth generation), and
the next generation (5G) is in the early implementation stage. Neither 4G nor 5G have been
tested for safety in any credible real-life scenarios. The current chapter assesses the medical and
biological studies that have been performed and then published in the biomedical literature, and
shows why they are deficient relative to identifying adverse health and safety effects.
However, even in the absence of the missing real-life components (which tend to
exacerbate the adverse effects of the wireless radiation shown in the biomedical literature), the
published literature shows there is much valid reason for concern about potential adverse health
effects from both 4G and 5G technology. The studies reported in the literature should be viewed
as extremely conservative, underestimating the adverse impacts substantially.
2A1. The Context of Wireless Radiation Health and Safety Research
Before addressing the technical and biological details of wireless radiation health and
safety research shown in the published literature, the context in which this literature has been
generated will be discussed.
The results shown in the literature cannot be separated from the context in which this
research has been sponsored, conducted, and disseminated!
In the USA (and in most, if not all, countries), the two major sponsors of wireless
radiation health and safety research are the Federal government and the wireless radiation
industry, in that order. Both of these organizations have a strong intrinsic conflict-of-interest
with respect to wireless radiation.
2A1a. Intrinsic Federal government wireless radiation conflict-of-interest
The Federal government is a strong
promoter
of wireless radiation infrastructure
development and rapid expansion, most recently supporting accelerated implementation of 5G
infrastructure. Every
•
•
•
•
Congressional evaluation of 5G I have heard (or read),
Congressperson’s statement on 5G I have heard (or read),
Presidential proclamation on 5G I have heard (or read), and
FCC proclamation on 5G I have heard (or read),
has unabashedly supported the
most accelerated implementation of 5G infrastructure.
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The Federal government that
promotes
accelerated implementation of wireless radiation
technology also 1)
sponsors
research examining
the technology’s
potential adverse effects
and 2)
regulates
the technology’s potentially adverse impacts on the public. The fact that
these development, regulation, and safety functions may be assigned to different Executive
Agencies within the Federal government is irrelevant from an independence perspective.
The separate Executive Agencies in the Federal government are like the tentacles of an
Octopus; they operate synchronously under one central command.
The wireless
promoters’ main objectives of developing and implementing the technology
rapidly are enabled by suppressing knowledge (to the public) of potential adverse effects from
the technology’s operation.
These fundamental conflicts impact the objectivity of the health
and safety R&D sponsors and performers. Any
Federal research sponsor
of wireless
radiation technology safety would be highly conflicted between 1) a desire to satisfy
Executive and Legislative objectives of accelerating expansion of wireless radiation
technology and implementation and 2) sponsoring objective research focused on identifying
and reporting adverse effects of wireless radiation expected under real-life conditions.
Likewise, any
sponsored research performer
addressing wireless radiation technology safety
would be highly conflicted between 1) reporting the actual adverse effects expected under
real-life conditions and 2) the desire to satisfy wireless radiation promotional objectives of the
research sponsors in order to maintain long-range funding.
2A1b. Intrinsic wireless radiation industry conflict-of-interest
The wireless radiation industry is obviously a strong promoter of accelerated
development and implementation of wireless radiation devices and infrastructure, and is a
sponsor of wireless radiation and safety research.
Trillions of dollars in revenues are
potentially at stake in successful promotion and adoption of wireless radiation infrastructure
and technology!
The industry’s
conflicts with respect to promotion and safety research are
similar to those of the Federal government listed above.
The wireless industry’s
role in suppressing information about the adverse impacts of
wireless radiation was described eloquently in a 2018 Nation article
(
https://www.thenation.com/article/how-big-wireless-made-us-think-that-cell-phones-are-safe-a-
special-investigation/
). As this exposé shows, studies on health effects were commissioned by the
wireless radiation industry in the 1990s under the management of Dr. George Carlo. The
adverse effects shown were downgraded and suppressed, in the spirit of similar suppression by
the tobacco and fossil energy industries, as stated in the Nation article:
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“Carlo’s story underscores the need for caution, however,
particularly since it evokes eerie
parallels with two of the most notorious cases of corporate deception on record: the
campaigns by the tobacco and fossil-fuel industries to obscure the dangers of smoking and
climate change, respectively. Just as tobacco executives were privately told by their own
scientists (in the 1960s) that smoking was deadly, and fossil-fuel executives were privately
told by their own scientists (in the 1980s) that burning oil, gas, and coal would cause a
“catastrophic” temperature rise, so Carlo’s testimony reveals that wireless executives were
privately told by their own scientists (in the 1990s) that cell phones could cause cancer and
genetic damage…..Like their tobacco and fossil-fuel brethren, wireless executives have
chosen not to publicize what their own scientists have said about the risks of their products.
On the contrary, the industry—in America, Europe, and Asia—has spent untold millions of
dollars in the past 25 years proclaiming that science is on its side, that the critics are quacks,
and that consumers have nothing to fear. This, even as the industry has worked behind the
scenes—again like its Big Tobacco counterpart—to deliberately addict its customers. Just as
cigarette companies added nicotine to hook smokers, so have wireless companies designed
cell phones to deliver a jolt of dopamine with each swipe of the screen.”
While the wireless radiation industry doesn’t play a formal role in regulating the safety
aspects of wireless radiation, it plays a strong de facto role. In addition to its lobbying efforts to
minimize regulations on wireless radiation exposure levels, it plays a revolving-door role with
respect to regulation.
The previous FCC Chairman had been President of the National Cable &
Telecommunications Association (NCTA) and CEO of the Cellular Telecommunications &
Internet Association (CTIA) before assuming his FCC Chairmanship. In recognition of his work
in promoting the wireless industry, he was inducted into the Wireless Hall of Fame in 2003 and
in 2009 (
https://en.wikipedia.org/wiki/Tom_Wheeler
). The present FCC Chairman served as
Associate General Counsel at Verizon Communications Inc., where he handled competition
matters, regulatory issues, and counseling of business units on broadband initiatives
(
https://en.wikipedia.org/wiki/Ajit_Pai#cite_note-Bio-2
). As is the case with so many other Federal
regulatory agencies [Kostoff, 2015-Chapter 9; 2016], the FCC is essentially an agency captured
by industry [Alster, 2015]!
So, in the two most recent Administrations, under two supposedly very different
Presidents, the FCC Chairmen had been, in different ways, lobbyists for the wireless radiation
technology industry. Both were (and are) extremely ardent promoters of the most rapid
acceleration of implementation of 5G infrastructure and associated devices and technologies.
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2A1c. Relation of
wireless radiation health and safety research to sponsors’ and performers’
conflicts-of-interest
The incentives for
sponsors
of wireless radiation health and safety research to fund
studies that will help promote accelerated expansion of wireless radiation devices and
infrastructure are many and the disincentives are essentially non-existent. Likewise, incentives
for
performers
of wireless radiation health and safety research to conduct studies that will help
promote accelerated expansion of wireless radiation devices and infrastructure are many and the
disincentives are few. Because of this unfortunate reality,
EVERY wireless radiation health and safety study/experiment whose results support the
wireless radiation promotion objectives of the organization(s) that sponsor these studies
must receive the highest level of scrutiny.
There is not a credibility symmetry between studies whose results 1) support the
promotional objectives of their sponsors or 2) do not support the promotional objectives of their
sponsors. For studies/experiments of equally high research/scientific quality, those studies that
do not support the promotional objectives of their sponsors should be assigned relatively higher
credibility priority than those that do support the promotional objectives of their sponsors. This
should not be interpreted as a lack of absolute credibility for studies that support the promotional
objectives of their sponsors. Many may very well be credible, as discussed further in section
2F.
However, research findings opposing the promotional objectives of the sponsors may
result in termination of further funding for the project, and adverse career and financial
consequences for the performer(s). Conversely, research findings supporting the promotional
objectives of the sponsors will most likely lead to continued and enhanced funding for the
project, and very positive career and financial impacts for the performer(s). Therefore, high
quality research studies whose results could impose serious career and financial risks for their
performers should rank higher in the credibility chain.
These conflicts-of-interest of researchers who accept funding from wireless radiation
promoters extend well beyond the papers and studies they publish. This category of wireless
radiation researchers tends to populate the Advisory Committees that help set the exposure safety
studies imposed by government regulatory agencies. Hardell has done a comprehensive
evaluation of some of the more influential Advisory Committees [Hardell, 2017], especially
ICNIRP and WHO, and has shown clearly the inter-locking linkages among these proxies of the
wireless radiation promoters.
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Operationally, the wireless radiation regulatory commissions, their advisory committees, their
health and safety research sponsors, and some of the researchers sponsored by the wireless
radiation promoters, along with the mainstream media, serve as
the de facto marketing arm
of the wireless radiation promoters,
in their attempts to mislead the public into believing
wireless radiation under present day exposure limits is safe!
2A1d. Relation
of wireless radiation health and safety research to publishers’ conflicts-of-
interest
Some journal publishers of articles concerning health and safety effects of wireless
radiation have similar conflicts of interest. Many journals are not independent from government
or industry sponsorship, in whole or in part, directly or indirectly. This conflict-of-interest is
addressed further in section
2F.
These journals control the review process by which articles are
selected for publication, and it is extremely easy for a journal to select articles for publication
that will align strongly with the promotional interests of the organizations or people that
contribute to their revenue stream. These direct or indirect journal sponsors include:
•
•
•
Promotional organizations that contribute directly to the journals;
Promotional organizations that contribute directly to professional societies that sponsor
many of the ‘leading’ journals;
Individuals who receive funding from industrial or governmental organizations
promoting wireless radiation technology and who
o
contribute directly to the journals and/or
o
contribute to professional societies
that sponsor many of the ‘leading’ journals
Anyone who has read thousands of wireless radiation journal article abstracts on health
and safety would have little problem in identifying those journals that rarely publish results
opposing the promotional objectives of government and industry (see Slesin [2006] for
allegations
of possible bias in one journal’s publication patterns of
microwave-induced
genotoxic results). Equally, they would have little problem in identifying those authors or author
institutions that even more rarely publish results opposing the promotional objectives of
government and industry. If we take into account the credibility asymmetry between studies
whose results 1) support the promotional objectives of their sponsors or 2) do not support the
promotional objectives of their sponsors, then a much different picture of the wireless radiation
health and safety research literature emerges. Many of the so-called conflicting results disappear
when credibility weightings are applied, and the true serious adverse effects resulting from this
harmful technology are shown in detail. The reader should keep this credibility asymmetry in
mind when evaluating the myriad adverse health effects shown in sections
2D
and
2E.
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2B. Wireless Radiation/Electromagnetic Spectrum
This section overviews the electromagnetic spectrum, and delineates the parts of the
spectrum on which this monograph will focus. The electromagnetic spectrum encompasses the
entire span of electromagnetic radiation. The spectrum includes: ionizing radiation (gamma rays,
x-rays, and the extreme ultraviolet, with wavelengths below ~10
-7
m and frequencies above
~3x10
15
Hz); non-ionizing visible radiation (wavelengths from ~4x10
-7
m to ~7x10
-7
m and
frequencies between ~4.2x10
14
Hz and ~7.7x10
14
Hz); non-ionizing non-visible radiation (short
wavelength radio waves and microwaves, with wavelengths between ~10
-3
m and ~10
5
m and
frequencies between ~3x10
11
to ~3x10
3
Hz; long wavelengths, ranging between ~10
5
m and ~10
8
m and frequencies ranging between 3x10
3
and 3 Hz).
The low frequencies (3 Hz–300 KHz) are used for electrical power line transmission (60
Hz in the U.S.) as well as maritime and submarine navigation and communications. Medium
frequencies (300 KHz–900 MHz) are used for AM/FM/TV broadcasts in North America. Lower
microwave frequencies (900 MHz–5 GHz) are used for telecommunications such as microwave
devices/communications, radio astronomy, mobile/cell phones, and wireless LANs. Higher
microwave frequencies (5 GHz– 300GHz) are used for radar and proposed for microwave WiFi,
and will be used for
‘high-band’
5G communications. Terahertz frequencies (300 GHz–3000
GHz) are used increasingly for imaging to supplement X-rays in some medical and security
scanning applications [Kostoff and Lau, 2017; Kostoff, 2019a; Kostoff et al, 2020].
In the study of non-ionizing EMF radiation health effects reported in this monograph, the
frequency spectrum ranging from 3 Hz to 300 GHz is covered, with particular emphasis on the
high frequency communications component ranging from ~1 GHz to ~300 GHz. A previous
review found that pulsed electromagnetic fields applied for relatively short periods of time could
sometimes be used for therapeutic purposes, whereas chronic exposure to electromagnetic fields
in the power frequency range (~60 Hz) and microwave frequency range (~1 GHz-tens GHz)
tended to result in detrimental health effects [Kostoff and Lau, 2013, 2017]. Because of present
concerns about the rapid expansion of new communications systems without adequate safety
testing, more emphasis will be placed on the communications frequencies in this monograph.
2C. Modern Non-Ionizing EMF Radiation Exposures
In ancient times, sunlight and its lunar reflections provided the bulk of the visible
spectrum for human beings (with fire a distant second and lightning a more distant third). Now,
many varieties of artificial light (incandescent, fluorescent, and light emitting
diode) have
replaced the sun as the main supplier of visible radiation during waking hours. Additionally,
EMF radiation from other parts of the non-ionizing spectrum has become ubiquitous in daily life,
such as from wireless computing and telecommunications. In the last two or three decades, the
explosive growth in the cellular telephone industry has placed many residences in metropolitan
areas within less than a mile of a cell tower. Future implementation of the next generation of
mobile networking technology, 5G, will increase the cell tower geographical densities by an
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order of magnitude. Health concerns have been raised about non-ionizing EMF radiation from
(1) mobile communication devices, (2) occupational exposure, (3) residential exposure, (4)
wireless networks in homes, businesses, and schools, and (5) other non-ionizing EMF radiation
sources such as ‘smart meters’ and ‘Internet of Things’.
2D. Demonstrated Biological and Health Effects from Prior Generations of Wireless Networking
Technology
2D1. Limitations of Previous Wireless Radiation Health Effects Studies
There have been two major types of studies performed to ascertain biological and health
effects of non-ionizing radiation: laboratory and epidemiology. The laboratory tests provide the
best scientific understanding of the effects of wireless radiation, but do not reflect the real-life
operating environment in which wireless radiation is embedded. There are three main reasons
that laboratory tests do not reflect real-life exposure conditions for human beings.
First, the laboratory tests have been performed mainly on animals, especially rats and
mice. Because of physiological differences, there have been continual concerns about
extrapolating small animal results to human beings. Additionally, while inhaled or ingested
substances can be scaled from small animals to human beings relatively straight-forwardly,
radiation may be more problematical. For non-ionizing radiation, penetration depth is a function
of frequency, tissue, and other parameters, and radiation of a given wavelength could penetrate
much deeper into the (small)
animal’s interior than similar wavelength radiation in humans.
Different organs and tissues would be affected, with different power densities.
Second, the typical incoming EMF signal for many/most laboratory tests performed in
the past consisted of the single carrier wave frequency; the lower frequency superimposed signal
containing the information was not always included. This omission may be important. As
Panagopoulos states: “It is important to note that except for the RF/microwave carrier frequency,
Extremely Low Frequencies
–
ELFs (0–3000Hz) are always present in all telecommunication
EMFs in the form of pulsing and modulation. There is significant evidence indicating that the
effects of telecommunication EMFs on living organisms are mainly due to the included ELFs….
While
∼50%
of the studies employing simulated exposures do not find any effects, studies
employing real-life exposures from commercially available devices display an almost 100%
consistency in showing adverse effects”. [Panogopoulos, 2019]. These effects may be
exacerbated further with 5G: “with every new generation of telecommunication devices…..the
amount of information transmitted each moment…..is increased, resulting in higher variability
and complexity of the signals with the living cells/ organisms even more unable to adapt
[Panogopoulos, 2019]”
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Third, these laboratory tests typically involved one stressor (wireless radiation) and were
performed under pristine conditions. This contradicts real-life exposures, where humans are
exposed to multiple toxic stimuli, in parallel or over time. In perhaps five percent of the wireless
radiation studies reported in the literature, a second stressor (mainly biological or chemical toxic
stimuli) was added, to ascertain whether additive, synergistic, potentiative, or antagonistic effects
were generated by the combination [Kostoff and Lau, 2013, 2017; Juutilainin et al, 2008;
Juutilainin et al, 2006].
Combination experiments are extremely important because, when other toxic stimuli are
considered in combination with non-ionizing EMF radiation, the synergies tend to enhance the
adverse effects of each stimulus in isolation. In other words, combined exposure to 1) toxic
stimuli and 2) non-ionizing EMF radiation translates into much lower levels of tolerance for each
toxic stimulus in the combination relative to its exposure levels that produce adverse effects in
isolation. So, the regulatory exposure limits for non-ionizing EMF radiation when examined in
combination with other potentially toxic stimuli should be far lower for safety purposes than
those derived from non-ionizing EMF radiation exposures in isolation [Kostoff et al, 2020].
Thus, almost all of the laboratory tests that have been performed are flawed with respect
to demonstrating the full adverse impact of the wireless radiation. Either 1) non-inclusion of
signal information or 2) using single stressors only 3) tends to underestimate the seriousness of
the adverse effects from non-ionizing radiation. Excluding
both
of these phenomena from
experiments, as was done in the vast majority of cases, tends to amplify this underestimation
substantially. Therefore, the results (of adverse effects from wireless radiation exposure)
reported in the biomedical literature should be viewed as 1) extremely conservative and 2) the
very low
‘floor’ of the seriousness of the adverse effects, not the ‘ceiling’.
The epidemiology studies typically involved human beings who had been subjected to
myriad known and unknown stressors prior to (and during) the study. The wireless radiation
exposure levels from e.g. the cell tower studies reported in Kostoff and Lau [2017] associated
with increased cancer incidence tended to be orders of magnitude lower than e.g. those exposure
levels generated in the recent highly-funded NTP studies [Melnick, 2019] and other laboratory
studies associated with increased cancer incidence. The inclusion of real-world effects in the cell
tower studies most likely accounted for the orders of magnitude wireless radiation exposure level
decreases that were associated with the initiation of increased cancer incidence.
Thus, the laboratory tests were conducted under very controlled conditions not
reflective of the real-world, while the epidemiology studies were performed in the presence of
many stressors, known and unknown, reflective of the real-world. The exposure levels of the
epidemiology studies were, for the most part, uncontrolled.
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2D2. Adverse Health Effects Identified in Major Review Studies
Many thousands of papers have been published over the past sixty+ years showing
adverse effects from wireless radiation applied in isolation or as part of a combination with other
toxic stimuli. Extensive reviews of these wireless radiation biological and health effects have
been published, including [Belpomme et al, 2018; Desai et al, 2009; Di Ciaula, 2018; Doyon and
Johansson, 2017; Havas, 2017; Kaplan et al, 2016; Kostoff and Lau, 2013, 2017; Kostoff et al,
2020; Lerchl et al, 2015; Levitt and Lai, 2010; Miller et al, 2019; Pall, 2016, 2018;
Panagopoulos, 2019; Panagopoulos et al, 2015; Russell, 2018; Sage and Burgio, 2018; Van
Rongen et al, 2009; Yakymenko et al, 2016; Bioinitiative, 2019].
In aggregate, for the high frequency (radiofrequency-RF) part of the spectrum, these
reviews show that RF radiation below the FCC guidelines can result in:
-carcinogenicity (brain tumors/glioma, breast cancer, acoustic neuromas, leukemia,
parotid gland tumors),
-genotoxicity (DNA damage, DNA repair inhibition, chromatin structure),
-mutagenicity, teratogenicity,
-neurodegenerative
diseases (Alzheimer’s Disease, Amyotrophic Lateral Sclerosis),
-neurobehavioral problems, autism,
-reproductive problems, pregnancy outcomes,
-oxidative stress, inflammation, apoptosis, blood-brain barrier disruption,
-pineal gland/melatonin production, sleep disturbance, headache,
-irritability, fatigue, concentration difficulties, depression, dizziness, tinnitus,
-burning and flushed skin, digestive disturbance, tremor, cardiac irregularities, and can
-adversely impact the neural, circulatory, immune, endocrine, and skeletal systems.
The effects range from myriad feelings of discomfort to life-threatening diseases. From
this perspective, RF exposure is a highly pervasive cause of disease!
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2D3. Adverse Health Effects from Open Literature Analysis
2D3a. Overview
To corroborate the findings from the major review studies of the previous section, an
analysis of a representative sample of the wireless radiation adverse health effects literature was
performed. A relatively simple query was used to retrieve records related to adverse health
effects from wireless radiation. Some filtering was done to remove records that did not identify
adverse health effects, but because of extensive use of titles (and sometimes abstracts) that
discuss methodologies rather than results, some/many records were retrieved that did not
demonstrate adverse health effects.
In all, 5311 records with abstracts were retrieved from Medline (Pubmed), and these
records were categorized by three different methods: manual taxonomy; factor analysis
taxonomy; text clustering taxonomy. The three methods and their results will be briefly
summarized here, and the more detailed results, including category record titles, will be
presented in Appendices 2-4.
2D3b. Manual taxonomy results
Based on the factor analysis (section 2D3c) and text clustering (2D3d) results, as well as
reading thousands of abstracts from the full database, a manual taxonomy of adverse health
effects from wireless radiation was constructed.
Appendix 2
presents this taxonomy (Table
A2-
1),
and the titles of the records that were assigned to each category in the taxonomy. The record
titles give a better appreciation for the contents of each category than the brief category heading.
This
manual taxonomy is the most relevant
(of the three taxonomies presented) to the
main objective of identifying and categorizing specific adverse health effects from wireless
technology, since it was not dependent on any algorithm to determine adverse effects categories
and received a
higher level of title filtering
than the other two.
Table A2-1
(reproduced in the
following) presents the categories in the taxonomy, and a strong condensation of the key phrases
1) used to define the category and 2) link to the record titles shown in
Appendix 2.
A more
detailed manual taxonomy, with orders-of-magnitude more phrases, is shown in
Appendix 2.
The adverse effects identified in the manual taxonomy cover those summarized in the
comprehensive review analyses described previously, and go well beyond. While all the
categories shown are problematical and harmful, the most researched categories with perhaps the
most serious adverse effects are
cancer/tumors, neurodegenerative diseases, reproduction
problems, and genotoxicity.
Thus, even confining these results to the non-classified open
literature, many of which are based on single stressor experiments that tend to downplay greatly
real-life adverse effects, there is more than enough hard evidence that wireless radiation 1)
can
be extremely harmful in real-life environments,
and 2)
needs to be subjected to orders-of-
magnitude harsher exposure limitations
than is the case today. In
Appendix 2,
the categories in
Table A2-1
are hyperlinked to their respective record title sections.
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Table A2-1
–
Manual Taxonomy
CATEGORY
Cancer/Tumors
Neurodegenerative
KEY PHRASES
cancer, leukemia, glioma, lymphoma, melanoma, Hodgkin's
disease, tumor, acoustic neuroma, meningioma
memory, central nervous system, learning, neurodegenerative,
Alzheimer's disease, cognition, amyotrophic lateral sclerosis,
dementia, epilepsy, multiple sclerosis, cognitive impairment,
seizures, autism
pregnancy, reproductive, sperm, embryos, testicular, fertility,
embryo, testosterone, infertility
DNA damage, genotoxic, micronuclei, mutagenic, strand breaks,
chromatin, mutation, chromosome aberrations,
Cardiac, cardiovascular, pacemaker, implanted, Cardiovascular
disease, arrhythmia, arterial blood pressure, ventricular fibrillation
lymphocytes, immune system, immunity, leukocytes, antibodies,
neutrophils, autoimmune, macrophage,
apoptosis, oxidative stress, Malondialdehyde, reactive oxygen
species, superoxide dismutase, lipid peroxidation, inflammation,
oxidation, ornithine decarboxylase, barrier permeability, atrophy,
C-reactive protein, oxidative damages
auditory, acoustic, hypersensitivity, electromagnetic
hypersensitivity, cataract, tinnitus, dermatitis, cataractogenic, pain
sensitivity, pain threshold
depression, anxiety, headache, dizziness, depressed, vertigo, nausea,
low back pain
malformations, teratogenic, congenital malformations, cleft palate,
melatonin, sleep, circadian, insomnia, pineal function
Reproduction
Genotoxicity
Cardiovascular
Immunity
Biomarkers
Sensory Disorders
Discomfort
Symptoms
Congenital
Abnormalities
Circadian
Rhythym and
Melatonin
Chronic
Conditions
metabolism, glucose, endocrine, cholesterol, Diabetes, calcium
homeostasis, obesity
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2D3b1. Adverse effects of wireless radiation on food chain
The above taxonomy (and its associated records) focuses on the direct linkage between
wireless radiation exposure and biomarkers, symptoms, and diseases. As such, these effects can
be viewed as direct effects. Equally important, but usually overlooked in any discussions of
adverse effects of wireless radiation, are the indirect effects, especially those on the ecological
infrastructure that supports human life.
An analogy to war and conflict may be instructive. When one examines the great wars
and battles of human history, especially those that persisted for more than very short periods, the
critical role of logistics in determining the outcome becomes obvious. Many wars/battles have
been won or lost by the adequacy and timeliness of logistical supplies and support.
The struggle for survival of human life on Earth is similarly dependent on the logistical
food supply chain. At the foundation of this supply chain (before the farmers become involved
in harvesting its bounty) are the insects, seeds, flora, trees, etc, that enable the bountiful growth
of the myriad potential foods. If the integrity of this foundational logistical supply chain is
threatened in any way, then both the animals and plant products we consume become
unavailable.
There is a substantial literature on the adverse impacts of wireless radiation on this
foundational logistical supply chain. These adverse effects are from the pre-5G exposures, and
would include enhanced coupling from the higher frequency harmonics. Many of these supply
chain elements (e.g., insects, seeds, larvae, etc) are very small, and we could expect enhanced
resonance/energy coupling from the shorter-wavelength 5G radiation when implemented. This
indirect impact of wireless radiation may turn out to be at least as important (if not more
important) as the direct impact of wireless radiation on human survival! At the
end of Chapter 3
are a few references showing the harmful effects of wireless radiation on the foundational food
supply chain. They are the tip of the iceberg of a much larger literature on adverse effects of
wireless radiation on the foundational food supply chain.
From a broader perspective, most of the laboratory experiment component of the wireless
radiation adverse effects literature can be viewed as related to the foundational food supply
chain. Much of this research is focused on mice, rats, insects, small birds, small fish, etc. These
species tend to be prey of larger animals/fowl/fish, and eventually make their way to the human
food table. Any environmental factor that affects the health of these species adversely will
eventually impacts the humans who are at the end of that chain. In reality, we have accumulated
a massive literature describing the adverse impacts of wireless radiation on myriad contributing
components to our food supply, and the results do not bode well for our future ability to feed the
existing
world’s population, much less the growing world’s population!
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2D3b2. Implants and Appendages
The adverse impacts of wireless radiation on myriad medical
implants don’t get much
discussion in the literature, especially passive implants (defined below), and especially with
regard to radiofrequency radiation. A number of articles in the database addressed non-organic
implants, which are foreign bodies inserted into humans and animals for medical purposes. Non-
organic implants addressed in the present database are typically not rejected by the immune
system like organic foreign substances (although some adjuvants such as metal could induce
autoimmune responses [Loyo et al, 2013]). Non-rejection does not mean they are safe,
especially from exposure to wireless radiation.
There were two major types of implants covered by the database articles showing adverse
effects: active implants that produced electrical signals mainly for controlling heart irregularities
(e.g., pacemakers, defibrillators) and hearing deficiencies (e.g., cochlear implants), and passive
metallic implants for structural support (e.g., dental implants, bone pins, plates, etc).
Additionally, there are articles addressing adverse effects from wireless radiation in the vicinity
of metallic appendages (e.g., metallic eyeglasses, metallic jewelry, etc).
The external EMF from microwaves (and other sources) could 1) impact the electrical
operation of the active implants adversely, 2) increase the Specific Absorption Rate (SAR)
values of tissue in the vicinity of the passive implants substantially because of resonance effects,
and 3) increase the flow and acidity of saliva in the vicinity of dental structures. While the EMF
effects on the cochlear implants could adversely affect auditory capability, EMF effects on the
heart-related implants could potentially be life-threatening. The increased SAR values around
the passive metal implants could result in increased tissue temperatures, and could adversely
impact integration and longevity of the passive metallic implants.
In the mouth, the combination of 1) increased tissue temperatures in proximity to the
implant or other orthodontic structures and 2) increased flow rate and acidity of saliva could lead
to 3) increased leaching of heavy metals. Exposure to heavy metals is a major contributor to
myriad chronic diseases [Kostoff, 2015]. The question then becomes: what other adverse health
effects from the exposure of both the active and passive implants to increasing levels of wireless
radiation have not been identified or addressed?
Appendix 7
addresses this issue of wireless radiation adverse effects related to medical
implants and appendages in more detail, and additionally addresses potential wireless radiation
adverse effects on tissues imbedded (deliberately or inadvertently) with exogenous-based
nanoparticles that effectively act as micro/nano-implants. These nanoparticle-imbedded tissues
may have the potential for enhanced energy absorption from the incoming RF signal, and may
exhibit potentially harmful thermal transients (over and above the potential thermal transients
resulting from the pulsed high peak-to-average power of the RF signal) that would be
camouflaged under the wide averaging time periods in the FCC Guidelines.
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2D3c. Factor analysis taxonomy results
The 5,311 records in the retrieved and
partially
filtered adverse health effects database
were imported into the VP software [VP, 2019], and a factor analysis was performed. Thousands
of MeSH Headings extracted by the VP software were inspected visually, and those directly
applicable to adverse health effects were selected. The software then used these selected MeSH
Headings to generate a factor matrix, which identified the main adverse health effects themes of
the database.
Appendix 3
presents this taxonomy (Table
A3-1),
and the titles of the records that
were assigned to each category in the taxonomy. The titles give a better appreciation for the
contents of each category than the brief category heading.
Table A3-1 (reproduced from Appendix 3) follows. It presents the factors/categories in
the taxonomy, and the key MeSH Headings used to define the factor/category and link to the
record titles shown in
Appendix 3.
In
Appendix 3,
the factors in
Table A3-1
are hyperlinked to
their respective record titles.
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Table A3-1 - Factor Analysis Taxonomy
FACTOR
THEME
1
Electromagnetic
hypersensitivity
and inflammation
2
Coronary artery
disease
3A
Congenital
abnormalities
3B
Mammary tumors
4
Male infertility
5
Brain neoplasms
MESH HEADINGS
C-Reactive Protein, Liver Diseases, Thyroid Diseases, Inflammation,
Tonsillitis, Hypersensitivity
Plaque, Atherosclerotic, Coronary Artery Disease, Diabetes Mellitus,
Carotid Artery Diseases, Inflammation, Hypertension
Cleft Lip, Cleft Palate, Calcification, Physiologic, Congenital
Abnormalities
Fibroadenoma, Adenoma, Mammary Neoplasms, Animal, Mammary
Neoplasms, Experimental, Adenocarcinoma
Sperm Count, Spermatozoa, Sperm Motility, Semen, Testis, Infertility,
Male, Spermatogenesis, Testosterone, Fertility
Meningioma, Glioma, Meningeal Neoplasms, Neuroma, Acoustic,
Brain Neoplasms, Glioblastoma, Neoplasms, Radiation-Induced,
Neuroma, Cranial Nerve Neoplasms, Parotid Neoplasms, Central
Nervous System Neoplasms
Burning Mouth Syndrome, Taste Disorders, Skin Diseases, Mouth
Diseases, Dizziness, Vision Disorders, Hypersensitivity, Delayed,
Fatigue
Carcinoma, Lobular, Carcinoma, Ductal, Breast, Breast Neoplasms,
Male, Adenoma
Oxidative Stress, Malondialdehyde, Glutathione Peroxidase, Lipid
Peroxidation, Reactive Oxygen Species, Apoptosis, DNA Damage,
Nitric Oxide, Protein Carbonylation
6
Sensory disorders
7
Breast neoplasms
8
Oxidative stress
9
Parkinson Disease, Neurodegenerative Diseases, Alzheimer Disease,
Neurodegenerative
Amyotrophic Lateral Sclerosis, Motor Neuron Disease, Occupational
diseases
Diseases, Dementia, Brain Diseases, Dementia, Vascular
10
Cerebrovascular
disorders
Cerebrovascular Disorders, Dementia, Migraine Disorders, Tinnitus,
Headache, Sleep Wake Disorders, Carotid Artery Diseases, Alzheimer
Disease, Dementia, Vascular
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11
Congenital
abnormalities and
glandular-based
tumors
12
Skin neoplasms
Cleft Lip, Cleft Palate, Fibroadenoma, Adenoma, Calcification,
Physiologic, Mammary Neoplasms, Animal, Mammary Neoplasms,
Experimental, Adenocarcinoma
Carcinoma, Basal Cell, Carcinoma, Squamous Cell, Skin Neoplasms,
Cocarcinogenesis, Neoplasms, Experimental, Neoplasms, Radiation-
Induced, Colonic Neoplasms
Leukemia, Myeloid, Acute, Leukemia, Lymphocytic, Chronic, B-Cell,
Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Leukemia,
Myeloid, Leukemia, Multiple Myeloma, Lymphoma, Leukemia,
Radiation-Induced, Acute Disease, Liver Neoplasms, Experimental,
Central Nervous System Neoplasms
Atrophy, Precancerous Conditions, Hyperplasia, Hypersensitivity,
Delayed, Thymus Gland, Capillary Permeability, Lymphoma
13
Leukemia
14
Precancerous
conditions
15
Melatonin, Circadian Rhythm, Pineal Gland
Circadian Rhythm
16
Eye diseases
Eye Diseases, Cataract, Vision Disorders, Sensation Disorders,
Neurotic Disorders, Lens, Crystalline, Corneal Diseases, Edema,
Hematologic Diseases
Tachycardia, Ventricular, Ventricular Fibrillation, Death, Sudden,
Cardiac, Arrhythmias, Cardiac
17
Electromagnetic
interference in
implanted
electronic devices
18
Liver Neoplasms
19
Symptoms of
discomfort
20
Neoplasms
Liver Neoplasms, Carcinoma, Hepatocellular, Neoplasm Recurrence,
Local, Lymphatic Metastasis
Headache, Dizziness, Fatigue, Depression, Anxiety, Tremor, Sleep
Wake Disorders, Neurotic Disorders, Stress, Psychological, Anxiety
Disorders, Nervous System Diseases
Lung Neoplasms, Ovarian Neoplasms, Pituitary Neoplasms,
Lymphoma, Prostatic Neoplasms, Colonic Neoplasms, Carcinoma,
Breast Neoplasms, Hematologic Neoplasms, Neoplasms, Liver
Neoplasms, Cell Transformation, Neoplastic, Nervous System
Neoplasms
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2D3d. Text clustering taxonomy results
The 5,311 records in the retrieved and
partially
filtered adverse health effects database
were imported into the CLUTO software [CLUTO, 2019], and a text clustering was performed.
Forty-eight lowest level clusters were selected, based on theme resolution desired (average ~100
records per lowest level category).
Appendix 4
presents this taxonomy (Table
A4-1, Table A4-
2),
and the titles of the records that were assigned to each lowest-level category in the taxonomy.
The titles give a better appreciation for the contents of each category than the brief category
theme shown.
Table A4-1 (reproduced from the Appendix) presents the high-level clusters in the
taxonomy, and the cluster themes. In
Appendix 4,
the fourth-level clusters in
Table A4-2
(repeated from the fourth level shown in Table A4-1) are hyperlinked to their respective record
titles.
Table A4-1 - CLUTO-Based Text Clustering Taxonomy
–
Top Levels
SECOND LEVEL FOURTH LEVEL
Cluster 92 (2561)
–
Cluster 78 (912) - Adverse impacts of wireless radiation, especially on
Adverse effects of
cataracts, cells, and cognitive functions
wireless radiation at Cluster 79 (428) - Microwave radiation absorption at different
cellular level,
frequencies
including radiation Cluster 82 (529) - Adverse effects of mobile phone radiation,
absorption at
especially oxidative stress
different
Cluster 84 (692) - Genotoxic effects of radiofrequency radiation
frequencies
Cluster 93 (2750)
–
Cluster 81 (673) - Adverse impacts of power-line EMF
Adverse health
Cluster 85 (540) - Adverse impacts of low-frequency EMF,
effects of EMF on
emphasizing cancer and neurodegenerative diseases
humans, especially Cluster 83 (668)
–
Adverse effects of mobile phone use, especially
cancer and
brain tumors, and brain and neural function
neurodegenerative
diseases, and on
Cluster 89 (869) - Human health risks from electromagnetic radiation,
implanted
including adverse effects on implanted electronic devices, and
electronic devices
possible protections
Note: Numbers in parentheses reflect numbers of records in cluster
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2D3e. Wireless radiation adverse health effects in closed literatures
It should be re-emphasized at this point that almost all of the wireless radiation findings
reported above reflect what is published in the open literature. That tends to emphasize basic
research, and tends to be produced by academia, with its strong incentives for publication.
There’s a much larger world of effort centered around wireless radiation technology and
engineering development (for surveillance, communications, and weaponry) performed in
organizations that have 1) few incentives to publish and 2) many prohibitions against publication
due to classification and/or proprietary issues. Publication of adverse effects of these wireless
systems could have severe financial consequences for all the stakeholders involved, and could
result in potential military operational constraints as well.
The Federal government and industry who sponsor and many times conduct these advanced
wireless radiation technology studies and demonstrations have 1) strong incentives to classify
and proprietarize any results detrimental to their promotional activities and 2) no incentives to
release results showing serious adverse health effects from wireless radiation to the public!
Consider the example shown in
section 2D4
concerning the Zalyubovskaya [1977]
reference, derived from Kostoff [2019a]. It shows some 1970s Soviet studies on EMF effects,
including millimeter-wave effects, that were classified for 35 years until declassification in 2012.
If relatively benign studies like those were classified for 35 years, one can only imagine the more
serious studies that remain classified until this day. Or, Soviet studies that were not presented in
an open forum because of their sensitivity. Or, USA studies that were performed decades ago (or
recently), and remain classified to this day.
Also, consider the following example, which came to light relatively recently.
On 30 October 2019, an article was published suggesting the presence of cancer clusters
among military pilots [
https://www.mcclatchydc.com/news/nation-world/national/national-
security/article236413708.html
]. This may be the tip of the iceberg, since there are latency
periods preceding the emergence of these cancers. It is unclear how well the health conditions
of these pilots are tracked once they leave the service (according to the article), or, more
specifically,
how well the public is informed
as to how well the health conditions of these
pilots are tracked once they leave the service, and, if they are tracked, what the results of this
tracking are. If there is tracking, who is funding the tracking, and what is its objectivity?
Severe recruiting consequences would result if it were shown that these serious diseases are in
fact associated with exposures to on-board avionics and other stressors unique to the aircraft
environment (EMF in combinations with other unique stressors [chemicals, psychological
stress, high and low-G forces, etc] that performance aircraft crews face). It would be valuable
to get EMF exposure data (using
an independent assessment)
under myriad flight conditions
for many different military aircraft, with all the onboard avionics in full operation.
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A similar article generated by the same organization addressing RF exposures of military
pilots [
https://www.mcclatchydc.com/news/nation-world/national/national-
security/article237797304.html
] complements the information contained in the above example, as
shown in the following:
The largest Grumman measurement reported in the article translates to
300 million
microwatts/square meter!
This is thirty times today's FCC general public exposure limit,
which itself is three-four orders-of-magnitude above levels shown by the cell tower studies to
increase cancer incidence substantially. In parallel, the pilots are also being exposed to
myriad other toxic stimuli, including EMF of other frequencies, cosmic radiation, perhaps fuel
odors, etc, increasing the possibility of adverse effect synergies.
These may be the tip of the iceberg of RF exposure measurements done in the aircraft cabin,
and there is no evidence that these were the highest occurring exposures. These types of
exposure measurements rarely, if ever, see the light of day in the open literature, and are not
advertised (for obvious purposes) by government-industry.
Additionally, while the gold coating mentioned may have kept a substantial amount of
external RF from entering the cabin, it also would have delayed RF (that was internally
generated or entered the cabin through non-gold coated non-metallic avenues) from leaving
the cockpit, mirroring a hohlraum effect.
This cockpit problem reflects a disturbing trend. The military services became network-
centric decades ago. They are almost completely dependent on wireless communications and
wireless detection/surveillance for all their operations. If they were to allow their labs and
contractors to report the possible damage from the levels of exposures happening in the field and
at their facilities, potentially resulting in much lower wireless radiation exposure limits, they
would be forced to eliminate many decades of so-called advances in their weaponry and
operations. It could also impact their recruitment efforts adversely. No different in kind from
their civilian counterparts, although the military may be operating at higher exposure levels
because of their ultra-high-performance requirements.
So, while the adverse health effects of wireless radiation listed above in the monograph
are very serious in their own right, they may be just the tip of the iceberg of the totality of
adverse health effects that have actually been demonstrated if the non-published or classified
studies had been taken into account.
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2D4. Adverse Wireless Radiation Health Effects from Former USSR Literature Analysis
2D4a. Overview
The Former Soviet Union/USSR was a major player in biomedical research on health
effects of non-ionizing radiation (both adverse and therapeutic) since at least the 1950s, and
perhaps well before. Some/much of the work was published in the Soviet open literature, and
available in Russian. Some/much of it was translated by USA intelligence agencies, and later
declassified. Some may still be classified. The major difference between the USA and Soviet
research on adverse effects of wireless radiation appears to be emphasis on thermal (USA) vs
athermal (Soviet) effects. This difference is reflected in the different wireless radiation exposure
limits imposed by each government.
2D4b. Glaser and Dodge review of East European radiofrequency literature
Glaser and Dodge addressed this issue within a comprehensive review of East European
radiofrequency and microwave radiation literature [Glaser and Dodge, 1976], as follows:
THERMAL VS ATHERMAL EFFECTS
–
USA-USSR
“The most significant difference between East and West relative to biological mechanisms of
effects of microwaves concerns the question of thermogenic versus nonthermogenic (or
athermal) effects…..The traditional Soviet and East European view from the earliest
publications of bio-studies has been that microwave and radio frequency fields can
functionally, and even morphologically in some cases, alter the organism at field flux or
power densities below those which cause measureable heating in tissues or biological
substrates. Thus, reversible changes in behavior, physiological function, and microstructures
are frequently reported at power densities of microwatts per square centimeter (muW/cm2),
well below the Western world’s “safe” exposure level of 10 milliwatts
per square centimeter
(10 mW/cm2)…..In contrast, the prevailing Western view, particularly in the United States, is
that the effects of microwave and radio frequency fields are attributable only to the heating
mechanism of those fields which are generally encountered at power densities in excess of 10
mW/cm2…..
The disparity between Eastern and Western views in this respect finds its most eloquent
expression in daily occupational exposure standards for microwaves. In the Soviet Union and
some East European countries, the standard for an occupational exposure day is 0.01
mW/cm2…..In the United States and some Western European countries, the value for
continuous exposure is 10 mW/cm2.
Prior to 1953, it was believed that 100 mW/cm2 was the lowest level at which significant
biological damage would occur…..Thus, 10 mW/cm2 is approximately one tenth the level
calculated to cause significant heating in human tissues, and agrees with physiologic and
metabolIc calculations . Intermediate standards between these values are practiced by some
European countries…...”
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This conclusion, presented 43 years ago in print, is particularly disheartening. Despite all
the evidence of adverse athermal effects of wireless radiation that was generated prior to 1976
(especially in the USSR, but in the USA as well), and the voluminous evidence (of adverse
athermal effects of wireless radiation) that has been reported from global research since 1976,
the USA government (along with many others) has refused to recognize the credibility of these
athermal wireless radiation effects in the setting of regulatory exposure standards.
2D4c. Glaser review of global radiofrequency literature circa 1972
What was the state of the open literature on adverse health effects of wireless radiation in
the 1970s, including what was known about Soviet and East European research? One partial
answer can be gleaned from a very comprehensive review of the global radiofrequency and
microwave biomedical effects literature published as a DTIC report in 1972 [Glaser, 1972]. The
abstract of this report states in part:
“More
than 2300 references on the biological responses to radio frequency and microwave
radiation, published up to April 1972, are included in this bibliography of the world literature.
Particular attention has been paid to the effects on man on non-ionizing radiation at these
frequencies. The citations are arranged alphabetically by author, and contain as much
information as possible so as to assure effective retrieval of the original documents.
Soviet
and East European literature is included in detail.
An outline of the effects which have been
attributed to radio frequency and microwave radiation is included as Chapter 1.”
The effects mentioned in the last sentence have been converted to a more readable form by Dr.
Magda Havas on her outstanding Web site (describing decades of global research on wireless
radiation health effects) [Havas, 2019]. As stated on her Web site, Dr. Havas has obtained hard
copies of Dr. Glaser’s references from Dr. Glaser, and is in the process of scanning them and
making them available to a wider audience.
Dr. Havas’ summary
of the effects mentioned in the
last sentence of the box above is repeated in the following table:
CATEGORY
A. Heating of
Organs*
[Applications:
Diathermy,
Electrosurgery,
Electrocoagulation,
Electrodesiccation,
Electrotomy]
ADVERSE EFFECTS
This includes heating of the whole body or part of the body like the
skin, bone and bone marrow, lens of the eye with cataracts and
damage to the cornea; genitalia causing tubular degeneration of
testicles; brains and sinuses; metal implants causing burns near hip
pins etc. These effects are reversible except for damage to the eye.
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This includes contraction of striated muscles; altered diameter of
blood vessels (increased vascular elasticity), dilation; changes in
oxidative processes in tissues and organs; liver enlargement; altered
sensitivity to drugs; decreased spermatogenesis leading to decreased
fertility and to sterility; altered sex ratio of births in favor of girls;
altered menstrual activity; altered fetal development; decreased
lactation in nursing mothers; reduction in diuresis resulting in sodium
excretion via urine output; altered renal function; changes in
conditioned reflexes; decreased electrical resistance of skin; changes
in the structure of skin receptors; altered rate of blood flow; altered
biocurrents in cerebral cortex in animals; changes in the rate of
clearance of tagged ions from tissues; reversible structural changes in
the cerebral cortex and diencephalon; changes in electrocardiographs;
altered sensitivity to light, sound, and olfactory stimuli; functional and
pathological changes in the eyes; myocardial necrosis; hemorrhage in
lungs, liver, gut and brain and generalized degeneration of body tissue
at fatal levels of radiation; loss of anatomical parts; death;
dehydration; altered rate of tissue calcification.
C. Central Nervous
This includes headaches; insomnia; restlessness (daytime and during
System Effects
sleep); changes in brain wave activity (EEG); cranial nerve disorders;
pyramidal tract lesions; disorders of conditioned reflexes;
vagomimetic and sympathomimetic action of the heart; seizure and
convulsions.
D. Autonomic
Altered heart rhythm; fatigue, structural alterations in synapses of the
Nervous System
vagus nerve; stimulation of the parasympathetic nervous system
Effects
leading to Bradycardia and inhibition of the sympathetic nervous
system.
E. Peripheral
Effects on locomotor nerves.
Nervous System
Effects
F. Psychological
Symptoms include neurasthenia (general bad feeling); depression;
Disorders
impotence; anxiety; lack of concentration; hypochondria; dizziness;
hallucinations; sleepiness or insomnia; irritability; decreased appetite;
loss of memory; scalp sensations; fatigue; chest pain, tremors.
G. Behavioral
Effects include changes in reflexive, operant, avoidance and
Changes in Animals
discrimination behaviors
Studies
H. Blood Disorders
Effects include changes in blood and bone marrow; increased
phagocytic and bactericidal functions; increased rate of hemolysis
(shorter lifespan of cells); increased blood sedimentation rate;
B. Changes in
Physiologic
Function
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I. Vascular
Disorders
J. Enzyme and
Other Biochemical
Changes (in vitro)
decreased erythrocytes; increased blood glucose concentrations;
altered blood histamine content; changes in lipids and cholesterol;
changes in Gamma Globulin and total protein concentration; changes
in number of eosinophils; decrease in albumin/globulin ratio; altered
hemopoiesis (rate of blood corpuscles formation); leukopenia
(increased number of white blood cells and leukocytosis;
reticulocytosis (increase in immature red blood cells).
This includes thrombosis and hypertension.
Changes in the activity of cholinesterase (also in vivo); phosphatase;
transaminase; amylase, carboxydismutase; denaturation of proteins;
inactivation of fungi, viruses, and bacteria; killed tissue cultures;
alterated rate of cell division; increased concentration of RNA in
lymphocytes and decreased concentration of RNA in brain, liver and
spleen; changes in pyruvic acid, lactic acid and creatinine excretions;
changes in concentration of glycogen in liver (hyperglycemia); altered
concentrationsof 17-ketosteroids in urine.
K. Metabolic
Effects include glycosuria (sugar in urne); increase in urinary phenols;
Disorders
altered processing of metabolic enzymes; altered carbohydrate
metabolism.
L. Gastro-Intestinal
Effects include anorexia; epigastric pan; constipation; altered secretion
Disorders
of stomach digestive juices.
M. Endocrine
Effects include altered functioning of pituitary gland, thyroid gland
Gland Changes
(hyper-thyroidism and enlarged thyroid, increased uptake of
radioactive iodine), and adrenal cortex; decreased corticosteroids in
blood; decreased glucocorticoidal activity; hypogonadism (with
decreased production of testosterone).
N. Histological
Changes in tubular epithelium of testicles and gross changes.
Changes
O. Genetic and
Effects include chromosomal aberrations (shortening, pseudochiasm,
Chromosomal
diploid structures, amitotic divisions, bridging, “stickiness”;
Changes
irregularities in chromosomal envelope); mutations; mongolism;
somatic alterations (not involving nucleus or chromosomes);
neoplastic diseases (tumors).
P. Pearl Chain
This refers to intracellular orientation of subcellular particles and
Effect
orientation of cellular and other (non-biologic particles, i.e. mini
magnetics) affecting orientation of animals, birds, and fish in
electromagnetic fields.
Q. Miscellaneous
These include sparking between dental fillings; metallic taste in
Effects
mouth; changes in optical activity of colloidal solutions; treatment for
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syphilis, poliomyelitis, skin diseases; loss and brittleness of hair;
sensations of buzzing, vibrations, pulsations, and tickling about head
and ears; copious perspiration, salivation, and protrusion of tongue;
changes in the operation of implanted cardiac pacemakers; changes in
circadian rhythms.
Thus, much was known about the adverse health effects of both thermal and athermal
high-frequency
wireless radiation even in the early 1970s (Glaser’s review did not address lower
frequency radiation effects, although we now know these lower frequency effects could be
equally damaging as those from high frequency), but this long-standing knowledge has not
translated into adequate protections for the public from wireless radiation, both in the USA and
the rest of the world.
2D4d. Joint Publications Research Service translations of East European research
Another avenue of insight into Soviet and East European research in the 1970s era was
provided by the Joint Publications Research Service (JPRS). A description of this organization
follows [
https://guides.library.harvard.edu/jprs
]:
The United States Joint Publications Research Service is a government agency which
translates foreign language books, newspapers, journals, unclassified foreign documents and
research reports. Approximately 80% of the documents translated are serial
publications. JPRS is the largest single producer of English language translations in the
world. More than 80,000 reports have been issued since 1957, and currently JPRS produces
over 300,000 pages of translations per year.
In its early years JPRS concentrated heavily on scientific and technical material
from communist countries. Gradually coverage has broadened to include more non-
scientific materials.
2D4d1. Maritime occupational radiofrequency exposures in USSR
One of the Soviet technical books translated by the JPRS
is listed on Dr. Havas’ Web site
[
https://magdahavas.com/pick-of-the-week-15-russian-translations-on-biological-effects-of-magnetic-
fields-and-radio-frequency-radiation/
]. This book [Kulikovskaya, 1970] is important because it
shows the levels of wireless radiation to which Soviets in some occupations were exposed fifty
years ago, numbers that many wireless radiation proponent countries do not readily advertise.
Whether these exposures are greater or less today is unclear; powers may be higher, but shielding
may be better.
In the introductory section of Chapter IV (Biological Effect of Radio Waves
–
p.70), the
following statement is made:
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“Foreign
researchers are giving basic attention to the effect of electromagnetic radio waves
beginning with the thermal effect, that is, heating the animate organism by the field energy.
The research performed in our country, in contrast to foreign research, is based on a complex of
dynamic studies of the reactions of the organism to the effect of low irradiation intensities, and,
especially, in the superhighfrequency range, recognition of the cumulative biological effect in the
case of chronic explosure to low power flux densities.”
This quoted statement confirms the statement of Glaser and Dodge in section 2D4b
above. Since the bulk of the references in Kulikovskaya’s
book are from the 1950s and 1960s,
one can surmise that
a decision was made by the Western powers (especially the USA, who led
the Western powers at that time) seventy years ago to downplay the adverse effects of athermal
wireless radiation, and promote the false concept that only the thermal effects of wireless
radiation are responsible for biomedical damage.
The decision-makers from the Western
powers recognized seventy years ago that
wide-ranging wireless communications and
surveillance were not possible if biologically protective exposure limits were promulgated.
Through countless Administrations and Legislatures since the days of President Eisenhower, all
USA (and most foreign) decision-makers have presented a consistent and unified front
promoting increased exposure to wireless radiation at the expense of
the health of the nation’s
citizens!
The following table shows examples (from Kulikovskaya [1970]) of maximum levels of
exposure to wireless radiation for Soviet citizens working in the marine environment. The
maximum electric field exposure levels exceed the Soviet regulatory limits at that time (which
were up to an order-of-magnitude lower than the USA regulatory limits) by up to two orders-of-
magnitude!
To place these numbers in perspective,
the Building Biologists’ recommendations for
safe long-term exposure limits in these frequency ranges is less than one volt per meter
(
https://mdsafetech.org/conversion-and-exposure-limits-emr-emf/
). Thus, the reported exposures
exceed safe levels by two-three orders of magnitude.
The research was performed at the Laboratory of Physical Factors of the State Scientific
Research Insitute of Labor Hygiene and Professional Diseases. The exposure levels reported are
what the Soviet government was willing to release to the public. Whether they were the most
severe exposures experienced by members of the civilian and military fleets remains unknown.
In terms
of personnel recruitment for these jobs, it was/is not in the government’s
(Soviet or
otherwise, including USA) best interests to release to the public exposure levels that would show
these jobs to be highly dangerous to health. The book attempts to make the point that most
exposures experienced by maritime personnel are much lower than the maximum, probably to
assuage the public. The results are disturbing nevertheless, and should be viewed as the ‘floor’
of exposures to be expected relative to measurements made by an 1)
independent objective
group
2)
on location during operations
3)
without having given advanced notice!
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REGION
Electromagnetic Fields Near Tube Generators for High-
Frequency Heating of Metals (P.23)
Electromagnetic Waves Near Tube Generators for High-
10-30
500+
20
Frequency Heating of Dielectrics (P.26)
Electromagnetic Fields in the Radio Rooms of Ships (P. 29)
.3-23
Passenger Ships (P. 32)
.4-.8
2,000
20
Ships of the Tanker Fleet (P. 36)
.4-.8
2,000
20
Dry Cargo Ships (P. 37)
.4-.8
1,600
20
Ships of the Auxiliary Fleet (P. 40)
.4-.8
420
20
Electromagnetic Fields of Radio Communications Antennas on
.3-3
880
20
the Decks and Superstructures of Ships (P. 44)
“In
conclusion, it can be stated that the highest intensity of an electric field up to hundreds and
sometimes
thousands and more volts per meter
occurs near the antenna drops and metal masses
on the top bridges and decks during operation of a medium wave radio. Here, the magnetic
component of the field can reach
ten and even fifteen amps/meter.”
P. 52)
Superhigh Frequency Electromagnetic Fields of Radar
3,000-
Antennas on the Decks of Ships (P. 52)
15,000
“Studies of the conditions of irradiation of the deck
crew with superhigh-frequency fields
performed on ships for various purposes show that when the radar antennas are installed on
co1umns 1.2-2.5 meters above the deck of the top bridge, the power flux density can be hundreds
and sometimes
thousands of microwatts per square centimeter.”
(P. 54)
FREQ
RANGE
MHz
.06-.8
MAX
EXPOS
V/m
1,000+
EXP
LIMIT
V/m
20
Some Adverse Health Effects of Marine Radio Operators (P. 80)
“The conditions of labor of marine radio operators are least favorable…..
a relatively large number of
people with various diseases appear among radio operators. Thus, out of 215 radio operators, 50 had
chronic diseases (23.2 percent)…..The primary disruption of the state of health of ship radio operators
is damage to the organs
of sight…..Among the diseases of the cardiovascular system occurring in ship
radio operators, hypertonic disease. myocardial distrophy and disruption of the blood circulation in the
brain play the leading role. All radio operators suffering from diseases of the cardiovascular system are
young (from 30 to 35 years old) with five to 10 years of service. Among the diseases of the nervous
system encountered in them, functional disorders of the central nervous system, vegetative neurosis,
and neurasthenic syndrome
are noted…..Thus, it is possible to consider it established that the largest
number of people with health impairments occur among ship radio operators as compared to other
marine professions.”
2D4d2. Biomedical effects of millimeter-wave exposures in some USSR research
Additionally, consider the following USSR reference [Zalyubovskaya, 1977] translated
by the JPRS and published as a classified document in 1977.
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SYSTEMIC ADVERSE EFFECTS FROM MILLIMETER-WAVE RADIATION
This is one of many translations of articles produced in the Former Soviet Union on wireless
radiation (also, see reviews of Soviet research on this topic by McRee [1979, 1980], Glazer
and Dodge [1976], Kositsky et al [2001]). On p. 57 of the pdf link, the article by
Zalyubovskaya addresses biological effects of millimeter radiowaves. Zalyubovskaya ran
experiments using power fluxes of 10,000,000 microwatts/square meter (the FCC guideline
limit for the general public today), and frequencies on the order of 60 GHz. Not only was
skin impacted adversely, but also heart, liver, kidney, spleen tissue as well, and blood and
bone marrow properties. These results reinforce the conclusion of Russell (see section
2E)
that systemic results may occur from millimeter-wave radiation. And, to re-emphasize, for
Zalyubovskaya’s experiments, the incoming signal was unmodulated carrier frequency only,
and the experiment was single stressor only. Thus, the expected real-world results (when
human beings are impacted, the signals are pulsed and modulated, and there is exposure to
many toxic stimuli) would be far more serious and would be initiated at lower (perhaps much
lower) power fluxes.
The Zalyubovskaya paper was published in 1977. What national security concerns
caused it (and the other papers in the linked pdf reference) to be classified in the first place, and
then kept classified for 35 years until declassification in 2012? What other papers on this topic
with similar findings were published in the USSR (and the USA) at that time, or even earlier, and
how many such papers never saw the light of day in the USSR (and the USA) at that time? It
appears that we have known about the potentially damaging effects of millimeter-wave radiation
on the skin (and other major systems in the body) for well over forty years, yet the discourse
today only revolves around the possibility of modest potential effects on the skin and perhaps
cataracts from millimeter-wave radiation.
2D4d3. Health effects from millimeter-wave exposures in Russian and Ukrainian
literature
The review by Kositsky referenced in section 2D4d2 [Kositsky et al, 2001] appears to be
based on 1) open literature publication of 2) wireless radiation biological effects 3) by Russian
and Ukrainian researchers, covering the publication time period of 1968-2000. It appears to be
quite comprehensive, and addresses both wireless radiation 1) adverse health effects and 2)
therapeutics. It covers millimeter-wave frequencies almost exclusively. Some important
takeaways from the Kositsky review are shown in the following box.
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BIOLOGICAL EFFECTS FROM MILLIMETER-WAVE RADIATION
“there
is a large probability of harmful effects from incidental generalized exposure, as
confirmed
in experiments on animals”
“Since
living organisms have evolved under conditions of low natural background EHF EMR,
they lack a ready-made mechanism of evolutionary adaptation to heightened levels of
radiation resulting from technogenic factors”
“The
results of clinical research showed that prolonged contact with EMF in the SHF band
can lead to development of diseases, the clinical profile of which is determined above all by
changes in the functional condition of the nervous and cardiovascular systems”
“Under
EFD of 60 µW/cm2, disturbance of female cycles; reduction in fertility, number and
weight of offspring; increase in postnatal deaths of the rat pups by a factor of 2.5; and
dystrophic changes in the reproductive organs of the animals were noted”
“The
results obtained give evidence that a single exposure to low-intensity EHF EMR without
modulation, and with modulation at low frequencies of 5-10 Hz, induce opposite effects in red
bone marrow (RBM). In the former case, we have pronounced stimulation of proliferative
processes in the RBM, which are reversible. In the latter case—progressive depression of the
process of blood production, right down to the formation of hypo- and aplastic conditions in
the RBM on the sixth day of observation.”
“biological
effects of millimeter waves (BEF MMW):…They do not depend on the intensity
of EMR, starting from the threshold to noticeable heating of tissue…..Irreversible BEF occur
only during prolonged or cyclical exposure…..During amplitude or frequency modulation of
MMW, bioeffects are maintained or strengthened as the power of exposure is significantly
reduced…..The
body “remembers” the effect of EMR for a relatively long time……In
some
cases, EMR influences sensitivity to other factors (chemicals,
ionizing radiation, etc.), and the
effects may persist through time.”
“In
epidemiological studies of the population of Ukraine, a connection was established
between leukemia in children and cancer in adults, and exposure to EMF at industrial
frequencies.”
“Specific injuries under radiowave exposure are development of cataracts, instability in
leukocyte make-up of peripheral blood, and vegeto-vascular disorder”
“the
likelihood of cancer was three times greater under SHF exposure”
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“It
can be proposed that the current increase in electromagnetic pollution of the environment
exceeds human adaptational capacities”
“The
danger of mobile telephones consists of the fact that in addition to direct effects on the
brain, the whole body is irradiated via the biologically active points of the concha of the ear”
“Observed
higher resonance frequencies of a living cell coincide with frequencies of radiation
of communications satellites. The power densities and duration of irradiation created by these
satellites will
significantly exceed…..the
energetic doses inducing changes in living cells……
there will be a likelihood of changes (including negative changes) in the genetic apparatus of
living cells during prolonged exposure to low-energy electromagnetic radiation from
communications satellites”
“Combination
with other deleterious factors: ionizing radiation, toxic substances,
geomagnetic anomalies and stress significantly increase the effects of HF EMR.”
“Occurrence
of a narcotic-type dependency (by stimulating production of endorphins) is
possible under regular irradiation with HF EMR.”
“in
animals irradiated with EMF, the nature of the infectious process changes—the course of
the infectious process is aggravated”
“Absorption
of EMF in biologically active points is many times more effective than in other
parts of the skin, and this energy influences the internal organs and the body as a whole
through the system of Chinese meridians.”
In summary, these excerpts show that
•
•
•
adverse effects can be initiated with very low doses of EMR,
millimeter-wave radiation can impact regions below the skin, and
adverse effects may be exacerbated when the EMR is combined with other toxic
stimuli.
Given Kositsky’s statement in
section 2D4
about the potential of a narcotic-type
dependency from exposure to EMR through stimulating production of endorphins, could EMR
be effectively
serving as one of the gateway ‘drugs’ to the increased opioid use we observe
today?
Appendix 5
addresses the potential impact of wireless radiation exposure on the opioid
crisis, and shows that wireless radiation could indeed be a contributing factor to the overuse of
opioids we are seeing today!
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Particularly troubling are Kositsky’s statements about the potential adverse effects of
communications satellites. He bases his conclusions on the matching of communications
satellites’ frequencies with living cell resonances, as follows:
“Observed
higher resonance frequencies of a living cell coincide with frequencies of
radiation of communications satellites. The power densities and duration of irradiation created
by these satellites will significantly exceed (by ten or more orders of magnitude—such
irradiation is possible over the course of a whole lifetime) the energetic doses inducing
changes in living cells.”
From some perspectives, the concept is counter-intuitive. Hormetic behavior of toxic
substances and vaccines tends to be observed at extremely low doses of toxic stimuli. The
average power fluxes from communications satellites are extremely low at the Earth’s surface,
and one would not expect adverse effects based on these low numbers. In the NTP experiments
that many people cite as the wireless radiation experimental Gold Standard [Melnick, 2019],
serious adverse effects were not observed until the power fluxes approached the FCC limit.
While his statements may seem counter-intuitive to some people, that does not mean they
are incorrect. The issue needs to be resolved, sooner rather than later. At this time, 5G satellites
are in fact being launched, and there are projections that tens of thousands of these satellites will
eventually be launched to complete the global terrestrial and space 5G network. Launching of
this number of satellites without the demonstrated evidence of safety would add to the unethical
and harmful nature of the mobile networking experiment already observed.
2D4d4. “Confirmation” of Soviet microwave effects studies forty years later
The Soviet studies on adverse health effects from athermal radiofrequency exposures
performed 40++ years ago showed clearly the dangers to human health from this toxic stimulus.
Even though there was voluminous non-Soviet research showing a wide spectrum of adverse
health effects from radiofrequency during that 40++ year period, some researchers undertook
studies under ‘similar’ conditions to purportedly ‘confirm’
or validate the results from the Soviet
studies [e.g., de Gannes et al, 2009; Repacholi et al, 2011; Grigoriev et al, 2010; Grigoriev,
2011]. This would require
“validation”
of health and safety research findings that were
generated forty years ago in a
completely different sponsorship and motivational context
than
has existed in the past decade. As one would expect, given the history of wireless radiation
health and safety research, the results were mixed.
What type of independence and objectivity would one expect from ‘confirmation’
research sponsored by the promoters of 2G, 3G, 4G and now 5G mobile networking technology?
Trillions of dollars in revenues are at stake in maintaining the fiction of wireless radiation safety
under current exposure limit regulations. While the results could be correct, they should be
interpreted with this context in mind.
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2E. Potential Adverse Health Effects Expected from 5G Mobile Networking Technology
The potential 5G adverse health effects derive from the intrinsic nature of the radiation,
and how this radiation interacts with tissue and other target structures. 4G networking
technology was associated mainly with carrier frequencies in the range of ~1-2.5 GHz (cell
phones, WiFi). The wavelength of 1 GHz radiation is 30 cm, and the penetration depth in human
tissue is a few centimeters. The highest performance 5G networking technology is mainly
associated with carrier frequencies at least an order of magnitude above the 4G frequencies,
although, as stated previously,
“ELFs (0–3000Hz)
are always present in all telecommunication
EMFs in the form of pulsing and modulation”. Penetration depths for the
high-performance
carrier frequency component of 5G radiation will be on the order of a few millimeters.
For much of the early implementation of 5G, and perhaps later, 5G will be integrated
with 4G. Some vendors will start out/have started out
with ‘low-band’ 5G (~600-900
MHz);
some will start out with ‘mid-band’ 5G (~2.5 GHz-4.2 GHz); and some will start out with ‘high
band’ 5G (~24-47
GHz). All these modes are associated with potentially severe adverse health
effects, and none have been tested for safety in any credible manner.
At the millimeter carrier wavelengths characteristic of high-band high performance 5G,
one can expect resonance phenomena with small-scale human structures [Betzalel, 2018;
Appendix 7B-3],
as well as resonances with insects/insect components [Thielens et al, 2018].
The common
‘wisdom’
being presented in the literature and the broader media is that, if
there are adverse impacts resulting from millimeter-wave 5G, the main impacts will be focused
on near-surface phenomena, such as skin cancer, cataracts, and other skin conditions, because of
shallow RF penetration depths. However, there is evidence that biological responses to
millimeter-wave irradiation can be initiated within the skin, and the subsequent systemic
signaling in the skin can result in physiological effects on the nervous system, heart, and immune
system [Russell, 2018]. There is additional evidence that adverse effects from millimeter-wave
radiation can occur in organs and tissue well below the skin surface (e.g., consider the example
shown in section 2D4d2 in the box titled
SYSTEMIC ADVERSE EFFECTS FROM
MILLIMETER-WAVE RADIATION,
or the example shown in section 2D4d3 in the box titled
BIOLOGICAL EFFECTS FROM MILLIMETER-WAVE RADIATION)
This should not be
surprising, since there are myriad signaling conduits connecting the skin to deeper structures in
the body.
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2F. Why is there not Full Consensus on Adverse Effects from Wireless Radiation?
2F1. Reasons for Lack of Full Consensus
Not all studies of wireless radiation have shown adverse effects. There are many
possibilities to explain this [Kostoff et al, 2020].
1) There could
be ‘windows’ in parameter space where adverse effects occur,
and
the studies/experiments were conducted outside these ‘windows’. Operation
outside these
windows could show i) no effects or ii) hormetic effects or iii) therapeutic effects.
For example, assume information content of the signal is a strong contributor to
adverse health effects [Panagopoulus, 2019]. Experiments that involve only the carrier
frequencies may be outside the ‘window’ where adverse health effects occur,
and no adverse
effects would be identified. Alternatively, in this specific example, the carrier signal and the
information signal could be viewed as a combination of potentially toxic stimuli, where the
adverse effects of each component are enabled because of the synergistic effects of the
combination. If only one of the members of the combination were studied, again, adverse
effects would not be identified.
As another example, an adverse health impact on one strain of rodent was shown for a
combination of 50 Hz EMF and DMBA, while no adverse health impact was shown on
another rodent strain for the same toxic stimuli combination [Fedrowitz et al, 2004]. From a
higher-order combination perspective, if genetics are viewed conceptually as potentially
equivalent to a toxic stimulus for combination purposes, then a synergistic three-constituent
combination of 50 Hz EMF, DMBA, and genetics was required to elicit adverse health
impacts in the above experiment. If these results can be extrapolated across species, then
human beings could exhibit different responses to the same electromagnetic stimuli based on
their genetic predispositions.
This particular experiment may be one of the most important conducted in wireless radiation
toxicology. It shows that adverse effects from wireless radiation could depend on
species/strain selection for the test subjects. This raises the question: which species or strain
is most representative of human populations with respect to mirroring the adverse effects of
wireless radiation. Is it rats; if so, is it Sprague-Dawley rats; if so, which strain of Sprague-
Dawley rats? Or, are myriad strains of rats required to simulate effects on human populations
with different genetic and other makeups? If not rats, is it dogs; if so, which species/strains of
dogs. For setting regulatory exposure limits, should laboratory tests be conducted on a wide
variety of species and strains, to determine which are the most representative of human
responses to wireless radiation? Would the optimal species differ for different types of
wireless radiation (e.g., high-frequency/low-frequency; high-power/low-power;
pulsed/continuous, etc) and/or different types of other toxic stimuli?
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The single stressor studies that constitute most of wireless radiation laboratory health
research, and indeed constitute most of the laboratory medical research literature, essentially
yield very narrow windows. Adverse effects are shown over very limited parameter ranges.
As the above examples show, as well as the examples in Kostoff and Lau [2017] and Kostoff
et al [2018], adverse effects shown by many combinations of stressors are not revealed when
these stressors are tested in isolation over the same parametric ranges.
One could conclude that, whether by design or accident,
the real-world impact of single
stressor studies is to conceal, rather than reveal, many of the more serious adverse health
effects of wireless radiation.
The stressor variables to be used for health studies should not be limited to single
stressors in isolation, but should include to the extent possible combinations of toxic stimuli
stressors, since these combinations reflect more accurately real-life exposures.
2)
3)
Research quality could be poor, and adverse effects were overlooked.
Or, the research team could have had a preconceived agenda
where finding no adverse effects from wireless radiation was the main objective of the
research.
2F2. The Role of Conflicts-of-Interest in Lack of Full Consensus
At this point, the reader would be well-advised to re-read
section 2A1
on conflicts-of-
interest relative to wireless radiation health and safety studies.
These conflicts pollute the well of knowledge relevant to health and safety, and are the
largest contributor to mis-informing the public about the serious adverse health and safety
impacts from wireless radiation.
For example, studies have shown that industry-funded research of wireless radiation
adverse health effects is far more likely to show no effects than funding from non-industry
sources [Huss et al, 2007; Slesin, 2006; Carpenter, 2019]. Studies in disciplines other than
wireless radiation have shown that, for products of high military, commercial, and political
sensitivity, ‘researchers’/organizations are hired to publish articles that conflict with the credible
science
(aka ‘product defense’
companies (
https://www.fastcompany.com/1139299/manufacturing-
doubt-product-defense
), ‘hired guns’,
etc), and therefore create doubt as to whether the product of
interest is harmful [Michaels, 2008, 2020; Oreskes and Conway, 2011; Ong and Glantz, 2000;
McGarity and Wagner, 2008; Walker, 2017].
Section 3.2.2 in a 2016 article on under-reporting of adverse effects of myriad substances
in the biomedical literature [Kostoff, 2016] shows clearly the collusion of the USA government
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and industry (and academia in some cases) in concealing harm of toxic substances (whose
continued use is of importance to one or both organizations). These examples, and many others
in the large USA government-industry candidate pool from which they were selected, show that
government-industry collusion to suppress adverse effects from technologies is endemic
across technologies;
it is not an aberration, but may be closer to the norm for technologies
that are sensitive commercially, militarily, and politically.
A comprehensive article in The New Yorker magazine
(
https://www.newyorker.com/magazine/2014/02/10/a-valuable-reputation?verso=true
) details the
travails that Prof. Tyrone Hays had to endure from industry in his quest to show that the
herbicide Atrazine contributes to severe adverse effects. While the European Union banned the
use of Atrazine almost two decades ago, the EPA has allowed its use to continue in the USA.
Finally,
Appendix 6
lists study references showing effects of industry funding on
research outcomes for myriad research disciplines (mainly within biomedical). What these
references don’t show (for the most part) is how industry convinced the regulators to incorporate
the results of these studies in setting the lax regulations we see in practice today [e.g., Kostoff,
2018a]. Given that the sponsor and performer incentives of those studies are no different from
the sponsor-performer incentives of wireless radiation health effects studies, there is little reason
for expecting less concealment of adverse effects in the wireless radiation studies. Given the
magnitude of revenues at stake for wireless radiation technology implementation, there is much
reason for expecting more concealment and/or neutralization of adverse effects in the wireless
radiation studies!
2F3. Interpreting Wireless Radiation Health Study Findings
Wireless radiation can play two roles as a contributor to adverse health effects:
initiator
and/or
promoter/accelerator.
The
initiator
role is reflected by single stressor studies (EMF
alone) that show adverse health effects. The
promoter/accelerator
role is reflected by 1)
combination studies that show no adverse effects from any of the constituents when tested in
isolation, but show adverse effects (synergies) when tested in combination or 2) accelerating
emergence of serious diseases. There can also be
initiator and promoter/accelerator
roles
shown by combination studies, where each constituent tested in isolation shows a modest adverse
effect, but the combination shows a much larger (i.e., synergistic) effect [Kostoff and Lau, 2013,
2017; Kostoff et al, 2018; Kostoff, 2018b].
So, if a study shows an adverse health effect from wireless radiation, and if it passes the
criteria for high quality research, then that specific adverse effect for the parameter range shown
could be accepted as credible. If a study shows no adverse health effects from wireless radiation
in a single stressor experiment, the study MAY reflect no
initiator
role
in the parameter window
selected,
if the study is deemed to be of high research quality. However, such an experiment
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offers little insight as to the
promoter/accelerator
role of the wireless radiation
in the parameter
range selected.
The same would hold true for no adverse effects shown in combination
experiments; there is no reason to believe that, even if wireless radiation serves as a
promoter/accelerator for some combinations, it would therefore serve as a promoter/accelerator
for all combinations.
In summary, the adverse effects of wireless radiation that result from credible high-
quality
studies published in the biomedical literature form the ‘floor’ for total adverse impacts of
this wireless radiation. Given the insights of synergies from toxic stimuli combination studies
evidenced in [Kostoff and Lau, 2013, 2017, Kostoff et al, 2018b, Juutiliin, 2006, 2008], many
more adverse impacts from wireless radiation can be expected if the parameter range of single
stressor studies is expanded and the numbers of combination studies are greatly expanded.
Further, there is little doubt that the biological effects of wireless radiation studies that
have been classified (by the organization promoting the expansion of this technology, the Federal
government,
for alleged ‘national security’ purposes)
show substantially more harmful effects
from this technology in real-life situations.
Even the Gold Standard for research credibility
–
independent replication of research
results
–
is questionable in politically, commercially, and militarily sensitive areas like wireless
radiation safety. Suppose there are two research groups (funded by the same government
agency) who both arrive at the same conclusion that just coincidentally coincides with what the
government sponsor wanted. Would this be considered independent? Or, these two research
groups received funding from different agencies of the same government. Would that be
considered independent? Or, these two research groups received funding from two different
governments that both had the same accelerated development objectives for the technology of
interest. Review articles tend to treat these types of
cases as independent, and don’t make the
distinction as long as the validation doesn’t arise from within the performer group/organization.
Given the broad support exhibited today by the USA Federal government, military, and
industry for the rapid implementation of 5G (and, indeed, the governments of most, if not all, the
major developed countries globally), all these organizations must present a united front in
declaring 5G (and previous generations of mobile networking technology) to be safe. If one
government lab, or one highly-funded performer, were to perform a credible real-life simulation
of wireless radiation effects and show the potential damage that might result, then the
government’s and industry’s
current fast-track effort to
implement 5G before the full extent
of the damage becomes known
would be derailed.
It is unrealistic that any government would allow this to happen!
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Even reporting of conflict-of-interest in wireless radiation research papers or evaluation
panels leaves much to be desired. Currently, potential research performer conflicts of interest are
identified by listing of funding sources in the published papers, or other formal documented
evidence of conflicts of interest. However, there are many potential conflicts of interest that may
not be as formal, but could be at least as influential as the formal conflicts in determining the
outcome of the research or proposal. To ascertain these other less formal conflicts of interest
would require vetting:
1) any elements of the researchers’/evaluators’
investment portfolio that would profit from
operation and expansion of the mobile telecommunications network, including impacts on
related industries;
2) any elements of their present business endeavors that would profit from operation and
expansion of this network, including impacts on related industries;
3) any elements of present or future pensions that would profit from operation and expansion of
this network, including impacts on related industries;
4) any proposals or future employment offers in the pipeline or being considered that would
profit from operation and expansion of this network, including impacts on related industries;
5) any other conflicts of interest by which they could profit from operation and expansion of the
mobile telecommunications network, including impacts on related industries.
2G. Conclusions
Wireless radiation offers the promise of improved 1) remote sensing, 2)
communications and data transfer, and 3) connectivity. Unfortunately, there is a large body of
data from laboratory and epidemiological studies showing that previous generations of wireless
networking technology have significant adverse health impacts. Much of this data was obtained
under conditions not reflective of the real-world. When real-world considerations are added,
such as 1) including the information content of signals along with the carrier frequencies, and 2)
including other toxic stimuli in combination with the wireless radiation,
the adverse effects are
increased substantially.
Superimposing 5G mobile networking technology on an imbedded
toxic wireless radiation environment (4G, 3G, etc) will exacerbate the myriad adverse health
effects already shown to exist. Far more research and testing of potential 5G health effects is
required before further rollout can be justified. Without this additional testing and demonstrated
safety of potential 5G health effects, we will be even further along in
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Chapter 4
–
Appendices
Appendix 1
–
Unethical Medical Experiments
A1-A. Overview
The biomedical literature reflects much good research. However, the world today is also
awash in unethical medical experiments. There are two major types. The first type is classical
unethical medical experiments, where test subjects are explicitly/proactively selected for
experiments on biological effects of drugs or potentially harmful substances, and participate in
these experiments without having given ‘informed consent’.
The second type may be far more
prevalent. Here, potentially harmful substances are introduced into commercial, military, or
other government practice without adequate demonstration of safety. Then, test subjects are
implicitly/reactively selected
‘a posteriori’
to participate in these de facto experiments, again
without having given informed consent. These latter studies are usually epidemiological studies.
In parallel with the burgeoning conduct of unethical medical experiments is production of
a literature that addresses the ethics of, and in many cases bemoans the prevalence and conduct
of, these myriad unethical medical experiments. The experiments and the accompanying ethics
literature form a symbiosis, where the literature feeds off the experiments, and the experiments
spawn an additional literature. It is not clear how much, if any, impact the ethics literature has
had/does have/will have on the conduct of the unethical medical experiments, especially those
unethical medical experiments of the second type defined above.
Appendix 1A
provides a few examples of mainly classical unethical medical
experiments, and
Appendix 1B
provides a few references that reflect the medical experiment
ethics literature.
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Appendix 1A
–
Unethical Medical Experiments - Examples
This Sub-Appendix provides examples of unethical medical experiments, conducted
mainly 1) over the last 100 years and 2) within the USA or under its auspices. The list is not
exhaustive, since an abbreviated search approach was used, covering both Medline and the Web.
Some of the more useful Web sources of information are shown in the following table:
https://en.wikipedia.org/wiki/Unethical_human_experimentation;
https://en.wikipedia.org/wiki/Human_subject_research;
https://en.wikipedia.org/wiki/Unethical_human_experimentation_in_the_United_States;
https://en.wikipedia.org/wiki/Medical_torture;
https://abuse.wikia.org/wiki/Unethical_human_experimentation_in_the_United_States;
https://www.amazon.com/s?k=human+experimentation&i=stripbooks&page=2&gclid=Cj0KCQiA89zv
BRDoARIsAOIePbBy8acwX6tfMZcGkZyi_UTov1I7_PxcFYDAgDWiAgHVc7anOyx57sIaAgtNEALw_wcB&
hvadid=241915884190&hvdev=c&hvlocphy=9007578&hvnetw=g&hvpos=2o1&hvqmt=b&hvrand=12
61052967636955269&hvtargid=kwd-
1053626641&hydadcr=22561_10346245&qid=1576539483&ref=sr_pg_2;
https://www.bibliotecapleyades.net/ciencia/ciencia_industryweapons173.htm
.
It should be noted that information of this type is not easy to obtain. The research
performers and their sponsors are not motivated to reveal such odious experiments to any
oversight organizations, and therefore tend to conceal these experiments to the largest extent
possible. There are three main routes by which this information eventually gets to the public:
whistle-blowers; discovery in legal lawsuits; inadvertent access by researchers examining other
topics. While we don’t know the extent of these
types of experiments that have not been
reported, it is probably a good assumption that there are huge numbers.
Following are some of the books and journal/magazine articles that describe these
experiments. It is by no means a complete list, and the interested reader would be well-advised
to read the articles with the Web links provided in the box.
Examples of Unethical Medical Experiments
Albarelli H.P, Kaye JS. The Hidden Tragedy of the CIA's Experiments on Children. 11 August
2010. Truthout.
Annas, George J.; Grodin, Michael A. The Nazi Doctors and the Nuremberg Code: Human
Rights in Human Experimentation. 1995. Oxford University Press. ISBN 978-0-19-510106-5.
Anon. History of the Human Subjects Protection System. Institutional Review Board
Guidebook. Office for Human Research Protections. 1993. Archived from the original on 2013-
02-18. Retrieved 2011-06-03.
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Anon. Institute of Medicine (U.S.). Committee on Thyroid Screening Related to I-131 Exposure,
National Research Council (U.S.). Committee on Exposure of the American People to I-131
from the Nevada Atomic Bomb Tests, ed. (1999). Exposure of the American people to Iodine-
131 from Nevada nuclear-bomb tests: review of the National Cancer Institute report and public
health implications. National Academies Press. pp. 113–114. ISBN 9780309061759.
Anon. Report on Search for Human Radiation Experiment Records. (PDF). U.S. Department of
Defense. 1997.
Anon. American Nuclear Guinea Pigs: Three Decades of Radiation Experiments on U.S.
Citizens. 1986. United States. Congress. House. of the Committee on Energy and Commerce.
Subcommittee on Energy Conservation and Power, published by U.S. Government Printing
Office.
Anon. How the U.S. government exposed thousands of Americans to lethal bacteria to test
biological warfare. 13 July 2005. Democracynow.org.
Anon. Institute of Medicine (U.S.). Committee on Thyroid Screening Related to I-131 Exposure,
National Research Council (U.S.). Committee on Exposure of the American People to I-131
from the Nevada Atomic Bomb Tests, ed. (1999). Exposure of the American people to Iodine-
131 from Nevada nuclear-bomb tests: review of the National Cancer Institute report and public
health implications. National Academies Press. ISBN 978-0-309-06175-9.
Anon. Jeder Mensch hat einen Name: Legal and ethical dimensions of human experiments under
National Socialism. Psychiatrie (Stuttgart, Germany). 2010;7(4):255-60.
Anon. National Commission for the Protection of Human Subjects of Biomedical and Behavioral
Research (1978-09-30), The Belmont Report: Ethical Principles and Guidelines for the
Protection of Human Subjects of Research (PDF), United States Department of Health,
Education and Welfare
Anon. Project MKUltra, the Central Intelligence Agency's Program of Research into Behavioral
Modification. 1977. Joint Hearing before the Select Committee on Intelligence and the
Subcommittee on Health and Scientific Research of the Committee on Human Resources, United
States Senate, Ninety-Fifth Congress, First Session. (PDF). U.S. Government Printing Office.
Ansell, BM, F. Antonini, L.E. Glynn: Cantharides blisters in children with rheumatic fever.
Clinical Science, November 1953, 12 (4): 367-373.
Barker HM. Bravo for the Marshallese: Regaining Control in a Post-Nuclear, Post-Colonial
World. 2004. Wadsworth, ISBN 0-534-61326-8
Barlett DL, Steele JB. Deadly Medicine. January 2011. Vanity Fair.
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Baumeister, Alan A. The Tulane Electrical Brain Stimulation Program. A historical Case Study
in Medical Ethics. 2000. Journal of the History of the Neurosciences. 9 (3): 262–278.
doi:10.1076/jhin.9.3.262.1787. PMID 11232368.
Baydala LT, Jill M. Starkes (2014). "Health research involving First Nations, Inuit and Métis
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Berenbaum, Michael. The world must know: the history of the Holocaust as told in the United
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Berger RL, M.D. (1990). Nazi Science
—
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Appendix 1B
–
Ethics of Medical Experiments
–
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Appendix 2
–
Manual Taxonomy of Adverse EMF Health Effects Database
A2-A. Category Themes
A query to retrieve Medline records showing adverse health effects of wireless radiation
was generated. The query was entered into the Medline search engine, and ~15,000 records were
retrieved. Filtering was applied to the retrieval to remove records not associated with adverse
health effects of wireless radiation, and 5311 records remained. Thousands of the highest
frequency title and abstract phrases were read, the categories from the factor analysis and text
clustering approaches of
Appendices 3
and
4
were evaluated, and a manual taxonomy of main
categories in the database was generated. The ~10,000 highest frequency abstract phrases were
visually inspected, and assigned to the appropriate categories in the taxonomy.
The following table (A2-1) shows the categories in the taxonomy, and the phrases
associated with each category. For each category, the records associated with the phrases
identified were highlighted, and the titles of those records were extracted. Following the table,
each category and representative record titles are shown in order to display the breadth of
coverage of the category.
In the
process of selecting the record titles to represent the category’s theme,
a second
level of filtering was done (visual inspection). Strong emphasis was placed on 1) records
associated with microwave frequencies; 2) exposures not exceeding FCC and ICNIRP-based
limits; 3) records that clearly showed adverse effects. This meant that
large numbers of records
showing adverse health effects from especially i) power/ELF frequencies and ii) high
microwave power exposures that had both thermal and athermal effects were not shown.
In the latter case (high microwave power exposures), where thermal effects exist, the
assumption is usually made that any adverse effects shown are due to thermal effects. This
may or may not be correct. Adverse effects could be due to thermal effects, they could be due
to higher radiation intensity athermal effects, or they could be due to some (potentially
synergistic) combination of thermal and athermal effects. In the record selection process, I
used the conservative approach of not selecting records where the radiation flux was
associated with increased temperatures.
The categories are not orthogonal; there is some overlap, especially among categories
that cover different levels of detail (e.g., cancer-genotoxicity, reproduction-biomarkers, etc).
Therefore, some representative record titles may appear in more than one category.
The major adverse effects are listed in the first column (Category), and the phrases
associated with the theme are listed in the second column (Key Phrases). These adverse effects
are self-explanatory. Each category in the taxonomy is hyper-linked to its respective record
titles. To obtain the full record, insert title into Pubmed, or similar Medline search engine.
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Table A2-1
–
Manual Taxonomy
CATEGORY
Cancer/Tumors
KEY PHRASES
cancer, leukemia, cancers, carcinogenic, breast cancer, malignant,
leukaemia, cancer risk, glioma, brain cancer, carcinogenesis, brain
tumours, lymphoma, carcinogen, childhood cancer, childhood
leukaemia, carcinoma, brain tumor, cancer incidence,
carcinogenicity, lymphoblastic, acute lymphoblastic, melanoma,
gliomas, neoplasms, acute lymphoblastic leukemia, breast cancer
risk, carcinogens, lymphoblastic leukemia, neoplastic, glioblastoma,
leukemia risk, malignancy, leukemias, malignancies,
neuroblastoma, cancer risks, lung cancer, childhood cancers,
lymphomas, astrocytoma, malignant brain, Acute leukemia,
mammary gland, brain cancers, glioma risk, Malignant melanoma,
malignant neoplasms, neoplasia, hyperplasia, myeloid leukemia,
carcinomas, neuroblastoma cells, testicular cancer, leukaemias,
neoplasm, mammary cancer, myeloma, nervous system cancers,
adenocarcinoma, cocarcinogenic, colorectal, glioblastoma
multiforme, Hodgkin's disease, multiple myeloma, non-Hodgkin's
lymphoma, seminoma, breast carcinoma, colon cancer, glioma
meningioma, larynx, neoplastic transformation, Non-Hodgkin
lymphoma, tumor, tumors, tumours, brain tumors, tumour,
neuroma, acoustic neuroma, meningioma, brain tumour, tumor risk,
tumor growth, tumor incidence, mammary tumors, tumor
promotion, intracranial tumors, tumor promoter, gland tumors,
meningiomas, tumorigenesis, tumour risk, benign tumors, nervous
system tumors, neuromas, acoustic neuromas, breast tumors, gland
tumours, parotid gland tumors, tumor-promoting
Neurodegenerative
memory, cognitive, central nervous system, learning,
neurodegenerative, Alzheimer's, learning and memory, Alzheimer's
disease, cognition, amyotrophic lateral sclerosis, neurodegenerative
diseases, cognitive function, cognitive functions, neurobehavioral,
dementia, spatial learning, acetylcholine, Parkinson's disease,
epilepsy, Glial fibrillary, motor activity, multiple sclerosis,
cognitive impairment, spatial learning and memory,
neurodegenerative disease, neuronal damage, Alzheimer disease,
cognitive effects, seizure, seizures, autism, cognitive functioning,
cognitive processing, memory function, memory impairment,
memory loss, neurological diseases, neuronal excitability, cognitive
dysfunction, memory deficit, memory functions, neurocognitive,
neuronal degeneration, spatial working memory
Reproduction
pregnancy, reproductive, pregnant, sperm, embryos, testicular,
fertility, embryo, testis, embryonic, fetuses, testosterone, motility,
infertility, reproduction, testes, semen, spermatozoa,
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Genotoxicity
Cardiovascular
spermatogenesis, reproductive system, sperm motility, male
fertility, sperm count, embryogenesis, abortion, male reproductive,
spermatogenic, embryonic development, mating, male infertility,
birth defects, serum testosterone, adverse reproductive, miscarriage,
reproductive organs, semen parameters, sperm concentration, sperm
parameters, testicular function, testosterone level, epididymis, male
reproductive system, spermatogenic cells, spermatogonia, fertilized
eggs, ovaries, reproductive capacity, reproductive outcomes, sperm
cells, sperm morphology, fertile, pregnancies, reproductive
function, testicular tissue, rat testes, rat testis, reproductive
functions, reproductive systems, sperm DNA, spermatogonial, testis
tissue, embryogeny, reproductive health, sperm cell, miscarriages,
offsprings, oocyte, oogenesis, preterm birth, seminal vesicles,
Sperm head, spermatids, sperms, testicles, fetal loss, genital,
gonads, reproductive hormones, semen analysis
DNA damage, genotoxic, micronuclei, chromosomal, micronucleus,
chromosome, genotoxicity, genotoxic effects, mutagenic, strand
breaks, chromatin, mutation, DNA strand, Chromatid, mutations,
chromosome aberrations, chromosomes, DNA fragmentation,
double-strand, chromosomal aberrations, DNA repair, DNA strand
breaks, micronucleus (MN), genetic damage, micronuclei (MN),
Sister Chromatid, genome, blood leukocytes, double-strand breaks,
oxidative DNA, chromosomal damage, DNA synthesis, mutant,
cellular stress, chromosome aberration, oxidative DNA damage,
Purkinje cells, DNA breaks, cell cycle arrest, clastogenic, genotoxic
potential, keratinocytes, micronucleated, single strand, cell division,
chromatid exchange, Chromatid Exchanges, genetic material,
micronucleus test, Mutagenesis, cell cycle progression, cellular
DNA, Cytochrome c, double strand, genetic effects, genomic
instability, micronucleus frequency, DNA single-strand, DNA-
damaging, Mutagen, mutagenicity, single strand breaks, chromatin
condensation, chromosomal aberration, double-strand breaks
(DSBs), strand breakage, cell cycle distribution, cell DNA,
genetically, strand DNA
Cardiac, cardiovascular, pacemaker, pacemakers, implanted, blood
pressure, implantable, vascular, heart rate variability, myocardial,
heart rate variability (HRV), implants, cardiac pacemakers,
implantation, defibrillators, implant, cardioverter, myocardium,
cardiovascular system, implantable cardioverter, Cardiovascular
disease, defibrillator, fibrillation, arrhythmia, arterial blood
pressure, autonomic nervous system, cardioverter defibrillators,
implanted pacemakers, cardiac pacemaker, hypertension,
arrhythmias, cardioverter-defibrillators, implantable cardioverter
defibrillators, implantable cardioverter-defibrillators, pacemaker
function, heart disease, implanted cardiac, tachycardia, cardiac
devices, circulatory system, microcirculation, blood vessels,
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Immunity
Biomarkers
Sensory Disorders
cardiomyocytes, cardiovascular effects, vascular permeability,
atherosclerosis, cardiovascular diseases, ventricular fibrillation,
arterial pressure, Atrial fibrillation, cardiac output, cardiovascular
function, Implantable cardioverter defibrillator (ICD), implantable
devices, arrhythmic, carotid artery, pacemaker dysfunction,
pacemaker malfunction
lymphocytes, immune, lymphocyte, immune system, immunity,
blood lymphocytes, leukocytes, antibodies, immune response,
human lymphocytes, antibody, peripheral blood lymphocytes,
immunological, leukocyte, neutrophils, lymphocytic, immune
functions, immunoreactivity, autoimmune, immunization,
monocytes, neutrophil, antigens, macrophage, immune parameters,
immune responses, immunocompetent, natural killer cells, spleen
lymphocytes, immunologic, immunoreactive, micronucleated cells,
monoclonal antibodies, spleen cells, splenocytes, T lymphocytes,
antibody production, antibody-forming, monoclonal antibody
apoptosis, oxidative stress, Malondialdehyde, reactive oxygen
species, apoptotic, superoxide dismutase, lipid peroxidation,
permeability, catalase, MDA, ROS, ROS), reactive oxygen species
(ROS), Malondialdehyde (MDA), SOD), cell death, glutathione
peroxidase, inflammatory, erythrocytes, oxidative damage, SOD,
caspase-3, free radical, nitric oxide, free radicals, biomarkers, bcl-2,
catalase (CAT), inflammation, corticosterone, edema, glutathione
peroxidase (GSH-Px), cytokine, cytokines, alkaline phosphatase,
cell apoptosis, protein kinase, ATP, glutathione (GSH), oxidation,
TNF-alpha, Bax, Ca2+, estrogen, ornithine decarboxylase, red
blood cells, intracellular calcium, cell damage, apoptotic cell,
hemoglobin, lactate dehydrogenase, cerebral blood flow, glutamate,
hydrogen peroxide, IL-1beta, Purkinje, serotonin, apoptotic cell
death, barrier permeability, carbonyl, hormone levels, ornithine
decarboxylase (ODC), acetylcholinesterase, calcium ion, Calcium
ions, endothelial cells, GABA, MDA levels, ODC, xanthine
oxidase, creatinine, intracellular ROS, cholinesterase, lipid
peroxidation levels, pro-inflammatory, protein kinase C,
adrenocorticotropic hormone, alanine aminotransferase, aspartate
aminotransferase, caspase 3, caspase-9, catalase activity,
glutathione levels, NF-kappaB, atrophy, nitric oxide synthase,
cAMP, acid phosphatase, adenosine deaminase, adrenocorticotropic
hormone (ACTH), blood cell count, blood platelets, Ca++,
adrenaline, C-reactive protein, oxidative damages, Reactive Oxygen
Species), vascular endothelial growth factor
auditory, acoustic, ear, hypersensitivity, EHS), EHS,
electromagnetic hypersensitivity, otoacoustic, vestibular,
hypersensitive, cataract, cochlea, auditory system, inner ear, lens
epithelial, corneal, tinnitus, vision, lenses, otoacoustic emissions,
hearing loss, otoacoustic emission, epidermis, rabbit lens,
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dermatitis, auditory stimuli, cataractogenic, Auditory brainstem
response (ABR), auditory evoked, electrohypersensitive,
electrosensitivity, vestibular system, cochlear implants,
dermatological, hearing function, hearing thresholds, pain
sensitivity, pain threshold, skin complaints
Discomfort
Symptoms
Congenital
Abnormalities
Circadian
Rhythym and
Melatonin
Chronic
Conditions
depression, anxiety, headache, headaches, dizziness, depressed,
depressive, vertigo, cataracts, behavioral effects, nausea, headache
dizziness, low back pain, behavioural effects,
malformations, teratogenic, congenital, congenital malformations,
teratogenicity, malformation, teratogens, teratologic, cleft palate,
congenital anomalies, malformed, teratological
melatonin, sleep, circadian, melatonin production, sleep
disturbances, insomnia, melatonin levels, melatonin secretion, sleep
disorders, sleep EEG, poor sleep, pineal function
metabolism, metabolic, glucose, endocrine, cholesterol, Diabetes,
calcium homeostasis, glucose levels, homeostatic, metabolic
activity, metabolic heat production, Diabetes Mellitus, diabetic,
glucose metabolism, obesity
All the records shown in this Appendix, and their relevant citing papers, were analyzed
further for most frequent keywords relating to serious symptoms/disease. In order of frequency,
they are: oxidative stress; Apoptosis; DNA damage; melatonin; Reactive oxygen species;
glioma; Testis; cancer; liver; Malondialdehyde; Brain cancer; testosterone; Anxiety; Depression;
Lipid peroxidation; ROS; Chromosomal aberrations; Learning and memory; oxidative damage;
sperm; testes; Infertility; spermatogenesis; Breast cancer; Cell cycle; Genotoxicity; Kidney;
Leukemia; Male infertility; micronuclei; Pregnancy; Sleep; sperm motility; acoustic neuroma;
carcinogenesis; carcinogenicity; Cognitive function; fertility; Heart rate variability;
Micronucleus; Reproduction; Spatial memory; Stress; Alzheimer's disease; astrocytoma;
Autophagy; Cognition; Cytotoxicity; free radicals.
These match well with the prior results shown for this strongly filtered database.
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A2-B. Category Record Titles
CANCER/TUMORS
Keywords
–
cancer, leukemia, cancers, carcinogenic, breast cancer, malignant, leukaemia, cancer
risk, glioma, brain cancer, carcinogenesis, brain tumours, lymphoma, carcinogen, childhood
cancer, childhood leukaemia, carcinoma, brain tumor, cancer incidence, carcinogenicity,
lymphoblastic, acute lymphoblastic, melanoma, gliomas, neoplasms, acute lymphoblastic
leukemia, breast cancer risk, carcinogens, lymphoblastic leukemia, neoplastic, glioblastoma,
leukemia risk, malignancy, leukemias, malignancies, neuroblastoma, cancer risks, lung cancer,
childhood cancers, lymphomas, astrocytoma, malignant brain, Acute leukemia, mammary gland,
brain cancers, glioma risk, Malignant melanoma, malignant neoplasms, neoplasia, hyperplasia,
myeloid leukemia, carcinomas, neuroblastoma cells, testicular cancer, leukaemias, neoplasm,
mammary cancer, myeloma, nervous system cancers, adenocarcinoma, cocarcinogenic,
colorectal, glioblastoma multiforme, Hodgkin's disease, multiple myeloma, non-Hodgkin's
lymphoma, seminoma, breast carcinoma, colon cancer, glioma meningioma, larynx, neoplastic
transformation, Non-Hodgkin lymphoma, tumor, tumors, tumours, brain tumors, tumour,
neuroma, acoustic neuroma, meningioma, brain tumour, tumor risk, tumor growth, tumor
incidence, mammary tumors, tumor promotion, intracranial tumors, tumor promoter, gland
tumors, meningiomas, tumorigenesis, tumour risk, benign tumors, nervous system tumors,
neuromas, acoustic neuromas, breast tumors, gland tumours, parotid gland tumors, tumor-
promoting
Titles
2.45-Gz wireless devices induce oxidative stress and proliferation through cytosolic Ca(2)(+)
influx in human leukemia cancer cells.
A case-case study of mobile phone use and acoustic neuroma risk in Japan.
A cluster of male breast cancer in office workers.
A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a
mobile phone base station.
A new electromagnetic exposure metric: high frequency voltage transients associated with
increased cancer incidence in teachers in a California school.
A population-based case-control study of radiofrequency exposure in relation to childhood
neoplasm.
Acceleration of the development of benzopyrene-induced skin cancer in mice by microwave
radiation.
Adult and childhood leukemia near a high-power radio station in Rome, Italy.
Association between exposure to pulsed electromagnetic fields and cancer in electric utility
workers in Quebec, Canada, and France.
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Association between number of cell phone contracts and brain tumor incidence in nineteen U.S.
States.
Association between radiation from mobile phones and tumour risk in adults].
Association between vestibular schwannomas and mobile phone use.
Biological effects from electromagnetic field exposure and public exposure standards.
Brain cancer and occupational exposure to magnetic fields among men: results from a Canadian
population-based case-control study.
Cancer in radar technicians exposed to radiofrequency/microwave radiation: sentinel episodes.
Cancer incidence and mortality and proximity to TV towers.
Cancer incidence near radio and television transmitters in Great Britain. I. Sutton Coldfield
transmitter.
Cancer incidence vs. FM radio transmitter density.
Cancer morbidity in subjects occupationally exposed to high frequency (radiofrequency and
microwave) electromagnetic radiation.
Cancer versus FM radio polarization types.
Case-control study of the association between malignant brain tumours diagnosed between 2007
and 2009 and mobile and cordless phone use.
Case-control study on the use of cellular and cordless phones and the risk for malignant brain
tumours.
Causes of death among Belgian professional military radar operators: a 37-year retrospective
cohort study.
Cell phone radiation exposure on brain and associated biological systems.
Cell phone use and acoustic neuroma: the need for standardized questionnaires and access to
industry data.
Cell phone use and risk of thyroid cancer: a population-based case-control study in Connecticut.
Cell phones and brain tumors: a review including the long-term epidemiologic data.
Cellular and cordless telephone use and the association with brain tumors in different age groups.
Cellular and cordless telephones and the risk for brain tumours.
Cellular neoplastic transformation induced by 916 MHz microwave radiation.
Cellular phone use and risk of benign and malignant parotid gland tumors--a nationwide case-
control study.
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Cellular telephones and their relay stations: a health risk?].
Commentary on the utility of the National Toxicology Program study on cell phone
radiofrequency radiation data for assessing human health risks despite unfounded criticisms
aimed at minimizing the findings of adverse health effects.
Connection between Cell Phone use, p53 Gene Expression in Different Zones of Glioblastoma
Multiforme and Survival Prognoses.
Current Understanding of the Health Effects of Electromagnetic Fields.
Danger of cellular telephones and their relay stations].
Decreased survival for childhood leukemia in proximity to television towers.
Decreased survival of glioma patients with astrocytoma grade IV (glioblastoma multiforme)
associated with long-term use of mobile and cordless phones.
Delayed biological effect of electromagnetic fields action].
Determining health policy for sensible mobile phone use--current world status].
Dirty electricity, chronic stress, neurotransmitters and disease.
Does cell phone use increase the chances of parotid gland tumor development? A systematic
review and meta-analysis.
Ecological study on residences in the vicinity of AM radio broadcasting towers and cancer death:
preliminary observations in Korea.
Effect of cell-phone radiofrequency on angiogenesis and cell invasion in human head and neck
cancer cells.
Effect of Exposure to 900 MHz GSM Mobile Phone Radiofrequency Radiation on Estrogen
Receptor Methylation Status in Colon Cells of Male Sprague Dawley Rats.
Effect of Mobile Phone-Induced Electromagnetic Field on Brain Hemodynamics and Human
Stem Cell Functioning: Possible Mechanistic Link to Cancer Risk and Early Diagnostic Value of
Electronphotonic Imaging.
Effects of Mobile Phones on Children's and Adolescents' Health: A Commentary.
Effects of the microwave radiation from the cellular phones on humans and animals].
Electromagnetic field exposure and male breast cancer risk: a meta-analysis of 18 studies.
Electromagnetic field exposures and childhood cancers in New Zealand.
Electromagnetic field induced biological effects in humans.
Electromagnetic fields and cancer: the cost of doing nothing.
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Enzymatic alterations in developing rat brain cells exposed to a low-intensity 16.5 GHz
microwave radiation.
Epidemiologic evidence relevant to radar (microwave) effects.
Epidemiological evidence for a health risk from mobile phone base stations.
EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
Evaluation of genotoxic effects in male Wistar rats following microwave exposure.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill
Viewpoints from 1965 on Association or Causation.
Evaluation of the cytogenotoxic damage in immature and mature rats exposed to 900 MHz
radiofrequency electromagnetic fields.
Evaluation of the genotoxicity of cell phone radiofrequency radiation in male and female rats and
mice following subchronic exposure.
Evidence for microwave carcinogenesis in vitro.
Exposure to low-intensive superhigh frequency electromagnetic field as a factor of
carcinogenesis in experimental animals.
Follow-up of radio and telegraph operators with exposure to electromagnetic fields and risk of
breast cancer.
Further aspects on cellular and cordless telephones and brain tumours.
Genotoxic and carcinogenic effects of non-ionizing electromagnetic fields.
Human disease resulting from exposure to electromagnetic fields.
Incidence of cancer in the vicinity of Korean AM radio transmitters.
Incidence of Seminoma Cancer in Staffs that Worked in Electromagnetic Waves Station; Three
Cases Report.
Increased incidence of cancer in a cohort of office workers exposed to strong magnetic fields.
Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies.
Indication of cocarcinogenic potential of chronic UMTS-modulated radiofrequency exposure in
an ethylnitrosourea mouse model.
Inferring the 1985-2014 impact of mobile phone use on selected brain cancer subtypes using
Bayesian structural time series and synthetic controls.
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Investigation of increased incidence in childhood leukemia near radio towers in Hawaii:
preliminary observations.
Leukemia mortality and incidence of infantile leukemia near the Vatican Radio Station of
Rome].
Long-term exposure to microwave radiation provokes cancer growth: evidences from radars and
mobile communication systems.
Long-term use of cellular phones and brain tumours: increased risk associated with use for > or
=10 years.
Melanoma incidence and frequency modulation (FM) broadcasting.
Melatonin and a spin-trap compound block radiofrequency electromagnetic radiation-induced
DNA strand breaks in rat brain cells.
Meta-analysis of association between mobile phone use and glioma risk.
Meta-analysis of long-term mobile phone use and the association with brain tumours.
Microwaves from Mobile Phones Inhibit 53BP1 Focus Formation in Human Stem Cells More
Strongly Than in Differentiated Cells: Possible Mechanistic Link to Cancer Risk.
Mitochondrial DNA damage and oxidative damage in HL-60 cells exposed to 900MHz
radiofrequency fields.
Mobile phone radiation causes brain tumors and should be classified as a probable human
carcinogen (2A) (review).
Mobile phone use and brain tumours in the CERENAT case-control study.
Mobile phone use and glioma risk: A systematic review and meta-analysis.
Mobile phone use and location of glioma: a case-case analysis.
Mobile phone use and risk for intracranial tumors and salivary gland tumors - A meta-analysis.
Mobile phone use and risk of brain tumours: a systematic review of association between study
quality, source of funding, and research outcomes.
Mobile phone use and risk of tumors: a meta-analysis.
Mobile phone use and the risk for malignant brain tumors: a case-control study on deceased
cases and controls.
Mobile phone use and the risk of acoustic neuroma.
Mobile Phone Use and the Risk of Parotid Gland Tumors: A Retrospective Case-Control Study.
Mobile phones and head tumours. The discrepancies in cause-effect relationships in the
epidemiological studies - how do they arise?
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Mobile phones and head tumours: it is time to read and highlight data in a proper way].
Mobile phones, cordless phones and the risk for brain tumours.
Mobile phones: time to rethink and limit usage.
Mobile telephones and cancer--a review of epidemiological evidence.
Modulation of wireless (2.45 GHz)-induced oxidative toxicity in laryngotracheal mucosa of rat
by melatonin.
Mortality by neoplasia and cellular telephone base stations in the Belo Horizonte municipality,
Minas Gerais state, Brazil.
Mutagenic response of 2.45 GHz radiation exposure on rat brain.
Neoplastic transformation of C3H/10T1/2 cells following exposure to 120-Hz modulated 2.45-
GHz microwaves and phorbol ester tumor promoter.
Neuroblastoma and paternal occupation. A case-control analysis.
New Zealand adolescents' cellphone and cordless phone user-habits: are they at increased risk of
brain tumours already? A cross-sectional study.
Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in
human endothelial cells: molecular mechanism for cancer- and blood-brain barrier-related
effects.
Occupational exposure to high-frequency electromagnetic fields and brain tumor risk in the
INTEROCC study: An individualized assessment approach.
Occupational exposures and brain cancer mortality: a preliminary study of east Texas residents.
Overproduction of free radical species in embryonal cells exposed to low intensity
radiofrequency radiation.
Oxidative and mutagenic effects of low intensity GSM 1800 MHz microwave radiation.
Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation.
Parental occupational exposures to electromagnetic fields and radiation and the incidence of
neuroblastoma in offspring.
Pooled analysis of case-control studies on acoustic neuroma diagnosed 1997-2003 and 2007-
2009 and use of mobile and cordless phones.
Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and
cordless phones including living and deceased subjects.
Pooled analysis of Swedish case-control studies during 1997-2003 and 2007-2009 on
meningioma risk associated with the use of mobile and cordless phones.
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Power-frequency magnetic fields and childhood brain tumors: a case-control study in Japan.
Probabilistic Multiple-Bias Modeling Applied to the Canadian Data From the Interphone Study
of Mobile Phone Use and Risk of Glioma, Meningioma, Acoustic Neuroma, and Parotid Gland
Tumors.
Proteomic analysis of continuous 900-MHz radiofrequency electromagnetic field exposure in
testicular tissue: a rat model of human cell phone exposure.
Radio frequency radiation-related cancer: assessing causation in the occupational/military
setting.
Radio-frequency radiation exposure from AM radio transmitters and childhood leukemia and
brain cancer.
Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering
factor.
Real versus Simulated Mobile Phone Exposures in Experimental Studies.
Real-world cell phone radiofrequency electromagnetic field exposures.
Report of final results regarding brain and heart tumors in Sprague-Dawley rats exposed from
prenatal life until natural death to mobile phone radiofrequency field representative of a 1.8GHz
GSM base station environmental emission.
Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five
Interphone countries.
Risks of carcinogenesis from electromagnetic radiation of mobile telephony devices.
Risks to Health and Well-Being From Radio-Frequency Radiation Emitted by Cell Phones and
Other Wireless Devices.
Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6:
microwaves act through voltage-gated calcium channel activation to induce biological impacts at
non-thermal levels, supporting a paradigm shift for microwave/lower frequency electromagnetic
field action.
Selenium reduces mobile phone (900 MHz)-induced oxidative stress, mitochondrial function,
and apoptosis in breast cancer cells.
Setting prudent public health policy for electromagnetic field exposures.
Simulation of the incidence of malignant brain tumors in birth cohorts that started using mobile
phones when they first became popular in Japan.
Synergism between sinusoidal-50Hz magnetic field and formaldehyde in triggering carcinogenic
effects in male Sprague-Dawley rats.
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Terahertz radiation increases genomic instability in human lymphocytes.
The effect of electromagnetic radiation on the rat brain: an experimental study.
The electromagnetic fields of cellular phones and the health of children and of teenagers (the
situation requiring to take an urgent measure)].
The Intracranial Distribution of Gliomas in Relation to Exposure From Mobile Phones: Analyses
From the INTERPHONE Study.
The possible role of radiofrequency radiation in the development of uveal melanoma.
The probability of developing brain tumours among users of cellular telephones (scientific
information to the decision of the International Agency for Research on Cancer (IARC)
announced on May 31, 2011)].
Thermal and non-thermal health effects of low intensity non-ionizing radiation: An international
perspective.
Towards 5G communication systems: Are there health implications?
Use of cellular or cordless telephones and the risk for non-Hodgkin's lymphoma.
Use of cellular telephones and brain tumour risk in urban and rural areas.
Use of electric bedding devices and risk of breast cancer in African-American women.
Use of electric blankets and association with prevalence of endometrial cancer.
Use of mobile and cordless phones and survival of patients with glioma.
Using the Hill viewpoints from 1965 for evaluating strengths of evidence of the risk for brain
tumors associated with use of mobile and cordless phones.
Wi-Fi technology--an uncontrolled global experiment on the health of mankind.
Wireless Phone Use and Risk of Adult Glioma: Evidence from a Meta-Analysis.
X-rays, microwaves and vinyl chloride monomer: their clastogenic and aneugenic activity, using
the micronucleus assay on human lymphocytes.
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NEURODEGENERATIVE
Keywords
–
memory, cognitive, central nervous system, learning, neurodegenerative,
Alzheimer's, learning and memory, Alzheimer's disease, cognition, amyotrophic lateral sclerosis,
neurodegenerative diseases, cognitive function, cognitive functions, neurobehavioral, dementia,
spatial learning, acetylcholine, Parkinson's disease, epilepsy, Glial fibrillary, motor activity,
multiple sclerosis, cognitive impairment, spatial learning and memory, neurodegenerative
disease, neuronal damage, Alzheimer disease, cognitive effects, seizure, seizures, autism,
cognitive functioning, cognitive processing, memory function, memory impairment, memory
loss, neurological diseases, neuronal excitability, cognitive dysfunction, memory deficit, memory
functions, neurocognitive, neuronal degeneration, spatial working memory
Titles
2.45 GHz Microwave Radiation Impairs Learning and Spatial Memory via Oxidative/Nitrosative
Stress Induced p53-Dependent/Independent Hippocampal Apoptosis: Molecular Basis and
Underlying Mechanism.
A case-control study on the risk factors of Alzheimer's disease in military elderly men].
A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a
mobile phone base station.
A meta-analysis for neurobehavioural effects due to electromagnetic field exposure emitted by
GSM mobile phones.
A possible association between fetal/neonatal exposure to radiofrequency electromagnetic
radiation and the increased incidence of autism spectrum disorders (ASD).
Activity and expression of acetylcholinesterase in PC12 cells exposed to intermittent 1.8 GHz
217-GSM mobile phone signal.
Acute exposure to GSM 900-MHz electromagnetic fields induces glial reactivity and
biochemical modifications in the rat brain.
Acute exposure to pulsed 2450-MHz microwaves affects water-maze performance of rats.
Adverse effects of excessive mobile phone use.
Alteration of adaptive behaviors of progeny after maternal mobile phone exposure.
Alterations of cognitive function and 5-HT system in rats after long term microwave exposure.
Altered cortical excitability in subjectively electrosensitive patients: results of a pilot study.
Amyotrophic lateral sclerosis and occupational exposure to electromagnetic fields.
Amyotrophic Lateral Sclerosis and Occupational Exposures: A Systematic Literature Review
and Meta-Analyses.
Assessment of auditory evoked potential in long-term mobile phone users.
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Behavioral Abnormality along with NMDAR-related CREB Suppression in Rat Hippocampus
after Shortwave Exposure.
Behavioral evaluation of microwave irradiation.
Biochemical modifications and neuronal damage in brain of young and adult rats after long-term
exposure to mobile phone radiations.
Biological effects from electromagnetic field exposure and public exposure standards.
Blood-brain barrier permeability and nerve cell damage in rat brain 14 and 28 days after
exposure to microwaves from GSM mobile phones.
Calcium-binding proteins and GFAP immunoreactivity alterations in murine hippocampus after
1 month of exposure to 835 MHz radiofrequency at SAR values of 1.6 and 4.0 W/kg.
Cell phone radiation exposure on brain and associated biological systems.
Cognitive and neurobiological alterations in electromagnetic hypersensitive patients: results of a
case-control study.
Cognitive impairment and neurogenotoxic effects in rats exposed to low-intensity microwave
radiation.
Cognitive impairment in rats after long-term exposure to GSM-900 mobile phone radiation.
Controversies on electromagnetic field exposure and the nervous systems of children.
Could myelin damage from radiofrequency electromagnetic field exposure help explain the
functional impairment electrohypersensitivity? A review of the evidence.
Cumulated biological effects of microwaves and their reflection in behavior, work capacity,
growth of body mass and state of brain neurons].
Dataset on significant role of Candesartan on cognitive functions in rats having memory
impairment induced by electromagnetic waves.
Effect of electromagnetic fields emitted by cellular phones on the latency of evoked
electrodermal activity.
Effect of electromagnetic radiation on discharge activity of neurons in the hippocampus CA1 in
rats].
Effect of low level microwave radiation exposure on cognitive function and oxidative stress in
rats.
Effect of Low Level Subchronic Microwave Radiation on Rat Brain.
Effect of Low-Intensity Microwave Radiation on Monoamine Neurotransmitters and Their Key
Regulating Enzymes in Rat Brain.
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Effect of Short-term 900 MHz low level electromagnetic radiation exposure on blood serotonin
and glutamate levels.
Effect of whole-body exposure to high-frequency electromagnetic field on the brain electrogeny
in neurodefective and healthy mice.
Effects of 2.4 GHz radiofrequency radiation emitted from Wi-Fi equipment on microRNA
expression in brain tissue.
Effects of 2G and 3G mobile phones on performance and electrophysiology in adolescents,
young adults and older adults.
Effects of 7 Hz-modulated 450 MHz electromagnetic radiation on human performance in visual
memory tasks.
Effects of cell phone radiation on lipid peroxidation, glutathione and nitric oxide levels in mouse
brain during epileptic seizure.
Effects of electromagnetic radiation from handsets of cellular telephone on neurobehavioral
function].
Effects of electromagnetic radiation on spatial memory and synapses in rat hippocampal CA1.
Effects of exposure to 2100MHz GSM-like radiofrequency electromagnetic field on auditory
system of rats.
Effects of fetal microwave radiation exposure on offspring behavior in mice.
Effects of millimeter wave irradiation with different frequency and power density on their
offsprings in mice].
Effects of mobile phone radiation (900 MHz radiofrequency) on structure and functions of rat
brain.
Effects of Mobile Phones on Children's and Adolescents' Health: A Commentary.
Effects of nano-selenium on cognition performance of mice exposed in 1800 MHz
radiofrequency fields].
Effects of pulsed electromagnetic fields on cognitive processes - a pilot study on pulsed field
interference with cognitive regeneration.
Effects of radiofrequency exposure emitted from a GSM mobile phone on proliferation,
differentiation, and apoptosis of neural stem cells.
Effects of radiofrequency exposure on the GABAergic system in the rat cerebellum: clues from
semi-quantitative immunohistochemistry.
Electromagnetic field and brain development.
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Electromagnetic Fields, Pulsed Radiofrequency Radiation, and Epigenetics: How Wireless
Technologies May Affect Childhood Development.
Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes
and multiple sclerosis.
Electromagnetic hypersensitivity--an increasing challenge to the medical profession.
Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through
activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats.
Electromagnetic radiation 2450 MHz exposure causes cognition deficit with mitochondrial
dysfunction and activation of intrinsic pathway of apoptosis in rats.
Electromagnetic radiation of non-thermal intensity and short exposition as a sub-threshold
irritant for the central nervous system].
Electrophysiological Assessment of the Impact of Mobile Phone Radiation on Cognition in
Persons With Epilepsy.
Elevated risk of Alzheimer's disease among workers with likely electromagnetic field exposure.
Epidemiological evidence for a health risk from mobile phone base stations.
EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.
Exposure to GSM 900-MHz mobile radiation impaired inhibitory avoidance memory
consolidation in rat: Involvements of opioidergic and nitrergic systems.
Exposure to radio-frequency electromagnetic waves alters acetylcholinesterase gene expression,
exploratory and motor coordination-linked behaviour in male rats.
Fetal radiofrequency radiation exposure from 800-1900 mhz-rated cellular telephones affects
neurodevelopment and behavior in mice.
From the Cover: 2.45-GHz Microwave Radiation Impairs Hippocampal Learning and Spatial
Memory: Involvement of Local Stress Mechanism-Induced Suppression of iGluR/ERK/CREB
Signaling.
Fundamentally new electromagnetic pollution and the lack of adequate regulatory framework--
on the risk assessment (analysis of modern domestic and foreign data)].
GFAP expression in the rat brain following sub-chronic exposure to a 900 MHz electromagnetic
field signal.
Glial markers and emotional memory in rats following acute cerebral radiofrequency exposures.
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Glucose administration attenuates spatial memory deficits induced by chronic low-power-density
microwave exposure.
GSM 900 MHz radiation inhibits ants' association between food sites and encountered cues.
GSM radiation triggers seizures and increases cerebral c-Fos positivity in rats pretreated with
subconvulsive doses of picrotoxin.
Health effects of living near mobile phone base transceiver station (BTS) antennae: a report from
Isfahan, Iran.
Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice
to GSM 1800 MHz mobile phone radiation: An exploratory study.
Influence of microwave radiation on synaptic structure and function of hippocampus in Wistar
rats].
Influence of pre- and postnatal exposure of rats to 2.45-GHz microwave radiation on
neurobehavioral function.
Interaction of microwaves and a temporally incoherent magnetic field on spatial learning in the
rat.
Investigation on the health of people living near mobile telephone relay stations: I/Incidence
according to distance and sex].
Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis,
mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root
ganglion of rats.
Long term impairment of cognitive functions and alterations of NMDAR subunits after
continuous microwave exposure.
Maternal cell phone use during pregnancy and child cognition at age 5years in 3 birth cohorts.
Maternal mobile phone exposure adversely affects the electrophysiological properties of Purkinje
neurons in rat offspring.
Maternal mobile phone exposure alters intrinsic electrophysiological properties of CA1
pyramidal neurons in rat offspring.
Melatonin and a spin-trap compound block radiofrequency electromagnetic radiation-induced
DNA strand breaks in rat brain cells.
Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric
effects including depression.
Microwave irradiation affects radial-arm maze performance in the rat.
Microwave radiation induced oxidative stress, cognitive impairment and inflammation in brain
of Fischer rats.
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Mobile phone electromagnetic radiation affects Amyloid Precursor Protein and alpha-synuclein
metabolism in SH-SY5Y cells.
Mobile phone use for 5 minutes can cause significant memory impairment in humans.
Motor activity of rabbits in conditions of chronic low-intensity pulse microwave irradiation].
Nerve cell damage in mammalian brain after exposure to microwaves from GSM mobile phones.
Neurobehavioral effects among inhabitants around mobile phone base stations.
Neuroprotective effects of melatonin and omega-3 on hippocampal cells prenatally exposed to
900 MHz electromagnetic fields.
Nonthermal effects of lifelong high-frequency electromagnetic field exposure on social memory
performance in rats.
Observations of changes in neurobehavioral functions in workers exposed to high-frequency
radiation].
Occupational Exposures and Neurodegenerative Diseases-A Systematic Literature Review and
Meta-Analyses.
Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout
adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-
day-old Sprague Dawley male rats.
Physiological changes in rats after exposure to low levels of microwaves.
Possible cause for altered spatial cognition of prepubescent rats exposed to chronic
radiofrequency electromagnetic radiation.
Protective Role of NMDAR for Microwave-Induced Synaptic Plasticity Injuries in Primary
Hippocampal Neurons.
Psychophysiological indicators for children using mobile phones. Communication 2. Results of
four-year monitoring].
Radiofrequency electromagnetic radiation-induced behavioral changes and their possible basis.
Reduction of phosphorylated synapsin I (ser-553) leads to spatial memory impairment by
attenuating GABA release after microwave exposure in Wistar rats.
Relationship between cognition function and hippocampus structure after long-term microwave
exposure.
Relationship between millimeter wave irradiation in pregnant mice and c-Fos protein expression
in hippocampus and learning and memory functions in their offsprings].
RKIP Regulates Neural Cell Apoptosis Induced by Exposure to Microwave Radiation Partly
Through the MEK/ERK/CREB Pathway.
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Setting prudent public health policy for electromagnetic field exposures.
Short-term memory in mice is affected by mobile phone radiation.
Spatial memory and learning performance and its relationship to protein synthesis of Swiss
albino mice exposed to 10 GHz microwaves.
Spatial memory performance of Wistar rats exposed to mobile phone.
Ten gigahertz microwave radiation impairs spatial memory, enzymes activity, and
histopathology of developing mice brain.
The chronic effect of pulsed 1800 MHz electromagnetic radiation on amino acid
neurotransmitters in three different areas of juvenile and young adult rat brain.
The effect of electromagnetic radiation in the mobile phone range on the behaviour of the rat.
The effect of pulsed electromagnetic radiation from mobile phone on the levels of monoamine
neurotransmitters in four different areas of rat brain.
The electromagnetic fields of cellular phones and the health of children and of teenagers (the
situation requiring to take an urgent measure)].
The implications of non-linear biological oscillations on human electrophysiology for
electrohypersensitivity (EHS) and multiple chemical sensitivity (MCS).
The Screening of Genes Sensitive to Long-Term, Low-Level Microwave Exposure and
Bioinformatic Analysis of Potential Correlations to Learning and Memory.
Thermal and non-thermal health effects of low intensity non-ionizing radiation: An international
perspective.
Transient and cumulative memory impairments induced by GSM 1.8 GHz cell phone signal in a
mouse model.
Upregulation of HIF-1alpha via activation of ERK and PI3K pathway mediated protective
response to microwave-induced mitochondrial injury in neuron-like cells.
Variations in electroencephalography with mobile phone usage in medical students.
Vitamin C protects rat cerebellum and encephalon from oxidative stress following exposure to
radiofrequency wave generated by a BTS antenna model.
What is the impact of electromagnetic waves on epileptic seizures?
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REPRODUCTION
Keywords
–
pregnancy, reproductive, pregnant, sperm, embryos, testicular, fertility, embryo,
testis, embryonic, fetuses, testosterone, motility, infertility, reproduction, testes, semen,
spermatozoa, spermatogenesis, reproductive system, sperm motility, male fertility, sperm count,
embryogenesis, abortion, male reproductive, spermatogenic, embryonic development, mating,
male infertility, birth defects, serum testosterone, adverse reproductive, miscarriage, reproductive
organs, semen parameters, sperm concentration, sperm parameters, testicular function,
testosterone level, epididymis, male reproductive system, spermatogenic cells, spermatogonia,
fertilized eggs, ovaries, reproductive capacity, reproductive outcomes, sperm cells, sperm
morphology, fertile, pregnancies, reproductive function, testicular tissue, rat testes, rat testis,
reproductive functions, reproductive systems, sperm DNA, spermatogonial, testis tissue,
embryogeny, reproductive health, sperm cell, miscarriages, offsprings, oocyte, oogenesis,
preterm birth, seminal vesicles, Sperm head, spermatids, sperms, testicles, fetal loss, genital,
gonads, reproductive hormones, semen analysis
Titles
1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53
dependent Bax mediated testicular apoptosis in mice, Mus musculus.
1950MHz Radio Frequency Electromagnetic Radiation Inhibits Testosterone Secretion of Mouse
Leydig Cells.
2.45 GHz microwave irradiation-induced oxidative stress affects implantation or pregnancy in
mice, Mus musculus.
2.45 GHz microwave radiation induced oxidative and nitrosative stress mediated testicular
apoptosis: Involvement of a p53 dependent bax-caspase-3 mediated pathway.
2.45-GHz microwave irradiation adversely affects reproductive function in male mouse, Mus
musculus by inducing oxidative and nitrosative stress.
900 MHz pulse-modulated radiofrequency radiation induces oxidative stress on heart, lung, testis
and liver tissues.
Activation of TLR signalling regulates microwave radiation-mediated impairment of
spermatogenesis in rat testis.
Alternating magnetic field damages the reproductive function of murine testes].
Are men talking their reproductive health away?
Are microwaves a co-teratogen? Experimental model concept and its verification].
Association between mobile phone use and semen quality: a systemic review and meta-analysis.
Association of excessive mobile phone use during pregnancy with birth weight: an adjunct study
in Kumamoto of Japan Environment and Children's Study.
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Autoimmune processes after long-term low-level exposure to electromagnetic fields (the results
of an experiment). Part 5. Impact of the blood serum from rats exposed to low-level
electromagnetic fields on pregnancy, foetus and offspring development of intact female rats].
Bioeffects of mobile telephony radiation in relation to its intensity or distance from the antenna.
Biological effects from electromagnetic field exposure and public exposure standards.
Biological effects of continuous exposure of embryos and young chickens to electromagnetic
fields emitted by video display units.
Biological effects of mobile phone electromagnetic field on chick embryo (risk assessment using
the mortality rate)].
Biophysical evaluation of radiofrequency electromagnetic field effects on male reproductive
pattern.
Biosomatic effects of the electromagnetic fields on view of the physiotherapy personnel health.
Cancer in radar technicians exposed to radiofrequency/microwave radiation: sentinel episodes.
Cell phone radiation exposure on brain and associated biological systems.
Cell phone usage and erectile function.
Cellphone electromagnetic radiation damages the testicular ultrastructure of male rats].
Chronic prenatal exposure to the 900 megahertz electromagnetic field induces pyramidal cell
loss in the hippocampus of newborn rats.
Chronotoxicity of 1800 MHz microwave radiation on sex hormones and spermatogenesis in male
mice].
Commentary on the utility of the National Toxicology Program study on cell phone
radiofrequency radiation data for assessing human health risks despite unfounded criticisms
aimed at minimizing the findings of adverse health effects.
Comparison of biological effects between continuous and intermittent exposure to GSM-900-
MHz mobile phone radiation: Detection of apoptotic cell-death features.
Comparison of native and microwave irradiated DNA.
Cranial and postcranial skeletal variations induced in mouse embryos by mobile phone radiation.
Cytokines produced by microwave-radiated Sertoli cells interfere with spermatogenesis in rat
testis.
Derangement of chick embryo retinal differentiation caused by radiofrequency electromagnetic
fields.
Disruption of the ovarian follicle reservoir of prepubertal rats following prenatal exposure to a
continuous 900-MHz electromagnetic field.
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Does prolonged radiofrequency radiation emitted from Wi-Fi devices induce DNA damage in
various tissues of rats?
Dose related shifts in the developmental progress of chick embryos exposed to mobile phone
induced electromagnetic fields.
Early and Delayed Effects of Radio Frequency Electromagnetic Fields on the Reproductive
Function and Functional Status of the Offspring of Experimental Animals].
Effect of 2.45 GHz microwave radiation on the fertility pattern in male mice.
Effect of 935-MHz phone-simulating electromagnetic radiation on endometrial glandular cells
during mouse embryo implantation.
Effect of cell phone usage on semen analysis in men attending infertility clinic: an observational
study.
Effect of early pregnancy electromagnetic field exposure on embryo growth ceasing].
Effect of electromagnetic irradiation produced by 3G mobile phone on male rat reproductive
system in a simulated scenario.
Effect of Electromagnetic Waves from Mobile Phones on Spermatogenesis in the Era of 4G-
LTE.
Effect of exposure to radio frequency radiation emitted by cell phone on the developing dorsal
root ganglion of chick embryo: a light microscopic study.
Effect of Guilingji Capsule on the fertility, liver functions, and serum LDH of male SD rats
exposed by 900 mhz cell phone].
Effect of long-term exposure of 2.4 GHz radiofrequency radiation emitted from Wi-Fi equipment
on testes functions.
Effect of low power microwave on the mouse genome: a direct DNA analysis.
Effect of low-intensity extremely high frequency radiation on reproductive function in wistar
rats.
Effect of Mobile Phone Radiation on Cardiovascular Development of Chick Embryo.
Effect of mobile telephones on sperm quality: a systematic review and meta-analysis.
Effect of Modified Wuzi Yanzong Pill () on Tip60-Mediated Apoptosis in Testis of Male Rats
after Microwave Radiation.
Effect of Radiofrequency Radiation Emitted from 2G and 3G Cell Phone on Developing Liver of
Chick Embryo - A Comparative Study.
Effect of radiofrequency radiation on reproductive health.
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Effect of rosmarinic acid on sertoli cells apoptosis and serum antioxidant levels in rats after
exposure to electromagnetic fields.
Effects of 1800-MHz radiofrequency fields on circadian rhythm of plasma melatonin and
testosterone in male rats.
Effects of cell phone use on semen parameters: Results from the MARHCS cohort study in
Chongqing, China.
Effects of cellular phone emissions on sperm motility in rats.
Effects of continuous low-level exposure to radiofrequency radiation on intrauterine
development in rats.
Effects of electromagnetic radiation from a cellular phone on human sperm motility: an in vitro
study.
Effects of electromagnetic waves emitted from 3G+wi-fi modems on human semen analysis.
Effects of exposure to a mobile phone on testicular function and structure in adult rabbit.
Effects of GSM-like radiofrequency irradiation during the oogenesis and spermiogenesis of
Xenopus laevis.
Effects of GSM-like radiofrequency on distortion product otoacoustic emissions in pregnant
adult rabbits.
Effects of millimeter wave irradiation with different frequency and power density on their
offsprings in mice].
Effects of mobile phone radiation on serum testosterone in Wistar albino rats.
Effects of prenatal 900 MHz electromagnetic field exposures on the histology of rat kidney.
Effects of radiofrequency electromagnetic fields on mammalian spermatogenesis].
Effects of radiofrequency electromagnetic wave exposure from cellular phones on the
reproductive pattern in male Wistar rats.
Effects of radiofrequency electromagnetic waves (RF-EMW) from cellular phones on human
ejaculated semen: an in vitro pilot study.
Effects of the exposure to mobile phones on male reproduction: a review of the literature.
Electromagnetic fields enhance chemically-induced hyperploidy in mammalian oocytes.
Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3
signaling pathways in rats.
Epidemiologic evidence relevant to radar (microwave) effects.
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EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
Evaluation of the effect of using mobile phones on male fertility.
Evidence for mobile phone radiation exposure effects on reproductive pattern of male rats: role
of ROS.
Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.
Exposure to a 900 MHz electromagnetic field for 1 hour a day over 30 days does change the
histopathology and biochemistry of the rat testis.
Exposure to cell phone induce oxidative stress in mice preantral follicles during in vitro
cultivation: An experimental study.
Exposure to non-ionizing electromagnetic radiation of public risk prevention instruments
threatens the quality of spermatozoids.
Fetal and neonatal responses following maternal exposure to mobile phones.
Fetal radiofrequency radiation exposure from 800-1900 mhz-rated cellular telephones affects
neurodevelopment and behavior in mice.
Growing concern over the safety of using mobile phones and male fertility.
GSM 900 MHz microwave radiation affects embryo development of Japanese quails.
GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant
rabbits.
Hazardous health effects of microwaves and radio waves].
Hypospermatogenesis and spermatozoa maturation arrest in rats induced by mobile phone
radiation.
Immunohistopathologic demonstration of deleterious effects on growing rat testes of
radiofrequency waves emitted from conventional Wi-Fi devices.
Immunomorphologic changes in the testes upon exposure to a microwave electromagnetic field].
Influence of microwave exposure on fertility of male rats.
Inhibition by Egb761 of the effect of cellphone radiation on the male reproductive system.
Interference of vitamin E on the brain tissue damage by electromagnetic radiation of cell phone
in pregnant and fetal rats].
Lethal and teratogenic effects of long-term low-intensity radio frequency radiation at 428 MHz
on developing chick embryo.
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Long-term effects of 900 MHz radiofrequency radiation emitted from mobile phone on testicular
tissue and epididymal semen quality.
Long-term exposure to 4G smartphone radiofrequency electromagnetic radiation diminished
male reproductive potential by directly disrupting Spock3-MMP2-BTB axis in the testes of adult
rats.
Long-term exposure to electromagnetic radiation from mobile phones and Wi-Fi devices
decreases plasma prolactin, progesterone, and estrogen levels but increases uterine oxidative
stress in pregnant rats and their offspring.
Long-term exposure to low intensity microwave radiation affects male reproductivity].
Long-term microwave radiation affects male reproduction in rats].
Maternal cell phone use during pregnancy and child behavioral problems in five birth cohorts.
Maternal cell phone use during pregnancy and child cognition at age 5years in 3 birth cohorts.
Maternal exposure to a continuous 900-MHz electromagnetic field provokes neuronal loss and
pathological changes in cerebellum of 32-day-old female rat offspring.
Maternal occupational exposure to extremely low frequency magnetic fields and the risk of brain
cancer in the offspring.
Maternal occupational exposure to extremely low frequency magnetic fields during pregnancy
and childhood leukemia.
Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA
damage and cell cycle arrest in germ cells of male Swiss albino mice.
Microwave exposure affecting reproductive system in male rats.
Microwave radiation (2.45 GHz)-induced oxidative stress: Whole-body exposure effect on
histopathology of Wistar rats.
Microwave radiation enhances teratogenic effect of cytosine arabinoside in mice.
Mobile phone (1800MHz) radiation impairs female reproduction in mice, Mus musculus,
through stress induced inhibition of ovarian and uterine activity.
Mobile phone radiation induces mode-dependent DNA damage in a mouse spermatocyte-derived
cell line: a protective role of melatonin.
Mobile phone radiation induces reactive oxygen species production and DNA damage in human
spermatozoa in vitro.
Mobile phone usage and male infertility in Wistar rats.
Morinda officialis how extract improves microwave-induced reproductive impairment in male
rats].
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Neuroprotective effects of melatonin and omega-3 on hippocampal cells prenatally exposed to
900 MHz electromagnetic fields.
Occupational exposure to magnetic fields in relation to male breast cancer and testicular cancer:
a Swedish case-control study.
Overproduction of free radical species in embryonal cells exposed to low intensity
radiofrequency radiation.
Oxidative and mutagenic effects of low intensity GSM 1800 MHz microwave radiation.
Oxidative changes and apoptosis induced by 1800-MHz electromagnetic radiation in NIH/3T3
cells.
Oxidative effects of extremely low frequency magnetic field and radio frequency radiation on
testes tissues of diabetic and healthy rats.
Oxidative stress-mediated alterations on sperm parameters in male Wistar rats exposed to 3G
mobile phone radiation.
Pathological effects of prenatal exposure to a 900 MHz electromagnetic field on the 21-day-old
male rat kidney.
Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male
reproductive system.
Postnatal development and behavior effects of in-utero exposure of rats to radiofrequency waves
emitted from conventional WiFi devices.
Prenatal and postnatal exposure to cell phone use and behavioral problems in children.
Probing the Origins of 1,800 MHz Radio Frequency Electromagnetic Radiation Induced Damage
in Mouse Immortalized Germ Cells and Spermatozoa in vitro.
Protective effect of Liuweidihuang Pills against cellphone electromagnetic radiation-induced
histomorphological abnormality, oxidative injury, and cell apoptosis in rat testes].
Protective effects of luteolin on rat testis following exposure to 900 MHz electromagnetic field.
Protective Effects of Zinc on 2.45 GHz Electromagnetic Radiation-Induced Oxidative Stress and
Apoptosis in HEK293 Cells.
Pulsed magnetic field from video display terminals enhances teratogenic effects of cytosine
arabinoside in mice.
Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling
pathway in mouse spermatogenic cells in vitro and thus may affect male fertility.
Radar radiation damages sperm quality].
Radiations and male fertility.
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Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones
induces oxidative stress and reduces sperm motility in rats.
Radiofrequency electromagnetic radiation from cell phone causes defective testicular function in
male Wistar rats.
Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular
germ cells in swiss albino mice.
Relationship between millimeter wave irradiation in pregnant mice and c-Fos protein expression
in hippocampus and learning and memory functions in their offsprings].
Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6:
microwaves act through voltage-gated calcium channel activation to induce biological impacts at
non-thermal levels, supporting a paradigm shift for microwave/lower frequency electromagnetic
field action.
Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the
HEK293 cells.
Towards 5G communication systems: Are there health implications?
Wi-Fi (2.45 GHz)- and mobile phone (900 and 1800 MHz)-induced risks on oxidative stress and
elements in kidney and testis of rats during pregnancy and the development of offspring.
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GENOTOXICITY
Keywords
–
DNA damage, genotoxic, micronuclei, chromosomal, micronucleus, chromosome,
genotoxicity, genotoxic effects, mutagenic, strand breaks, chromatin, mutation, DNA strand,
Chromatid, mutations, chromosome aberrations, chromosomes, DNA fragmentation, double-
strand, chromosomal aberrations, DNA repair, DNA strand breaks, micronucleus (MN), genetic
damage, micronuclei (MN), Sister Chromatid, genome, blood leukocytes, double-strand breaks,
oxidative DNA, chromosomal damage, DNA synthesis, mutant, cellular stress, chromosome
aberration, oxidative DNA damage, Purkinje cells, DNA breaks, cell cycle arrest, clastogenic,
genotoxic potential, keratinocytes, micronucleated, single strand, cell division, chromatid
exchange, Chromatid Exchanges, genetic material, micronucleus test, Mutagenesis, cell cycle
progression, cellular DNA, Cytochrome c, double strand, genetic effects, genomic instability,
micronucleus frequency, DNA single-strand, DNA-damaging, Mutagen, mutagenicity, single
strand breaks, chromatin condensation, chromosomal aberration, double-strand breaks (DSBs),
strand breakage, cell cycle distribution, cell DNA, genetically, strand DNA
Titles
1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53
dependent Bax mediated testicular apoptosis in mice, Mus musculus.
1950MHz Radio Frequency Electromagnetic Radiation Inhibits Testosterone Secretion of Mouse
Leydig Cells.
2.45 GHz microwave irradiation-induced oxidative stress affects implantation or pregnancy in
mice, Mus musculus.
2.45 GHz radiofrequency fields alter gene expression in cultured human cells.
60 Hz magnetic field exposure induces DNA crosslinks in rat brain cells.
8-Oxo-7, 8-dihydro-2'-deoxyguanosine as a biomarker of DNA damage by mobile phone
radiation.
8-oxoG DNA glycosylase-1 inhibition sensitizes Neuro-2a cells to oxidative DNA base damage
induced by 900 MHz radiofrequency electromagnetic radiation.
915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci
in human lymphocytes from hypersensitive and healthy persons.
954 MHz microwaves enhance the mutagenic properties of mitomycin C.
A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a
mobile phone base station.
A non-thermal effect of millimeter wave radiation on the puffing of giant chromosomes.
Acute low-intensity microwave exposure increases DNA single-strand breaks in rat brain cells.
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Assessment of cytogenetic damage and oxidative stress in personnel occupationally exposed to
the pulsed microwave radiation of marine radar equipment.
Assessment of DNA sensitivity in peripheral blood leukocytes after occupational exposure to
microwave radiation: the alkaline comet assay and chromatid breakage assay.
Assessment of radio-frequency electromagnetic radiation by the micronucleus test in bovine
peripheral erythrocytes.
Biochemical and histological studies on adverse effects of mobile phone radiation on rat's brain.
Biochemical modifications and neuronal damage in brain of young and adult rats after long-term
exposure to mobile phone radiations.
Biological effects from electromagnetic field exposure and public exposure standards.
Biophysical evaluation of radiofrequency electromagnetic field effects on male reproductive
pattern.
Cell phone radiation exposure on brain and associated biological systems.
Chromosomal damage in human diploid fibroblasts by intermittent exposure to extremely low-
frequency electromagnetic fields.
Chromosome damage and micronucleus formation in human blood lymphocytes exposed in vitro
to radiofrequency radiation at a cellular telephone frequency (847.74 MHz, CDMA).
Cognitive impairment and neurogenotoxic effects in rats exposed to low-intensity microwave
radiation.
Combinative exposure effect of radio frequency signals from CDMA mobile phones and
aphidicolin on DNA integrity.
Combined exposure of ELF magnetic fields and x-rays increased mutant yields compared with x-
rays alone in pTN89 plasmids.
Commentary on the utility of the National Toxicology Program study on cell phone
radiofrequency radiation data for assessing human health risks despite unfounded criticisms
aimed at minimizing the findings of adverse health effects.
Comparison of biological effects between continuous and intermittent exposure to GSM-900-
MHz mobile phone radiation: Detection of apoptotic cell-death features.
Comparison of chromosome aberrations in peripheral blood lymphocytes from people
occupationally exposed to ionizing and radiofrequency radiation.
Connection between Cell Phone use, p53 Gene Expression in Different Zones of Glioblastoma
Multiforme and Survival Prognoses.
Cytogenetic changes induced by low-intensity microwaves in the species Triticum aestivum].
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Cytogenetic consequences of microwave irradiation on mammalian cells incubated in vitro.
Cytogenetic damage in human lymphocytes following GMSK phase modulated microwave
exposure.
Cytotoxic and genotoxic effects of high-frequency electromagnetic fields (GSM 1800 MHz) on
immature and mature rats.
DNA Damage of Lymphocytes in Volunteers after 4 hours Use of Mobile Phone.
Effect of 2.45 GHz microwave radiation on the fertility pattern in male mice.
Effect of 3G cell phone exposure with computer controlled 2-D stepper motor on non-thermal
activation of the hsp27/p38MAPK stress pathway in rat brain.
Effect of 900-, 1800-, and 2100-MHz radiofrequency radiation on DNA and oxidative stress in
brain.
Effect of 950 MHz UHF electromagnetic radiation on biomarkers of oxidative damage,
metabolism of UFA and antioxidants in the livers of young rats of different ages.
Effect of acute exposure to microwave from mobile phone on DNA damage and repair of
cultured human lens epithelial cells in vitro].
Effect of early pregnancy electromagnetic field exposure on embryo growth ceasing].
Effect of electromagnetic irradiation produced by 3G mobile phone on male rat reproductive
system in a simulated scenario.
Effect of electromagnetic radiation of millimetric wave band on genome of somatic cells].
Effect of exposure to radio frequency radiation emitted by cell phone on the developing dorsal
root ganglion of chick embryo: a light microscopic study.
Effect of GSTM1 and GSTT1 Polymorphisms on Genetic Damage in Humans Populations
Exposed to Radiation From Mobile Towers.
Effect of Low Level Subchronic Microwave Radiation on Rat Brain.
Effect of low power microwave on the mouse genome: a direct DNA analysis.
Effect of low-intensity microwave radiation on proliferation of cultured epithelial cells of rabbit
lens].
Effect of Mobile Phone Radiation on Cardiovascular Development of Chick Embryo.
Effect of Radiofrequency Radiation Emitted from 2G and 3G Cell Phone on Developing Liver of
Chick Embryo - A Comparative Study.
Effect of Radiofrequency Radiation on Human Hematopoietic Stem Cells.
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Effect of whole-body exposure to high-frequency electromagnetic field on the brain electrogeny
in neurodefective and healthy mice.
Effects of GSM 1800 MHz radiofrequency electromagnetic fields on DNA damage in Chinese
hamster lung cells].
Effects of low-intensity extremely high frequency electromagnetic radiation on chromatin
structure of lymphoid cells in vivo and in vitro].
Effects of microwave radiation on thymocytes in mice at different power densities].
Effects of radiofrequency electromagnetic wave exposure from cellular phones on the
reproductive pattern in male Wistar rats.
Effects of radiofrequency electromagnetic waves (RF-EMW) from cellular phones on human
ejaculated semen: an in vitro pilot study.
Effects of the Effect of Ultra High Frequency Mobile Phone Radiation on Human Health.
Electromagnetic fields and health: DNA-based dosimetry.
Electromagnetic fields at a mobile phone frequency (900 MHz) trigger the onset of general stress
response along with DNA modifications in Eisenia fetida earthworms.
Electromagnetic fields enhance chemically-induced hyperploidy in mammalian oocytes.
Electromagnetic noise inhibits radiofrequency radiation-induced DNA damage and reactive
oxygen species increase in human lens epithelial cells.
Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3
signaling pathways in rats.
Epidemiologic evidence relevant to radar (microwave) effects.
Erythropoietic changes in rats after 2.45 GJz nonthermal irradiation.
Evaluation of basal DNA damage and oxidative stress in Wistar rat leukocytes after exposure to
microwave radiation.
Evaluation of genotoxic and/or co-genotoxic effects in cells exposed in vitro to extremely-low
frequency electromagnetic fields].
Evaluation of selected biochemical parameters in the saliva of young males using mobile phones.
Evaluation of the cytogenotoxic damage in immature and mature rats exposed to 900 MHz
radiofrequency electromagnetic fields.
Evaluation of the genotoxicity of cell phone radiofrequency radiation in male and female rats and
mice following subchronic exposure.
Exposure of human peripheral blood lymphocytes to electromagnetic fields associated with
cellular phones leads to chromosomal instability.
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Exposure to 1800 MHz radiofrequency electromagnetic radiation induces oxidative DNA base
damage in a mouse spermatocyte-derived cell line.
Exposure to 915 MHz radiation induces micronuclei in Vicia faba root tips.
Exposure to global system for mobile communication (GSM) cellular phone radiofrequency
alters gene expression, proliferation, and morphology of human skin fibroblasts.
Exposure to low-intensive superhigh frequency electromagnetic field as a factor of
carcinogenesis in experimental animals.
Exposure to non-ionizing electromagnetic fields emitted from mobile phones induced DNA
damage in human ear canal hair follicle cells.
Exposure to non-ionizing electromagnetic radiation of public risk prevention instruments
threatens the quality of spermatozoids.
Fifty-gigahertz microwave exposure effect of radiations on rat brain.
GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant
rabbits.
Immunohistopathologic demonstration of deleterious effects on growing rat testes of
radiofrequency waves emitted from conventional Wi-Fi devices.
Impact of radio frequency electromagnetic radiation on DNA integrity in the male germline.
Increased levels of numerical chromosome aberrations after in vitro exposure of human
peripheral blood lymphocytes to radiofrequency electromagnetic fields for 72 hours.
Increased ornithine decarboxylase activity in cultured cells exposed to low energy modulated
microwave fields and phorbol ester tumor promoters.
Influence of 1.8 GHz microwave on DNA damage induced by 4 chemical mutagens].
Influence of electromagnetic fields on reproductive system of male rats.
Interference of vitamin E on the brain tissue damage by electromagnetic radiation of cell phone
in pregnant and fetal rats].
Long-term microwave radiation affects male reproduction in rats].
Low intensity microwave radiation induced oxidative stress, inflammatory response and DNA
damage in rat brain.
Maternal exposure to a continuous 900-MHz electromagnetic field provokes neuronal loss and
pathological changes in cerebellum of 32-day-old female rat offspring.
Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA
damage and cell cycle arrest in germ cells of male Swiss albino mice.
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Melatonin protects rat thymus against oxidative stress caused by exposure to microwaves and
modulates proliferation/apoptosis of thymocytes.
Microwaves from Mobile Phones Inhibit 53BP1 Focus Formation in Human Stem Cells More
Strongly Than in Differentiated Cells: Possible Mechanistic Link to Cancer Risk.
Mobile phone radiation induces mode-dependent DNA damage in a mouse spermatocyte-derived
cell line: a protective role of melatonin.
Mobile phone radiation induces reactive oxygen species production and DNA damage in human
spermatozoa in vitro.
Mobile phones, heat shock proteins and cancer.
Mutagenic and morphologic impacts of 1.8GHz radiofrequency radiation on human peripheral
blood lymphocytes (hPBLs) and possible protective role of pre-treatment with Ginkgo biloba
(EGb 761).
Mutagenic response of 2.45 GHz radiation exposure on rat brain.
Neural cell apoptosis induced by microwave exposure through mitochondria-dependent caspase-
3 pathway.
Oxidative and mutagenic effects of low intensity GSM 1800 MHz microwave radiation.
Oxidative changes and apoptosis induced by 1800-MHz electromagnetic radiation in NIH/3T3
cells.
Probing the Origins of 1,800 MHz Radio Frequency Electromagnetic Radiation Induced Damage
in Mouse Immortalized Germ Cells and Spermatozoa in vitro.
Protective effects of Genistein on human renal tubular epithelial cells damage of microwave
radiation].
Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling
pathway in mouse spermatogenic cells in vitro and thus may affect male fertility.
Purkinje cell number decreases in the adult female rat cerebellum following exposure to 900
MHz electromagnetic field.
Quantitative patterns in the cytogenetic action of microwaves].
Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic effects in vitro in
human fibroblasts but not in lymphocytes.
Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular
germ cells in swiss albino mice.
Radioprotective effects of honeybee venom (Apis mellifera) against 915-MHz microwave
radiation-induced DNA damage in wistar rat lymphocytes: in vitro study.
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RAPD Profiling, DNA Fragmentation, and Histomorphometric Examination in Brains of Wistar
Rats Exposed to Indoor 2.5 Ghz Wi-Fi Devices Radiation.
Reactive oxygen species levels and DNA fragmentation on astrocytes in primary culture after
acute exposure to low intensity microwave electromagnetic field.
Risks to Health and Well-Being From Radio-Frequency Radiation Emitted by Cell Phones and
Other Wireless Devices.
RKIP Regulates Neural Cell Apoptosis Induced by Exposure to Microwave Radiation Partly
Through the MEK/ERK/CREB Pathway.
Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6:
microwaves act through voltage-gated calcium channel activation to induce biological impacts at
non-thermal levels, supporting a paradigm shift for microwave/lower frequency electromagnetic
field action.
Significance of micronuclei in buccal smears of mobile phone users: A comparative study.
Single- and double-strand DNA breaks in rat brain cells after acute exposure to radiofrequency
electromagnetic radiation.
Single strand DNA breaks in rat brain cells exposed to microwave radiation.
Single-strand DNA breaks in human hair root cells exposed to mobile phone radiation.
Status quo of the researches on the biological effect of electromagnetic radiation on the testis and
epididymal sperm].
Study of low-intensity 2450-MHz microwave exposure enhancing the genotoxic effects of
mitomycin C using micronucleus test and comet assay in vitro.
Studying the synergistic damage effects induced by 1.8 GHz radiofrequency field radiation
(RFR) with four chemical mutagens on human lymphocyte DNA using comet assay in vitro.
Terahertz radiation increases genomic instability in human lymphocytes.
The effect of mobile phone on the number of Purkinje cells: a stereological study.
The effect of radiofrequency radiation on DNA and lipid damage in female and male infant
rabbits.
The Effects of Melatonin on Oxidative Stress Parameters and DNA Fragmentation in Testicular
Tissue of Rats Exposed to Microwave Radiation.
The effects of radiofrequency electromagnetic radiation on sperm function.
The effects of radiofrequency fields on cell proliferation are non-thermal.
The genomic effects of cell phone exposure on the reproductive system.
The genotoxic effect of radiofrequency waves on mouse brain.
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The influence of 1800 MHz GSM-like signals on hepatic oxidative DNA and lipid damage in
nonpregnant, pregnant, and newly born rabbits.
The influence of direct mobile phone radiation on sperm quality.
The link between radiofrequencies emitted from wireless technologies and oxidative stress.
The therapeutic effect of a pulsed electromagnetic field on the reproductive patterns of male
Wistar rats exposed to a 2.45-GHz microwave field.
Tinnitus and cell phones: the role of electromagnetic radiofrequency radiation.
Wi-Fi is an important threat to human health.
X-rays, microwaves and vinyl chloride monomer: their clastogenic and aneugenic activity, using
the micronucleus assay on human lymphocytes.
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CARDIOVASCULAR
Keywords
–
Cardiac, cardiovascular, pacemaker, pacemakers, implanted, blood pressure,
implantable, vascular, heart rate variability, myocardial, heart rate variability (HRV), implants,
cardiac pacemakers, implantation, defibrillators, implant, cardioverter, myocardium,
cardiovascular system, implantable cardioverter, Cardiovascular disease, defibrillator,
fibrillation, arrhythmia, arterial blood pressure, autonomic nervous system, cardioverter
defibrillators, implanted pacemakers, cardiac pacemaker, hypertension, arrhythmias,
cardioverter-defibrillators, implantable cardioverter defibrillators, implantable cardioverter-
defibrillators, pacemaker function, heart disease, implanted cardiac, tachycardia, cardiac devices,
circulatory system, microcirculation, blood vessels, cardiomyocytes, cardiovascular effects,
vascular permeability, atherosclerosis, cardiovascular diseases, ventricular fibrillation, arterial
pressure, Atrial fibrillation, cardiac output, cardiovascular function, Implantable cardioverter
defibrillator (ICD), implantable devices, arrhythmic, carotid artery, pacemaker dysfunction,
pacemaker malfunction
Titles
2.45 GHz microwave irradiation-induced oxidative stress affects implantation or pregnancy in
mice, Mus musculus.
5-HT contents change in peripheral blood of workers exposed to microwave and high frequency
radiation].
Activation of VEGF/Flk-1-ERK Pathway Induced Blood-Brain Barrier Injury After Microwave
Exposure.
AduoLa Fuzhenglin down-regulates microwave-induced expression of beta1-adrenergic receptor
and muscarinic type 2 acetylcholine receptor in myocardial cells of rats.
An update on mobile phones interference with medical devices.
Analysis of ECG on the staffs exposed to microwave in the radio calling signal station].
Biochemical and histological studies on adverse effects of mobile phone radiation on rat's brain.
Biological effects and health risks of electromagnetic fields at levels classified by INCRIP ans
admissible among occupationally exposed workers: a study of the Nofer Institute of
Occupational Medicine, Lodz].
Biological effects from electromagnetic field exposure and public exposure standards.
Biosomatic effects of the electromagnetic fields on view of the physiotherapy personnel health.
Cardiac devices and electromagnetic interference revisited: new radiofrequency technologies and
implications for dermatologic surgery.
Cardiovascular risk in operators under radiofrequency electromagnetic radiation.
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Cell Phone Radiation Effect on Bone-to-Implant Osseointegration: A Preliminary Histologic
Evaluation in Rabbits.
Cell phone radiation exposure on brain and associated biological systems.
Cellular Phone Irradiation of the Head Affects Heart Rate Variability Depending on
Inspiration/Expiration Ratio.
Danger of cellular telephones and their relay stations].
Dataset on significant role of Candesartan on cognitive functions in rats having memory
impairment induced by electromagnetic waves.
Dirty electricity, chronic stress, neurotransmitters and disease.
Disturbances in the function of cardiac pacemaker caused by short wave and microwave
diathermies and pulsed high frequency current.
ECG changes in factory workers exposed to 27.2 MHz radiofrequency radiation.
Effect of mobile phone electromagnetic emission on characteristics of cerebral blood circulation
and neurohumoral regulations in humans].
Effect of Mobile Phone Radiation on Cardiovascular Development of Chick Embryo.
Effect of qindan fuzheng capsule on ultrastructure of microwave radiation injured
cardiomyocytes and hepatocytes in rats].
Effects of 900-MHz electromagnetic field emitted from cellular phone on brain oxidative stress
and some vitamin levels of guinea pigs.
Electromagnetic compatibility study of the in-vitro interaction of wireless phones with cardiac
pacemakers.
Electromagnetic energy radiated from mobile phone alters electrocardiographic records of
patients with ischemic heart disease.
Electromagnetic field induced biological effects in humans.
Electromagnetic fields produced by incubators influence heart rate variability in newborns.
Electromagnetic fields promote severe and unique vascular calcification in an animal model of
ectopic calcification.
Electromagnetic interference of communication devices on ECG machines.
Electromagnetic interference of implantable cardiac devices from a shoulder massage machine.
Electromagnetic interference of implantable unipolar cardiac pacemakers by an induction oven.
Electronic article surveillance systems and interactions with implantable cardiac devices: risk of
adverse interactions in public and commercial spaces.
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Electrosmog and autoimmune disease.
Epidemiological risk assessment of pathology development in occupational exposure to
radiofrequency electromagnetic fields].
Evaluation of occupational risk caused by exposure to electromagnetic rays].
Evaluation of selected functional circulation parameters of workers from various occupational
groups exposed to electromagnetic fields of high frequency. III. 24-h monitoring of arterial blood
pressure (ABP)].
Evaluation of selected parameters of circulatory system function in various occupational groups
exposed to high frequency electromagnetic fields. II. Electrocardiographic changes].
Evaluation of the safety of users of active implantable medical devices (AIMD) in the working
environment in terms of exposure to electromagnetic fields - Practical approach to the
requirements of European Directive 2013/35/EU.
Fetal and neonatal responses following maternal exposure to mobile phones.
Health Council Report 'Radiofrequency electromagnetic fields (300 Hz-300 GHz). The Health
Council of the Netherlands].
Heart rate variability (HRV) analysis in radio and TV broadcasting stations workers.
Heart rate variability affected by radiofrequency electromagnetic field in adolescent students.
Hospital pager systems may cause interference with pacemaker telemetry.
Implanted medical devices in workers exposed to radio-frequency radiation.
In vitro and in vivo study of electromagnetic compatibility of cellular phones and pacemakers].
Influence of digital and analogue cellular telephones on implanted pacemakers.
Inter-beat intervals of cardiac-cell aggregates during exposure to 2.45 GHz CW, pulsed, and
square-wave-modulated microwaves.
Interference of vitamin E on the brain tissue damage by electromagnetic radiation of cell phone
in pregnant and fetal rats].
Leukemia mortality and incidence of infantile leukemia near the Vatican Radio Station of
Rome].
Long-term exposure to microwave radiation provokes cancer growth: evidences from radars and
mobile communication systems.
Mobile phone interference with medical equipment and its clinical relevance: a systematic
review.
Occupational exposure to non-ionizing radiation and an association with heart disease: an
exploratory study.
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Replication of heart rate variability provocation study with 2.4-GHz cordless phone confirms
original findings.
Report of final results regarding brain and heart tumors in Sprague-Dawley rats exposed from
prenatal life until natural death to mobile phone radiofrequency field representative of a 1.8GHz
GSM base station environmental emission.
Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6:
microwaves act through voltage-gated calcium channel activation to induce biological impacts at
non-thermal levels, supporting a paradigm shift for microwave/lower frequency electromagnetic
field action.
Selective interference with pacemaker activity by electrical dental devices.
Subjective symptoms reported by people living in the vicinity of cellular phone base stations:
review].
The effect of cell phones on pacemaker function].
The effects of the duration of mobile phone use on heart rate variability parameters in healthy
subjects.
The health problems of computer operators].
The influence of the call with a mobile phone on heart rate variability parameters in healthy
volunteers.
Use of mobile phones in ICU--why not ban?
A Journal Course: update for nurse anesthetists. Arrhythmia management devices and
electromagnetic interference.
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IMMUNITY
Keywords
–
lymphocytes, immune, lymphocyte, immune system, immunity, blood lymphocytes,
leukocytes, antibodies, immune response, human lymphocytes, antibody, peripheral blood
lymphocytes, immunological, leukocyte, neutrophils, lymphocytic, immune functions,
immunoreactivity, autoimmune, immunization, monocytes, neutrophil, antigens, macrophage,
immune parameters, immune responses, immunocompetent, natural killer cells, spleen
lymphocytes, immunologic, immunoreactive, micronucleated cells, monoclonal antibodies,
spleen cells, splenocytes, T lymphocytes, antibody production, antibody-forming, monoclonal
antibody
Titles
954 MHz microwaves enhance the mutagenic properties of mitomycin C.
Cellphone electromagnetic radiation damages the testicular ultrastructure of male rats].
Electromagnetic fields may act via calcineurin inhibition to suppress immunity, thereby
increasing risk for opportunistic infection: Conceivable mechanisms of action.
Exposure to 1.8 GHz electromagnetic fields affects morphology, DNA-related Raman spectra
and mitochondrial functions in human lympho-monocytes.
Exposure to 900 MHz radiofrequency radiation induces caspase 3 activation in proliferating
human lymphocytes.
Exposure to radiation from single or combined radio frequencies provokes macrophage
dysfunction in the RAW 264.7 cell line.
Gene expression changes in the skin of rats induced by prolonged 35 GHz millimeter-wave
exposure.
Immune responses of a wall lizard to whole-body exposure to radiofrequency electromagnetic
radiation.
Immunobiological effect of bitemporal exposure of rabbits to microwaves].
Immunomorphologic changes in the testes upon exposure to a microwave electromagnetic field].
Immunosuppressive effect of the decimeter-band electromagnetic field].
Impact of radiofrequency radiation on DNA damage and antioxidants in peripheral blood
lymphocytes of humans residing in the vicinity of mobile phone base stations.
Increased levels of numerical chromosome aberrations after in vitro exposure of human
peripheral blood lymphocytes to radiofrequency electromagnetic fields for 72 hours.
Individual responsiveness to induction of micronuclei in human lymphocytes after exposure in
vitro to 1800-MHz microwave radiation.
Influence of 1.8 GHz microwave on DNA damage induced by 4 chemical mutagens].
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Morphological changes in the thyroid and adrenals under the bitemporal action of a UHF
electrical field and decimeter waves (experimental research)].
Mutagenic and morphologic impacts of 1.8GHz radiofrequency radiation on human peripheral
blood lymphocytes (hPBLs) and possible protective role of pre-treatment with Ginkgo biloba
(EGb 761).
Radiofrequency radiation and the immune system. Part 3. In vitro effects on human
immunoglobin and on murine T- and B-lymphocytes.
Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering
factor.
Radioprotective effects of honeybee venom (Apis mellifera) against 915-MHz microwave
radiation-induced DNA damage in wistar rat lymphocytes: in vitro study.
Reaction of the immune system to low-level RF/MW exposures.
Study of low-intensity 2450-MHz microwave exposure enhancing the genotoxic effects of
mitomycin C using micronucleus test and comet assay in vitro.
Studying the synergistic damage effects induced by 1.8 GHz radiofrequency field radiation
(RFR) with four chemical mutagens on human lymphocyte DNA using comet assay in vitro.
Terahertz radiation increases genomic instability in human lymphocytes.
The effect of electromagnetic radiation with extremely high frequency and low intensity on
cytotoxic activity of human natural killer cells].
The effects of 2100-MHz radiofrequency radiation on nasal mucosa and mucociliary clearance in
rats.
The immune response of women with prolonged exposure to electromagnetic fields produced by
radiotelevision broadcasting stations.
Effect of electromagnetic radiation on T-lymphocyte subpopulations and immunoglobulin level
in human blood serum after occupational exposure].
Effect of electromagnetic waves from mobile phone on immune status of male rats: possible
protective role of vitamin D.
Effect of extremely high frequency electromagnetic radiation of low intensity on parameters of
humoral immunity in healthy mice].
Effect of low intensity and very high frequency electromagnetic radiation on occupationally
exposed personnel].
Effect of low-intensity microwave of on mitomycin C-induced genotoxicity in vitro].
Effect of microwave radiation on cellular immunity indices in conditions of chronic exposure].
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Effect of wide-band modulated electromagnetic fields on the workers of high-frequency
telephone exchanges].
Effects of 2000 muW/cm2; electromagnetic radiation on expression of immunoreactive protein
and mRNA of NMDA receptor 2A subunit in rats hippocampus].
Effects of electromagnetic radiation on health and immune function of operators].
Effects of GSM 1800 MHz radiofrequency electromagnetic fields on DNA damage in Chinese
hamster lung cells].
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BIOMARKERS
Keywords
–
apoptosis, oxidative stress, Malondialdehyde, reactive oxygen species, apoptotic,
superoxide dismutase, lipid peroxidation, permeability, catalase, MDA, ROS, ROS), reactive
oxygen species (ROS), Malondialdehyde (MDA), SOD), cell death, glutathione peroxidase,
inflammatory, erythrocytes, oxidative damage, SOD, caspase-3, free radical, nitric oxide, free
radicals, biomarkers, bcl-2, catalase (CAT), inflammation, corticosterone, edema, glutathione
peroxidase (GSH-Px), cytokine, cytokines, alkaline phosphatase, cell apoptosis, protein kinase,
ATP, glutathione (GSH), oxidation, TNF-alpha, Bax, Ca2+, estrogen, ornithine decarboxylase,
red blood cells, intracellular calcium, cell damage, apoptotic cell, hemoglobin, lactate
dehydrogenase, cerebral blood flow, glutamate, hydrogen peroxide, IL-1beta, Purkinje,
serotonin, apoptotic cell death, barrier permeability, carbonyl, hormone levels, ornithine
decarboxylase (ODC), acetylcholinesterase, calcium ion, Calcium ions, endothelial cells, GABA,
MDA levels, ODC, xanthine oxidase, creatinine, intracellular ROS, cholinesterase, lipid
peroxidation levels, pro-inflammatory, protein kinase C, adrenocorticotropic hormone, alanine
aminotransferase, aspartate aminotransferase, caspase 3, caspase-9, catalase activity, glutathione
levels, NF-kappaB, atrophy, nitric oxide synthase, cAMP, acid phosphatase, adenosine
deaminase, adrenocorticotropic hormone (ACTH), blood cell count, blood platelets, Ca++,
adrenaline, C-reactive protein, oxidative damages, Reactive Oxygen Species), vascular
endothelial growth factor
Titles
1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53
dependent Bax mediated testicular apoptosis in mice, Mus musculus.
1950MHz Radio Frequency Electromagnetic Radiation Inhibits Testosterone Secretion of Mouse
Leydig Cells.
2.45 GHz microwave irradiation-induced oxidative stress affects implantation or pregnancy in
mice, Mus musculus.
2.45 GHz Microwave Radiation Impairs Learning and Spatial Memory via Oxidative/Nitrosative
Stress Induced p53-Dependent/Independent Hippocampal Apoptosis: Molecular Basis and
Underlying Mechanism.
2.45 GHz microwave radiation induced oxidative and nitrosative stress mediated testicular
apoptosis: Involvement of a p53 dependent bax-caspase-3 mediated pathway.
2.45-GHz microwave irradiation adversely affects reproductive function in male mouse, Mus
musculus by inducing oxidative and nitrosative stress.
8-oxoG DNA glycosylase-1 inhibition sensitizes Neuro-2a cells to oxidative DNA base damage
induced by 900 MHz radiofrequency electromagnetic radiation.
900 MHz pulse-modulated radiofrequency radiation induces oxidative stress on heart, lung, testis
and liver tissues.
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900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat
endometrium: protection by vitamins E and C.
900-MHz microwave radiation enhances gamma-ray adverse effects on SHG44 cells.
900-MHz microwave radiation promotes oxidation in rat brain.
915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci
in human lymphocytes from hypersensitive and healthy persons.
Activation of VEGF/Flk-1-ERK Pathway Induced Blood-Brain Barrier Injury After Microwave
Exposure.
Acute ocular injuries caused by 60-Ghz millimeter-wave exposure.
Alterations of cognitive function and 5-HT system in rats after long term microwave exposure.
Alternating magnetic field damages the reproductive function of murine testes].
Apoptosis is induced by radiofrequency fields through the caspase-independent mitochondrial
pathway in cortical neurons.
Biochemical and histological studies on adverse effects of mobile phone radiation on rat's brain.
Biochemical and pathological changes in the male rat kidney and bladder following exposure to
continuous 900-MHz electromagnetic field on postnatal days 22-59<sup/>.
Biochemical changes in rat brain exposed to low intensity 9.9 GHz microwave radiation.
Biochemical modifications and neuronal damage in brain of young and adult rats after long-term
exposure to mobile phone radiations.
Bioeffects induced by exposure to microwaves are mitigated by superposition of ELF noise.
Bioeffects of mobile telephony radiation in relation to its intensity or distance from the antenna.
Biological effects from electromagnetic field exposure and public exposure standards.
Biological effects of continuous exposure of embryos and young chickens to electromagnetic
fields emitted by video display units.
Biological oxidation in cells exposed to microwaves in the millimeter range].
Blood-brain barrier permeability and nerve cell damage in rat brain 14 and 28 days after
exposure to microwaves from GSM mobile phones.
Calreticulin attenuated microwave radiation-induced human microvascular endothelial cell injury
through promoting actin acetylation and polymerization.
Cell phone electromagnetic field radiations affect rhizogenesis through impairment of
biochemical processes.
Cellphone electromagnetic radiation damages the testicular ultrastructure of male rats].
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Changes in mitochondrial functioning with electromagnetic radiation of ultra high frequency as
revealed by electron paramagnetic resonance methods.
Changes in serum alkaline phosphatase activity during in vitro exposure to amplitude-modulated
electromagnetic field of ultrahigh frequency (2375 MHz) in guinea pigs].
Comparison of biological effects between continuous and intermittent exposure to GSM-900-
MHz mobile phone radiation: Detection of apoptotic cell-death features.
Cytotoxic and genotoxic effects of high-frequency electromagnetic fields (GSM 1800 MHz) on
immature and mature rats.
DNA Damage of Lymphocytes in Volunteers after 4 hours Use of Mobile Phone.
Effect of 2.45 GHz microwave radiation on the fertility pattern in male mice.
Effect of 3G cell phone exposure with computer controlled 2-D stepper motor on non-thermal
activation of the hsp27/p38MAPK stress pathway in rat brain.
Effect of 835 MHz radiofrequency radiation exposure on calcium binding proteins in the
hippocampus of the mouse brain.
Effect of 900 MHz Electromagnetic Radiation on the Induction of ROS in Human Peripheral
Blood Mononuclear Cells.
Effect of 900 MHz radio frequency radiation on beta amyloid protein, protein carbonyl, and
malondialdehyde in the brain.
Effect of 900 MHz radiofrequency radiation on oxidative stress in rat brain and serum.
Effect of 900-, 1800-, and 2100-MHz radiofrequency radiation on DNA and oxidative stress in
brain.
Effect of 900Mhz electromagnetic fields on energy metabolism in postnatal rat cerebral cortical
neurons].
Effect of 910-MHz electromagnetic field on rat bone marrow.
Effect of American Ginseng Capsule on the liver oxidative injury and the Nrf2 protein
expression in rats exposed by electromagnetic radiation of frequency of cell phone].
Effect of cell phone use on salivary total protein, enzymes and oxidative stress markers in young
adults: a pilot study.
Effect of Exposure to 900 MHz GSM Mobile Phone Radiofrequency Radiation on Estrogen
Receptor Methylation Status in Colon Cells of Male Sprague Dawley Rats.
Effect of Guilingji Capsule on the fertility, liver functions, and serum LDH of male SD rats
exposed by 900 mhz cell phone].
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Effect of low level microwave radiation exposure on cognitive function and oxidative stress in
rats.
Effect of Low-Intensity Microwave Radiation on Monoamine Neurotransmitters and Their Key
Regulating Enzymes in Rat Brain.
Effect of mobile phone electromagnetic emission on characteristics of cerebral blood circulation
and neurohumoral regulations in humans].
Effect of Mobile Phone-Induced Electromagnetic Field on Brain Hemodynamics and Human
Stem Cell Functioning: Possible Mechanistic Link to Cancer Risk and Early Diagnostic Value of
Electronphotonic Imaging.
Effect of radiofrequency electromagnetic field exposure on in vitro models of neurodegenerative
disease.
Effect of Short-term 900 MHz low level electromagnetic radiation exposure on blood serotonin
and glutamate levels.
Effects of 1800 MHz GSM-like exposure on the gonadal function and hematological parameters
of male mice].
Effects of 2.4 GHz radiofrequency radiation emitted from Wi-Fi equipment on microRNA
expression in brain tissue.
Effects of 2.45 GHz microwave exposures on the peroxidation status in Wistar rats.
Effects of 900-MHz electromagnetic field emitted from cellular phone on brain oxidative stress
and some vitamin levels of guinea pigs.
Effects of 900-MHz electromagnetic fields exposure throughout middle/late adolescence on the
kidney morphology and biochemistry of the female rat.
Effects of acute exposure to the radiofrequency fields of cellular phones on plasma lipid peroxide
and antioxidase activities in human erythrocytes.
Effects of cell phone radiation on lipid peroxidation, glutathione and nitric oxide levels in mouse
brain during epileptic seizure.
Electromagnetic fields (1.8 GHz) increase the permeability to sucrose of the blood-brain barrier
in vitro.
Electromagnetic fields (UHF) increase voltage sensitivity of membrane ion channels; possible
indication of cell phone effect on living cells.
Electromagnetic fields at a mobile phone frequency (900 MHz) trigger the onset of general stress
response along with DNA modifications in Eisenia fetida earthworms.
Electromagnetic fields may act via calcineurin inhibition to suppress immunity, thereby
increasing risk for opportunistic infection: Conceivable mechanisms of action.
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Electromagnetic fields, such as those from mobile phones, alter regional cerebral blood flow and
sleep and waking EEG.
Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats.
Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through
activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats.
Electromagnetic radiation 2450 MHz exposure causes cognition deficit with mitochondrial
dysfunction and activation of intrinsic pathway of apoptosis in rats.
Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3
signaling pathways in rats.
Electromagnetic-pulse-induced activation of p38 MAPK pathway and disruption of blood-retinal
barrier.
Enhanced cytotoxic and genotoxic effects of gadolinium following ELF-EMF irradiation in
human lymphocytes.
Enhancement of X-ray Induced Apoptosis by Mobile Phone-Like Radio-Frequency
Electromagnetic Fields in Mouse Spermatocyte-Derived Cells.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Evidence for mobile phone radiation exposure effects on reproductive pattern of male rats: role
of ROS.
Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.
Exposure to 1800 MHz radiofrequency electromagnetic radiation induces oxidative DNA base
damage in a mouse spermatocyte-derived cell line.
Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial
DNA in primary cultured neurons.
Exposure to 1950-MHz TD-SCDMA electromagnetic fields affects the apoptosis of astrocytes
via caspase-3-dependent pathway.
Exposure to 900 MHz radiofrequency radiation induces caspase 3 activation in proliferating
human lymphocytes.
Exposure to a 900 MHz electromagnetic field for 1 hour a day over 30 days does change the
histopathology and biochemistry of the rat testis.
Exposure to cell phone induce oxidative stress in mice preantral follicles during in vitro
cultivation: An experimental study.
Exposure to cell phone radiation up-regulates apoptosis genes in primary cultures of neurons and
astrocytes.
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Exposure to ELF-pulse modulated X band microwaves increases in vitro human astrocytoma cell
proliferation.
Exposure to global system for mobile communication (GSM) cellular phone radiofrequency
alters gene expression, proliferation, and morphology of human skin fibroblasts.
Exposure to GSM 900-MHz mobile radiation impaired inhibitory avoidance memory
consolidation in rat: Involvements of opioidergic and nitrergic systems.
Exposure to pulse-modulated radio frequency electromagnetic fields affects regional cerebral
blood flow.
Exposure to radiation from single or combined radio frequencies provokes macrophage
dysfunction in the RAW 264.7 cell line.
Exposure to radiofrequency radiation induces oxidative stress in duckweed Lemna minor L.
Extremely low-frequency electromagnetic field exposure enhances inflammatory response and
inhibits effect of antioxidant in RAW 264.7 cells.
From the Cover: 2.45-GHz Microwave Radiation Impairs Hippocampal Learning and Spatial
Memory: Involvement of Local Stress Mechanism-Induced Suppression of iGluR/ERK/CREB
Signaling.
GSM 900 MHz microwave radiation affects embryo development of Japanese quails.
GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant
rabbits.
Histological and histochemical study of the protective role of rosemary extract against harmful
effect of cell phone electromagnetic radiation on the parotid glands.
Immunohistopathologic demonstration of deleterious effects on growing rat testes of
radiofrequency waves emitted from conventional Wi-Fi devices.
Immunomorphologic changes in the testes upon exposure to a microwave electromagnetic field].
Impact of electromagnetic radiation emitted by monitors on changes in the cellular membrane
structure and protective antioxidant effect of vitamin A - In vitro study.
In vivo exposure of rats to a weak alternating magnetic field increases ornithine decarboxylase
activity in the mammary gland by a similar extent as the carcinogen DMBA.
Increased ornithine decarboxylase activity in cultured cells exposed to low energy modulated
microwave fields and phorbol ester tumor promoters.
Interference of vitamin E on the brain tissue damage by electromagnetic radiation of cell phone
in pregnant and fetal rats].
Japanese encephalitis virus (JEV): potentiation of lethality in mice by microwave radiation.
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Lipid peroxide damage in retinal ganglion cells induced by microwave].
Long term and excessive use of 900 MHz radiofrequency radiation alter microRNA expression
in brain.
Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis,
mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root
ganglion of rats.
Long-term exposure of 2450MHz electromagnetic radiation induces stress and anxiety like
behavior in rats.
Long-term exposure to electromagnetic radiation from mobile phones and Wi-Fi devices
decreases plasma prolactin, progesterone, and estrogen levels but increases uterine oxidative
stress in pregnant rats and their offspring.
Long-term exposure to microwave radiation provokes cancer growth: evidences from radars and
mobile communication systems.
Low intensity microwave radiation induced oxidative stress, inflammatory response and DNA
damage in rat brain.
Low power density microwave radiation induced early changes in rabbit lens epithelial cells.
Magnetic-field-induced DNA strand breaks in brain cells of the rat.
Maternal exposure to a continuous 900-MHz electromagnetic field provokes neuronal loss and
pathological changes in cerebellum of 32-day-old female rat offspring.
Maternal mobile phone exposure adversely affects the electrophysiological properties of Purkinje
neurons in rat offspring.
Microwave exposure impairs synaptic plasticity in the rat hippocampus and PC12 cells through
over-activation of the NMDA receptor signaling pathway.
Microwave radiation (2.45 GHz)-induced oxidative stress: Whole-body exposure effect on
histopathology of Wistar rats.
Microwave radiation induced oxidative stress, cognitive impairment and inflammation in brain
of Fischer rats.
Microwave radiation induces injury to GC-2spd cells].
Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling.
Mobile phone (1800MHz) radiation impairs female reproduction in mice, Mus musculus,
through stress induced inhibition of ovarian and uterine activity.
Mobile phone affects cerebral blood flow in humans.
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Mobile phone radiation induces reactive oxygen species production and DNA damage in human
spermatozoa in vitro.
Mobile phone radiation-induced free radical damage in the liver is inhibited by the antioxidants
N-acetyl cysteine and epigallocatechin-gallate.
Neural cell apoptosis induced by microwave exposure through mitochondria-dependent caspase-
3 pathway.
Neurodegenerative changes and apoptosis induced by intrauterine and extrauterine exposure of
radiofrequency radiation.
Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in
human endothelial cells: molecular mechanism for cancer- and blood-brain barrier-related
effects.
Overproduction of free radical species in embryonal cells exposed to low intensity
radiofrequency radiation.
Oxidative stress-mediated alterations on sperm parameters in male Wistar rats exposed to 3G
mobile phone radiation.
Oxidative stress-mediated skin damage in an experimental mobile phone model can be prevented
by melatonin.
p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic
field exposure.
Pathological study of testicular injury induced by high power microwave radiation in rats].
Permeability of the blood-brain barrier induced by 915 MHz electromagnetic radiation,
continuous wave and modulated at 8, 16, 50, and 200 Hz.
Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout
adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-
day-old Sprague Dawley male rats.
Protective effect of Liuweidihuang Pills against cellphone electromagnetic radiation-induced
histomorphological abnormality, oxidative injury, and cell apoptosis in rat testes].
Protective effects of beta-glucan against oxidative injury induced by 2.45-GHz electromagnetic
radiation in the skin tissue of rats.
Protective effects of Genistein on human renal tubular epithelial cells damage of microwave
radiation].
Protective effects of luteolin on rat testis following exposure to 900 MHz electromagnetic field.
Pulse modulated 900 MHz radiation induces hypothyroidism and apoptosis in thyroid cells: a
light, electron microscopy and immunohistochemical study.
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Pulsed electromagnetic fields accelerate apoptotic rate in osteoclasts.
Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling
pathway in mouse spermatogenic cells in vitro and thus may affect male fertility.
Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones
induces oxidative stress and reduces sperm motility in rats.
Radiofrequency electromagnetic radiation from cell phone causes defective testicular function in
male Wistar rats.
Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular
germ cells in swiss albino mice.
Radiofrequency radiation emitted from Wi-Fi (2.4 GHz) causes impaired insulin secretion and
increased oxidative stress in rat pancreatic islets.
Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering
factor.
Reactive oxygen species formation and apoptosis in human peripheral blood mononuclear cell
induced by 900 MHz mobile phone radiation.
Reactive oxygen species levels and DNA fragmentation on astrocytes in primary culture after
acute exposure to low intensity microwave electromagnetic field.
Reduction of phosphorylated synapsin I (ser-553) leads to spatial memory impairment by
attenuating GABA release after microwave exposure in Wistar rats.
Role of Mitochondria in the Oxidative Stress Induced by Electromagnetic Fields: Focus on
Reproductive Systems.
Selenium reduces mobile phone (900 MHz)-induced oxidative stress, mitochondrial function,
and apoptosis in breast cancer cells.
Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the
HEK293 cells.
Ten gigahertz microwave radiation impairs spatial memory, enzymes activity, and
histopathology of developing mice brain.
Testicular apoptosis and histopathological changes induced by a 2.45 GHz electromagnetic field.
The antioxidant effect of Green Tea Mega EGCG against electromagnetic radiation-induced
oxidative stress in the hippocampus and striatum of rats.
Ultrastructural change of rabbit lens epithelial cells induced by low power level microwave
radiation].
Vitamin C protects rat cerebellum and encephalon from oxidative stress following exposure to
radiofrequency wave generated by a BTS antenna model.
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Zinc supplementation ameliorates electromagnetic field-induced lipid peroxidation in the rat
brain.
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SENSORY DISORDERS
Keywords
–
auditory, acoustic, ear, hypersensitivity, EHS, electromagnetic hypersensitivity,
otoacoustic, vestibular, hypersensitive, cataract, cochlea, auditory system, inner ear, lens
epithelial, corneal, tinnitus, vision, lenses, otoacoustic emissions, hearing loss, otoacoustic
emission, epidermis, rabbit lens, dermatitis, auditory stimuli, cataractogenic, Auditory brainstem
response (ABR), auditory evoked, electrohypersensitive, electrosensitivity, vestibular system,
cochlear implants, dermatological, hearing function, hearing thresholds, pain sensitivity, pain
threshold, skin complaints
Titles
A quantitative study on early changes in rabbit lens capsule epithelium induced by low power
density microwave radiation].
A study on the effect of prolonged mobile phone use on pure tone audiometry thresholds of
medical students of Sikkim.
Acceleration of the development of benzopyrene-induced skin cancer in mice by microwave
radiation.
Alteration of glycine receptor immunoreactivity in the auditory brainstem of mice following
three months of exposure to radiofrequency radiation at SAR 4.0 W/kg.
Assessment of intermittent UMTS electromagnetic field effects on blood circulation in the
human auditory region using a near-infrared system.
Association between vestibular schwannomas and mobile phone use.
Audiologic disturbances in long-term mobile phone users.
Blocking 1800 MHz mobile phone radiation-induced reactive oxygen species production and
DNA damage in lens epithelial cells by noise magnetic fields].
Cell phone use and acoustic neuroma: the need for standardized questionnaires and access to
industry data.
Changes in gap junctional intercellular communication in rabbits lens epithelial cells induced by
low power density microwave radiation.
Cognitive and neurobiological alterations in electromagnetic hypersensitive patients: results of a
case-control study.
Contribution of physical factors to the complex anthropogenic load in an industrial town].
Decrease in the intensity of the cellular immune response and nonspecific inflammation upon
exposure to extremely high frequency electromagnetic radiation].
DNA damage and repair induced by acute exposure of microwave from mobile phone on
cultured human lens epithelial cells].
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EEG Changes Due to Experimentally Induced 3G Mobile Phone Radiation.
Effect Of Electromagnetic Waves Emitted From Mobile Phone On Brain Stem Auditory Evoked
Potential In Adult Males.
Effect of low-intensity microwave radiation on proliferation of cultured epithelial cells of rabbit
lens].
Effect of superposed electromagnetic noise on DNA damage of lens epithelial cells induced by
microwave radiation.
Effect of wide-band modulated electromagnetic fields on the workers of high-frequency
telephone exchanges].
Effects of 2.45-GHz microwaves on primate corneal endothelium.
Effects of different dose microwave radiation on protein components of cultured rabbit lens].
Effects of exposure to 2100MHz GSM-like radiofrequency electromagnetic field on auditory
system of rats.
Effects of GSM-like radiofrequency on distortion product otoacoustic emissions in pregnant
adult rabbits.
Effects of intensive and moderate cellular phone use on hearing function.
Effects of low level electromagnetic field exposure at 2.45 GHz on rat cornea.
Effects of microwave radiation on the eye: the occupational health perspective.
Effects of mobile phones on oxidant/antioxidant balance in cornea and lens of rats.
Effects of pulsed electromagnetic fields on cognitive processes - a pilot study on pulsed field
interference with cognitive regeneration.
Electromagnetic field induced biological effects in humans.
Electromagnetic hypersensitivity--an increasing challenge to the medical profession.
Experimental studies on the influence of millimeter radiation on light transmission through the
lens].
Increased sensitivity of the non-human primate eye to microwave radiation following ophthalmic
drug pretreatment.
Intraoperative observation of changes in cochlear nerve action potentials during exposure to
electromagnetic fields generated by mobile phones.
Is human saliva an indicator of the adverse health effects of using mobile phones?
Low power density microwave radiation induced early changes in rabbit lens epithelial cells.
Mobile phone induced sensorineural hearing loss.
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Mobile phone related-hazards and subjective hearing and vision symptoms in the Saudi
population.
Non-thermal electromagnetic radiation damage to lens epithelium.
Occupational safety: effects of workplace radiofrequencies on hearing function.
Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple
chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder.
Replication of heart rate variability provocation study with 2.4-GHz cordless phone confirms
original findings.
Single-strand DNA breaks in human hair root cells exposed to mobile phone radiation.
Some ocular symptoms and sensations experienced by long term users of mobile phones.
Some ocular symptoms experienced by users of mobile phones.
The acute auditory effects of exposure for 60 minutes to mobile`s electromagnetic field.
The effect of radiofrequency radiation generated by a Global System for Mobile
Communications source on cochlear development in a rat model.
The effect of very low dose pulsed magnetic waves on cochlea.
The effects of pulsed low-level EM fields on memory processes].
The electromagnetic fields of cellular phones and the health of children and of teenagers (the
situation requiring to take an urgent measure)].
Tinnitus and cell phones: the role of electromagnetic radiofrequency radiation.
Tinnitus and mobile phone use.
Ultrastructural change of rabbit lens epithelial cells induced by low power level microwave
radiation].
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DISCOMFORT SYMPTOMS
Keywords
–
depression, anxiety, headache, headaches, dizziness, depressed, depressive, vertigo,
cataracts, behavioral effects, nausea, headache dizziness, low back pain, behavioural effects
Titles
A study on the biological effects of exposure mobile-phone frequency EMF].
A survey study on some neurological symptoms and sensations experienced by long term users
of mobile phones.
Adverse effects of excessive mobile phone use.
Anxiogenic effect of chronic exposure to extremely low frequency magnetic field in adult rats.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep
disturbance in Saudi population.
Chronic exposure to ELF fields may induce depression.
Clinical features of headache associated with mobile phone use: a cross-sectional study in
university students.
Effect of electromagnetic radiations from mobile phone base stations on general health and
salivary function.
Effect of high-frequency EMF on public health and its neuro-chemical investigations].
Effect of low intensity and very high frequency electromagnetic radiation on occupationally
exposed personnel].
Effects of electromagnetic radiation from cellular telephone handsets on symptoms of
neurasthenia].
Effects of electromagnetic radiation on health and immune function of operators].
Effects of GSM-Frequency Electromagnetic Radiation on Some Physiological and Biochemical
Parameters in Rats.
Effects of low intensity radiofrequency electromagnetic fields on electrical activity in rat
hippocampal slices.
Effects of microwave radiation on the eye: the occupational health perspective.
Effects of mobile phone radiation (900 MHz radiofrequency) on structure and functions of rat
brain.
Exposure to mobile phone electromagnetic field radiation, ringtone and vibration affects anxiety-
like behaviour and oxidative stress biomarkers in albino wistar rats.
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Exposure to radio-frequency electromagnetic waves alters acetylcholinesterase gene expression,
exploratory and motor coordination-linked behaviour in male rats.
Long-term exposure of 2450MHz electromagnetic radiation induces stress and anxiety like
behavior in rats.
Magnetic fields of transmission lines and depression.
Microwave radiation and chlordiazepoxide: synergistic effects on fixed-interval behavior.
Microwave sickness: a reappraisal.
Mobile phone use and health symptoms in children.
Mobile Phone Use and The Risk of Headache: A Systematic Review and Meta-analysis of Cross-
sectional Studies.
Mobile phone use, school electromagnetic field levels and related symptoms: a cross-sectional
survey among 2150 high school students in Izmir.
Motor activity of rabbits in conditions of chronic low-intensity pulse microwave irradiation].
MRI magnetic field stimulates rotational sensors of the brain.
Neurobehavioral effects among inhabitants around mobile phone base stations.
Postnatal development and behavior effects of in-utero exposure of rats to radiofrequency waves
emitted from conventional WiFi devices.
Preliminary report: symptoms associated with mobile phone use.
Prevalence of headache among handheld cellular telephone users in Singapore: a community
study.
Radiofrequency electromagnetic radiation-induced behavioral changes and their possible basis.
Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6:
microwaves act through voltage-gated calcium channel activation to induce biological impacts at
non-thermal levels, supporting a paradigm shift for microwave/lower frequency electromagnetic
field action.
Self-reported symptoms associated with exposure to electromagnetic fields: a questionnaire
study.
Self-reporting of symptom development from exposure to radiofrequency fields of wireless
smart meters in victoria, australia: a case series.
Subjective complaints of people living near mobile phone base stations in Poland.
Subjective symptoms, sleeping problems, and cognitive performance in subjects living near
mobile phone base stations.
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CONGENITAL ABNORMALITIES
Keywords
–
malformations, teratogenic, congenital, congenital malformations, teratogenicity,
teratogens, teratologic, cleft palate, congenital anomalies, malformed, teratological
Titles
Are microwaves a co-teratogen? Experimental model concept and its verification].
Effect of early pregnancy electromagnetic field exposure on embryo growth ceasing].
Effects of continuous low-level exposure to radiofrequency radiation on intrauterine
development in rats.
Effects of GSM-like radiofrequency irradiation during the oogenesis and spermiogenesis of
Xenopus laevis.
Effects of MR exposure at 1.5 T on early embryonic development of the chick.
First cell cycles of sea urchin Paracentrotus lividus are dramatically impaired by exposure to
extremely low-frequency electromagnetic field.
Lethal and teratogenic effects of long-term low-intensity radio frequency radiation at 428 MHz
on developing chick embryo.
Microwave radiation enhances teratogenic effect of cytosine arabinoside in mice.
Morinda officialis how extract improves microwave-induced reproductive impairment in male
rats].
MRI effects on craniofacial size and crown-rump length in C57BL/6J mice in 1.5T fields.
Pathological study of testicular injury induced by high power microwave radiation in rats].
Pulsed magnetic field from video display terminals enhances teratogenic effects of cytosine
arabinoside in mice.
Reproductive hazards among workers at high voltage substations.
Studies of the teratogenic potential of exposure of rats to 6000-MHz microwave radiation. I.
Morphologic analysis at term.
Studies of the teratogenic potential of exposure of rats to 6000-MHz microwave radiation. II.
Postnatal psychophysiologic evaluations.
Teratogenic effects of sinusoidal extremely low frequency electromagnetic fields on morphology
of 24 hr chick embryos.
Teratogenic, biochemical, and histological studies with mice prenatally exposed to 2.45-GHz
microwave radiation.
VDT pulse magnetic field enhances teratogenic effect of ara-c in mice.
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CIRCADIAN RHYTHYM AND MELATONIN
Keywords
–
melatonin, sleep, circadian, melatonin production, sleep disturbances, insomnia,
melatonin levels, melatonin secretion, sleep disorders, sleep EEG, poor sleep, pineal function
Titles
900-MHz microwave radiation promotes oxidation in rat brain.
A 50-Hz electromagnetic field impairs sleep.
Association between Excessive Use of Mobile Phone and Insomnia and Depression among
Japanese Adolescents.
Association between overuse of mobile phones on quality of sleep and general health among
occupational health and safety students.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep
disturbance in Saudi population.
Bedtime mobile phone use and sleep in adults.
Biological effects of continuous exposure of embryos and young chickens to electromagnetic
fields emitted by video display units.
Breast cancer and electric power.
Cellular phones: are they detrimental?
Chronic exposure to ELF fields may induce depression.
Chronotoxicity of 1800 MHz microwave radiation on sex hormones and spermatogenesis in male
mice].
Circadian rhythmicity of antioxidant markers in rats exposed to 1.8 GHz radiofrequency fields.
Direct suppressive effects of weak magnetic fields (50 Hz and 16 2/3 Hz) on melatonin synthesis
in the pineal gland of Djungarian hamsters (Phodopus sungorus).
Do magnetic fields cause increased risk of childhood leukemia via melatonin disruption?
Effect of electromagnetic radiations from mobile phone base stations on general health and
salivary function.
Effect of low intensity and very high frequency electromagnetic radiation on occupationally
exposed personnel].
Effects of 1800-MHz radiofrequency fields on circadian rhythm of plasma melatonin and
testosterone in male rats.
Effects of electromagnetic fields exposure on plasma hormonal and inflammatory pathway
biomarkers in male workers of a power plant.
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Effects of melatonin on Wi-Fi-induced oxidative stress in lens of rats.
Effects of Mobile Phones on Children's and Adolescents' Health: A Commentary.
Effects of prenatal 900 MHz electromagnetic field exposures on the histology of rat kidney.
EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
Exposure to electromagnetic fields and suicide among electric utility workers: a nested case-
control study.
Health effects of living near mobile phone base transceiver station (BTS) antennae: a report from
Isfahan, Iran.
Individual differences in the effects of mobile phone exposure on human sleep: rethinking the
problem.
Investigation on the health of people living near mobile telephone relay stations: I/Incidence
according to distance and sex].
Melatonin and a spin-trap compound block radiofrequency electromagnetic radiation-induced
DNA strand breaks in rat brain cells.
Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA
damage and cell cycle arrest in germ cells of male Swiss albino mice.
Melatonin modulates 900 Mhz microwave-induced lipid peroxidation changes in rat brain.
Melatonin protects rat thymus against oxidative stress caused by exposure to microwaves and
modulates proliferation/apoptosis of thymocytes.
Melatonin reduces oxidative stress induced by chronic exposure of microwave radiation from
mobile phones in rat brain.
Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric
effects including depression.
Mitochondrial DNA damage and oxidative damage in HL-60 cells exposed to 900MHz
radiofrequency fields.
Mobile phone radiation induces mode-dependent DNA damage in a mouse spermatocyte-derived
cell line: a protective role of melatonin.
Mobile phone use, school electromagnetic field levels and related symptoms: a cross-sectional
survey among 2150 high school students in Izmir.
Mobile phones: time to rethink and limit usage.
Modulation of wireless (2.45 GHz)-induced oxidative toxicity in laryngotracheal mucosa of rat
by melatonin.
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Neurobehavioral effects among inhabitants around mobile phone base stations.
Neuroprotective effects of melatonin and omega-3 on hippocampal cells prenatally exposed to
900 MHz electromagnetic fields.
Non-thermal biomarkers of exposure to radiofrequency/microwave radiation.
Non-thermal continuous and modulated electromagnetic radiation fields effects on sleep EEG of
rats.
Oxidative stress-mediated skin damage in an experimental mobile phone model can be prevented
by melatonin.
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CHRONIC CONDITIONS
Keywords - metabolism, metabolic, glucose, endocrine, cholesterol, Diabetes, calcium
homeostasis, glucose levels, homeostatic, metabolic activity, metabolic heat production, Diabetes
Mellitus, diabetic, glucose metabolism, obesity
Titles
Assessment of biological changes of continuous whole-body exposure to static magnetic field
and extremely low frequency electromagnetic fields in mice.
Association of exposure to radio-frequency electromagnetic field radiation (RF-EMFR)
generated by mobile phone base stations with glycated hemoglobin (HbA1c) and risk of Type 2
Diabetes Mellitus.
Biological accounts emerging from some kinds of electromagnetic waves in the environment.
Calreticulin attenuated microwave radiation-induced human microvascular endothelial cell injury
through promoting actin acetylation and polymerization.
Cardiovascular risk in operators under radiofrequency electromagnetic radiation.
Cell oxidation-reduction imbalance after modulated radiofrequency radiation.
Changes in mitochondrial functioning with electromagnetic radiation of ultra high frequency as
revealed by electron paramagnetic resonance methods.
Common behaviors alterations after extremely low-frequency electromagnetic field exposure in
rat animal model.
Dirty electricity, chronic stress, neurotransmitters and disease.
Disordered redox metabolism of brain cells in rats exposed to low doses of ionizing radiation or
UHF electromagnetic radiation.
Disturbances of glucose tolerance in workers exposed to electromagnetic radiation].
Dynamics of metabolic parameters in rats during repeated exposure to modulated low-intensity
UHF radiation.
Effect of a 20 kHz sawtooth magnetic field exposure on the estrous cycle in mice.
Effect of coherent extremely high-frequency and low-intensity electromagnetic radiation on the
activity of membrane systems in Escherichia coli].
Effect of discontinuous short-wave electromagnetic field irradiation on the state of the endocrine
glands].
Effect of Exposure to 900 MHz GSM Mobile Phone Radiofrequency Radiation on Estrogen
Receptor Methylation Status in Colon Cells of Male Sprague Dawley Rats.
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Effects of continuous low-level exposure to radiofrequency radiation on intrauterine
development in rats.
Effects of continuous-wave, pulsed, and sinusoidal-amplitude-modulated microwaves on brain
energy metabolism.
Effects of electromagnetic fields on the immune systems of occupationally exposed humans and
mice.
Effects of electromagnetic radiation exposure on bone mineral density, thyroid, and oxidative
stress index in electrical workers.
Effects of exposure to electromagnetic field radiation (EMFR) generated by activated mobile
phones on fasting blood glucose.
Effects of extremely low frequency electromagnetic field and its combination with lead on the
antioxidant system in mouse].
Effects of microwave radiation on the eye: the occupational health perspective.
Effects of RF-EMF Exposure from GSM Mobile Phones on Proliferation Rate of Human
Adipose-derived Stem Cells: An In-vitro Study.
Endocrine mechanism of placental circulatory disturbances induced by microwave in pregnant
rats].
Evidence that dirty electricity is causing the worldwide epidemics of obesity and diabetes.
Exposure to GSM 900 MHz electromagnetic fields affects cerebral cytochrome c oxidase
activity.
Functional activity and metabolism of blood neutrophils exposed to low-intensity microwaves].
Glucose administration attenuates spatial memory deficits induced by chronic low-power-density
microwave exposure.
GSM mobile phone radiation suppresses brain glucose metabolism.
High-frequency electromagnetic field exposure on reproductive and endocrine functions of
female workers].
Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice
to GSM 1800 MHz mobile phone radiation: An exploratory study.
Long-term exposure to microwave radiation provokes cancer growth: evidences from radars and
mobile communication systems.
Metabolic changes in cells under electromagnetic radiation of mobile communication systems].
Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer's
disease.
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Pulse modulated 900 MHz radiation induces hypothyroidism and apoptosis in thyroid cells: a
light, electron microscopy and immunohistochemical study.
Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones
induces oxidative stress and reduces sperm motility in rats.
Radiofrequency radiation emitted from Wi-Fi (2.4 GHz) causes impaired insulin secretion and
increased oxidative stress in rat pancreatic islets.
Towards 5G communication systems: Are there health implications?
Wi-Fi is an important threat to human health.
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A2-C. Citing Papers
Essentially all the papers referenced in A2-B show adverse effects. The papers that cite
these adverse effects papers (and some associated papers) were retrieved, and were filtered by
visual inspection. The references to these citing papers that also show adverse effects from
wireless radiation are presented in the following. The combination of relevant papers in A2-B
and their citing papers in A2-C constitutes a representative sample of the wireless radiation
adverse effects literature.
The actual literature is far larger. The query used to retrieve relevant papers for A2-B was
quite simple, and mainly the citing papers component of the citation network (citing papers, cited
papers, related records, etc) was used to expand the relevant papers.
CITING PAPERS
Abdi S, Dorranian D, Naderi GA, Razavi AE. Changes in physico-chemical characteristics of
human low density lipoprotein nano-particles by electromagnetic field exposure. Studia
Universitatis Babes-Bolyai Chemia. 2016;61(1):185-97.
Abedalqader F, Alhuarrat MA, Ibrahim G, Taha F, Al Tamimi A, Shukur M, et al. The
correlation between smart device usage & sleep quality among UAE residents. Sleep Medicine.
2019;63:18-23.
Aberumand M, Mansouri E, Pourmotahari F, Mirlohi M, Abdoli Z. Biochemical and
Histological Effects of Mobile Phone Radiation on Enzymes and Tissues of Mice. Research
Journal of Pharmaceutical Biological and Chemical Sciences. 2016;7(5):1962-71.
Abu-Elsaoud PAM, Qari SH. Influence of Microwave Irradiations on Germination, Seedling
Growth and Electrolyte Leakage of Barley (Hordeum vulgare L.). Catrina-the International
Journal of Environmental Sciences. 2017;16(1):11-24.
Acharya R, Kumar D, Mathur G. Study of Electromagnetic Radiation Effects on Human Body
and Reduction Techniques. In: Janyani V, Tiwari M, Singh G, Minzioni P, editors. Optical and
Wireless Technologies, Owt 2017. Lecture Notes in Electrical Engineering. 4722018. p. 497-
505.
Adebayo EA, Adeeyo AO, Ogundiran MA, Olabisi O. Bio-physical effects of radiofrequency
electromagnetic radiation (RF-EMR) on blood parameters, spermatozoa, liver, kidney and heart
of albino rats. Journal of King Saud University Science. 2019;31(4):813-21.
Agrawal Y, Gupta V. To treat the patient and not the telemetry: Electric toothbrush causing
hospital admission. International Journal of Cardiology. 2016;221:112-3.
Ahamed VIT, Karthick NG, Joseph PK. Effect of mobile phone radiation on heart rate
variability. Computers in Biology and Medicine. 2008;38(6):709-12.
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Ahmadi SS, Khaki AA, Alihemmati A, Rajabzadeh A, Giasi GS. The Effects of 50 Hz
Electromagnetic Fields Induction of Apoptosis in Rat Follicles. Crescent Journal of Medical and
Biological Sciences. 2017;4(2):64-8.
Akbal A, Kiran Y, Sahin A, Turgut-Balik D, Balik HH. Effects of Electromagnetic Waves
Emitted by Mobile Phones on Germination, Root Growth, and Root Tip Cell Mitotic Division of
Lens culinaris Medik. Polish Journal of Environmental Studies. 2012;21(1):23-9.
Akefe IO, Yusuf IL, Adegoke VA. C-glycosyl flavonoid orientin alleviates learning and memory
impairment by radiofrequency electromagnetic radiation in mice via improving antioxidant
defence mechanism. Asian Pacific Journal of Tropical Biomedicine. 2019;9(12):518-23.
Al Taweel YA, Kamel AE, Abd El Ghany AAM, Nageeb RS, Bolbol SA, Elsayed MIR.
Prevalence of risk factors including cell phone use among patients with brain tumors. Egyptian
Journal of Neurology Psychiatry and Neurosurgery. 2016;53(2):111-8.
Al-Bayyari N. The effect of cell phone usage on semen quality and fertility among Jordanian
males. Middle East Fertility Society Journal. 2017;22(3):178-82.
Al-Damegh MA. Rat testicular impairment induced by electromagnetic radiation from a
conventional cellular telephone and the protective effects of the antioxidants vitamins C and E.
Clinics. 2012;67(7):785-92.
Al-Quzwini OF, Al-Taee HA, Al-Shaikh SF. Male fertility and its association with occupational
and mobile phone towers hazards: An analytic study. Middle East Fertility Society Journal.
2016;21(4):236-40.
Al-Serori H, Ferk F, Kundi M, Bileck A, Gerner C, Misik M, et al. Mobile phone specific
electromagnetic fields induce transient DNA damage and nucleotide excision repair in serum-
deprived human glioblastoma cells. Plos One. 2018;13(4).
Al-Serori H, Kundi M, Ferk F, Misik M, Nersesyan A, Murbach M, et al. Evaluation of the
potential of mobile phone specific electromagnetic fields (UMTS) to produce micronuclei in
human glioblastoma cell lines. Toxicology in Vitro. 2017;40:264-71.
Alchalabi ASH. Gene expression of certain heat shock proteins and antioxidant enzymes in
microwave exposed rats. Gene Reports. 2019;16.
Alexiou GA, Sioka C. Mobile phone use and risk for intracranial tumors. Journal of Negative
Results in Biomedicine. 2015;14.
Ali AH, Salman MD, Saleh R, Fayadh EN, abd Al-Hameed S, Falah H, et al. The Effect of the
Electronic Devices on Children. International Workshop in Physics Applications. Journal of
Physics Conference Series. 11782019.
Aliyari H, Hosseinian SH, Menhaj MB, Sahraei H. Analysis of the Effects of High-Voltage
Transmission Line on Human Stress and Attention Through Electroencephalography (EEG).
Iranian Journal of Science and Technology-Transactions of Electrical Engineering. 2019;43:211-
8.
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Aliyari H, Hosseinian SH, Sahraei H, Menhaj MB. Effect of proximity to high-voltage fields:
results of the neural network model and experimental model with macaques. International
Journal of Environmental Science and Technology. 2019;16(8):4315-26.
Alkis ME, Akdag MZ, Dasdag S, Yegin K, Akpolat V. Single-strand DNA breaks and oxidative
changes in rat testes exposed to radiofrequency radiation emitted from cellular phones.
Biotechnology & Biotechnological Equipment. 2019;33(1):1733-40.
Altun G, Deniz OG, Yurt KK, Davis D, Kaplan S. Effects of mobile phone exposure on
metabolomics in the male and female reproductive systems. Environmental Research.
2018;167:700-7.
An K, Wang QL, Zhang Y, Guo DM, Cui X. The preventative effects of zinc and vitamin E
supplementation on cellular phone radiation-induced oxidative stress in brain tissues of rats and
their fetuses. Trace Elements and Electrolytes. 2015;32(3):119-25.
Asgari A, Shoja E, Barzegar S. The Effect of Electromagnetic Waves and Workplace Lighting
on Job Stress in Employees of Power Distribution Company. Pakistan Journal of Medical &
Health Sciences. 2019;13(3):889-92.
Asl JF, Larijani B, Zakerkish M, Rahim F, Shirbandi K, Akbari R. The possible global hazard of
cell phone radiation on thyroid cells and hormones: a systematic review of evidences.
Environmental Science and Pollution Research. 2019;26(18):18017-31.
Aslan A, Ikinci A, Bas O, Sonmez OF, Kaya H, Odaci E. Long-term exposure to a continuous
900 MHz electromagnetic field disrupts cerebellar morphology in young adult male rats.
Biotechnic & Histochemistry. 2017;92(5):324-30.
Aslankoc R, Gumral N, Saygin M, Senol N, Asci H, Cankara FN, et al. The impact of electric
fields on testis physiopathology, sperm parameters and DNA integrityThe role of resveratrol.
Andrologia. 2018;50(4).
Auger N, Bilodeau-Bertrand M, Marcoux S, Kosatsky T. Residential exposure to
electromagnetic fields during pregnancy and risk of child cancer: A longitudinal cohort study.
Environmental Research. 2019;176.
Azimipour F, Zavareh S, Lashkarbolouki T. The Effect of Radiation Emitted by Cell Phone on
The Gelatinolytic Activity of Matrix Metalloproteinase-2 and-9 of Mouse Pre-Antral Follicles
during In Vitro Culture. Cell Journal. 2020;22(1):1-8.
Azimzadeh M, Jelodar G. Alteration of testicular regulatory and functional molecules following
long-time exposure to 900 MHz RFW emitted from BTS. Andrologia. 2019;51(9).
Azimzadeh M, Jelodar GA, Namazi F, Soleimani F. Exposure to radiofrequency wave (RFW)
generated by a base transceiver stations (BTS) antenna model affects learning and memory in
female more than male rats. International Journal of Radiation Research. 2018;16(4):487-91.
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Azizi SMY, Sarghein SH, Majd A, Peyvandi M. The effects of the electromagnetic fields on the
biochemical components, enzymatic and non-enzymatic antioxidant systems of tea Camellia
sinensis L. Physiology and Molecular Biology of Plants. 2019;25(6):1445-56.
Bahar L, Eralp A, Rumevleklioglu Y, Erturk SE, Yuncu M. THE EFFECT OF
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Baiden P, Tadeo SK, Peters KE. The association between excessive screen-time behaviors and
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Balik MS, Tumkaya L, Sehitoglu I, Kalkan Y, Yilmaz A, Balik G, et al. Effects of 900 MHz
electromagnetic field on prenatal locomotor development in rats. International Journal of Clinical
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Balmori A. Anthropogenic radiofrequency electromagnetic fields as an emerging threat to
wildlife orientation. Science of the Total Environment. 2015;518:58-60.
Balmori A. Radiotelemetry and wildlife: Highlighting a gap in the knowledge on radiofrequency
radiation effects. Science of the Total Environment. 2016;543:662-9.
Bamdad K, Adel Z, Esmaeili M. Complications of nonionizing radiofrequency on divided
attention. Journal of Cellular Biochemistry. 2019;120(6):10572-5.
Bamikole AO, Olukayode OA, Obajuluwa T, Pius O, Ibidun OO, Adewale FO, et al. Exposure to
a 2.5 GHz Non-ionizing Electromagnetic Field Alters Hematological Profiles, Biochemical
Parameters, and Induces Oxidative Stress in Male Albino Rats. Biomedical and Environmental
Sciences. 2019;32(11):860-3.
Bandara P. Mobile phone use and the brain cancer incidence rate in Australia. Cancer
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Bandara P, Carpenter DO. Causes of cancer: Perceptions vs. the scientific evidence. European
Journal of Cancer. 2020;124:214-6.
Bandara P, Weller S. Cardiovascular disease: Time to identify emerging environmental risk
factors. European Journal of Preventive Cardiology. 2017;24(17):1819-23.
Banerjee S, Singh NN, Sreedhar G, Mukherjee S. Analysis of the Genotoxic Effects of Mobile
Phone Radiation using Buccal Micronucleus Assay: A Comparative Evaluation. Journal of
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Barcal J, Stopka P, Krizova J, Vrba J, Vozeh F. High-frequency electromagnetic radiation and
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Barthelemy A, Mouchard A, Villegier AS, Ieee. Glial markers and emotional memory in rats
following cerebral radiofrequency exposures2016.
Bartos P, Netusil R, Slaby P, Dolezel D, Ritz T, Vacha M. Weak radiofrequency fields affect the
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Bas O, Sonmez OF, Aslan A, Ikinci A, Hanci H, Yildirim M, et al. Pyramidal Cell Loss in the
Cornu Ammonis of 32-day-old Female Rats Following Exposure to a 900 Megahertz
Electromagnetic Field During Prenatal Days 13-21. Neuroquantology. 2013;11(4):591-9.
Bayat M, Hemati S, Soleimani-Estyar R, Shahin-Jafari A. Effect of long-term exposure of mice
to 900 MHz GSM radiation on experimental cutaneous candidiasis. Saudi Journal of Biological
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Bedir R, Tumkaya L, Mercantepe T, Yilmaz A. Pathological Findings Observed in the Kidneys
of Postnatal Male Rats Exposed to the 2100 MHz Electromagnetic Field. Archives of Medical
Research. 2018;49(7):432-40.
Bektas H, Bektas MS, Dasdag S. Effects of mobile phone exposure on biochemical parameters
of cord blood: A preliminary study. Electromagnetic Biology and Medicine. 2018;37(4):184-91.
Bellieni CV, Nardi V, Buonocore G, Di Fabio S, Pinto I, Verrotti A. Electromagnetic fields in
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Belyaev I, Dean A, Eger H, Hubmann G, Jandrisovits R, Johansson O, et al. EUROPAEM EMF
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Bhatia S, Vashisth S, Salhan A. Cellular Radiations Effect on Human Health. In: Satapathy SC,
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Bhattacharya D, Gangopadhyay S, Bhakta MS. MOBILE PHONE RADIATION EXPOSURE
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Biagi PF, Boffola S, Stefanelli R, Schiavulli L, Ligonzo T, Casamassima G, et al.
Morphometrical and Morphological Alterations of Human Leukocytes Exposed to 1.8 GHz
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Borovkova M, Serebriakova M, Fedorov V, Sedykh E, Vaks V, Lichutin A, et al. Investigation
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Bortkiewicz A. MOBILE PHONE USE AND RISK FOR INTRACRANIAL TUMORS AND
SALIVARY GLAND TUMORSA META-ANALYSIS (vol 30, pg 27, 2017). International
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Cetkin M, Kizilkan N, Demirel C, Bozdag Z, Erkilic S, Erbagci H. Quantitative changes in
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Chandel S, Kaur S, Issa M, Singh HP, Batish DR, Kohli RK. Appraisal of immediate and late
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Cornacchione M, Pellegrini M, Fassina L, Mognaschi ME, Di Siena S, Gimmelli R, et al. beta-
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Ding Z, Li JT, Li F, Mephryar MM, Wu SC, Zhang C, et al. The Protection of Vitamin C and
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Djindjic B, Dzopalic T, Dunjic M, Krstic D, Radovanovic Z, Milenkovic J, et al. Effects of
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Dogan MS, Yavas MC, Gunay A, Yavuz I, Deveci E, Akkus Z, et al. The protective effect of
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Appendix 3
–
Factor Analysis of Adverse EMF Effects Database
A3-A. Factor Themes
A query to retrieve Medline records showing adverse health effects of wireless radiation
was generated. The query was entered into the Medline search engine, and ~15,000 records were
retrieved. Filtering was applied to the retrieval to remove records not associated with adverse
health effects of wireless radiation, and 5311 records remained. These records did not receive
the further filtering as the database in Appendix 2.
Thousands of the highest frequency MeSH terms were read, and those strongly related to
adverse health effects of wireless radiation were selected. A factor analysis was performed using
these terms, and a 21-factor taxonomy was generated.
The following table (A3-1) shows the categories/factors in the taxonomy, and the highest
weighted (most influential in determining the factor theme) MeSH Headings associated with
each category/factor. For each category, the records associated with the highest weighted MeSH
Headings identified were highlighted, and the titles of those records were extracted. Following
the table, each category and associated record titles are shown in order to display the breadth of
coverage of the category. The categories in
Table A3-1
are hyperlinked to their respective titles.
Because of the limitations on record filtering, most of the records show adverse health effects,
but not all do. Some of the records go beyond the FCC exposure limits, and some address
frequencies much lower than microwave. There is some overlap among factors, since some
MeSH Headings may be influential in determining the themes of multiple factors.
Major themes from the table include cancer, breast cancer, liver cancer, skin cancer, brain
cancer, leukemia, tumors, precancerous conditions, neurodegenerative diseases, cardiovascular
disease, electronic implant dysfunction, cerebrovascular disorders, inflammation, oxidative
stress, male infertility, electrohypersensitivity, sleep, congenital abnormalities, sensory disorders,
symptoms of discomfort, eye diseases.
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Table A3-1 - Factor Analysis Taxonomy
FACTOR
THEME
1
Electromagnetic
hypersensitivity
and inflammation
2
Coronary artery
disease
3A
Congenital
abnormalities
3B
Mammary tumors
4
Male infertility
5
Brain neoplasms
MESH HEADINGS
C-Reactive Protein, Liver Diseases, Thyroid Diseases, Inflammation,
Tonsillitis, Hypersensitivity
Plaque, Atherosclerotic, Coronary Artery Disease, Diabetes Mellitus,
Carotid Artery Diseases, Inflammation, Hypertension
Cleft Lip, Cleft Palate, Calcification, Physiologic, Congenital
Abnormalities
Fibroadenoma, Adenoma, Mammary Neoplasms, Animal, Mammary
Neoplasms, Experimental, Adenocarcinoma
Sperm Count, Spermatozoa, Sperm Motility, Semen, Testis, Infertility,
Male, Spermatogenesis, Testosterone, Fertility
Meningioma, Glioma, Meningeal Neoplasms, Neuroma, Acoustic,
Brain Neoplasms, Glioblastoma, Neoplasms, Radiation-Induced,
Neuroma, Cranial Nerve Neoplasms, Parotid Neoplasms, Central
Nervous System Neoplasms
Burning Mouth Syndrome, Taste Disorders, Skin Diseases, Mouth
Diseases, Dizziness, Vision Disorders, Hypersensitivity, Delayed,
Fatigue
Carcinoma, Lobular, Carcinoma, Ductal, Breast, Breast Neoplasms,
Male, Adenoma
Oxidative Stress, Malondialdehyde, Glutathione Peroxidase, Lipid
Peroxidation, Reactive Oxygen Species, Apoptosis, DNA Damage,
Nitric Oxide, Protein Carbonylation
6
Sensory disorders
7
Breast neoplasms
8
Oxidative stress
9
Parkinson Disease, Neurodegenerative Diseases, Alzheimer Disease,
Neurodegenerative
Amyotrophic Lateral Sclerosis, Motor Neuron Disease, Occupational
diseases
Diseases, Dementia, Brain Diseases, Dementia, Vascular
10
Cerebrovascular
disorders
Cerebrovascular Disorders, Dementia, Migraine Disorders, Tinnitus,
Headache, Sleep Wake Disorders, Carotid Artery Diseases, Alzheimer
Disease, Dementia, Vascular
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11
Congenital
abnormalities and
glandular-based
tumors
12
Skin neoplasms
Cleft Lip, Cleft Palate, Fibroadenoma, Adenoma, Calcification,
Physiologic, Mammary Neoplasms, Animal, Mammary Neoplasms,
Experimental, Adenocarcinoma
Carcinoma, Basal Cell, Carcinoma, Squamous Cell, Skin Neoplasms,
Cocarcinogenesis, Neoplasms, Experimental, Neoplasms, Radiation-
Induced, Colonic Neoplasms
Leukemia, Myeloid, Acute, Leukemia, Lymphocytic, Chronic, B-Cell,
Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Leukemia,
Myeloid, Leukemia, Multiple Myeloma, Lymphoma, Leukemia,
Radiation-Induced, Acute Disease, Liver Neoplasms, Experimental,
Central Nervous System Neoplasms
Atrophy, Precancerous Conditions, Hyperplasia, Hypersensitivity,
Delayed, Thymus Gland, Capillary Permeability, Lymphoma
13
Leukemia
14
Precancerous
conditions
15
Melatonin, Circadian Rhythm, Pineal Gland
Circadian Rhythm
16
Eye diseases
Eye Diseases, Cataract, Vision Disorders, Sensation Disorders,
Neurotic Disorders, Lens, Crystalline, Corneal Diseases, Edema,
Hematologic Diseases
Tachycardia, Ventricular, Ventricular Fibrillation, Death, Sudden,
Cardiac, Arrhythmias, Cardiac
17
Electromagnetic
interference in
implanted
electronic devices
18
Liver Neoplasms
19
Symptoms of
discomfort
20
Neoplasms
Liver Neoplasms, Carcinoma, Hepatocellular, Neoplasm Recurrence,
Local, Lymphatic Metastasis
Headache, Dizziness, Fatigue, Depression, Anxiety, Tremor, Sleep
Wake Disorders, Neurotic Disorders, Stress, Psychological, Anxiety
Disorders, Nervous System Diseases
Lung Neoplasms, Ovarian Neoplasms, Pituitary Neoplasms,
Lymphoma, Prostatic Neoplasms, Colonic Neoplasms, Carcinoma,
Breast Neoplasms, Hematologic Neoplasms, Neoplasms, Liver
Neoplasms, Cell Transformation, Neoplastic, Nervous System
Neoplasms
210
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Largest Unethical Medical Experiment in Human History
Copyright 2020
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A3-B. Factor Record Titles
FACTOR 1
Theme
–
Electromagnetic hypersensitivity and inflammation
Key MeSH Headings - C-Reactive Protein, Liver Diseases, Thyroid Diseases, Inflammation,
Tonsillitis, Hypersensitivity
Titles
915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci
in human lymphocytes from hypersensitive and healthy persons.
A cognitive-behavioral treatment of patients suffering from "electric hypersensitivity".
Subjective effects and reactions in a double-blind provocation study.
A systematic review of treatments for electromagnetic hypersensitivity.
Activation of TLR signalling regulates microwave radiation-mediated impairment of
spermatogenesis in rat testis.
Analysis of the effect of a 60 Hz AC field on histamine release by rat peritoneal mast cells.
Are thyroid dysfunctions related to stress or microwave exposure (900 MHz)?
Bilateral symmetry of local inflammatory activation in human carotid atherosclerotic plaques.
Biological effects of low-level environmental agents.
Blood laboratory findings in patients suffering from self-perceived electromagnetic
hypersensitivity (EHS).
Changes in antioxidant capacity of blood due to mutual action of electromagnetic field (1800
MHz) and opioid drug (tramadol) in animal model of persistent inflammatory state.
Changes in the chromatin structure of lymphoid cells under the influence of low-intensity
extremely high-frequency electromagnetic radiation against the background of inflammatory
process].
Clinical significance of tonsillar provocation test in diagnosis of tonsillar focal infection--by
indirect irradiation of ultra-micro waves].
Controversies around electromagnetic fields and electromagnetic hypersensitivity. The
construction of "low noise" public problems].
Decrease in the intensity of the cellular immune response and nonspecific inflammation upon
exposure to extremely high frequency electromagnetic radiation].
Dependence of anti-inflammatory effects of high peak-power pulsed electromagnetic radiation of
extremely high frequency on exposure parameters].
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Description of persons with symptoms presumed to be caused by electricity or visual display
units--oral aspects.
Development and evaluation of the electromagnetic hypersensitivity questionnaire.
Earthing: health implications of reconnecting the human body to the Earth's surface electrons.
Effect of high frequency electromagnetic wave stimulation on muscle injury in a rat model.
Effect of mobile phone use on salivary concentrations of protein, amylase, lipase,
immunoglobulin A, lysozyme, lactoferrin, peroxidase and C-reactive protein of the parotid
gland.
Effect of quinacrine on inflammatory reaction of blood system induced by microwave
irradiation].
Effect of the pulsed electromagnetic field on the release of inflammatory mediators from
adipose-derived stem cells (ADSCs) in rats.
Effects of low-intensity ultrahigh frequency electromagnetic radiation on inflammatory
processes.
Effects of personalised exposure on self-rated electromagnetic hypersensitivity and sensibility -
A double-blind randomised controlled trial.
Effects of RF fields emitted from smart phones on cardio-respiratory parameters: a preliminary
provocation study.
Electrical hypersensitivity in humans--fact or fiction?
Electrohypersensitivity: a functional impairment due to an inaccessible environment.
Electromagnetic fields (EMF): do they play a role in children's environmental health (CEH)?
Electromagnetic fields and health outcomes.
Electromagnetic fields hypersensitivity].
Electromagnetic hypersensitivity (EHS) and subjective health complaints associated with
electromagnetic fields of mobile phone communication--a literature review published between
2000 and 2004.
Electromagnetic hypersensitivity--an increasing challenge to the medical profession.
Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes
and multiple sclerosis.
Electromagnetic hypersensitivity: fact or fiction?
Epidemiology and etiology of gliomas.
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Extremely low-frequency electromagnetic field exposure enhances inflammatory response and
inhibits effect of antioxidant in RAW 264.7 cells.
Features of anti-inflammatory effects of modulated extremely high-frequency electromagnetic
radiation.
Functional brain MRI in patients complaining of electrohypersensitivity after long term exposure
to electromagnetic fields.
Heavy metal exposure in patients suffering from electromagnetic hypersensitivity.
Hsp70 is an independent stress marker among frequent users of mobile phones.
Hypersensitivity symptoms associated with exposure to cellular telephones: no causal link.
Hypersensitivity syndrome].
Hypersensitivity to electricity: working definition and additional characterization of the
syndrome.
Idiopathic environmental intolerance attributed to electromagnetic fields (formerly
'electromagnetic hypersensitivity'): An updated systematic review of provocation studies.
Increased mercury release from dental amalgam restorations after exposure to electromagnetic
fields as a potential hazard for hypersensitive people and pregnant women.
Induction of macrophage migration inhibitory factor precedes the onset of acute tonsillitis.
Microwaves from GSM mobile telephones affect 53BP1 and gamma-H2AX foci in human
lymphocytes from hypersensitive and healthy persons.
Mobile-phone-based home exercise training program decreases systemic inflammation in COPD:
a pilot study.
Physiological variables and subjective symptoms by 60 Hz magnetic field in EHS and non-EHS
persons.
Prevalence of self-reported hypersensitivity to electric or magnetic fields in a population-based
questionnaire survey.
Provocation of electric hypersensitivity under everyday conditions.
Provocation study of persons with perceived electrical hypersensitivity and controls using
magnetic field exposure and recording of electrophysiological characteristics.
Provocation with stress and electricity of patients with "sensitivity to electricity".
Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple
chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder.
Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic
radiation will increase in lipopolysaccharide-induced inflammation in vitro model.
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Some ocular symptoms and sensations experienced by long term users of mobile phones.
The amelioration of phagocytic ability in microglial cells by curcumin through the inhibition of
EMF-induced pro-inflammatory responses.
The effect of melatonin on the liver of rats exposed to microwave radiation.
The implications of non-linear biological oscillations on human electrophysiology for
electrohypersensitivity (EHS) and multiple chemical sensitivity (MCS).
The microwave syndrome or electro-hypersensitivity: historical background.
The role of fatty acids in anti-inflammatory effects of low-intensity extremely high-frequency
electromagnetic radiation.
The role of microwave radiometry in carotid artery disease. Diagnostic and clinical prospective.
Thermal and non-thermal health effects of low intensity non-ionizing radiation: An international
perspective.
Thermal Response of In Vivo Human Skin to Fractional Radiofrequency Microneedle Device.
Use of terahertz electromagnetic radiation at nitric oxide frequencies for the correction of thyroid
functional state during stress].
Wireless communication fields and non-specific symptoms of ill health: a literature review.
Women growing older with environmental sensitivities: A grounded theory model of meeting
one's needs.
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FACTOR 2
Theme
–
Coronary artery disease
Key MeSH Headings - Plaque, Atherosclerotic, Coronary Artery Disease, Diabetes Mellitus,
Carotid Artery Diseases, Inflammation, Hypertension
Titles
A study on the biological effects of exposure mobile-phone frequency EMF].
A survey on diabetes mellitus in the staff of electric power system in Baotou city].
Activation of TLR signalling regulates microwave radiation-mediated impairment of
spermatogenesis in rat testis.
Analysis of the effect of a 60 Hz AC field on histamine release by rat peritoneal mast cells.
Bilateral symmetry of local inflammatory activation in human carotid atherosclerotic plaques.
Blood laboratory findings in patients suffering from self-perceived electromagnetic
hypersensitivity (EHS).
Cardiovascular risk in operators under radiofrequency electromagnetic radiation.
Changes in antioxidant capacity of blood due to mutual action of electromagnetic field (1800
MHz) and opioid drug (tramadol) in animal model of persistent inflammatory state.
Changes in the chromatin structure of lymphoid cells under the influence of low-intensity
extremely high-frequency electromagnetic radiation against the background of inflammatory
process].
Decrease in the intensity of the cellular immune response and nonspecific inflammation upon
exposure to extremely high frequency electromagnetic radiation].
Dependence of anti-inflammatory effects of high peak-power pulsed electromagnetic radiation of
extremely high frequency on exposure parameters].
Development of hypertension after long-term exposure to static magnetic fields among workers
from a magnetic resonance imaging device manufacturing facility.
Earthing: health implications of reconnecting the human body to the Earth's surface electrons.
Effect of electromagnetic irradiation of the millimetric range on hemodynamics in patients with
arterial hypertension].
Effect of high frequency electromagnetic wave stimulation on muscle injury in a rat model.
Effect of quinacrine on inflammatory reaction of blood system induced by microwave
irradiation].
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RN Kostoff
Effect of the pulsed electromagnetic field on the release of inflammatory mediators from
adipose-derived stem cells (ADSCs) in rats.
Effects of low-intensity ultrahigh frequency electromagnetic radiation on inflammatory
processes.
Electromagnetic effects on people.
Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes
and multiple sclerosis.
Epidemiological risk assessment of pathology development in occupational exposure to
radiofrequency electromagnetic fields].
Evaluation of occupational risk caused by exposure to electromagnetic rays].
Evidence that dirty electricity is causing the worldwide epidemics of obesity and diabetes.
Exacerbation of hypertension and disturbances of the geomagnetic field].
Exposure to radio-frequency radiation from an aircraft radar unit.
Extremely low-frequency electromagnetic field exposure enhances inflammatory response and
inhibits effect of antioxidant in RAW 264.7 cells.
Features of anti-inflammatory effects of modulated extremely high-frequency electromagnetic
radiation.
Health care utilisation and attitudes towards health care in subjects reporting environmental
annoyance from electricity and chemicals.
Mobile-phone-based home exercise training program decreases systemic inflammation in COPD:
a pilot study.
Psychological symptoms and intermittent hypertension following acute microwave exposure.
Radiofrequency Scanning for Retained Surgical Items Can Cause Electromagnetic Interference
and Pacing Inhibition if an Asynchronous Pacing Mode Is Not Applied.
Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple
chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder.
Role of ultrasonic dopplerography in monitoring the effectiveness of treatment of patients who
have sustained a stroke with decimeter-range electromagnetic waves].
Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic
radiation will increase in lipopolysaccharide-induced inflammation in vitro model.
Some ocular symptoms and sensations experienced by long term users of mobile phones.
The amelioration of phagocytic ability in microglial cells by curcumin through the inhibition of
EMF-induced pro-inflammatory responses.
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The heliogeophysical aspects of circumpolar health.
The role of fatty acids in anti-inflammatory effects of low-intensity extremely high-frequency
electromagnetic radiation.
The role of microwave radiometry in carotid artery disease. Diagnostic and clinical prospective.
Thermal Response of In Vivo Human Skin to Fractional Radiofrequency Microneedle Device.
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FACTOR 3A
Theme
–
Congenital abnormalities
Key MeSH Headings - Cleft Lip, Cleft Palate, Calcification, Physiologic, Congenital
Abnormalities
Titles
A confirmation study of Russian and Ukrainian data on effects of 2450 MHz microwave
exposure on immunological processes and teratology in rats.
Adverse human reproductive outcomes and electromagnetic fields: a brief summary of the
epidemiologic literature.
Age diseases depending on geomagnetic field activity inside the womb period].
Alternative functional relationships between ELF field exposure and possible health effects:
report on an expert workshop.
An evaluation of the mutagenic, carcinogenic and teratogenic potential of microwaves.
An international project to confirm Soviet-era results on immunological and teratological effects
of RF field exposure in Wistar rats and comments on Grigoriev et al. [2010].
Anesthesia as an effective agent against the production of congenital anomalies in mouse fetuses
exposed to electromagnetic radiation.
Are microwaves a co-teratogen? Experimental model concept and its verification].
Case-control study on maternal residential proximity to high voltage power lines and congenital
anomalies in France.
Chick embryo development can be irreversibly altered by early exposure to weak extremely-low-
frequency magnetic fields.
Clinical teratology.
Congenital anomalies in the offspring of rats after exposure of the testis to an electrostatic field.
Contribution of physical factors to the complex anthropogenic load in an industrial town].
Development of chicken embryos in a pulsed magnetic field.
Development of preincubated chicken eggs following exposure to 50 Hz electromagnetic fields
with 1.33-7.32 mT flux densities.
Developmental changes in Drosophila melanogaster following exposure to alternating
electromagnetic fields.
Developmental toxicity interactions of salicylic acid and radiofrequency radiation or 2-
methoxyethanol in rats.
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Effects of 2.45 GHz CW microwave radiation on embryofetal development in mice.
Effects of gestational exposure to 1.95-GHz W-CDMA signals for IMT-2000 cellular phones:
Lack of embryotoxicity and teratogenicity in rats.
Effects of noise and electromagnetic fields on reproductive outcomes.
Electromagnetic poles and reproduction].
EMF and health.
Epidemiological studies of work with video display terminals and adverse pregnancy outcomes
(1984-1992).
Evaluation of the developmental toxicity of 60 Hz magnetic fields and harmonic frequencies in
Sprague-Dawley rats.
Interaction of static and extremely low frequency electric and magnetic fields with living
systems: health effects and research needs.
Joint actions of environmental nonionizing electromagnetic fields and chemical pollution in
cancer promotion.
Maternal exposure to magnetic fields from high-voltage power lines and the risk of birth defects.
Maternal proximity to extremely low frequency electromagnetic fields and risk of birth defects.
Mouse early embryos obtained by natural breeding or in vitro fertilization display a differential
sensitivity to extremely low-frequency electromagnetic fields.
Mutagenic, carcinogenic and teratogenic effects induced by radiofrequency electromagnetic field
of mobile phone].
Neural and behavioral teratological evaluation of rats exposed to ultra-wideband electromagnetic
fields.
Paternal work in the power industry: effects on children at delivery.
Possible effects of electric blankets and heated waterbeds on fetal development.
Prospective study of pregnancy outcomes after parental cell phone exposure: the Norwegian
Mother and Child Cohort Study.
Pulsed magnetic field from video display terminals enhances teratogenic effects of cytosine
arabinoside in mice.
Recent advances in research on radiofrequency fields and health.
Reproductive and teratologic effects of electromagnetic fields.
Risk of birth defects by parental occupational exposure to 50 Hz electromagnetic fields: a
population based study.
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Search for teratogenic risks with the aid of malformation registries.
Some effects of exposure of the Japanese quail embryo to 2.45-GHz microwave radiation.
Teratogenic effects of sinusoidal extremely low frequency electromagnetic fields on morphology
of 24 hr chick embryos.
Teratology, survival, and reversal learning after fetal irradiation of mice by 2450-MHz
microwave energy.
The effects of ionizing radiation, microwaves, and ultrasound on the developing embryo: clinical
interpretations and applications of the data.
The influence of electromagnetic radiation generated by a mobile phone on the skeletal system of
rats.
VDT pulse magnetic field enhances teratogenic effect of ara-c in mice].
Video display terminal use during pregnancy and reproductive outcome--a meta-analysis.
Video display terminals: risk of electromagnetic radiation.
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FACTOR 3B
Theme
–
Mammary tumors
Key MeSH Headings - Fibroadenoma, Adenoma, Mammary Neoplasms, Animal, Mammary
Neoplasms, Experimental, Adenocarcinoma
Titles
A histopathological study on alterations in DMBA-induced mammary carcinogenesis in rats with
50 Hz, 100 muT magnetic field exposure.
Acceleration of mammary tumorigenesis by exposure of 7,12-dimethylbenz[a]anthracene-treated
female rats in a 50-Hz, 100-microT magnetic field: replication study.
Bioelectromagnetic field effects on cancer cells and mice tumors.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in F344/N
rats.
Chronic, low-level (1.0 W/kg) exposure of mice prone to mammary cancer to 2450 MHz
microwaves.
Do cocarcinogenic effects of ELF electromagnetic fields require repeated long-term interaction
with carcinogens? Characteristics of positive studies using the DMBA breast cancer model in
rats.
Effect of 13 week magnetic field exposures on DMBA-initiated mammary gland carcinomas in
female Sprague-Dawley rats.
Effect of 26 week magnetic field exposures in a DMBA initiation-promotion mammary gland
model in Sprague-Dawley rats.
Effect of a 9 mT pulsed magnetic field on C3H/Bi female mice with mammary carcinoma. A
comparison between the 12 Hz and the 460 Hz frequencies.
Effects of 50- or 60-hertz, 100 microT magnetic field exposure in the DMBA mammary cancer
model in Sprague-Dawley rats: possible explanations for different results from two laboratories.
Effects of 900 MHz GSM wireless communication signals on DMBA-induced mammary tumors
in rats.
Effects of GSM-900 microwaves on DMBA-induced mammary gland tumors in female Sprague-
Dawley rats.
Effects of magnetic fields on mammary tumor development induced by 7,12-
dimethylbenz(a)anthracene in rats.
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Effects of mobile-phone microwave on dimethylbenz (a) anthracene induced mammary
carcinoma development in rats].
Effects of weak alternating magnetic fields on nocturnal melatonin production and mammary
carcinogenesis in rats.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Evaluation of the potential carcinogenicity of 60 Hz linear sinusoidal continuous-wave magnetic
fields in Fischer F344 rats.
Low-frequency electromagnetic radiation enhances the induction of rat mammary tumors by
nitrosomethyl urea.
Magnetic fields and mammary cancer in rodents: a critical review and evaluation of published
literature.
Male breast tumors in railway engine drivers: investigation of 5 cases].
Microwave absorption by normal and tumor cells.
Modifying effect of light and electromagnetic field on development of mammary tumors induced
by N-nitrosomethyl urea in female rats].
Non dietetic environmental risk factors in prostate cancer].
Occupational exposure to magnetic fields in relation to male breast cancer and testicular cancer:
a Swedish case-control study.
On the role of the interactions of ions with external magnetic fields in physiologic processes and
their importance in chronobiology.
Repeated exposure of C3H/HeJ mice to ultra-wideband electromagnetic pulses: lack of effects on
mammary tumors.
Significant differences in the effects of magnetic field exposure on 7,12-
dimethylbenz(a)anthracene-induced mammary carcinogenesis in two substrains of Sprague-
Dawley rats.
Study on potential effects of "902-MHz GSM-type Wireless Communication Signals" on
DMBA-induced mammary tumours in Sprague-Dawley rats.
The effect of low-frequency electromagnetic fields on the development of experimental
mammary tumors].
Transferrin receptors and natural killer cell lysis. A study using Colo 205 cells exposed to 60 Hz
electromagnetic fields.
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FACTOR 4
Theme
–
Male infertility
Key MeSH Headings - Sperm Count, Spermatozoa, Sperm Motility, Semen, Testis, Infertility,
Male, Spermatogenesis, Testosterone, Fertility
Titles
1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53
dependent Bax mediated testicular apoptosis in mice, Mus musculus.
1950MHz Radio Frequency Electromagnetic Radiation Inhibits Testosterone Secretion of Mouse
Leydig Cells.
2.45 GHz microwave radiation induced oxidative and nitrosative stress mediated testicular
apoptosis: Involvement of a p53 dependent bax-caspase-3 mediated pathway.
2.45-GHz microwave irradiation adversely affects reproductive function in male mouse, Mus
musculus by inducing oxidative and nitrosative stress.
900 MHz pulse-modulated radiofrequency radiation induces oxidative stress on heart, lung, testis
and liver tissues.
A 50-Hz electromagnetic field impairs sleep.
Abnormal physical architecture of the lipophilic domains of human sperm membrane in
oligospermia: a logical cause for low fertility profiles.
Action of UHF microwaves on the germ and somatic cells of mammals].
Activation of TLR signalling regulates microwave radiation-mediated impairment of
spermatogenesis in rat testis.
Acute, whole-body microwave exposure and testicular function of rats.
Adolescent in-school cellphone habits: a census of rules, survey of their effectiveness, and
fertility implications.
Alternating magnetic field damages the reproductive function of murine testes].
An evaluation of the effects of long-term cell phone use on the testes via light and electron
microscope analysis.
An ultrastructural analysis of the testes in mice subjected to long-term exposure to a 17-kHz
electrical field].
Analysis of Gene Expression in Mice Testes Exposed to 1.765 GHz Microwave in Utero.
Are men talking their reproductive health away?
Association between mobile phone use and semen quality: a systemic review and meta-analysis.
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Biologic effects of prolonged exposure to ELF electromagnetic fields in rats: II. 50 Hz magnetic
fields.
Biological and morphological effects on the reproductive organ of rats after exposure to
electromagnetic field.
Biological effects of non-ionizing electromagnetic fields: Two sides of a coin.
Biophysical evaluation of radiofrequency electromagnetic field effects on male reproductive
pattern.
Cell phones and male infertility: a review of recent innovations in technology and consequences.
Cell phones and male infertility: dissecting the relationship.
Cell phones: modern man's nemesis?
Cellphone electromagnetic radiation damages the testicular ultrastructure of male rats].
Challenging cell phone impact on reproduction: a review.
Changes of rat testicular germ cell apoptosis after high power microwave radiation].
Chronotoxicity of 1800 MHz microwave radiation on sex hormones and spermatogenesis in male
mice].
Combined effects of traffic and electromagnetic fields on the immune system of fertile atopic
women.
Combined effects of varicocele and cell phones on semen and hormonal parameters.
Comparative effectiveness of different tests to determine the mutagenicity of certain factors in
mammals. II. Frequency of anomalous sperm head in mice exposed to different factors].
Comparison of native and microwave irradiated DNA.
Congenital anomalies in the offspring of rats after exposure of the testis to an electrostatic field.
Cytogenetic effects of microwave irradiation on male germ cells of the mouse.
Cytokines produced by microwave-radiated Sertoli cells interfere with spermatogenesis in rat
testis.
DNA damage, cell kinetics and ODC activities studied in CBA mice exposed to electromagnetic
fields generated by transmission lines.
Does exposure to computers affect the routine parameters of semen quality?
Does prolonged radiofrequency radiation emitted from Wi-Fi devices induce DNA damage in
various tissues of rats?
Does static electric field from ultra-high voltage direct-current transmission lines affect male
reproductive capacity? Evidence from a laboratory study on male mice.
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Dominant lethal studies in male mice after exposure to 2.45 GHz microwave radiation.
Dominant lethal studies in male mice after exposure to a 50 Hz magnetic field.
Dominant lethal studies in male mice after exposure to a 50-Hz electric field.
Dosimetry for a study of effects of 2.45-GHz microwaves on mouse testis.
Effect of 2.45 GHz microwave radiation on the fertility pattern in male mice.
Effect of 2450 MHz microwaves on the fertility of Swiss female mice].
Effect of cell phone usage on semen analysis in men attending infertility clinic: an observational
study.
Effect of discontinuous short-wave electromagnetic field irradiation on the state of the endocrine
glands].
Effect of electromagnetic irradiation produced by 3G mobile phone on male rat reproductive
system in a simulated scenario.
Effect of Electromagnetic Waves from Mobile Phones on Spermatogenesis in the Era of 4G-
LTE.
Effect of Guilingji Capsule on the fertility, liver functions, and serum LDH of male SD rats
exposed by 900 mhz cell phone].
Effect of long-term exposure of 2.4 GHz radiofrequency radiation emitted from Wi-Fi equipment
on testes functions.
Effect of low power microwave on the mouse genome: a direct DNA analysis.
Effect of low-intensity extremely high frequency radiation on reproductive function in wistar
rats.
Effect of mobile telephones on sperm quality: a systematic review and meta-analysis.
Effect of Modified Wuzi Yanzong Pill () on Tip60-Mediated Apoptosis in Testis of Male Rats
after Microwave Radiation.
Effect of rosmarinic acid on sertoli cells apoptosis and serum antioxidant levels in rats after
exposure to electromagnetic fields.
Effect of whole-body 1800MHz GSM-like microwave exposure on testicular steroidogenesis and
histology in mice.
Effects of 1800-MHz radiofrequency fields on circadian rhythm of plasma melatonin and
testosterone in male rats.
Effects of 2.45 GHz CW microwave radiation on embryofetal development in mice.
Effects of 2.45 GHz microwave radiation and heat on mouse spermatogenic epithelium.
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Effects of 2.45 GHz microwaves on meiotic chromosomes of male CBA/CAY mice.
Effects of 60 Hz electromagnetic field exposure on testicular germ cell apoptosis in mice.
Effects of a unique electromagnetic field system on the fertility of rats.
Effects of cellular phone emissions on sperm motility in rats.
Effects of electromagnetic fields exposure on plasma hormonal and inflammatory pathway
biomarkers in male workers of a power plant.
Effects of electromagnetic fields on fecundity in the chicken.
Effects of electromagnetic fields on the reproductive success of American kestrels.
Effects of electromagnetic pulses on apoptosis and TGF-beta3 expression of mouse testis tissue].
Effects of electromagnetic radiation from a cellular phone on human sperm motility: an in vitro
study.
Effects of electromagnetic radiation on morphology and TGF-beta3 expression in mouse
testicular tissue.
Effects of electromagnetic waves emitted from 3G+wi-fi modems on human semen analysis.
Effects of exposure to a mobile phone on sexual behavior in adult male rabbit: an observational
study.
Effects of exposure to a mobile phone on testicular function and structure in adult rabbit.
Effects of exposure to electromagnetic field (1.8/0.9 GHz) on testicular function and structure in
growing rats.
Effects of extremely low-frequency electromagnetic fields (ELF-EMF) exposure on B6C3F1
mice.
Effects of GSM-like radiofrequency irradiation during the oogenesis and spermiogenesis of
Xenopus laevis.
Effects of high power microwave on the expressions of Bcl-2 and C-myc proteins in the rat
testis].
Effects of microwaves (950 MHZ mobile phone) on morphometric and apoptotic changes of
rabbit epididymis.
Effects of mobile phone radiation on serum testosterone in Wistar albino rats.
Effects of radiofrequency electromagnetic fields (UMTS) on reproduction and development of
mice: a multi-generation study.
Effects of radiofrequency electromagnetic fields on mammalian spermatogenesis].
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Effects of radiofrequency electromagnetic wave exposure from cellular phones on the
reproductive pattern in male Wistar rats.
Effects of radiofrequency electromagnetic waves (RF-EMW) from cellular phones on human
ejaculated semen: an in vitro pilot study.
Effects of the exposure to mobile phones on male reproduction: a review of the literature.
Effects of whole-body 50-Hz magnetic field exposure on mouse Leydig cells.
Effects on rat testis of 1.95-GHz W-CDMA for IMT-2000 cellular phones.
Electric power, pineal function, and the risk of breast cancer.
Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3
signaling pathways in rats.
Environmental risk factors in the history of male patients of an infertility clinic.
Evaluation of changes in electrophysiological and hormonal parameters in rabbits resulting from
short-term low-intensity ultra-high-frequency irradiation].
Evaluation of testicular degeneration induced by low-frequency electromagnetic fields.
Evaluation of the effect of using mobile phones on male fertility.
Evidence for mobile phone radiation exposure effects on reproductive pattern of male rats: role
of ROS.
Examination of electric field effects on tissues by using back propagation neural network.
Exercise testing in the evaluation of human responses to powerline frequency fields.
Experimental research on the biological action of the pulse-modulated microwave radiation
created by shipboard radar stations].
Exposure to a 900 MHz electromagnetic field for 1 hour a day over 30 days does change the
histopathology and biochemistry of the rat testis.
Exposure to magnetic fields and the risk of poor sperm quality.
Exposure to non-ionizing electromagnetic radiation of public risk prevention instruments
threatens the quality of spermatozoids.
Extremely low frequency electromagnetic field exposure affects fertilization outcome in swine
animal model.
Extremely low-frequency magnetic fields can impair spermatogenesis recovery after reversible
testicular damage induced by heat.
Flow cytometric analysis of the effects of 50 Hz magnetic fields on mouse spermatogenesis].
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Germ cell degeneration in normal and microwave-irradiated rats: potential sperm production
rates at different developmental steps in spermatogenesis.
Growing concern over the safety of using mobile phones and male fertility.
Habits of cell phone usage and sperm quality - does it warrant attention?
Health problems among workers of iron welding machines: an effect of electromagnetic fields.
Histological and cytological examination of rat reproductive tissue after short-time intermittent
radiofrequency exposure.
How does long term exposure to base stations and mobile phones affect human hormone
profiles?
Human disease resulting from exposure to electromagnetic fields.
Hygienic standardization of electromagnetic radiation from two-channel meteorological radar
stations].
Hypospermatogenesis and spermatozoa maturation arrest in rats induced by mobile phone
radiation.
Immunohistopathologic demonstration of deleterious effects on growing rat testes of
radiofrequency waves emitted from conventional Wi-Fi devices.
Immunomorphologic changes in the testes upon exposure to a microwave electromagnetic field].
Impact of 2.45 GHz microwave radiation on the testicular inflammatory pathway biomarkers in
young rats: The role of gallic acid.
Impact of cell phone radiation on male reproduction].
Impact of cell phone use on men's semen parameters.
Impact of microwave at X-band in the aetiology of male infertility.
Impact of mobile phone radiation on the quality and DNA methylation of human sperm in vitro].
Impact of radio frequency electromagnetic radiation on DNA integrity in the male germline.
In vitro effect of pulsed 900 MHz GSM radiation on mitochondrial membrane potential and
motility of human spermatozoa.
In vitro effects of radiofrequency electromagnetic waves on bovine spermatozoa motility.
In vitro fertilization of mouse ova by spermatozoa exposed isothermally to radio-frequency
radiation.
Influence of a 50 hz extra low frequency electromagnetic field on spermatozoa motility and
fertilization rates in rabbits.
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Influence of electromagnetic fields emitted by GSM-900 cellular telephones on the circadian
patterns of gonadal, adrenal and pituitary hormones in men.
Influence of electromagnetic fields on reproductive system of male rats.
Influence of in vitro microwave radiation on the fertilizing capacity of turkey sperm.
Influence of microwave exposure on fertility of male rats.
Influence of radiofrequency-electromagnetic waves from 3rd-generation cellular phones on
fertilization and embryo development in mice.
Inhibition by Egb761 of the effect of cellphone radiation on the male reproductive system.
Inhibitory effects of low doses of melatonin on induction of preneoplastic liver lesions in a
medium-term liver bioassay in F344 rats: relation to the influence of electromagnetic near field
exposure.
Interaction of microwave radiation with turkey sperm.
Is there a relationship between cell phone use and semen quality?
Long-term effects of 900 MHz radiofrequency radiation emitted from mobile phone on testicular
tissue and epididymal semen quality.
Long-term exposure of male and female mice to 50 Hz magnetic field: effects on fertility.
Long-term exposure to low intensity microwave radiation affects male reproductivity].
Long-term microwave radiation affects male reproduction in rats].
Low frequency electromagnetic waves increase human sperm motility - A pilot study revealing
the potent effect of 43 kHz radiation.
Mechanisms of biological effects of radiofrequency electromagnetic fields: an overview.
Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA
damage and cell cycle arrest in germ cells of male Swiss albino mice.
Metabolic and ultrastructural adaptation mechanisms during the primary prophylactic action of
low-intensity electromagnetic radiation under normal and radiation conditions].
Microwave emissions from police radar.
Microwave exposure affecting reproductive system in male rats.
Microwave radiation decreases the expressions of occludin and JAM-1 in rats].
Mobile phone radiation induces reactive oxygen species production and DNA damage in human
spermatozoa in vitro.
Mobile phone usage and male infertility in Wistar rats.
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Morinda officialis how extract improves microwave-induced reproductive impairment in male
rats].
Multigeneration reproductive toxicity assessment of 60-Hz magnetic fields using a continuous
breeding protocol in rats.
Occupational exposures obtained by questionnaire in clinical practice and their association with
semen quality.
Occupational hazards for the male reproductive system.
Occupational influences on male fertility and sexuality. I.
Oxidative effects of extremely low frequency magnetic field and radio frequency radiation on
testes tissues of diabetic and healthy rats.
Oxidative stress-mediated alterations on sperm parameters in male Wistar rats exposed to 3G
mobile phone radiation.
PARAMETERS OF SPERMATOGENESIS IN MEN EXPOSED TO DIFFICULT
ENVIRONMENTS].
Pathological study of testicular injury induced by high power microwave radiation in rats].
Poly ADP ribosylation as a possible mechanism of microwave--biointeraction.
Prospective study of pregnancy outcomes after parental cell phone exposure: the Norwegian
Mother and Child Cohort Study.
Protective effect of Liuweidihuang Pills against cellphone electromagnetic radiation-induced
histomorphological abnormality, oxidative injury, and cell apoptosis in rat testes].
Protective effects of luteolin on rat testis following exposure to 900 MHz electromagnetic field.
Proteomic analysis of continuous 900-MHz radiofrequency electromagnetic field exposure in
testicular tissue: a rat model of human cell phone exposure.
Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling
pathway in mouse spermatogenic cells in vitro and thus may affect male fertility.
Quantitative changes in testicular structure and function in rat exposed to mobile phone
radiation.
Radar radiation damages sperm quality].
Radiations and male fertility.
Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones
induces oxidative stress and reduces sperm motility in rats.
Radiofrequency electromagnetic fields; male infertility and sex ratio of offspring.
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Radiofrequency electromagnetic radiation from cell phone causes defective testicular function in
male Wistar rats.
Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular
germ cells in swiss albino mice.
Rat fertility and embryo fetal development: influence of exposure to the Wi-Fi signal.
Reaction of Reproductive System and Epididymal Spermatozoa .of Rats to Electromagnetic
Radiation from Mobile Phone (1745 MHz) of Various Duration].
Recent reports of Wi-Fi and mobile phone-induced radiation on oxidative stress and reproductive
signaling pathways in females and males.
Reproduction in male Japanese quail exposed to microwave radiation during embryogeny.
Reproductive hazards among workers at high voltage substations.
Response of Caenorhabditis elegans to wireless devices radiation exposure.
Response of the seminiferous epithelium of the mouse exposed to low dose high energy (HZE)
and electromagnetic radiation.
Scientometric study of the effects of exposure to non-ionizing electromagnetic fields on fertility:
A contribution to understanding the reasons of partial failure.
Self-reported mobile phone use and semen parameters among men from a fertility clinic.
Semen analysis of military personnel associated with military duty assignments.
Sperm count and sperm abnormality in male mice after exposure to 2.45 GHz microwave
radiation.
State of the reproductive systemin in male rats of 1st generation obtained from irradiated parents
and exposed to electromagnetic radiation (897 MHz) during embryogenesis and postnatal
development].
Status quo of the researches on the biological effect of electromagnetic radiation on the testis and
epididymal sperm].
Structural and ultrastructural study of rat testes influenced by electromagnetic radiation.
Studies of the induction of dominant lethals and translocations in male mice after chronic
exposure to microwave radiation.
Studies of the teratogenic potential of exposure of rats to 6000-MHz microwave radiation. II.
Postnatal psychophysiologic evaluations.
Study of bioeffects of ship-borne microwave navigation radar in chronic experiments].
Testicular apoptosis and histopathological changes induced by a 2.45 GHz electromagnetic field.
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Testicular development evaluation in rats exposed to 60 Hz and 1 mT electromagnetic field.
Testicular function of rats following exposure to microwave radiation.
Tests of mutagenesis and reproduction in male rats exposed to 2,450-MHz (CW) microwaves.
The biological effects of radiofrequency radiation: a critical review and recommendations.
The combined action of drinking mineral water and low-intensity electromagnetic radiation
under the immobilization stress conditions (an experimental study)].
The effect of acute far field exposure at 2.45 GHz on the mouse testis.
The effect of alternating electric field of industrial frequency on testicles of white mice].
The effect of low-intensity prolonged impulse electromagnetic irradiation in the UHF range on
the testes and the appendages of the testis in rats].
The effect of male occupational exposure in infertile couples in Norway.
The effect of prenatal exposure to 900-MHz electromagnetic field on the 21-old-day rat testicle.
The effect of pulsed 900-MHz GSM mobile phone radiation on the acrosome reaction, head
morphometry and zona binding of human spermatozoa.
The effects of an electromagnetic field on the boundary tissue of the seminiferous tubules of the
rat: A light and transmission electron microscope study.
The effects of electromagnetic waves emitted by the cell phones on the testicular tissue.
The effects of extremely low frequency electromagnetic field exposure on the pH of the adult
male semen and the motoricity parameters of spermatozoa in vitro].
The Effects of Melatonin on Oxidative Stress Parameters and DNA Fragmentation in Testicular
Tissue of Rats Exposed to Microwave Radiation.
The effects of radiofrequency electromagnetic radiation on sperm function.
The effects of simultaneous combined exposure to CDMA and WCDMA electromagnetic fields
on rat testicular function.
The genomic effects of cell phone exposure on the reproductive system.
The influence of electromagnetic radiation of industrial frequency on Daphnia magna (Straus)].
The influence of ultrasound and constant magnetic field on gametes, zygotes, and embryos of the
sea urchin].
The interaction of changes in the genitalia in the pathogenesis of sterility in men].
The mobile phone decreases fructose but not citrate in rabbit semen: a longitudinal study.
The semen quality of the mobile phone users.
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The specific features of the development of metabolic and regenerative processes under the
action of low-intensity electromagnetic radiation in radiation exposure conditions (an
experimental study)].
The therapeutic effect of a pulsed electromagnetic field on the reproductive patterns of male
Wistar rats exposed to a 2.45-GHz microwave field.
The use of FDTD in establishing in vitro experimentation conditions representative of lifelike
cell phone radiation on the spermatozoa.
Therapeutic approaches of melatonin in microwave radiations-induced oxidative stress-mediated
toxicity on male fertility pattern of Wistar rats.
Whole-body microwave exposure emitted by cellular phones and testicular function of rats.
Wi-Fi (2.45 GHz)- and mobile phone (900 and 1800 MHz)-induced risks on oxidative stress and
elements in kidney and testis of rats during pregnancy and the development of offspring.
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FACTOR 5
Theme
–
Brain neoplasms
Key MeSH Headings - Meningioma, Glioma, Meningeal Neoplasms, Neuroma, Acoustic, Brain
Neoplasms, Glioblastoma, Neoplasms, Radiation-Induced, Neuroma, Cranial Nerve Neoplasms,
Parotid Neoplasms, Central Nervous System Neoplasms
Titles
50-Hz electromagnetic environment and the incidence of childhood tumors in Stockholm
County.
A Bayesian approach to hazard identification. The case of electromagnetic fields and cancer.
A case-case study of mobile phone use and acoustic neuroma risk in Japan.
A cerebral primitive neuroectodermal tumor in a squirrel monkey (Saimiri sciureus).
A literature review of medical side effects from radio-frequency energy in the human
environment: involving cancer, tumors, and problems of the central nervous system.
A pooled analysis of extremely low-frequency magnetic fields and childhood brain tumors.
A population-based case-control study of radiofrequency exposure in relation to childhood
neoplasm.
A review of in vitro studies: low-frequency electromagnetic fields.
A three-dimensional point process model for the spatial distribution of disease occurrence in
relation to an exposure source.
Acoustic neuroma risk in relation to mobile telephone use: results of the INTERPHONE
international case-control study.
Adult glioma in relation to residential power frequency electromagnetic field exposures in the
San Francisco Bay area.
Adult mortality from leukemia, brain cancer, amyotrophic lateral sclerosis and magnetic fields
from power lines: a case-control study in Brazil.
Alternative functional relationships between ELF field exposure and possible health effects:
report on an expert workshop.
An epidemiological review of mobile telephones and cancer.
An international prospective cohort study of mobile phone users and health (Cosmos): design
considerations and enrolment.
Analyses of temporal and spatial patterns of glioblastoma multiforme and other brain cancer
subtypes in relation to mobile phones using synthetic counterfactuals.
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Analysis of ear side of mobile phone use in the general population of Japan.
Analysis of gene expression in two human-derived cell lines exposed in vitro to a 1.9 GHz pulse-
modulated radiofrequency field.
Analysis of mobile phone use among young patients with brain tumors in Japan.
Anthropogenic Radio-Frequency Electromagnetic Fields Elicit Neuropathic Pain in an
Amputation Model.
Application criteria of the precautionary principle].
Assessing the potential carcinogenic activity of magnetic fields using animal models.
Assessment of cellular telephone and other radio frequency exposure for epidemiologic research.
Association between number of cell phone contracts and brain tumor incidence in nineteen U.S.
States.
Association between radiation from mobile phones and tumour risk in adults].
Association between vestibular schwannomas and mobile phone use.
Association of childhood cancer with residential traffic density.
Berkson error adjustment and other exposure surrogates in occupational case-control studies,
with application to the Canadian INTEROCC study.
Bioeffects of electromagnetic fields--safety limits of each frequency band, especially less than
radio one].
Biological effects from electromagnetic field exposure and public exposure standards.
Biological effects of amplitude-modulated radiofrequency radiation.
Biological effects of electromagnetic fields and radiation.
Biological effects of extremely low-frequency electromagnetic fields: in vivo studies.
Biological effects on human health due to radiofrequency/microwave exposure: a synopsis of
cohort studies.
Biological indicators in response to radiofrequency/microwave exposure.
Biological interactions and potential health effects of extremely-low-frequency magnetic fields
from power lines and other common sources.
Biological responses to electromagnetic fields.
Biomarkers of induced electromagnetic field and cancer.
Biophysical estimation of the environmental importance of electromagnetic fields.
Biophysical mechanisms of electromagnetic fields interaction and health effects].
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Brain cancer and occupational exposure to magnetic fields among men: results from a Canadian
population-based case-control study.
Brain cancer incidence trends in relation to cellular telephone use in the United States.
Brain cancer risk and electromagnetic fields (EMFs): assessing the geomagnetic component.
Brain tumor risk in children in relation to use of electric blankets and water bed heaters. Results
from the United States West Coast Childhood Brain Tumor Study.
Brain tumor risk in offspring of men occupationally exposed to electric and magnetic fields.
Calcium protects differentiating neuroblastoma cells during 50 Hz electromagnetic radiation.
Cancer in radar technicians exposed to radiofrequency/microwave radiation: sentinel episodes.
Cancer incidence among welders: possible effects of exposure to extremely low frequency
electromagnetic radiation (ELF) and to welding fumes.
Cancer incidence and magnetic field exposure in industries using resistance welding in Sweden.
Cancer incidence and mortality and proximity to TV towers.
Cancer incidence vs. FM radio transmitter density.
Cancer morbidity in subjects occupationally exposed to high frequency (radiofrequency and
microwave) electromagnetic radiation.
Cancer risks related to low-level RF/MW exposures, including cell phones.
Carcinogenic risk of extremely-low-frequency electromagnetic fields: state of the art].
Carcinogenicity study of 217 Hz pulsed 900 MHz electromagnetic fields in Pim1 transgenic
mice.
Carcinogenicity study of GSM and DCS wireless communication signals in B6C3F1 mice.
Carcinogenicity test of 50 Hz sinusoidal magnetic fields in rats.
Case-control study of childhood cancer and exposure to 60-Hz magnetic fields.
Case-control study of the association between malignant brain tumours diagnosed between 2007
and 2009 and mobile and cordless phone use.
Case-control study on occupational exposure to extremely low-frequency electromagnetic fields
and glioma risk.
Case-Control Study on Occupational Exposure to Extremely Low-Frequency Electromagnetic
Fields and the Association with Meningioma.
Case-control study on the use of cellular and cordless phones and the risk for malignant brain
tumours.
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Case-control study on uveal melanoma (RIFA): rational and design.
Cell phone radiation exposure on brain and associated biological systems.
Cell phone use and acoustic neuroma: the need for standardized questionnaires and access to
industry data.
Cell phone use and risk of thyroid cancer: a population-based case-control study in Connecticut.
Cell phones and brain tumors: a review including the long-term epidemiologic data.
Cell phones and cancer: what is the evidence for a connection?
Cell phones and children: follow the precautionary road.
Cell Phones and Risk of brain and acoustic nerve tumours: the French INTERPHONE case-
control study].
Cell phones: health risks and prevention].
Cellular and cordless telephone use and the association with brain tumors in different age groups.
Cellular and cordless telephones and the risk for brain tumours.
Cellular phone use and brain tumor: a meta-analysis.
Cellular phone use and risk of benign and malignant parotid gland tumors--a nationwide case-
control study.
Cellular phones and risk of brain tumors.
Cellular phones and their hazards: the current evidence.
Cellular phones, cordless phones, and the risks of glioma and meningioma (Interphone Study
Group, Germany).
Cellular telephone use and risk of intratemporal facial nerve tumor.
Cellular telephone use and time trends for brain, head and neck tumours.
Cellular telephones and risk for brain tumors: a population-based, incident case-control study.
Cellular-telephone use and brain tumors.
Changes in brain glioma incidence and laterality correlates with use of mobile phones--a
nationwide population based study in Israel.
Childhood brain tumors and residential electromagnetic fields (EMF).
Childhood brain tumour risk and its association with wireless phones: a commentary.
Childhood brain tumours and use of mobile phones: comparison of a case-control study with
incidence data.
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Childhood cancer and magnetic fields from high-voltage power lines in England and Wales: a
case-control study.
Childhood cancer and residential proximity to power lines. UK Childhood Cancer Study
Investigators.
Childhood cancer in relation to a modified residential wire code.
Childhood cancer in relation to distance from high voltage power lines in England and Wales: a
case-control study.
Childhood cancer in relation to indicators of magnetic fields from ground current sources.
Childhood cancer occurrence in relation to power line configurations: a study of potential
selection bias in case-control studies.
Childhood leukaemia and distance from power lines in California: a population-based case-
control study.
Children's health and RF EMF exposure. Views from a risk assessment and risk communication
perspective.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in F344/N
rats.
Chronic, low-level (1.0 W/kg) exposure of mice prone to mammary cancer to 2450 MHz
microwaves.
Cochlear implants in the etiopathogenesis of glioblastoma--an interesting observation or
independent finding?
Cohort and nested case-control studies of hematopoietic cancers and brain cancer among electric
utility workers.
Comparative analyses of the studies of magnetic fields and cancer in electric utility workers:
studies from France, Canada, and the United States.
Comparative health risk assessment of electromagnetic fields.
Computer screens and brain cancer.
Concern that "EMF" magnetic fields from power lines cause cancer.
Correlation between cellular phone use and epithelial parotid gland malignancies.
Current state of our knowledge on brain tumor epidemiology.
Cytotoxicity of temozolomide on human glioblastoma cells is enhanced by the concomitant
exposure to an extremely low-frequency electromagnetic field (100Hz, 100G).
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Danger of cellular telephones and their relay stations].
Decreased survival of glioma patients with astrocytoma grade IV (glioblastoma multiforme)
associated with long-term use of mobile and cordless phones.
Do people understand IARC's 2B categorization of RF fields from cell phones?
Does cell phone use increase the chances of parotid gland tumor development? A systematic
review and meta-analysis.
Ecological study on residences in the vicinity of AM radio broadcasting towers and cancer death:
preliminary observations in Korea.
Effect of magnetic field exposure on anchorage-independent growth of a promoter-sensitive
mouse epidermal cell line (JB6).
Effect of Mobile Phone-Induced Electromagnetic Field on Brain Hemodynamics and Human
Stem Cell Functioning: Possible Mechanistic Link to Cancer Risk and Early Diagnostic Value of
Electronphotonic Imaging.
Effect of radiofrequency radiation exposure on mouse skin tumorigenesis initiated by 7,12-
dimethybenz[alpha]anthracene.
Effects of 2.45-GHz microwave radiation and phorbol ester 12-O-tetradecanoylphorbol-13-
acetate on dimethylhydrazine-induced colon cancer in mice.
Effects of 2450 MHz electromagnetic fields with a wide range of SARs on methylcholanthrene-
induced transformation in C3H10T1/2 cells.
Effects of 900 MHz GSM wireless communication signals on DMBA-induced mammary tumors
in rats.
Effects of a 2450 MHz high-frequency electromagnetic field with a wide range of SARs on the
induction of heat-shock proteins in A172 cells.
Effects of electromagnetic fields on health].
Effects of electromagnetic radiation of mobile phones on the central nervous system.
Effects of exposure to a 1950 MHz radio frequency field on expression of Hsp70 and Hsp27 in
human glioma cells.
Effects of GSM-900 microwaves on DMBA-induced mammary gland tumors in female Sprague-
Dawley rats.
Effects of low level microwave radiation on carcinogenesis in Swiss Albino mice.
Effects of mobile phone radiation on UV-induced skin tumourigenesis in ornithine
decarboxylase transgenic and non-transgenic mice.
Electric and magnetic field exposure and brain cancer: a review.
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Electric blanket or mattress cover use and breast cancer incidence in women 50-79 years of age.
Electric Blanket Use and Risk of Thyroid Cancer in the Women's Health Initiative Observational
Cohort.
Electrical field exposure and human health. Risk assessment and problems relative to
bureaucratic procedures and to the role of instituitional organizations in control and prevention].
Electromagnetic field exposures and childhood cancers in New Zealand.
Electromagnetic fields and brain tumours: a commentary.
Electromagnetic fields and cancer risks.
Electromagnetic fields and cancer: the cost of doing nothing.
Electromagnetic fields and cells.
Electromagnetic fields and female breast cancer.
Electromagnetic fields and health effects--epidemiologic studies of cancer, diseases of the central
nervous system and arrhythmia-related heart disease.
Electromagnetic fields and public health.
Electromagnetic fields from high-voltage installations and cancer in childhood].
Electromagnetic fields of mobile telephone systems--thresholds, effects and risks for cochlear
implant patients and healthy people].
Electromagnetic fields--effects on health].
Electromagnetic fields: a cancer promoter?
Electromagnetic radiations and cancer. Cause and prevention.
Electromagnetic-field exposure and cancer.
Electrosmog as a health risk factor: sources of artificial electromagnetic fields, evaluation of
health risk, prevention methods].
EMF and health.
Environmental risk factors for brain tumors.
Environmental risk factors for sporadic acoustic neuroma (Interphone Study Group, Germany).
Epidemiologic evidence on mobile phones and tumor risk: a review.
Epidemiologic evidence relevant to radar (microwave) effects.
Epidemiologic study of residential proximity to transmission lines and childhood cancer in
California: description of design, epidemiologic methods and study population.
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Epidemiological appraisal of studies of residential exposure to power frequency magnetic fields
and adult cancers.
Epidemiological studies of human exposures to radiofrequency radiation. A critical review.
Epidemiological studies of radio frequency exposures and human cancer.
Epidemiological study of power lines and childhood cancer in the UK: further analyses.
Epidemiology and etiology of gliomas.
Epidemiology of brain tumors.
Epidemiology of health effects of radiofrequency exposure.
Epidemiology of Intracranial Gliomas.
Estimates of Environmental Exposure to Radiofrequency Electromagnetic Fields and Risk of
Lymphoma Subtypes.
Estimating associations of mobile phone use and brain tumours taking into account laterality: a
comparison and theoretical evaluation of applied methods.
Estimating exposure in studies of residential magnetic fields and cancer: importance of short-
term variability, time interval between diagnosis and measurement, and distance to power line.
Evaluation of carcinogenic effects of electromagnetic fields (EMF).
Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill
Viewpoints from 1965 on Association or Causation.
Evaluation of potential confounders in planning a study of occupational magnetic field exposure
and female breast cancer.
Evaluation of residential exposure to intermediate frequency magnetic fields.
Evaluation of the effects of electric and magnetic fields in humans].
Evaluation of the potential carcinogenicity of 60 Hz linear sinusoidal continuous-wave magnetic
fields in Fischer F344 rats.
Evaluation of the potential of mobile phone specific electromagnetic fields (UMTS) to produce
micronuclei in human glioblastoma cell lines.
Experimental data on radiofrequency].
Exposure to 2.45 GHz electromagnetic fields induces hsp70 at a high SAR of more than 20 W/kg
but not at 5W/kg in human glioma MO54 cells.
Exposure to 50-Hz electric field and incidence of leukemia, brain tumors, and other cancers
among French electric utility workers.
Exposure to 60-Hz magnetic fields and proliferation of human astrocytoma cells in vitro.
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Exposure to low electromagnetic fields and the carcinogenesis process].
Exposure to power frequency electric fields and the risk of childhood cancer in the UK.
Exposure to power-frequency magnetic fields and the risk of childhood cancer. UK Childhood
Cancer Study Investigators.
Exposure to radio-frequency electromagnetic fields from broadcast transmitters and risk of
childhood cancer: a census-based cohort study.
Extremely low frequency electromagnetic fields (EMF) and brain cancer in adults and children:
review and comment.
Extremely low frequency electromagnetic fields and cancer: the epidemiologic evidence.
Extremely low-frequency electromagnetic fields exposure and female breast cancer risk: a meta-
analysis based on 24,338 cases and 60,628 controls.
Fifty Hertz electromagnetic field exposure stimulates secretion of beta-amyloid peptide in
cultured human neuroglioma.
Follow-up of radio and telegraph operators with exposure to electromagnetic fields and risk of
breast cancer.
Further aspects on cellular and cordless telephones and brain tumours.
Future needs of occupational epidemiology of extremely low frequency electric and magnetic
fields: review and recommendations.
Genetic, carcinogenic and teratogenic effects of radiofrequency fields.
GSM and DCS wireless communication signals: combined chronic toxicity/carcinogenicity study
in the Wistar rat.
Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29
years ago?
Health effects of electromagnetic fields].
Health effects of microwave exposures: a review of the recent (1995-1998) literature.
Health risks from the use of mobile phones.
Health risks of electric and magnetic fields caused by high-voltage systems in Finland.
Health risks of electromagnetic fields. Part I: Evaluation and assessment of electric and magnetic
fields.
Health risks of exposure to non-ionizing radiation--myths or science-based evidence.
Health risks of mobile phones].
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Hematopoietic neoplasia in C57BL/6 mice exposed to split-dose ionizing radiation and circularly
polarized 60 Hz magnetic fields.
High-voltage overhead power lines in epidemiology: patterns of time variations in current load
and magnetic fields.
How dangerous are mobile phones, transmission masts, and electricity pylons?
Human disease resulting from exposure to electromagnetic fields.
Immunotropic effects of electromagnetic fields in the range of radio- and microwave
frequencies].
Impact of random and systematic recall errors and selection bias in case--control studies on
mobile phone use and brain tumors in adolescents (CEFALO study).
Improved classification of evidence for EMF health risks.
In vitro and in vivo studies of the "VITA" device].
Incidence of breast cancer in a Norwegian cohort of women with potential workplace exposure
to 50 Hz magnetic fields.
Incidence of cancer in the vicinity of Korean AM radio transmitters.
Incidence of leukaemia and brain tumours in some "electrical occupations".
Incorporation of epidemiological findings into radiation protection standards.
Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies.
Indication of cocarcinogenic potential of chronic UMTS-modulated radiofrequency exposure in
an ethylnitrosourea mouse model.
Inferring the 1985-2014 impact of mobile phone use on selected brain cancer subtypes using
Bayesian structural time series and synthetic controls.
Influence of low frequency electromagnetic fields on the nervous system].
Interactions between occupational exposure to extremely low frequency magnetic fields and
chemicals for brain tumour risk in the INTEROCC study.
Interactive effect of chemical substances and occupational electromagnetic field exposure on the
risk of gliomas and meningiomas in Swedish men.
Invited commentary: electromagnetic fields and cancer in railway workers.
Leukaemia, brain tumours and exposure to extremely low frequency magnetic fields: cohort
study of Swiss railway employees.
Leukemia, brain tumors, and exposure to extremely low frequency electromagnetic fields in
Swiss railway employees.
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Location of gliomas in relation to mobile telephone use: a case-case and case-specular analysis.
Long-term and frequent cellular phone use and risk of acoustic neuroma.
Long-term mobile phone use and acoustic neuroma risk.
Long-term mobile phone use and brain tumor risk.
Long-term mobile phone use and the risk of vestibular schwannoma: a Danish nationwide cohort
study.
Long-term use of cellular phones and brain tumours: increased risk associated with use for > or
=10 years.
Long-term use of mobile phone and its association with glioma: a systematic review and meta-
analysis].
Long-term, low-level microwave irradiation of rats.
Los Angeles study of residential magnetic fields and childhood brain tumors.
Lost in laterality: interpreting ''preferred side of the head during mobile phone use and risk of
brain tumour'' associations.
Low frequency electromagnetic fields in the working environment--exposure and health effects.
Elevated risk of cancer, reproductive hazards or other unwanted health effects?].
Low-frequency electromagnetic radiation enhances the induction of rat mammary tumors by
nitrosomethyl urea.
Low-level exposure to radiofrequency electromagnetic fields: health effects and research needs.
Lymphoma development of simultaneously combined exposure to two radiofrequency signals in
AKR/J mice.
Magnetic field exposure in relation to leukemia and brain cancer mortality among electric utility
workers.
Magnetic fields and brain tumour risks in UK electricity supply workers.
Magnetic fields and breast cancer in Swedish adults residing near high-voltage power lines.
Magnetic fields and childhood cancer--a pooled analysis of two Scandinavian studies.
Magnetic fields and childhood cancer: an epidemiological investigation of the effects of high-
voltage underground cables.
Magnetic fields of high voltage power lines and risk of cancer in Finnish adults: nationwide
cohort study.
Magnetic fields, leukemia, and central nervous system tumors in Swedish adults residing near
high-voltage power lines.
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Malignant melanoma of the skin - not a sunshine story!
Maternal occupational exposure to extremely low frequency magnetic fields and the risk of brain
cancer in the offspring.
Medical aspects of radiofrequency radiation overexposure.
Medical exposure to ionising radiation and the risk of brain tumours: Interphone study group,
Germany.
Melanoma incidence and frequency modulation (FM) broadcasting.
Melatonin suppression by static and extremely low frequency electromagnetic fields: relationship
to the reported increased incidence of cancer.
Meningioma and mobile phone use--a collaborative case-control study in five North European
countries.
Meningioma patients diagnosed 2007-2009 and the association with use of mobile and cordless
phones: a case-control study.
Meta-analysis of association between mobile phone use and glioma risk.
Meta-analysis of long-term mobile phone use and the association with brain tumours.
Meta-analysis of mobile phone use and intracranial tumors.
Methods used to calculate exposures in two epidemiological studies of power lines in the UK.
Mobile phone base stations and early childhood cancers: case-control study.
Mobile phone radiation and the risk of cancer; a review.
Mobile phone radiation causes brain tumors and should be classified as a probable human
carcinogen (2A) (review).
Mobile Phone Radiation: Physiological & Pathophysiologcal Considerations.
Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide
excision repair in serum-deprived human glioblastoma cells.
Mobile phone use and acoustic neuroma risk in Japan.
Mobile phone use and brain tumors in children and adolescents: a multicenter case-control study.
Mobile phone use and brain tumours in the CERENAT case-control study.
Mobile phone use and glioma risk: A systematic review and meta-analysis.
Mobile phone use and glioma risk: comparison of epidemiological study results with incidence
trends in the United States.
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Mobile phone use and incidence of brain tumour histological types, grading or anatomical
location: a population-based ecological study.
Mobile phone use and incidence of glioma in the Nordic countries 1979-2008: consistency
check.
Mobile phone use and location of glioma: a case-case analysis.
Mobile phone use and risk for intracranial tumors and salivary gland tumors - A meta-analysis.
Mobile phone use and risk for intracranial tumors.
Mobile phone use and risk of acoustic neuroma: results of the Interphone case-control study in
five North European countries.
Mobile phone use and risk of brain neoplasms and other cancers: prospective study.
Mobile phone use and risk of brain tumours: a systematic review of association between study
quality, source of funding, and research outcomes.
Mobile phone use and risk of glioma in 5 North European countries.
Mobile phone use and risk of glioma in adults: case-control study.
Mobile phone use and risk of intracranial tumors: a consistency analysis.
Mobile phone use and risk of parotid gland tumor.
Mobile phone use and risk of tumors: a meta-analysis.
Mobile phone use and the risk for malignant brain tumors: a case-control study on deceased
cases and controls.
Mobile phone use and the risk of acoustic neuroma.
Mobile Phone Use and the Risk of Parotid Gland Tumors: A Retrospective Case-Control Study.
Mobile phone use and the risk of skin cancer: a nationwide cohort study in Denmark.
Mobile phone use, exposure to radiofrequency electromagnetic field, and brain tumour: a case-
control study.
Mobile phones and brain tumours: a review of epidemiological research.
Mobile phones and head tumours. The discrepancies in cause-effect relationships in the
epidemiological studies - how do they arise?
Mobile phones and head tumours: it is time to read and highlight data in a proper way].
Mobile phones, brain tumors, and the interphone study: where are we now?
Mobile phones, cordless phones and rates of brain tumors in different age groups in the Swedish
National Inpatient Register and the Swedish Cancer Register during 1998-2015.
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Mobile phones, cordless phones and the risk for brain tumours.
Mobile phones, mobile phone base stations and cancer: a review.
Mobile phones: influence on auditory and vestibular systems.
Mortality from brain cancer and leukaemia among electrical workers.
Mortality in workers exposed to electromagnetic fields.
Mortality indices for hemoblastoses in Rivno Province before and after the accident at the
Chernobyl Atomic Electric Power Station].
Motivation and significance of IARC classification for mobile phone].
Need for a European approach to the effects of extremely low-frequency electromagnetic fields
on cancer. ELF-EMF European Feasibility Study Group.
New Zealand adolescents' cellphone and cordless phone user-habits: are they at increased risk of
brain tumours already? A cross-sectional study.
Non dietetic environmental risk factors in prostate cancer].
Non-ionizing electromagnetic radiation and cancer--is there a relationship?
Non-ionizing electromagnetic radiation: a study of carcinogenic and cancer treatment potential.
Non-thermal bioeffects of static and extremely low frequency electromagnetic fields].
Nonionizing electromagnetic fields and cancer: a review.
Normal doses of visible light can cause mutations in skin].
Occupational and residential exposure to electromagnetic fields and risk of brain tumors in
adults: a case-control study in Gironde, France.
Occupational and residential magnetic field exposure and leukemia and central nervous system
tumors.
Occupational electric and magnetic field exposure and brain cancer: a meta-analysis.
Occupational exposure to electromagnetic fields and its health effects in electric energy
workers].
Occupational exposure to electromagnetic fields and sex-differential risk of uveal melanoma.
Occupational exposure to electromagnetic fields and the occurrence of brain tumors. An analysis
of possible associations.
Occupational exposure to high-frequency electromagnetic fields and brain tumor risk in the
INTEROCC study: An individualized assessment approach.
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Occupational exposure to ionizing and non-ionizing radiation and risk of non-Hodgkin
lymphoma.
Occupational exposure to ionizing radiation and electromagnetic fields in relation to the risk of
thyroid cancer in Sweden.
Occupational exposure to low frequency magnetic fields and the risk of low grade and high
grade glioma.
Occupational exposure to magnetic fields and brain tumours in central Sweden.
Occupational exposure to magnetic fields and the risk of brain tumors.
Occupational exposure to non-ionizing radiation and an association with heart disease: an
exploratory study.
Occupational exposure to power frequency magnetic fields and risk of non-Hodgkin lymphoma.
Occupational exposure to radio frequency/microwave radiation and the risk of brain tumors:
Interphone Study Group, Germany.
Occupational exposures and brain cancer mortality: a preliminary study of east Texas residents.
Occupational magnetic field exposure and the risk of acoustic neuroma.
Occupational risk factors for cancer of the central nervous system: a case-control study on death
certificates from 24 U.S. states.
Overview of epidemiologic research on electric and magnetic fields and cancer.
p53 immunoreactivity in cutaneous PUVA tumors is similar to that in other non-melanoma skin
neoplasms.
Panel exploring pro and con arguments as to whether EMFs cause childhood brain cancer.
Parental occupational exposure to magnetic fields and childhood cancer (Sweden).
Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male
reproductive system.
Physical basis of adverse and therapeutic effects of low intensity microwave radiation.
Pooled analysis of case-control studies on acoustic neuroma diagnosed 1997-2003 and 2007-
2009 and use of mobile and cordless phones.
Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and
cordless phones including living and deceased subjects.
Pooled analysis of Swedish case-control studies during 1997-2003 and 2007-2009 on
meningioma risk associated with the use of mobile and cordless phones.
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Possible cocarcinogenic effects of ELF electromagnetic fields may require repeated long-term
interaction with known carcinogenic factors.
Possible effects of radiofrequency electromagnetic fields on in vivo C6 brain tumors in Wistar
rats.
Possible health hazards from exposure to power-frequency electric and magnetic fields--a
COMAR Technical Information Statement.
Power-frequency magnetic fields and childhood brain tumors: a case-control study in Japan.
Primary brain cancer in adults and the use of common household appliances: a case-control
study.
Probabilistic Multiple-Bias Modeling Applied to the Canadian Data From the Interphone Study
of Mobile Phone Use and Risk of Glioma, Meningioma, Acoustic Neuroma, and Parotid Gland
Tumors.
Public health and the radio frequency radiation emitted by cellphone technology, smart meters
and WiFi.
Quantifying the impact of selection bias caused by nonparticipation in a case-control study of
mobile phone use.
Radiation exposure, socioeconomic status, and brain tumor risk in the US Air Force: a nested
case-control study.
Radio and microwave frequency radiation and health--an analysis of the literature].
Radio frequency electromagnetic fields: cancer, mutagenesis, and genotoxicity.
Radio-frequency radiation exposure from AM radio transmitters and childhood leukemia and
brain cancer.
Radiofrequency and microwave radiation in the microelectronics industry.
Radiofrequency electromagnetic fields emitted from base stations of DECT cordless phones and
the risk of glioma and meningioma (Interphone Study Group, Germany).
Radiofrequency exposure and mammalian cell toxicity, genotoxicity, and transformation.
Radiofrequency exposure and mortality from cancer of the brain and lymphatic/hematopoietic
systems.
Radiofrequency field exposure and cancer: what do the laboratory studies suggest?
Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering
factor.
Rate of occurrence of transient magnetic field events in U.S. residences.
Reanalysis of risks of childhood leukaemia with distance from overhead power lines in the UK.
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Recent advances in research on radiofrequency fields and health: 2001-2003.
Recent advances in research on radiofrequency fields and health: 2004-2007.
Recent data from the literature on the biological and pathologic effects of electromagnetic
radiation, radio waves and stray currents].
Refinements in magnetic field exposure assignment for a case-cohort study of electrical utility
workers.
Repeated exposure of C3H/HeJ mice to ultra-wideband electromagnetic pulses: lack of effects on
mammary tumors.
Report of final results regarding brain and heart tumors in Sprague-Dawley rats exposed from
prenatal life until natural death to mobile phone radiofrequency field representative of a 1.8GHz
GSM base station environmental emission.
Residential electric consumption and childhood cancer in Canada (1971-1986)
Residential exposure to 60-Hertz magnetic fields and adult cancers in Taiwan.
Residential magnetic field exposure and childhood brain cancer: a meta-analysis.
Residential mobility of populations near UK power lines and implications for childhood
leukaemia.
Review of four publications on the Danish cohort study on mobile phone subscribers and risk of
brain tumors.
Review of possible modulation-dependent biological effects of radiofrequency fields.
Review of the epidemiologic literature on EMF and Health.
Review on health effects related to mobile phones. Part II: results and conclusions.
Risk for leukaemia and brain and breast cancer among Danish utility workers: a second follow-
up.
Risk of brain tumors from wireless phone use.
Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five
Interphone countries.
Risk of cancer among Danish electricity workers. A cohort study].
Risk of neoplastic diseases in conditions of exposure to power magnetic fields--epidemiologic
investigations].
Risk of neoplastic diseases in conditions of exposure to radio- and microwave fields--
epidemiologic investigations].
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Selection bias due to differential participation in a case-control study of mobile phone use and
brain tumors.
Selection bias from differential residential mobility as an explanation for associations of wire
codes with childhood cancer.
Self-reported electrical appliance use and risk of adult brain tumors.
Setting prudent public health policy for electromagnetic field exposures.
Should the threshold limit value for power frequency (60 Hz) magnetic fields be changed?
Perceptions among scientists and other risk experts.
Significant differences in the effects of magnetic field exposure on 7,12-
dimethylbenz(a)anthracene-induced mammary carcinogenesis in two substrains of Sprague-
Dawley rats.
Simulation of the incidence of malignant brain tumors in birth cohorts that started using mobile
phones when they first became popular in Japan.
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer
344 rats chronically exposed to 836 MHz modulated microwaves.
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer
344 rats exposed to frequency-modulated microwave fields.
Studies of childhood brain tumors using immunohistochemistry and microwave technology:
methodological considerations.
Studying the effects of mobile phone use on the auditory system and the central nervous system:
a review of the literature and future directions.
Survival and cancer in laboratory mammals exposed to radiofrequency energy.
Survival of glioma patients in relation to mobile phone use in Denmark, Finland and Sweden.
Symptomatic complex partial status epilepticus manifesting as utilization behavior of a mobile
phone.
Systematic review of wireless phone use and brain cancer and other head tumors.
The anatomical distribution of cerebral gliomas in mobile phone users.
The controversy about a possible relationship between mobile phone use and cancer.
The controversy about a possible relationship between mobile phone use and cancer.
The design, construction and calibration of a carefully controlled source for exposure of
mammalian cells to extremely low-frequency electromagnetic fields.
The effect of 60-Hz magnetic fields on co-promotion of chemically induced skin tumors on
SENCAR mice: a discussion of three studies.
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The effect of chronic exposure to 835.62 MHz FDMA or 847.74 MHz CDMA radiofrequency
radiation on the incidence of spontaneous tumors in rats.
The effect of embryonic and fetal exposure to x-ray, microwaves, and ultrasound: counseling the
pregnant and nonpregnant patient about these risks.
The effects of 860 MHz radiofrequency radiation on the induction or promotion of brain tumors
and other neoplasms in rats.
The effects of embryonic and fetal exposure to x-ray, microwaves, and ultrasound.
The effects of ionizing radiation, microwaves, and ultrasound on the developing embryo: clinical
interpretations and applications of the data.
The effects of pulsed 860 MHz radiofrequency radiation on the promotion of neurogenic tumors
in rats.
The epidemiology of electric and magnetic field exposures in the power frequency range and
reproductive outcomes.
The estimation of 3D SAR distributions in the human head from mobile phone compliance
testing data for epidemiological studies.
The IARC carcinogenicity evaluation of radio-frequency electromagnetic field: with special
reference to epidemiology of mobile phone use and brain tumor risk].
The incidence rate and mortality of malignant brain tumors after 10 years of intensive cell phone
use in Taiwan.
The Intracranial Distribution of Gliomas in Relation to Exposure From Mobile Phones: Analyses
From the INTERPHONE Study.
The possible role of contact current in cancer risk associated with residential magnetic fields.
The possible role of radiofrequency radiation in the development of uveal melanoma.
The potential carcinogenic hazards of electromagnetic radiation: a review.
The precautionary principle and electric and magnetic fields.
The probability of developing brain tumours among users of cellular telephones (scientific
information to the decision of the International Agency for Research on Cancer (IARC)
announced on May 31, 2011)].
The problem of hygienic standardization of commercial electric and magnetic fields in Russia
and other countries].
The question of health effects from exposure to electromagnetic fields.
The role of chemical and physical factors in cancer development].
The sensitivity of children to electromagnetic fields.
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Thermal and non-thermal health effects of low intensity non-ionizing radiation: An international
perspective.
Time trend in incidence of malignant neoplasms of the central nervous system in relation to
mobile phone use among young people in Japan.
Time trends (1998-2007) in brain cancer incidence rates in relation to mobile phone use in
England.
Trends in incidence of primary brain cancer in New Zealand, 1995 to 2010.
Uncertainty in the relation between exposure to magnetic fields and brain cancer due to
assessment and assignment of exposure and analytical methods in dose-response modeling.
Use of cellular and cordless telephones and risk of testicular cancer.
Use of cellular telephones and brain tumour risk in urban and rural areas.
Use of cellular telephones and risk of cancer. A Danish cohort study].
Use of cellular telephones and the risk for brain tumours: A case-control study.
Use of mobile and cordless phones and survival of patients with glioma.
Use of mobile phones and cancer risk.
Use of mobile phones and risk of brain tumours: update of Danish cohort study.
Use of mobile phones in Norway and risk of intracranial tumours.
Use of wireless phones and the risk of salivary gland tumours: a case-control study.
Using the Hill viewpoints from 1965 for evaluating strengths of evidence of the risk for brain
tumors associated with use of mobile and cordless phones.
Validation of self-reported start year of mobile phone use in a Swedish case-control study on
radiofrequency fields and acoustic neuroma risk.
Variation in cancer risk estimates for exposure to powerline frequency electromagnetic fields: a
meta-analysis comparing EMF measurement methods.
Vestibular schwannoma and cell-phones. Results, limits and perspectives of clinical studies.
Wire codes, magnetic fields, and childhood cancer.
Wireless Phone Use and Risk of Adult Glioma: Evidence from a Meta-Analysis.
World Health Organization, radiofrequency radiation and health - a hard nut to crack (Review).
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FACTOR 6
Theme
–
Sensory disorders
Key MeSH Headings - Burning Mouth Syndrome, Taste Disorders, Skin Diseases, Mouth
Diseases, Dizziness, Vision Disorders, Hypersensitivity, Delayed, Fatigue
Titles
A method for in vivo detection of abnormal subepidermal tissues based on dielectric properties.
A survey study on some neurological symptoms and sensations experienced by long term users
of mobile phones.
Adverse cutaneous effects of ionizing and non-ionizing electromagnetic radiation.
Association between exposure to radiofrequency electromagnetic fields assessed by dosimetry
and acute symptoms in children and adolescents: a population based cross-sectional study.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep
disturbance in Saudi population.
Bedtime mobile phone use and sleep in adults.
Can exposure to a terrestrial trunked radio (TETRA)-like signal cause symptoms? A randomised
double-blind provocation study.
Cardiac devices and electromagnetic interference revisited: new radiofrequency technologies and
implications for dermatologic surgery.
Description of persons with symptoms presumed to be caused by electricity or visual display
units--oral aspects.
Effect of millimeter waves on cyclophosphamide induced suppression of the immune system.
Effect of stress and intesity of mobile phone using on the health and subjective symptoms in
GSM workers].
Electromagnetic hypersensitivity (EHS) and subjective health complaints associated with
electromagnetic fields of mobile phone communication--a literature review published between
2000 and 2004.
Environmental illness: fatigue and cholinesterase activity in patients reporting hypersensitivity to
electricity.
Health response of two communities to military antennae in Cyprus.
Health status of the workers exposed to strong, constant magnetic fields].
Human exposure to 4.0-Tesla magnetic fields in a whole-body scanner.
Immune function and host defense in rodents exposed to 60-Hz magnetic fields.
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Immunomorphologic changes in the testes upon exposure to a microwave electromagnetic field].
Interference with cardiac pacemakers by cellular telephones.
Microwave sickness: a reappraisal.
Mobile communication: radiobiology problems and evaluation of danger].
Mobile phone use and subjective symptoms. Comparison of symptoms experienced by users of
analogue and digital mobile phones.
Mobile phone use, school electromagnetic field levels and related symptoms: a cross-sectional
survey among 2150 high school students in Izmir.
Neurobehavioral effects among inhabitants around mobile phone base stations.
Non-specific physical symptoms and electromagnetic field exposure in the general population:
can we get more specific? A systematic review.
Odontologic survey of referred patients with symptoms allegedly caused by electricity or visual
display units.
Provocation with stress and electricity of patients with "sensitivity to electricity".
Psychologic aspects of patients with symptoms presumed to be caused by electricity or visual
display units.
Some ocular symptoms and sensations experienced by long term users of mobile phones.
Some ocular symptoms experienced by users of mobile phones.
Specific patterns of weak (1 microTesla) transcerebral complex magnetic fields differentially
affect depression, fatigue, and confusion in normal volunteers.
Study of human neurovegetative and hematologic effects of environmental low-frequency (50-
Hz) electromagnetic fields produced by transformers.
Subjective symptoms related to mobile phone use--a pilot study].
Symptoms experienced by people in vicinity of base stations: II/ Incidences of age, duration of
exposure, location of subjects in relation to the antennas and other electromagnetic factors].
Symptoms of ill health ascribed to electromagnetic field exposure--a questionnaire survey.
Symptoms, personality traits, and stress in people with mobile phone-related symptoms and
electromagnetic hypersensitivity.
The effects of cell phone use on peripheral vision.
The effects of multivitamin supplementation on mood and general well-being in healthy young
adults. A laboratory and at-home mobile phone assessment.
The risk of subjective symptoms in mobile phone users in Poland--an epidemiological study.
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Video display terminals: risk of electromagnetic radiation.
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FACTOR 7
Theme
–
Breast neoplasms
Key MeSH Headings - Carcinoma, Lobular, Carcinoma, Ductal, Breast, Breast Neoplasms,
Male, Adenoma
Titles
A cluster of male breast cancer in office workers.
A meta-analysis of epidemiologic studies of electric and magnetic fields and breast cancer in
women and men.
Breast cancer, occupation, and exposure to electromagnetic fields among Swedish men.
Carcinogenic risk of extremely-low-frequency electromagnetic fields: state of the art].
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in F344/N
rats.
Effect of 13 week magnetic field exposures on DMBA-initiated mammary gland carcinomas in
female Sprague-Dawley rats.
Electromagnetic field exposure and male breast cancer risk: a meta-analysis of 18 studies.
Epidemiology and aetiological factors of male breast cancer: a ten years retrospective study in
eastern Turkey.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Magnetic fields and breast cancer in Swedish adults residing near high-voltage power lines.
Magnetic fields and mammary cancer in rodents: a critical review and evaluation of published
literature.
Male breast tumors in railway engine drivers: investigation of 5 cases].
Occupational exposure to magnetic fields in relation to male breast cancer and testicular cancer:
a Swedish case-control study.
Risk for leukaemia and brain and breast cancer among Danish utility workers: a second follow-
up.
The relationship between electromagnetic field and light exposures to melatonin and breast
cancer risk: a review of the relevant literature.
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FACTOR 8
Theme
–
Oxidative stress
Key MeSH Headings - Oxidative Stress, Malondialdehyde, Glutathione Peroxidase, Lipid
Peroxidation, Reactive Oxygen Species, Apoptosis, DNA Damage, Nitric Oxide, Protein
Carbonylation
Titles
14.6 mT ELF magnetic field exposure yields no DNA breaks in model system Salmonella, but
provides evidence of heat stress protection.
1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53
dependent Bax mediated testicular apoptosis in mice, Mus musculus.
1950MHz Radio Frequency Electromagnetic Radiation Inhibits Testosterone Secretion of Mouse
Leydig Cells.
2.1 GHz electromagnetic field does not change contractility and intracellular Ca2+ transients but
decreases beta-adrenergic responsiveness through nitric oxide signaling in rat ventricular
myocytes.
2.45 GHz microwave irradiation-induced oxidative stress affects implantation or pregnancy in
mice, Mus musculus.
2.45 GHz Microwave Radiation Impairs Learning and Spatial Memory via Oxidative/Nitrosative
Stress Induced p53-Dependent/Independent Hippocampal Apoptosis: Molecular Basis and
Underlying Mechanism.
2.45 GHz microwave radiation induced oxidative and nitrosative stress mediated testicular
apoptosis: Involvement of a p53 dependent bax-caspase-3 mediated pathway.
2.45-GHz microwave irradiation adversely affects reproductive function in male mouse, Mus
musculus by inducing oxidative and nitrosative stress.
2.45-Gz wireless devices induce oxidative stress and proliferation through cytosolic Ca(2)(+)
influx in human leukemia cancer cells.
50 Hz extremely low frequency electromagnetic fields enhance protein carbonyl groups content
in cancer cells: effects on proteasomal systems.
50-Hertz electromagnetic fields induce gammaH2AX foci formation in mouse preimplantation
embryos in vitro.
8-Oxo-7, 8-dihydro-2'-deoxyguanosine as a biomarker of DNA damage by mobile phone
radiation.
8-oxoG DNA glycosylase-1 inhibition sensitizes Neuro-2a cells to oxidative DNA base damage
induced by 900 MHz radiofrequency electromagnetic radiation.
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900 MHz pulse-modulated radiofrequency radiation induces oxidative stress on heart, lung, testis
and liver tissues.
900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat
endometrium: protection by vitamins E and C.
900-MHz microwave radiation enhances gamma-ray adverse effects on SHG44 cells.
900-MHz microwave radiation promotes oxidation in rat brain.
915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci
in human lymphocytes from hypersensitive and healthy persons.
A 700 MHz 1H-NMR study reveals apoptosis-like behavior in human K562 erythroleukemic
cells exposed to a 50 Hz sinusoidal magnetic field.
A comparative analysis of the biological action of microwaves and laser radiation].
A critical review of the genotoxic potential of electric and magnetic fields.
A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a
mobile phone base station.
A cross-sectional study on oxidative stress in workers exposed to extremely low frequency
electromagnetic fields.
A histopathological and biochemical evaluation of oxidative injury in the sciatic nerves of male
rats exposed to a continuous 900-megahertz electromagnetic field throughout all periods of
adolescence.
Acute exposure to 930 MHz CW electromagnetic radiation in vitro affects reactive oxygen
species level in rat lymphocytes treated by iron ions.
Acute exposure to a 60 Hz magnetic field increases DNA strand breaks in rat brain cells.
Acute low-intensity microwave exposure increases DNA single-strand breaks in rat brain cells.
Adaptive response in mice exposed to 900 MHZ radiofrequency fields: bleomycin-induced DNA
and oxidative damage/repair.
Adaptive response in mice exposed to 900 MHz radiofrequency fields: primary DNA damage.
Adaptive response in mouse bone-marrow stromal cells exposed to 900-MHz radiofrequency
fields: Gamma-radiation-induced DNA strand breaks and repair.
Adverse and beneficial effects in Chinese hamster lung fibroblast cells following radiofrequency
exposure.
Age diseases depending on geomagnetic field activity inside the womb period].
Age-related effects on induction of DNA strand breaks by intermittent exposure to
electromagnetic fields.
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An evaluation of genotoxicity in human neuronal-type cells subjected to oxidative stress under
an extremely low frequency pulsed magnetic field.
An in vitro study of the effects of exposure to a GSM signal in two human cell lines: monocytic
U937 and neuroblastoma SK-N-SH.
Analysis of proto-oncogene and heat-shock protein gene expression in human derived cell-lines
exposed in vitro to an intermittent 1.9 GHz pulse-modulated radiofrequency field.
Antioxidants alleviate electric field-induced effects on lung tissue based on assays of heme
oxygenase-1, protein carbonyl content, malondialdehyde, nitric oxide, and hydroxyproline.
Anxiety-like behavioural effects of extremely low-frequency electromagnetic field in rats.
Apoptosis in haemopoietic progenitor cells exposed to extremely low-frequency magnetic fields.
Apoptosis induced by microwave radiation in pancreatic cancer JF305 cells.
Apoptosis induced by ultraviolet radiation is enhanced by amplitude modulated radiofrequency
radiation in mutant yeast cells.
Apoptosis is induced by radiofrequency fields through the caspase-independent mitochondrial
pathway in cortical neurons.
Apoptosis of Lewis Lung Carcinoma Cells Induced by Microwave via p53 and Proapoptotic
Proteins In vivo.
Apoptotic cell death during Drosophila oogenesis is differentially increased by electromagnetic
radiation depending on modulation, intensity and duration of exposure.
Assessment of biological changes of continuous whole body exposure to static magnetic field
and extremely low frequency electromagnetic fields in mice.
Assessment of cytogenetic damage and oxidative stress in personnel occupationally exposed to
the pulsed microwave radiation of marine radar equipment.
Assessment of DNA sensitivity in peripheral blood leukocytes after occupational exposure to
microwave radiation: the alkaline comet assay and chromatid breakage assay.
Assessment of genetic damage in peripheral blood of human volunteers exposed (whole-body) to
a 200 muT, 60 Hz magnetic field.
Assessment of genotoxicity and genomic instability in rat primary astrocytes exposed to 872
MHz radiofrequency radiation and chemicals.
Assessment of nuclear abnormalities in exfoliated cells from the oral epithelium of mobile phone
users.
Assessment of oxidant/antioxidant status in saliva of cell phone users.
Association of microwaves and ionizing radiation: potentiation of teratogenic effects in the rat.
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Autoimmune processes after long-term low-level exposure to electromagnetic fields (the results
of an experiment). Part 4. Manifestation of oxidative intracellular stress-reaction after long-term
non-thermal EMF exposure of rats].
Biochemical and histological studies on adverse effects of mobile phone radiation on rat's brain.
Biochemical and pathological changes in the male rat kidney and bladder following exposure to
continuous 900-MHz electromagnetic field on postnatal days 22-59<sup/>.
Biochemical modifications and neuronal damage in brain of young and adult rats after long-term
exposure to mobile phone radiations.
Bioeffects of microwave--a brief review.
Bioelectromagnetic field effects on cancer cells and mice tumors.
Biological effects of non-ionizing electromagnetic fields: Two sides of a coin.
Biological responses of mobile phone frequency exposure.
Biological stress responses to radio frequency electromagnetic radiation: are mobile phones
really so (heat) shocking?
Biophysical evaluation of radiofrequency electromagnetic field effects on male reproductive
pattern.
Blocking 1800 MHz mobile phone radiation-induced reactive oxygen species production and
DNA damage in lens epithelial cells by noise magnetic fields].
Calreticulin protects rat microvascular endothelial cells against microwave radiation-induced
injury by attenuating endoplasmic reticulum stress.
Cell oxidation-reduction imbalance after modulated radiofrequency radiation.
Cell phone electromagnetic field radiations affect rhizogenesis through impairment of
biochemical processes.
Cell phone radiation exposure on brain and associated biological systems.
Cell phones and cancer: what is the evidence for a connection?
Cell type-specific genotoxic effects of intermittent extremely low-frequency electromagnetic
fields.
Cellphone electromagnetic radiation damages the testicular ultrastructure of male rats].
Cellular effects of electromagnetic fields.
Changes in antioxidant capacity of blood due to mutual action of electromagnetic field (1800
MHz) and opioid drug (tramadol) in animal model of persistent inflammatory state.
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Changes of apoptosis, mitochondrion membrane potential and Ca2+ of hypothalamic neurons
induced by high power microwave].
Changes of rat testicular germ cell apoptosis after high power microwave radiation].
Chromosomal damage in human diploid fibroblasts by intermittent exposure to extremely low-
frequency electromagnetic fields.
Chronic exposure to 50Hz magnetic fields causes a significant weakening of antioxidant defence
systems in aged rat brain.
Cognitive impairment and neurogenotoxic effects in rats exposed to low-intensity microwave
radiation.
Combinative exposure effect of radio frequency signals from CDMA mobile phones and
aphidicolin on DNA integrity.
Combined effects of 872 MHz radiofrequency radiation and ferrous chloride on reactive oxygen
species production and DNA damage in human SH-SY5Y neuroblastoma cells.
Combined exposure of ELF magnetic fields and x-rays increased mutant yields compared with x-
rays alone in pTN89 plasmids.
Comments on "Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic
effects in vitro in human fibroblasts but not in lymphocytes" by Schwarz et al. (Int Arch Occup
Environ Health 2008: doi: 10.1007/s00420-008-0305-5).
Comparative study of cell cycle kinetics and induction of apoptosis or necrosis after exposure of
human Mono Mac 6 cells to radiofrequency radiation.
Comparison of biological effects between continuous and intermittent exposure to GSM-900-
MHz mobile phone radiation: Detection of apoptotic cell-death features.
Comparison of cytotoxic and genotoxic effects of plutonium-239 alpha particles and mobile
phone GSM 900 radiation in the Allium cepa test.
Correction of microcirculatory disturbances with terahertz electromagnetic radiation at nitric
oxide frequencies in albino rats under conditions of acute stress.
Corrective effects of electromagnetic radiation in a millimeter wavelength range on the
parameters of oxidative stress after standard anti-helicobacterial therapy in patients with ulcer
disease].
Critical comments on DNA breakage by mobile-phone electromagnetic fields [Diem et al.,
Mutat. Res. 583 (2005) 178-183].
Cytogenetic effects of 18.0 and 16.5 GHz microwave radiation on human lymphocytes in vitro.
Cytogenetic effects of 935.2-MHz (GSM) microwaves alone and in combination with mitomycin
C.
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Cytogenetic studies in human blood lymphocytes exposed in vitro to 2.45 GHz or 8.2 GHz
radiofrequency radiation.
Cytogenetic studies in human cells exposed in vitro to GSM-900 MHz radiofrequency radiation
using R-banded karyotyping.
Cytokines produced by microwave-radiated Sertoli cells interfere with spermatogenesis in rat
testis.
Cytotoxic and genotoxic effect in RTG-2 cell line exposed to selected biocides used in the
disinfection of cooling towers.
Cytotoxic and genotoxic effects of high-frequency electromagnetic fields (GSM 1800 MHz) on
immature and mature rats.
Decreased DNA repair rates and protection from heat induced apoptosis mediated by
electromagnetic field exposure.
Dependence of microwave effect on the secondary structure of DNA on molecular weight of
polynucleotide].
Developmental effects of perinatal exposure to extremely weak 7 Hz magnetic fields and nitric
oxide modulation in the Wistar albino rat.
Different methods for evaluating the effects of microwave radiation exposure on the nervous
system.
Disordered redox metabolism of brain cells in rats exposed to low doses of ionizing radiation or
UHF electromagnetic radiation.
DNA and chromosomal damage in response to intermittent extremely low-frequency magnetic
fields.
DNA damage and repair induced by acute exposure of microwave from mobile phone on
cultured human lens epithelial cells].
DNA damage in rat brain cells after in vivo exposure to 2450 MHz electromagnetic radiation and
various methods of euthanasia.
DNA damage induced in brain cells of CBA mice exposed to magnetic fields.
DNA damage, cell kinetics and ODC activities studied in CBA mice exposed to electromagnetic
fields generated by transmission lines.
Do extremely low frequency magnetic fields enhance the effects of environmental carcinogens?
A meta-analysis of experimental studies.
Do naturally occurring magnetic nanoparticles in the human body mediate increased risk of
childhood leukaemia with EMF exposure?
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Does MW Radiation Affect Gene Expression, Apoptotic Level, and Cell Cycle Progression of
Human SH-SY5Y Neuroblastoma Cells?
Does prolonged radiofrequency radiation emitted from Wi-Fi devices induce DNA damage in
various tissues of rats?
Drosophila oogenesis as a bio-marker responding to EMF sources.
Effect of 0.2 T static magnetic field on human neurons: remodeling and inhibition of signal
transduction without genome instability.
Effect of 2.45 GHz microwave radiation on the fertility pattern in male mice.
Effect of 3G cell phone exposure with computer controlled 2-D stepper motor on non-thermal
activation of the hsp27/p38MAPK stress pathway in rat brain.
Effect of 7 mT static magnetic field and iron ions on rat lymphocytes: apoptosis, necrosis and
free radical processes.
Effect of 900 MHz radio frequency radiation on beta amyloid protein, protein carbonyl, and
malondialdehyde in the brain.
Effect of 900 MHz radiofrequency radiation on oxidative stress in rat brain and serum.
Effect of 900-, 1800-, and 2100-MHz radiofrequency radiation on DNA and oxidative stress in
brain.
Effect of 950 MHz UHF electromagnetic radiation on biomarkers of oxidative damage,
metabolism of UFA and antioxidants in the livers of young rats of different ages.
Effect of acute exposure to microwave from mobile phone on DNA damage and repair of
cultured human lens epithelial cells in vitro].
Effect of American Ginseng Capsule on the liver oxidative injury and the Nrf2 protein
expression in rats exposed by electromagnetic radiation of frequency of cell phone].
Effect of coexposure to 50 Hz magnetic fields and an aneugen on human lymphocytes,
determined by the cytokinesis block micronucleus assay.
Effect of continuous irradiation with terahertz electromagnetic waves of the NO frequency range
on behavioral reactions of male albino rats under stress conditions.
Effect of electromagnetic field produced by mobile phones on the activity of superoxide
dismutase (SOD-1) and the level of malonyldialdehyde (MDA)--in vitro study].
Effect of electromagnetic field produced by mobile phones on the activity of superoxide
dismutase (SOD-1)--in vitro researches].
Effect of electromagnetic microwave radiation on the growth of Ehrlich ascites carcinoma.
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Effect of exposure and withdrawal of 900-MHz-electromagnetic waves on brain, kidney and
liver oxidative stress and some biochemical parameters in male rats.
Effect of exposure to the edge signal on oxidative stress in brain cell models.
Effect of extremely low frequency magnetic field on antioxidant activity in plasma and red blood
cells in spot welders.
Effect of extremely low-frequency electromagnetic fields on antioxidant activity in the human
keratinocyte cell line NCTC 2544.
Effect of GSTM1 and GSTT1 Polymorphisms on Genetic Damage in Humans Populations
Exposed to Radiation From Mobile Towers.
Effect of handportable mobiletelephone microwave radiation on rat central neuron apoptosis].
Effect of intermittent and continuous exposure to electromagnetic fields on cultured hippocampal
cells.
Effect of long-term power frequency electromagnetic field exposure on proliferation and
apoptosis of SRA01/04 cells].
Effect of low level microwave radiation exposure on cognitive function and oxidative stress in
rats.
Effect of Low Level Subchronic Microwave Radiation on Rat Brain.
Effect of microwave radiation on primary cultured Sertoli cells].
Effect of mobile phone exposure on apoptotic glial cells and status of oxidative stress in rat
brain.
Effect of Mobile Phone Radiation on Cardiovascular Development of Chick Embryo.
Effect of mobile phones on micronucleus frequency in human exfoliated oral mucosal cells.
Effect of Modified Wuzi Yanzong Pill () on Tip60-Mediated Apoptosis in Testis of Male Rats
after Microwave Radiation.
Effect of pulsed electromagnetic field with different frequencies on the proliferation, apoptosis
and migration of human ovarian cancer cells].
Effect of Radiofrequency Radiation on Human Hematopoietic Stem Cells.
Effect of radiofrequency radiation on reproductive health.
Effect of rosmarinic acid on sertoli cells apoptosis and serum antioxidant levels in rats after
exposure to electromagnetic fields.
Effect of selenium pre-treatment on plasma antioxidant vitamins A (retinol) and E (alpha-
tocopherol) in static magnetic field-exposed rats.
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Effect of static magnetic field on development toxicity of rat embryonic midbrain neurons cells].
Effect of superposed electromagnetic noise on DNA damage of lens epithelial cells induced by
microwave radiation.
Effects of 10-GHz microwaves on hematological parameters in Swiss albino mice and their
modulation by Prunus avium.
Effects of 1800 MHz RF-EMF exposure on DNA damage and cellular functions in primary
cultured neurogenic cells.
Effects of 2,450 MHz microwave on DNA damage induced by three chemical mutagens in
vitro].
Effects of 2.45 GHz electromagnetic fields with a wide range of SARs on bacterial and HPRT
gene mutations.
Effects of 2.45 GHz microwave exposures on the peroxidation status in Wistar rats.
Effects of 50 Hz electromagnetic fields on the histology, apoptosis, and expression of c-Fos and
beta-catenin on the livers of preincubated white Leghorn chicken embryos.
Effects of 50-Hz magnetic field exposure on hormone secretion and apoptosis-related gene
expression in human first trimester villous trophoblasts in vitro.
Effects of 60 Hz electromagnetic field exposure on testicular germ cell apoptosis in mice.
Effects of 60-Hz fields, estradiol and xenoestrogens on human breast cancer cells.
Effects of 837 and 1950 MHz radiofrequency radiation exposure alone or combined on oxidative
stress in MCF10A cells.
Effects of 900-MHz electromagnetic field emitted from cellular phone on brain oxidative stress
and some vitamin levels of guinea pigs.
Effects of 900-MHz electromagnetic fields exposure throughout middle/late adolescence on the
kidney morphology and biochemistry of the female rat.
Effects of acute electromagnetic field exposure and movement restraint on antioxidant system in
liver, heart, kidney and plasma of Wistar rats: a preliminary report.
Effects of acute exposure to the radiofrequency fields of cellular phones on plasma lipid peroxide
and antioxidase activities in human erythrocytes.
Effects of aluminum and extremely low frequency electromagnetic radiation on oxidative stress
and memory in brain of mice.
Effects of broad band electromagnetic fields on HSP70 expression and ischemia-reperfusion in
rat hearts.
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Effects of cell phone radiation on lipid peroxidation, glutathione and nitric oxide levels in mouse
brain during epileptic seizure.
Effects of centimeter waves on the immune system of mice in endotoxic shock].
Effects of chronic exposure to 950 MHz ultra-high-frequency electromagnetic radiation on
reactive oxygen species metabolism in the right and left cerebral cortex of young rats of different
ages.
Effects of co-exposure to extremely low frequency (ELF) magnetic fields and benzene or
benzene metabolites determined in vitro by the alkaline comet assay.
Effects of dietary green tea polyphenol supplementation on the health of workers exposed to
high-voltage power lines.
Effects of electromagnetic field produced by mobile phones on the oxidant and antioxidant status
of rats.
Effects of electromagnetic pulses on apoptosis and TGF-beta3 expression of mouse testis tissue].
Effects of electromagnetic radiation from a cellular telephone on the oxidant and antioxidant
levels in rabbits.
Effects of electromagnetic radiation on morphology and TGF-beta3 expression in mouse
testicular tissue.
Effects of electromagnetic radiation on RAF/MEK/ERK signaling pathway in rats
hippocampus].
Effects of electromagnetic radiation produced by 3G mobile phones on rat brains: magnetic
resonance spectroscopy, biochemical, and histopathological evaluation.
Effects of exposure to 2100MHz GSM-like radiofrequency electromagnetic field on auditory
system of rats.
Effects of exposure to 50 Hz electric field at different strengths on oxidative stress and
antioxidant enzyme activities in the brain tissue of guinea pigs.
Effects of extremely low frequency electromagnetic field and its combination with lead on the
antioxidant system in mouse].
Effects of extremely low-frequency pulsed electromagnetic fields on morphological and
biochemical properties of human breast carcinoma cells (T47D).
Effects of GSM 1800 MHz radiofrequency electromagnetic fields on DNA damage in Chinese
hamster lung cells].
Effects of high power microwave on the expressions of Bcl-2 and C-myc proteins in the rat
testis].
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Effects of in vitro exposure to power frequency magnetic fields on UV-induced DNA damage of
rat lymphocytes.
Effects of long-term 50Hz power-line frequency electromagnetic field on cell behavior in Balb/c
3T3 cells.
Effects of Long-Term Exposure to 60 GHz Millimeter-Wavelength Radiation on the
Genotoxicity and Heat Shock Protein (Hsp) Expression of Cells Derived from Human Eye.
Effects of Low-Frequency Electromagnetic Field on Oxidative Stress in Selected Structures of
the Central Nervous System.
Effects of low-intensity ultrahigh frequency electromagnetic radiation on inflammatory
processes.
Effects of melatonin on Wi-Fi-induced oxidative stress in lens of rats.
Effects of microwave radiation on lipid peroxidation and the content of neurotransmitters in
mice].
Effects of microwave radiation on thymocytes in mice at different power densities].
Effects of microwaves (950 MHZ mobile phone) on morphometric and apoptotic changes of
rabbit epididymis.
Effects of mobile phone exposure on metabolomics in the male and female reproductive systems.
Effects of mobile phone radiation (900 MHz radiofrequency) on structure and functions of rat
brain.
Effects of mobile phone use on brain tissue from the rat and a possible protective role of vitamin
C - a preliminary study.
Effects of mobile phones on oxidant/antioxidant balance in cornea and lens of rats.
Effects of prenatal and postnatal exposure of Wi-Fi on development of teeth and changes in teeth
element concentration in rats. [corrected].
Effects of prenatal and postnatal exposure to GSM-like radiofrequency on blood chemistry and
oxidative stress in infant rabbits, an experimental study.
Effects of prenatal exposure to WIFI signal (2.45GHz) on postnatal development and behavior in
rat: Influence of maternal restraint.
Effects of pulsed 2.856 GHz microwave exposure on BM-MSCs isolated from C57BL/6 mice.
Effects of pulsed electric fields on DNA of human lymphocytes.
Effects of pulsed electromagnetic fields on cartilage apoptosis signalling pathways in
ovariectomised rats.
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Effects of pulsed magnetic field treatment of soybean seeds on calli growth, cell damage, and
biochemical changes under salt stress.
Effects of radiofrequency electromagnetic wave exposure from cellular phones on the
reproductive pattern in male Wistar rats.
Effects of radiofrequency electromagnetic waves (RF-EMW) from cellular phones on human
ejaculated semen: an in vitro pilot study.
Effects of sinusoidal electromagnetic fields on histopathology and structures of brains of
preincubated white Leghorn chicken embryos.
Effects of static magnetic field and cadmium on oxidative stress and DNA damage in rat cortex
brain and hippocampus.
Effects of the ELF-MFs on the development of spleens of preincubated chicken embryos.
Effects of the exposure to mobile phones on male reproduction: a review of the literature.
Effects of third generation mobile phone-emitted electromagnetic radiation on oxidative stress
parameters in eye tissue and blood of rats.
Effects on protein kinase C and gene expression in a human mast cell line, HMC-1, following
microwave exposure.
Electric and/or magnetic field effects on DNA structure and function in cultured human cells.
Electromagnetic fields and health: DNA-based dosimetry.
Electromagnetic fields at a mobile phone frequency (900 MHz) trigger the onset of general stress
response along with DNA modifications in Eisenia fetida earthworms.
Electromagnetic fields at mobile phone frequency induce apoptosis and inactivation of the multi-
chaperone complex in human epidermoid cancer cells.
Electromagnetic fields may act directly on DNA.
Electromagnetic fields may act via calcineurin inhibition to suppress immunity, thereby
increasing risk for opportunistic infection: Conceivable mechanisms of action.
Electromagnetic noise inhibits radiofrequency radiation-induced DNA damage and reactive
oxygen species increase in human lens epithelial cells.
Electromagnetic pulse activated brain microglia via the p38 MAPK pathway.
Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats.
Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through
activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats.
Electromagnetic radiation 2450 MHz exposure causes cognition deficit with mitochondrial
dysfunction and activation of intrinsic pathway of apoptosis in rats.
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Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3
signaling pathways in rats.
Electromagnetic wave emitting products and "Kikoh" potentiate human leukocyte functions.
Electromagnetic wave irradiation promotes osteoblastic cell proliferation and up-regulates
growth factors via activation of the ERK1/2 and p38 MAPK pathways.
Enhanced cytotoxic and genotoxic effects of gadolinium following ELF-EMF irradiation in
human lymphocytes.
Epinephrine, DNA integrity and oxidative stress in workers exposed to extremely low-frequency
electromagnetic fields (ELF-EMFs) at 132 kV substations.
EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
Evaluating the combinative effects on human lymphocyte DNA damage induced by ultraviolet
ray C plus 1.8 GHz microwaves using comet assay in vitro.
Evaluation of basal DNA damage and oxidative stress in Wistar rat leukocytes after exposure to
microwave radiation.
Evaluation of DNA damage in spinal cord and mutagenic effect of a Phalpha1beta recombinant
toxin with analgesic properties from the Phoneutria nigriventer spider.
Evaluation of genotoxic and/or co-genotoxic effects in cells exposed in vitro to extremely-low
frequency electromagnetic fields].
Evaluation of genotoxic effects in human fibroblasts after intermittent exposure to 50 Hz
electromagnetic fields: a confirmatory study.
Evaluation of genotoxic effects in human leukocytes after in vitro exposure to 1950 MHz UMTS
radiofrequency field.
Evaluation of genotoxic effects in human peripheral blood leukocytes following an acute in vitro
exposure to 900 MHz radiofrequency fields.
Evaluation of genotoxic effects in male Wistar rats following microwave exposure.
Evaluation of hormonal change, biochemical parameters, and histopathological status of uterus
in rats exposed to 50-Hz electromagnetic field.
Evaluation of HSP70 expression and DNA damage in cells of a human trophoblast cell line
exposed to 1.8 GHz amplitude-modulated radiofrequency fields.
Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill
Viewpoints from 1965 on Association or Causation.
Evaluation of selected biochemical parameters in the saliva of young males using mobile phones.
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Evaluation of the cytogenotoxic damage in immature and mature rats exposed to 900 MHz
radiofrequency electromagnetic fields.
Evaluation of the effects of mobile phones on the neural tube development of chick embryos.
Evaluation of the potential of mobile phone specific electromagnetic fields (UMTS) to produce
micronuclei in human glioblastoma cell lines.
Evidence for mobile phone radiation exposure effects on reproductive pattern of male rats: role
of ROS.
Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.
Examination of electric field effects on tissues by using back propagation neural network.
Exposure of magnetic bacteria to simulated mobile phone-type RF radiation has no impact on
mortality.
Exposure of mammalian cells to 60-Hz magnetic or electric fields: analysis for DNA single-
strand breaks.
Exposure of rat brain to 915 MHz GSM microwaves induces changes in gene expression but not
double stranded DNA breaks or effects on chromatin conformation.
Exposure to 1.8 GHz electromagnetic fields affects morphology, DNA-related Raman spectra
and mitochondrial functions in human lympho-monocytes.
Exposure to 1800 MHz radiofrequency electromagnetic radiation induces oxidative DNA base
damage in a mouse spermatocyte-derived cell line.
Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial
DNA in primary cultured neurons.
Exposure to 1950-MHz TD-SCDMA electromagnetic fields affects the apoptosis of astrocytes
via caspase-3-dependent pathway.
Exposure to 900 MHz electromagnetic field induces an unbalance between pro-apoptotic and
pro-survival signals in T-lymphoblastoid leukemia CCRF-CEM cells.
Exposure to 900 MHz radiofrequency radiation induces caspase 3 activation in proliferating
human lymphocytes.
Exposure to acute electromagnetic radiation of mobile phone exposure range alters transiently
skin homeostasis of a model of pigmented reconstructed epidermis.
Exposure to cell phone radiation up-regulates apoptosis genes in primary cultures of neurons and
astrocytes.
Exposure to GSM 900-MHz mobile radiation impaired inhibitory avoidance memory
consolidation in rat: Involvements of opioidergic and nitrergic systems.
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Exposure to mobile phone (900-1800 MHz) during pregnancy: tissue oxidative stress after
childbirth.
Exposure to mobile phone electromagnetic field radiation, ringtone and vibration affects anxiety-
like behaviour and oxidative stress biomarkers in albino wistar rats.
Exposure to non-ionizing electromagnetic fields emitted from mobile phones induced DNA
damage in human ear canal hair follicle cells.
Exposure to radiation from single or combined radio frequencies provokes macrophage
dysfunction in the RAW 264.7 cell line.
Exposure to radiofrequency radiation induces oxidative stress in duckweed Lemna minor L.
Exposure to static magnetic field of pregnant rats induces hepatic GSH elevation but not
oxidative DNA damage in liver and kidney.
Extremely low frequency (ELF) magnetic fields and apoptosis: a review.
Extremely low frequency (ELF) magnetic fields enhance chemically induced formation of
apurinic/apyrimidinic (AP) sites in A172 cells.
Extremely low frequency electromagnetic field reduces oxidative stress during the rehabilitation
of post-acute stroke patients.
Extremely low frequency electromagnetic radiation enhanced energy metabolism and induced
oxidative stress in Caenorhabditis elegans].
Extremely low frequency magnetic field induces hyperalgesia in mice modulated by nitric oxide
synthesis.
Extremely low-frequency magnetic fields modulate nitric oxide signaling in rat brain.
From the Cover: 2.45-GHz Microwave Radiation Impairs Hippocampal Learning and Spatial
Memory: Involvement of Local Stress Mechanism-Induced Suppression of iGluR/ERK/CREB
Signaling.
Gene expression and reproductive abilities of male Drosophila melanogaster subjected to ELF-
EMF exposure.
Gene expression changes in the skin of rats induced by prolonged 35 GHz millimeter-wave
exposure.
Genetic damage in human cells exposed to non-ionizing radiofrequency fields: a meta-analysis
of the data from 88 publications (1990-2011).
Genetic damage in humans exposed to extremely low-frequency electromagnetic fields.
Genetic damage in mammalian somatic cells exposed to extremely low frequency electro-
magnetic fields: a meta-analysis of data from 87 publications (1990-2007).
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Genetic damage in mammalian somatic cells exposed to radiofrequency radiation: a meta-
analysis of data from 63 publications (1990-2005).
Genetic damage in subjects exposed to radiofrequency radiation.
Genotoxic and carcinogenic effects of non-ionizing electromagnetic fields.
Genotoxic Effects in Human Fibroblasts Exposed to Microwave Radiation.
Genotoxicity evaluation of electromagnetic fields generated by 835-MHz mobile phone
frequency band.
Genotoxicity of radiofrequency signals. I. Investigation of DNA damage and micronuclei
induction in cultured human blood cells.
Ginkgo biloba prevents mobile phone-induced oxidative stress in rat brain.
GSM base station electromagnetic radiation and oxidative stress in rats.
GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant
rabbits.
Hematological and toxicogenomic effects of ferromagnetic screening of natural electromagnetic
fields.
Histological and histochemical study of the protective role of rosemary extract against harmful
effect of cell phone electromagnetic radiation on the parotid glands.
Human fibroblasts and 900 MHz radiofrequency radiation: evaluation of DNA damage after
exposure and co-exposure to 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5h)-furanone (MX).
Human health consequences of environmentally-modulated gene expression: potential roles of
ELF-EMF induced epigenetic versus mutagenic mechanisms of disease.
Human mesenchymal stem cells are sensitive to abnormal gravity and exhibit classic apoptotic
features.
Human skin cell stress response to GSM-900 mobile phone signals. In vitro study on isolated
primary cells and reconstructed epidermis.
Immunohistopathologic demonstration of deleterious effects on growing rat testes of
radiofrequency waves emitted from conventional Wi-Fi devices.
Immunomodulating action of low intensity millimeter waves on primed neutrophils.
Impact of 2.45 GHz microwave radiation on the testicular inflammatory pathway biomarkers in
young rats: The role of gallic acid.
Impact of cell phone radiation on male reproduction].
Impact of electromagnetic radiation emitted by monitors on changes in the cellular membrane
structure and protective antioxidant effect of vitamin A - In vitro study.
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Impact of microwave at X-band in the aetiology of male infertility.
Impact of radio frequency electromagnetic radiation on DNA integrity in the male germline.
Impact of radiofrequency radiation on DNA damage and antioxidants in peripheral blood
lymphocytes of humans residing in the vicinity of mobile phone base stations.
Impacts of exposure to 900 MHz mobile phone radiation on liver function in rats.
Importance of DNA fragmentation in apoptosis with regard to TUNEL specificity.
In vitro free radical scavenging activities and effect of synthetic oligosaccharides on antioxidant
enzymes and lipid peroxidation in aged mice.
In vitro non-thermal oxidative stress response after 1800 MHz radiofrequency radiation.
Increased apoptosis, changes in intracellular Ca2+, and functional alterations in lymphocytes and
macrophages after in vitro exposure to static magnetic field.
Induction of adaptive response in mice exposed to 900MHz radiofrequency fields: application of
micronucleus assay.
Induction of apoptotic cell death in human leukemic cell line, HL-60, by extremely low
frequency electric magnetic fields: analysis of the possible mechanisms in vitro.
Induction of DNA strand breaks by intermittent exposure to extremely-low-frequency
electromagnetic fields in human diploid fibroblasts.
Influence of 1.8 GHz microwave on DNA damage induced by 4 chemical mutagens].
Influence of 1.8 GHz microwave on DNA damage induced by ultraviolet C ray].
Influence of 1.8-GHz (GSM) radiofrequency radiation (RFR) on DNA damage and repair
induced by X-rays in human leukocytes in vitro.
Influence of 900 MHz frequency electromagnetic radiation on some blood indices].
Influence of a static magnetic field (250 mT) on the antioxidant response and DNA integrity in
THP1 cells.
Influence of electromagnetic field (1800 MHz) on lipid peroxidation in brain, blood, liver and
kidney in rats.
Influence of extremely-low-frequency magnetic field on antioxidative melatonin properties in
AT478 murine squamous cell carcinoma culture.
Influence of high-frequency electromagnetic fields on different modes of cell death and gene
expression.
Influence of low magnetic field on lipid peroxidation].
Influence of microwave exposure on fertility of male rats.
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Influence of microwaves on different types of receptors and the role of peroxidation of lipids on
receptor-protein shedding.
Inhibition by Egb761 of the effect of cellphone radiation on the male reproductive system.
Inhibitory effect of microwave radiation on proliferation of human pancreatic cancer JF305 cells
and its mechanism].
Intermittent extremely low frequency electromagnetic fields cause DNA damage in a dose-
dependent way.
Investigation of co-genotoxic effects of radiofrequency electromagnetic fields in vivo.
Investigation of potential genotoxic effects of low frequency electromagnetic fields on
Escherichia coli.
Investigation of the effects of 2.1 GHz microwave radiation on mitochondrial membrane
potential (DeltaPsim), apoptotic activity and cell viability in human breast fibroblast cells.
Investigation of the effects of distance from sources on apoptosis, oxidative stress and cytosolic
calcium accumulation via TRPV1 channels induced by mobile phones and Wi-Fi in breast cancer
cells.
Is human saliva an indicator of the adverse health effects of using mobile phones?
Lasting hepatotoxic effects of prenatal mobile phone exposure.
Lipid peroxide damage in retinal ganglion cells induced by microwave].
Liver antioxidant stores protect the brain from electromagnetic radiation (900 and 1800 MHz)-
induced oxidative stress in rats during pregnancy and the development of offspring.
Local vasodilator response to mobile phones.
Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis,
mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root
ganglion of rats.
Long-term exposure to electromagnetic radiation from mobile phones and Wi-Fi devices
decreases plasma prolactin, progesterone, and estrogen levels but increases uterine oxidative
stress in pregnant rats and their offspring.
Loss of transforming activity of plasmid DNA (pBR322) in E. coli caused by singlet molecular
oxygen.
Low intensity and frequency pulsed electromagnetic fields selectively impair breast cancer cell
viability.
Low intensity microwave radiation induced oxidative stress, inflammatory response and DNA
damage in rat brain.
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Low power density microwave radiation induced early changes in rabbit lens epithelial cells.
Low-Frequency Electromagnetic Field Exposure Enhances Extracellular Trap Formation by
Human Neutrophils through the NADPH Pathway.
Low-intensity electromagnetic fields induce human cryptochrome to modulate intracellular
reactive oxygen species.
Magnetic-field-induced DNA strand breaks in brain cells of the rat.
Measurement of DNA damage after acute exposure to pulsed-wave 2450 MHz microwaves in rat
brain cells by two alkaline comet assay methods.
Measurement of DNA damage after exposure to 2450 MHz electromagnetic radiation.
Measurement of DNA damage after exposure to electromagnetic radiation in the cellular phone
communication frequency band (835.62 and 847.74 MHz).
Measurement of DNA damage and apoptosis in Molt-4 cells after in vitro exposure to
radiofrequency radiation.
Measurement of the 100MHz EMF radiation in vivo effects on zebrafish D. rerio embryonic
development: A multidisciplinary study.
Measurements of alkali-labile DNA damage and protein-DNA crosslinks after 2450 MHz
microwave and low-dose gamma irradiation in vitro.
Mechanism of short-term ERK activation by electromagnetic fields at mobile phone frequencies.
Mechanisms of electromagnetic radiation damaging male reproduction].
Melatonin and a spin-trap compound block radiofrequency electromagnetic radiation-induced
DNA strand breaks in rat brain cells.
Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA
damage and cell cycle arrest in germ cells of male Swiss albino mice.
Melatonin modulates 900 Mhz microwave-induced lipid peroxidation changes in rat brain.
Melatonin protects rat thymus against oxidative stress caused by exposure to microwaves and
modulates proliferation/apoptosis of thymocytes.
Melatonin reduces oxidative stress induced by chronic exposure of microwave radiation from
mobile phones in rat brain.
Metabolic changes in cells under electromagnetic radiation of mobile communication systems].
Microwave absorption by magnetite: a possible mechanism for coupling nonthermal levels of
radiation to biological systems.
Microwave effects on plasmid DNA.
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Microwave electromagnetic field regulates gene expression in T-lymphoblastoid leukemia
CCRF-CEM cell line exposed to 900 MHz.
Microwave exposure affecting reproductive system in male rats.
Microwave exposure of neuronal cells in vitro: Study of apoptosis.
Microwave induces apoptosis in A549 human lung carcinoma cell line.
Microwave radiation (2.45 GHz)-induced oxidative stress: Whole-body exposure effect on
histopathology of Wistar rats.
Microwave radiation induced oxidative stress, cognitive impairment and inflammation in brain
of Fischer rats.
Microwave radiation induces injury to GC-2spd cells].
Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling.
Mitochondrial DNA damage and oxidative damage in HL-60 cells exposed to 900MHz
radiofrequency fields.
Mitochondrial hyperpolarization and cytochrome-c release in microwave-exposed MCF-7 cells.
Mobile phone (1800MHz) radiation impairs female reproduction in mice, Mus musculus,
through stress induced inhibition of ovarian and uterine activity.
Mobile phone radiation induces mode-dependent DNA damage in a mouse spermatocyte-derived
cell line: a protective role of melatonin.
Mobile phone radiation induces reactive oxygen species production and DNA damage in human
spermatozoa in vitro.
Mobile phone radiation-induced free radical damage in the liver is inhibited by the antioxidants
N-acetyl cysteine and epigallocatechin-gallate.
Mobile phone signal exposure triggers a hormesis-like effect in Atm(+/+) and Atm(-/-) mouse
embryonic fibroblasts.
Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide
excision repair in serum-deprived human glioblastoma cells.
Mobile phone usage and male infertility in Wistar rats.
Mobile phones, heat shock proteins and cancer.
Mobile-phone radiation-induced perturbation of gene-expression profiling, redox equilibrium
and sporadic-apoptosis control in the ovary of Drosophila melanogaster.
Modulation of cell death in the rat thymus. Light and electron microscopic investigations.
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Modulation of wireless (2.45 GHz)-induced oxidative toxicity in laryngotracheal mucosa of rat
by melatonin.
Morphological and antioxidant impairments in the spinal cord of male offspring rats following
exposure to a continuous 900MHz electromagnetic field during early and mid-adolescence.
Mutagenic response of 2.45 GHz radiation exposure on rat brain.
Neural cell apoptosis induced by microwave exposure through mitochondria-dependent caspase-
3 pathway.
Neurodegenerative changes and apoptosis induced by intrauterine and extrauterine exposure of
radiofrequency radiation.
Neuroprotective effects of lotus seedpod procyanidins on extremely low frequency
electromagnetic field-induced neurotoxicity in primary cultured hippocampal neurons.
Non-thermal bioeffects of static and extremely low frequency electromagnetic fields].
Non-thermal cellular effects of lowpower microwave radiation on the lens and lens epithelial
cells.
Non-thermal DNA breakage by mobile-phone radiation (1800 MHz) in human fibroblasts and in
transformed GFSH-R17 rat granulosa cells in vitro.
Non-thermal effects of 2.45 GHz microwaves on spindle assembly, mitotic cells and viability of
Chinese hamster V-79 cells.
Non-thermal effects of continuous 2.45 GHz microwaves on Fas-induced apoptosis in human
Jurkat T-cell line.
Normal doses of visible light can cause mutations in skin].
Overproduction of free radical species in embryonal cells exposed to low intensity
radiofrequency radiation.
Oxidative and mutagenic effects of low intensity GSM 1800 MHz microwave radiation.
Oxidative changes and apoptosis induced by 1800-MHz electromagnetic radiation in NIH/3T3
cells.
Oxidative DNA damage in rats exposed to extremely low frequency electro magnetic fields.
Oxidative effects of extremely low frequency magnetic field and radio frequency radiation on
testes tissues of diabetic and healthy rats.
Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation.
Oxidative stress and prevention of the adaptive response to chronic iron overload in the brain of
young adult rats exposed to a 150 kilohertz electromagnetic field.
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Oxidative stress effects on the central nervous system of rats after acute exposure to ultra high
frequency electromagnetic fields.
Oxidative stress-mediated alterations on sperm parameters in male Wistar rats exposed to 3G
mobile phone radiation.
Oxidative stress-mediated skin damage in an experimental mobile phone model can be prevented
by melatonin.
p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic
field exposure.
PARAMETERS OF SPERMATOGENESIS IN MEN EXPOSED TO DIFFICULT
ENVIRONMENTS].
Pathological effects of prenatal exposure to a 900 MHz electromagnetic field on the 21-day-old
male rat kidney.
Pathological Findings Observed in the Kidneys of Postnatal Male Rats Exposed to the 2100 MHz
Electromagnetic Field.
Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male
reproductive system.
Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout
adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-
day-old Sprague Dawley male rats.
Post-continuous whole body exposure of rabbits to 650 MHz electromagnetic fields: effects on
liver, spleen, and brain.
Postnatal development and behavior effects of in-utero exposure of rats to radiofrequency waves
emitted from conventional WiFi devices.
Preliminary evaluation of nanoscale biogenic magnetite-based ferromagnetic transduction
mechanisms for mobile phone bioeffects.
Prevalence of nuclear cataract in Swiss veal calves and its possible association with mobile
telephone antenna base stations.
Pro- and antioxidant effect of electromagnetic fields of extremely high frequency (460 MHz) on
brain tissues in experiment].
Proliferation and apoptosis in a neuroblastoma cell line exposed to 900 MHz modulated
radiofrequency field.
Propagation of electromagnetic radiation in mitochondria?
Protective effect of Liuweidihuang Pills against cellphone electromagnetic radiation-induced
histomorphological abnormality, oxidative injury, and cell apoptosis in rat testes].
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Protective effect of melatonin and vitamin E against prooxidative action of iron ions and static
magnetic field].
Protective effects of beta-glucan against oxidative injury induced by 2.45-GHz electromagnetic
radiation in the skin tissue of rats.
Protective effects of Genistein on human renal tubular epithelial cells damage of microwave
radiation].
Protective effects of luteolin on rat testis following exposure to 900 MHz electromagnetic field.
Protein oxidation under extremely low frequency electric field in guinea pigs. Effect of N-acetyl-
L-cysteine treatment.
Pulse modulated 900 MHz radiation induces hypothyroidism and apoptosis in thyroid cells: a
light, electron microscopy and immunohistochemical study.
Pulse-modulated Electromagnetic Radiation of Extremely High Frequencies Protects Cellular
DNA against Damaging Effect of Physico-Chemical Factors in vitro].
Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in
Doxorubicin-treated Mouse Osteosarcoma Cells.
Pulsed electromagnetic fields accelerate apoptotic rate in osteoclasts.
Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling
pathway in mouse spermatogenic cells in vitro and thus may affect male fertility.
Purkinje cell number decreases in the adult female rat cerebellum following exposure to 900
MHz electromagnetic field.
Quality Matters: Systematic Analysis of Endpoints Related to "Cellular Life" in Vitro Data of
Radiofrequency Electromagnetic Field Exposure.
Radiation protection and possible mechanisms for low intensity microwave].
Radiations and male fertility.
Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones
induces oxidative stress and reduces sperm motility in rats.
Radiofrequency (microwave) radiation exposure of mammalian cells during UV-induced DNA
repair synthesis.
Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic effects in vitro in
human fibroblasts but not in lymphocytes.
Radiofrequency electromagnetic radiation exposure effects on amygdala morphology, place
preference behavior and brain caspase-3 activity in rats.
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Radiofrequency electromagnetic radiation from cell phone causes defective testicular function in
male Wistar rats.
Radiofrequency exposure and mammalian cell toxicity, genotoxicity, and transformation.
Radiofrequency radiation (900 MHz) induces Egr-1 gene expression and affects cell-cycle
control in human neuroblastoma cells.
Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular
germ cells in swiss albino mice.
Radiofrequency radiation emitted from Wi-Fi (2.4 GHz) causes impaired insulin secretion and
increased oxidative stress in rat pancreatic islets.
Radioprotective effects of honeybee venom (Apis mellifera) against 915-MHz microwave
radiation-induced DNA damage in wistar rat lymphocytes: in vitro study.
RAPD Profiling, DNA Fragmentation, and Histomorphometric Examination in Brains of Wistar
Rats Exposed to Indoor 2.5 Ghz Wi-Fi Devices Radiation.
Reactive oxygen species elevation and recovery in Drosophila bodies and ovaries following
short-term and long-term exposure to DECT base EMF.
Reactive oxygen species formation and apoptosis in human peripheral blood mononuclear cell
induced by 900 MHz mobile phone radiation.
Reactive oxygen species levels and DNA fragmentation on astrocytes in primary culture after
acute exposure to low intensity microwave electromagnetic field.
Recent advances in research on radiofrequency fields and health.
Recent advances in the effects of microwave radiation on brains.
Recent reports of Wi-Fi and mobile phone-induced radiation on oxidative stress and reproductive
signaling pathways in females and males.
Relationship between activation of microglia and Jaks phosphorylation induced by microwave
irradiation].
Response of Caenorhabditis elegans to wireless devices radiation exposure.
Resveratrol may reverse the effects of long-term occupational exposure to electromagnetic fields
on workers of a power plant.
RKIP Regulates Neural Cell Apoptosis Induced by Exposure to Microwave Radiation Partly
Through the MEK/ERK/CREB Pathway.
Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca2+ signaling
molecular pathways in breast cancer.
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Role of Mitochondria in the Oxidative Stress Induced by Electromagnetic Fields: Focus on
Reproductive Systems.
Role of radical pairs and feedback in weak radio frequency field effects on biological systems.
Saccharomyces cerevisiae as a model organism for studying the carcinogenicity of non-ionizing
electromagnetic fields and radiation].
Searching for the perfect wave: the effect of radiofrequency electromagnetic fields on cells.
Selenium reduces mobile phone (900 MHz)-induced oxidative stress, mitochondrial function,
and apoptosis in breast cancer cells.
Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the
HEK293 cells.
Selenium supplementation ameliorates static magnetic field-induced disorders in antioxidant
status in rat tissues.
Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic
radiation will increase in lipopolysaccharide-induced inflammation in vitro model.
Short-term exposure to 50 Hz ELF-EMF alters the cisplatin-induced oxidative response in
AT478 murine squamous cell carcinoma cells.
Single strand DNA breaks in rat brain cells exposed to microwave radiation.
Single- and double-strand DNA breaks in rat brain cells after acute exposure to radiofrequency
electromagnetic radiation.
Static magnetic field affects oxidative stress in mouse cochlea.
Studies on the injury effects of hippocampus induced by high power microwave radiation in rat].
Study of low-intensity 2450-MHz microwave exposure enhancing the genotoxic effects of
mitomycin C using micronucleus test and comet assay in vitro.
Study of p53 expression and post-transcriptional modifications after GSM-900 radiofrequency
exposure of human amniotic cells.
Studying the protein expression in human B lymphoblastoid cells exposed to 1.8-GHz (GSM)
radiofrequency radiation (RFR) with protein microarray.
Synergism between electricity and ionizing radiation.
Ten gigahertz microwave radiation impairs spatial memory, enzymes activity, and
histopathology of developing mice brain.
Teratogenic effect of broad-band electromagnetic field on neonatal mice (Mus musculus).
Testicular apoptosis and histopathological changes induced by a 2.45 GHz electromagnetic field.
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The 2100MHz radiofrequency radiation of a 3G-mobile phone and the DNA oxidative damage in
brain.
The activity of prooxidant-antioxidant system in loach embryos under the action of microwave
radiation].
The amelioration of phagocytic ability in microglial cells by curcumin through the inhibition of
EMF-induced pro-inflammatory responses.
The antioxidant effect of Green Tea Mega EGCG against electromagnetic radiation-induced
oxidative stress in the hippocampus and striatum of rats.
The apoptotic effect and the plausible mechanism of microwave radiation on rat myocardial
cells.
The cardiac injury effect of microwave radiation on rabbit and its mechanism].
The effect of 50 hz magnetic field of different shape on oxygen metabolism in blood platelets: in
vitro studies.
The effect of decimeter waves on the metabolism of the myocardium and its hormonal regulation
in rabbits with experimental ischemia].
The effect of electromagnetic field exposure on the formation of DNA lesions.
The effect of electromagnetic field exposure on the formation of DNA single strand breaks in
human cells.
The effect of electromagnetic field on reactive oxygen species production in human neutrophils
in vitro.
The effect of electromagnetic radiation on the rat brain: an experimental study.
The effect of electromagnetic waves of very high frequency of molecular spectra of radiation and
absorption of nitric oxide on the functional activity of platelets].
The effect of exposure of rats during prenatal period to radiation spreading from mobile phones
on renal development.
The effect of melatonin on the liver of rats exposed to microwave radiation.
The effect of microwave irradiation on the peroxide modification of low density lipoproteins in
human blood serum].
The effect of microwave radiation on the levels of MDA and the activity of SOD of
nasopharyngeal carcinoma cells].
The effect of microwaves on lipid peroxidation and on lipid and mineral metabolism in warm-
blooded animals (experimental research)].
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The effect of prenatal exposure to 1800 MHz electromagnetic field on calcineurin and bone
development in rats.
The effect of prenatal exposure to 900-MHz electromagnetic field on the 21-old-day rat testicle.
The effect of radiofrequency radiation on DNA and lipid damage in female and male infant
rabbits.
The effect of radiofrequency radiation on DNA and lipid damage in non-pregnant and pregnant
rabbits and their newborns.
The effects of electromagnetic fields from power lines on avian reproductive biology and
physiology: a review.
The effects of electromagnetic radiation (2450 MHz wireless devices) on the heart and blood
tissue: role of melatonin.
The effects of exposure to electromagnetic field on rat myocardium.
The effects of long-term exposure to a 2450 MHz electromagnetic field on growth and pubertal
development in female Wistar rats.
The Effects of Melatonin on Oxidative Stress Parameters and DNA Fragmentation in Testicular
Tissue of Rats Exposed to Microwave Radiation.
The effects of mobile phones on apoptosis in cerebral tissue: an experimental study on rats.
The effects of N-acetylcysteine and epigallocatechin-3-gallate on liver tissue protein oxidation
and antioxidant enzyme levels after the exposure to radiofrequency radiation.
The effects of prenatal exposure to a 900-MHz electromagnetic field on the 21-day-old male rat
heart.
The effects of prenatal long-duration exposure to 900-MHz electromagnetic field on the 21-day-
old newborn male rat liver.
The effects of radiofrequency electromagnetic radiation on sperm function.
The effects of simultaneous combined exposure to CDMA and WCDMA electromagnetic fields
on rat testicular function.
The genotoxic effect of radiofrequency waves on mouse brain.
The impact of electromagnetic radiation (2.45 GHz, Wi-Fi) on the female reproductive system:
The role of vitamin C.
The impact of electromagnetic radiation of different parameters on platelet oxygen metabolism -
in vitro studies.
The influence of 1800 MHz GSM-like signals on blood chemistry and oxidative stress in non-
pregnant and pregnant rabbits.
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The influence of 1800 MHz GSM-like signals on hepatic oxidative DNA and lipid damage in
nonpregnant, pregnant, and newly born rabbits.
The influence of microwave radiation from cellular phone on fetal rat brain.
The injury effects of microwave exposure on visual performance and retinal ganglion cells
(RGCs) in rats].
The link between radiofrequencies emitted from wireless technologies and oxidative stress.
The pathogenesis of central nervous system functional disordersafter exposure to microwave
radiation].
The physiopathological effects of quercetin on oxidative stress in radiation of 4.5 g mobile phone
exposed liver tissue of rat.
The preventive effect of lotus seedpod procyanidins on cognitive impairment and oxidative
damage induced by extremely low frequency electromagnetic field exposure.
The prophylactic effect of vitamin C on oxidative stress indexes in rat eyes following exposure
to radiofrequency wave generated by a BTS antenna model.
The protective effect of autophagy on mouse spermatocyte derived cells exposure to 1800MHz
radiofrequency electromagnetic radiation.
The protective effect of caffeic acid phenethyl ester (CAPE) on oxidative stress in rat liver
exposed to the 900 MHz electromagnetic field.
The protective effects of N-acetyl-L-cysteine and epigallocatechin-3-gallate on electric field-
induced hepatic oxidative stress.
The repair of gamma-ray-induced chromosomal damage in human lymphocytes after exposure to
extremely low frequency electromagnetic fields.
The role of chemical and physical factors in cancer development].
The role of electromagnetic fields in neurological disorders.
The role of heat shock proteins HSP90 in the response of immune cells to centimeter
microwaves].
The role of zinc supplementation in the inhibition of tissue damage caused by exposure to
electromagnetic field in rat lung and liver tissues.
The study of retinal ganglion cell apoptosis induced by different intensities of microwave
irradiation.
The therapeutic effect of a pulsed electromagnetic field on the reproductive patterns of male
Wistar rats exposed to a 2.45-GHz microwave field.
The use of millimeter wavelength electromagnetic waves in cardiology.
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Therapeutic approaches of melatonin in microwave radiations-induced oxidative stress-mediated
toxicity on male fertility pattern of Wistar rats.
Thermal and non-thermal health effects of low intensity non-ionizing radiation: An international
perspective.
Ultra-wideband pulses increase nitric oxide production by RAW 264.7 macrophages incubated in
nitrate.
Upregulation of HIF-1alpha via activation of ERK and PI3K pathway mediated protective
response to microwave-induced mitochondrial injury in neuron-like cells.
Use of terahertz electromagnetic radiation at nitric oxide frequencies for the correction of thyroid
functional state during stress].
Vitamin C protects rat cerebellum and encephalon from oxidative stress following exposure to
radiofrequency wave generated by a BTS antenna model.
Wi-Fi (2.45 GHz)- and mobile phone (900 and 1800 MHz)-induced risks on oxidative stress and
elements in kidney and testis of rats during pregnancy and the development of offspring.
Wi-Fi is an important threat to human health.
Zinc protective effects on pig retinal pigment epithelial cell damage of lipid peroxide induced by
2450 MHz microwave].
Zinc supplementation ameliorates electromagnetic field-induced lipid peroxidation in the rat
brain.
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FACTOR 9
Theme
–
Neurodegenerative diseases
Key MeSH Headings - Parkinson Disease, Neurodegenerative Diseases, Alzheimer Disease,
Amyotrophic Lateral Sclerosis, Motor Neuron Disease, Occupational Diseases, Dementia, Brain
Diseases, Dementia, Vascular
Titles
5-HT contents change in peripheral blood of workers exposed to microwave and high frequency
radiation].
60 Hertz magnetic field exposure assessment for an investigation of leukemia in telephone
lineworkers.
A case-control study on the risk factors of Alzheimer's disease in military elderly men].
A cluster of male breast cancer in office workers.
A cognitive-behavioral treatment of patients suffering from "electric hypersensitivity".
Subjective effects and reactions in a double-blind provocation study.
A literature review: the cardiovascular effects of exposure to extremely low frequency
electromagnetic fields.
A methodological approach to studying the values of 50-Hz electromagnetic fields that influence
the workers of power enterprises].
A mortality study of electrical utility workers in Quebec.
A population-based cohort study of occupational exposure to magnetic fields and cardiovascular
disease mortality.
A study on the biological effects of exposure mobile-phone frequency EMF].
Absenteeism and mortality of workers exposed to electromagnetic fields in the French Electricity
Company.
Acute effects of ELF electromagnetic fields: a field study of linesmen working with 400 kV
power lines.
Acute effects of pulsed microwaves and 3-nitropropionic acid on neuronal ultrastructure in the
rat caudate-putamen.
Acute leukaemia in workers exposed to electromagnetic fields.
Acute leukemia in electrical workers: a New Zealand case-control study.
Adult mortality from leukemia, brain cancer, amyotrophic lateral sclerosis and magnetic fields
from power lines: a case-control study in Brazil.
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Amyotrophic lateral sclerosis (ALS) and extremely-low frequency (ELF) magnetic fields: a
study in the SOD-1 transgenic mouse model.
Amyotrophic lateral sclerosis and environmental factors.
Amyotrophic lateral sclerosis and exposure to metals and other occupational/environmental
hazardous materials: state of the art].
Amyotrophic lateral sclerosis and occupational exposure to electromagnetic fields.
Amyotrophic Lateral Sclerosis and Occupational Exposures: A Systematic Literature Review
and Meta-Analyses.
An apparently incongruous exposure-response relationship resulting from the use of job
description to assess magnetic field exposure.
Annals of conflicting results: looking back on electromagnetic field research.
Are occupational, hobby, or lifestyle exposures associated with Philadelphia chromosome
positive chronic myeloid leukaemia?
Are thyroid dysfunctions related to stress or microwave exposure (900 MHz)?
Assessment of cellular telephone and other radio frequency exposure for epidemiologic research.
Assessment of magnetic field exposures for a mortality study at a uranium enrichment plant.
ASSESSMENT OF OCCUPATIONAL EXPOSURE TO RADIO FREQUENCY
ELECTROMAGNETIC FIELDS].
Association between exposure to pulsed electromagnetic fields and cancer in electric utility
workers in Quebec, Canada, and France.
Association between extremely low-frequency electromagnetic fields occupations and
amyotrophic lateral sclerosis: a meta-analysis.
Association between occupational exposure to power frequency electromagnetic fields and
amyotrophic lateral sclerosis: a review.
Berkson error adjustment and other exposure surrogates in occupational case-control studies,
with application to the Canadian INTEROCC study.
Biologic effects and health consequences of low and high (radio) frequency electromagnetic
fields.
Biological effects on human health due to radiofrequency/microwave exposure: a synopsis of
cohort studies.
Biological indicators in response to radiofrequency/microwave exposure.
Biophysical mechanisms of electromagnetic fields interaction and health effects].
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Brain cancer and occupational exposure to magnetic fields among men: results from a Canadian
population-based case-control study.
Breast cancer and electromagnetic fields--a review.
Can exposure to a terrestrial trunked radio (TETRA)-like signal cause symptoms? A randomised
double-blind provocation study.
Cancer in the electric power industry.
Cancer incidence among Norwegian airline pilots.
Cancer incidence among welders: possible effects of exposure to extremely low frequency
electromagnetic radiation (ELF) and to welding fumes.
Cancer incidence and magnetic field exposure in industries using resistance welding in Sweden.
Carcinogenic risk of extremely-low-frequency electromagnetic fields: state of the art].
Cardiovascular diseases and the work environment. A critical review of the epidemiologic
literature on nonchemical factors.
Causes of death among Belgian professional military radar operators: a 37-year retrospective
cohort study.
Chromosome studies of personnel exposed to electromagnetic radiation at radar centers].
Clinical monitoring in areas of exposure to radiofrequency electromagnetic fields].
Clinical variants of the disease caused by exposure to radio-frequency electromagnetic fields].
Cohort and nested case-control studies of hematopoietic cancers and brain cancer among electric
utility workers.
Computer screens and brain cancer.
Contemporary state of hygienic regulation of electromagnetic fields and prospective harmonizing
with foreign standards].
Criterial parameter of hygienic regulation for exposure to rarely repeated ultrashort
electromagnetic impulses].
Current problems of nonionizing radiation.
Dementia and occupational exposure to magnetic fields.
Depression in high voltage power line workers.
Description of persons with symptoms presumed to be caused by electricity or visual display
units--oral aspects.
Development and evaluation of a tool for retrospective exposure assessment of selected
endocrine disrupting chemicals and EMF in the car manufacturing industry.
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Difficulties of expert testimony in microwave disease].
Ecological and hygienic studies of electromagnetic irradiation of navigation safety system in
Eastern area of the Finnish Gulf].
Effect of electromagnetic radiation on T-lymphocyte subpopulations and immunoglobulin level
in human blood serum after occupational exposure].
Effect of radiofrequency electromagnetic field exposure on in vitro models of neurodegenerative
disease.
Effect of ultra high frequency electromagnetic waves and lead on the workers' health;
phytotherapy of the disorders].
Effect of wide-band modulated electromagnetic fields on the workers of high-frequency
telephone exchanges].
Effects of 60 Hz electromagnetic field exposure on APP695 transcription levels in differentiating
human neuroblastoma cells.
Effects of exposure to microwaves: problems and perspectives.
Effects of exposure to very high frequency radiofrequency radiation on six antenna engineers in
two separate incidents.
Electric and magnetic fields and health outcomes--an overview.
Electric and magnetic fields at power frequencies.
Electrical occupations and neurodegenerative disease: analysis of U.S. mortality data.
Electromagnetic field exposure and cancer: a review of epidemiologic evidence.
Electromagnetic interference of GSM mobile phones with the implantable deep brain stimulator,
ITREL-III.
Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats.
Elevated risk of Alzheimer's disease among workers with likely electromagnetic field exposure.
EMF and health.
Environmental risk factors for non-Hodgkin's lymphoma: a population-based case-control study
in Languedoc-Roussillon, France.
Epidemiologic studies of electric and magnetic fields and cancer: a case study of distortions by
the media.
Epidemiologic studies of the effect of microwaves (neurophysiologic, hematologic and
ophthalmologic aspects)].
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Epidemiological risk assessment of pathology development in occupational exposure to
radiofrequency electromagnetic fields].
Evaluation of occupational risk caused by exposure to electromagnetic rays].
Evaluation of various psychologic parameters in a group of workers occupationally exposed to
radiofrequency].
Evaluation of vital activity of workers with obliterating diseases of lower extremities servicing
electric transmission lines].
Exposure from occupational versus other sources.
Exposure to electromagnetic fields and risk of central nervous system diseases among employees
at Danish electric companies].
Exposure to extremely-low-frequency electromagnetic fields and radiofrequency radiation:
cardiovascular effects in humans.
Exposure to low-frequency electromagnetic fields--a health hazard?
Exposure to magnetic fields among electrical workers in relation to leukemia risk in Los Angeles
County.
Exposure to VHF and UHF electromagnetic fields among workers employed in radio and TV
broadcast centers. I. Assessment of exposure].
Exposure, health complaints and cognitive performance among employees of an MRI scanners
manufacturing department.
Fifty Hertz electromagnetic field exposure stimulates secretion of beta-amyloid peptide in
cultured human neuroglioma.
Follow-up of radio and telegraph operators with exposure to electromagnetic fields and risk of
breast cancer.
Future needs of occupational epidemiology of extremely low frequency electric and magnetic
fields: review and recommendations.
Health Effects of Electromagnetic Fields on Reproductive-Age Female Operators of Plastic
Welding Machines in Fuzhou, China.
Health effects of electromagnetic fields].
Health effects relevant to the setting of EMF exposure limits.
Health of workers exposed to electric fields.
Health problems among operators of plastic welding machines and exposure to radiofrequency
electromagnetic fields.
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Health state and performance of operators in electric discharge facilities--sources of
electromagnetic impulses].
HEALTH STATUS OF ELECTROTECHNICAL PERSONNEL EXPOSED TO THE
COMBINED IMPACT OF ELECTROMAGNETIC FIELDS OF 50 HZ AND CHEMICALS].
Health status of railway workers using magnetic powder flaw detectors].
Health status of the workers exposed to strong, constant magnetic fields].
Hygienic assessment of working conditions and functional resistance in electric power station
workers].
HYGIENIC ASSESSMENT OF WORKING CONDITIONS OF EMPLOYEES OF
BROADCASTING CENTER].
Hygienic evaluation of work conditions for shielded compartments staff].
Hygienic optimization of the use of chemical protective means on railway transport].
Idiopathic environmental intolerance: 2 disabling entities to recognize].
Impact of electromagnetic fields on a computer user].
Incidence of breast cancer in a Norwegian cohort of women with potential workplace exposure
to 50 Hz magnetic fields.
Incidence of cancer among workers in Norwegian hydroelectric power companies.
Incidence of cancer in Norwegian workers potentially exposed to electromagnetic fields.
Incidence of cancer in persons with occupational exposure to electromagnetic fields in Denmark.
Incidence of leukaemia and brain tumours in some "electrical occupations".
Increased incidence of cancer in a cohort of office workers exposed to strong magnetic fields.
Influence of power frequency electric and magnetic fields on human health.
Interactions between occupational exposure to extremely low frequency magnetic fields and
chemicals for brain tumour risk in the INTEROCC study.
Interactive effect of chemical substances and occupational electromagnetic field exposure on the
risk of gliomas and meningiomas in Swedish men.
Leukaemia, brain tumours and exposure to extremely low frequency magnetic fields: cohort
study of Swiss railway employees.
Leukemia and occupational exposure to electromagnetic fields: review of epidemiologic surveys.
Leukemia following occupational exposure to 60-Hz electric and magnetic fields among Ontario
electric utility workers.
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Leukemia in electric utility workers: the evaluation of alternative indices of exposure to 60 Hz
electric and magnetic fields.
Leukemia in telephone linemen.
Long term and excessive use of 900 MHz radiofrequency radiation alter microRNA expression
in brain.
Low frequency electromagnetic fields in the working environment--exposure and health effects.
Elevated risk of cancer, reproductive hazards or other unwanted health effects?].
Low-back pain among electric power supply workers and their attitude toward its prevention and
the treatment.
Magnetic field exposure and neurodegenerative disease mortality among electric utility workers.
Magnetic field exposure and neurodegenerative diseases--recent epidemiological studies.
Magnetic field exposure in relation to leukemia and brain cancer mortality among electric utility
workers.
Magnetic field exposure related to cancer subtypes.
Magnetic field on the deranged accommodation of visual detector terminal operators].
Magnetic fields and brain tumour risks in UK electricity supply workers.
Magnetic fields and leukaemia risks in UK electricity supply workers.
Magnetic fields exposure from high-voltage power lines and risk of amyotrophic lateral sclerosis
in two Italian populations.
Male breast tumors in railway engine drivers: investigation of 5 cases].
Microwave antigen retrieval of beta-amyloid precursor protein immunoreactivity.
Microwave sickness: a reappraisal.
Mobile phone use and brain tumours in the CERENAT case-control study.
Modern concepts and methodology of means, methods of protection, and safety measures for
servicemen affected by nonionizing radiation].
Mortality among workers in the geothermal power plants at Larderello, Italy.
Mortality from amyotrophic lateral sclerosis, other chronic disorders, and electric shocks among
utility workers.
Mortality from brain cancer and leukaemia among electrical workers.
Mortality from neurodegenerative disease and exposure to extremely low-frequency magnetic
fields: 31 years of observations on Swiss railway employees.
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Mortality of personnel operating electric power objects with 500 kV voltage].
Myeloid leukemias and myelodysplastic syndromes: chemical exposure, histologic subtype and
cytogenetics in a case-control study.
Neurodegenerative disease and magnetic field exposure in UK electricity supply workers.
Neurodegenerative diseases in welders and other workers exposed to high levels of magnetic
fields.
Neurodegenerative diseases, suicide and depressive symptoms in relation to EMF.
Neurological effects of microwave exposure related to mobile communication.
Neurological effects of radiofrequency radiation.
News in occupational cancers].
Non-Hodgkin's lymphoma among electric utility workers in Ontario: the evaluation of alternate
indices of exposure to 60 Hz electric and magnetic fields.
Non-ionizing radiation exposure causing ill-health and alopecia areata.
Novelties in hygienic evaluation of electromagnetic conditions on computerized workplaces].
Occupation and malignant lymphoma: a population based case control study in Germany.
Occupational assessment of computer placement in school areas].
Occupational electromagnetic field exposures associated with sleep quality: a cross-sectional
study.
Occupational exposure and amyotrophic lateral sclerosis in a prospective cohort.
Occupational exposure of healthcare and research staff to static magnetic stray fields from 1.5-7
Tesla MRI scanners is associated with reporting of transient symptoms.
Occupational exposure to electromagnetic field and breast cancer risk in a large, population-
based, case-control study in the United States.
Occupational exposure to electromagnetic fields and Alzheimer disease.
Occupational exposure to electromagnetic fields and its health effects in electric energy
workers].
Occupational exposure to electromagnetic fields and sex-differential risk of uveal melanoma.
Occupational exposure to electromagnetic fields and the occurrence of brain tumors. An analysis
of possible associations.
Occupational exposure to electromagnetic fields of extremely low frequency (with particular
regard to power plants) and the health status of workers, based on a literature review].
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Occupational exposure to extremely low frequency electric and magnetic fields and Alzheimer
disease: a meta-analysis.
Occupational exposure to extremely low frequency magnetic fields and risk of Alzheimer
disease: A systematic review and meta-analysis.
Occupational exposure to ionizing radiation and electromagnetic fields in relation to the risk of
thyroid cancer in Sweden.
Occupational exposure to low frequency magnetic fields and dementia: a case-control study.
Occupational exposure to low frequency magnetic fields and the risk of low grade and high
grade glioma.
Occupational exposure to magnetic fields in case-referent studies of neurodegenerative diseases.
Occupational exposure to non-ionizing radiation and an association with heart disease: an
exploratory study.
Occupational exposure to physical agents: the new Italian database for risk assessment and
control.
Occupational exposure to power frequency magnetic fields and risk of non-Hodgkin lymphoma.
Occupational exposures and brain cancer mortality: a preliminary study of east Texas residents.
Occupational Exposures and Neurodegenerative Diseases-A Systematic Literature Review and
Meta-Analyses.
Occupational exposures and the risk of amyotrophic lateral sclerosis.
Occupational exposures obtained by questionnaire in clinical practice and their association with
semen quality.
Occupational exposures to extremely low frequency magnetic fields and postmenopausal breast
cancer.
Occupational factors of anxiety and depressive disorders in the French National Electricity and
Gas Company. The Anxiety-Depression Group.
Occupational hazards for the male reproductive system.
Occupational health evaluation of electromagnetic fields in electric trains and subway
technologic areas].
Occupational magnetic field exposure and neurodegenerative disease.
Occupational magnetic field exposure and site-specific cancer incidence: a Swedish cohort study.
Occupational risk and its prophylaxis for female workers engaged in radio-electronic instrument
industry].
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Occupational risk factors for acute leukaemia: a case-control study.
Occupational risk factors for cancer of the central nervous system: a case-control study on death
certificates from 24 U.S. states.
Occupational risk factors in Alzheimer's disease: a review assessing the quality of published
epidemiological studies.
Occupational risks in grocery stores].
Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer's
disease.
Ocular medical surveillance on microwave and laser workers.
On prevention of a combined impact of electromagnetic radiation and climatic/weather factors
on worker's organism].
On prevention of electromagnetic rays effects in workers exposed to extreme climate
conditions].
On the microwave exposure.
Optimization of methods for measurement and assessment of occupational exposure to
electromagnetic fields in physiotherapy (SW diathermy)].
Overview of epidemiologic research on electric and magnetic fields and cancer.
Perspectives on health effects of electric and magnetic fields.
Physical factors and stress].
Physicians appeals on the dangers of mobile communication--what is the evidence? Assessment
of public health data.
Prevalence of depression among electrical workers.
Prevalence of musculoskeletal disorders and related occupational causative factors among
electricity linemen: A narrative review.
Problem of studying influence of electric and magnetic fields on human health. Results and
prospects].
Provocation of the electromagnetic distress syndrome.
Radiofrequency (RF) sickness in the Lilienfeld Study: an effect of modulated microwaves?
Radiofrequency electromagnetic fields; male infertility and sex ratio of offspring.
Radiofrequency fields, transthyretin, and Alzheimer's disease.
Relationship between amyloid beta protein and melatonin metabolite in a study of electric utility
workers.
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Relationships between occupational history and serum concentrations of organochlorine
compounds in exocrine pancreatic cancer.
Remote effects of occupational and non-occupational exposure to electromagnetic fields of
power-line frequency. Epidemiological studies].
Reports on electromagnetic field strength measurements issued for occupational health and
safety needs in the opinion of radio communication station users].
Residence near power lines and mortality from neurodegenerative diseases: longitudinal study of
the Swiss population.
Residential and occupational exposures to 50-Hz magnetic fields and breast cancer in women: a
population-based study.
Residential distance to high-voltage power lines and risk of neurodegenerative diseases: a Danish
population-based case-control study.
Review of the epidemiologic literature on EMF and Health.
Risk agents related to work and amyotrophic lateral sclerosis: An occupational medicine focus.
Risk factors for Alzheimer disease: a population-based case-control study in Istanbul, Turkey.
Risk factors, health risks, and risk management for aircraft personnel and frequent flyers.
Risk for leukaemia and brain and breast cancer among Danish utility workers: a second follow-
up.
Risk of severe cardiac arrhythmia in male utility workers: a nationwide danish cohort study.
Searching for the perfect wave: the effect of radiofrequency electromagnetic fields on cells.
Setting prudent public health policy for electromagnetic field exposures.
Socioeconomic status, social mobility and cancer occurrence during working life: a case-control
study among French electricity and gas workers.
State of peripheral blood of technical personnel exposed to constant magnetic fields].
Symptoms of the musculoskeletal system and exposure to magnetic fields in an aluminium plant.
Systematic analysis of the state of man exposed to radio wave irradiation for a long time].
The effect of various occupational exposures to microwave radiation on the concentrations of
immunoglobulins and T lymphocyte subsets].
The evaluation of the consequences of electromagnetic irradiation of hands in operators of high-
frequency welding devices].
The evaluation of the exposure of seamstresses to electromagnetic fields, emitted by sewing
machines].
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The health problems of computer operators].
The possible role of radiofrequency radiation in the development of uveal melanoma.
The potential hazard for the development of leukemia from exposure to electromagnetic
radiation (a review of the literature)].
The psychosocial work environment and skin symptoms among visual display terminal workers:
a case referent study.
The strategy of targetted health surveillance. II. Genetically determined susceptibility to
chemical substances and other issues related to health surveillance.
Trends in nonionizing electomagnetic radiation bioeffects research and related occupational
health aspects.
Various psychological parameters in subjects occupationally exposed to radiofrequencies].
Work environment and cardiovascular diseases. A short review of the literature.
Work related etiology of amyotrophic lateral sclerosis (ALS): a meta-analysis.
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FACTOR 10
Theme - Cerebrovascular disorders
Key MeSH Headings - Cerebrovascular Disorders, Dementia, Migraine Disorders, Tinnitus,
Headache, Sleep Wake Disorders, Carotid Artery Diseases, Alzheimer Disease, Dementia,
Vascular
Titles
A 50-Hz electromagnetic field impairs sleep.
A case-control study on the risk factors of Alzheimer's disease in military elderly men].
A literature review of medical side effects from radio-frequency energy in the human
environment: involving cancer, tumors, and problems of the central nervous system.
A study on the biological effects of exposure mobile-phone frequency EMF].
A survey study on some neurological symptoms and sensations experienced by long term users
of mobile phones.
Association between exposure to radiofrequency electromagnetic fields assessed by dosimetry
and acute symptoms in children and adolescents: a population based cross-sectional study.
Association between overuse of mobile phones on quality of sleep and general health among
occupational health and safety students.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep
disturbance in Saudi population.
Association of tinnitus and electromagnetic hypersensitivity: hints for a shared pathophysiology?
Cell phones: modern man's nemesis?
Clinical features of headache associated with mobile phone use: a cross-sectional study in
university students.
Cohort study on the effects of everyday life radio frequency electromagnetic field exposure on
non-specific symptoms and tinnitus.
Dementia and occupational exposure to magnetic fields.
Do mobile phone base stations affect sleep of residents? Results from an experimental double-
blind sham-controlled field study.
Effect of stress and intesity of mobile phone using on the health and subjective symptoms in
GSM workers].
Effects of 60 Hz electromagnetic field exposure on APP695 transcription levels in differentiating
human neuroblastoma cells.
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Effects of Millimeter-Wave Electromagnetic Radiation on the Experimental Model of Migraine.
Effects of Sleep Quality on the Association between Problematic Mobile Phone Use and Mental
Health Symptoms in Chinese College Students.
Electrical occupations and neurodegenerative disease: analysis of U.S. mortality data.
Electromagnetic hypersensitivity (EHS) and subjective health complaints associated with
electromagnetic fields of mobile phone communication--a literature review published between
2000 and 2004.
Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats.
Elevated risk of Alzheimer's disease among workers with likely electromagnetic field exposure.
Exposure to electromagnetic fields and risk of central nervous system diseases among employees
at Danish electric companies].
Fifty Hertz electromagnetic field exposure stimulates secretion of beta-amyloid peptide in
cultured human neuroglioma.
Headache and sferics.
Health of workers exposed to electric fields.
Individual variation in temporal relationships between exposure to radiofrequency
electromagnetic fields and non-specific physical symptoms: A new approach in studying
'electrosensitivity'.
Investigation of sleep disorders in the vicinity of high frequency transmitters].
Long term and excessive use of 900 MHz radiofrequency radiation alter microRNA expression
in brain.
Long-term and frequent cellular phone use and risk of acoustic neuroma.
Magnetic field exposure and neurodegenerative disease mortality among electric utility workers.
Magnetic field exposure and neurodegenerative diseases--recent epidemiological studies.
Microwave antigen retrieval of beta-amyloid precursor protein immunoreactivity.
Microwave sickness: a reappraisal.
Mobile communication: radiobiology problems and evaluation of danger].
Mobile phone headache: a double blind, sham-controlled provocation study.
Mobile phone use and health symptoms in children.
Mobile phone use and stress, sleep disturbances, and symptoms of depression among young
adults--a prospective cohort study.
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Mobile phone use and subjective symptoms. Comparison of symptoms experienced by users of
analogue and digital mobile phones.
Mobile Phone Use and The Risk of Headache: A Systematic Review and Meta-analysis of Cross-
sectional Studies.
Mobile phone use, school electromagnetic field levels and related symptoms: a cross-sectional
survey among 2150 high school students in Izmir.
Natural very-low-frequency sferics and headache.
Neurobehavioral effects among inhabitants around mobile phone base stations.
Neurodegenerative diseases in welders and other workers exposed to high levels of magnetic
fields.
Neurodegenerative diseases, suicide and depressive symptoms in relation to EMF.
Neurological changes induced by a mobile phone.
Non-specific physical symptoms and electromagnetic field exposure in the general population:
can we get more specific? A systematic review.
Occupational electromagnetic field exposures associated with sleep quality: a cross-sectional
study.
Occupational exposure to electromagnetic fields and Alzheimer disease.
Occupational exposure to extremely low frequency electric and magnetic fields and Alzheimer
disease: a meta-analysis.
Occupational exposure to extremely low frequency magnetic fields and risk of Alzheimer
disease: A systematic review and meta-analysis.
Occupational exposure to low frequency magnetic fields and dementia: a case-control study.
Occupational exposure to magnetic fields in case-referent studies of neurodegenerative diseases.
Occupational Exposures and Neurodegenerative Diseases-A Systematic Literature Review and
Meta-Analyses.
Occupational magnetic field exposure and neurodegenerative disease.
Occupational risk factors in Alzheimer's disease: a review assessing the quality of published
epidemiological studies.
Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer's
disease.
Physicians appeals on the dangers of mobile communication--what is the evidence? Assessment
of public health data.
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Preliminary report: symptoms associated with mobile phone use.
Prevalence of headache among handheld cellular telephone users in Singapore: a community
study.
Psychological symptoms and intermittent hypertension following acute microwave exposure.
Radio and microwave frequency radiation and health--an analysis of the literature].
Radiofrequency fields, transthyretin, and Alzheimer's disease.
Relationship between amyloid beta protein and melatonin metabolite in a study of electric utility
workers.
Residence near power lines and mortality from neurodegenerative diseases: longitudinal study of
the Swiss population.
Residential distance to high-voltage power lines and risk of neurodegenerative diseases: a Danish
population-based case-control study.
Risk factors for Alzheimer disease: a population-based case-control study in Istanbul, Turkey.
Role of ultrasonic dopplerography in monitoring the effectiveness of treatment of patients who
have sustained a stroke with decimeter-range electromagnetic waves].
Subjective symptoms related to mobile phone use--a pilot study].
Subjective symptoms, sleeping problems, and cognitive performance in subjects living near
mobile phone base stations.
Survey of mobile phone use and their chronic effects on the hearing of a student population.
Symptom prevalence and worry about high voltage transmission lines.
Symptoms experienced by people in vicinity of base stations: II/ Incidences of age, duration of
exposure, location of subjects in relation to the antennas and other electromagnetic factors].
Symptoms of ill health ascribed to electromagnetic field exposure--a questionnaire survey.
Symptoms reported by mobile cellular telephone users].
The association between use of mobile phones after lights out and sleep disturbances among
Japanese adolescents: a nationwide cross-sectional survey.
The effects of 884 MHz GSM wireless communication signals on headache and other symptoms:
an experimental provocation study.
The prevalence of symptoms attributed to electromagnetic field exposure: a cross-sectional
representative survey in Switzerland.
The relationship between adolescents' well-being and their wireless phone use: a cross-sectional
study.
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The risk of subjective symptoms in mobile phone users in Poland--an epidemiological study.
The role of microwave radiometry in carotid artery disease. Diagnostic and clinical prospective.
Time-dependent hematological changes in workers exposed to electromagnetic fields.
Tinnitus and cell phones: the role of electromagnetic radiofrequency radiation.
Tinnitus and mobile phone use.
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FACTOR 11
Theme - Congenital abnormalities and glandular-based tumors
Key MeSH Headings - Cleft Lip, Cleft Palate, Fibroadenoma, Adenoma, Calcification,
Physiologic, Mammary Neoplasms, Animal, Mammary Neoplasms, Experimental,
Adenocarcinoma
Titles
A histopathological study on alterations in DMBA-induced mammary carcinogenesis in rats with
50 Hz, 100 muT magnetic field exposure.
Acceleration of mammary tumorigenesis by exposure of 7,12-dimethylbenz[a]anthracene-treated
female rats in a 50-Hz, 100-microT magnetic field: replication study.
Are microwaves a co-teratogen? Experimental model concept and its verification].
Bioelectromagnetic field effects on cancer cells and mice tumors.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in F344/N
rats.
Chronic, low-level (1.0 W/kg) exposure of mice prone to mammary cancer to 2450 MHz
microwaves.
Do cocarcinogenic effects of ELF electromagnetic fields require repeated long-term interaction
with carcinogens? Characteristics of positive studies using the DMBA breast cancer model in
rats.
Effect of 13 week magnetic field exposures on DMBA-initiated mammary gland carcinomas in
female Sprague-Dawley rats.
Effect of 26 week magnetic field exposures in a DMBA initiation-promotion mammary gland
model in Sprague-Dawley rats.
Effect of a 9 mT pulsed magnetic field on C3H/Bi female mice with mammary carcinoma. A
comparison between the 12 Hz and the 460 Hz frequencies.
Effects of 50- or 60-hertz, 100 microT magnetic field exposure in the DMBA mammary cancer
model in Sprague-Dawley rats: possible explanations for different results from two laboratories.
Effects of 900 MHz GSM wireless communication signals on DMBA-induced mammary tumors
in rats.
Effects of GSM-900 microwaves on DMBA-induced mammary gland tumors in female Sprague-
Dawley rats.
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Effects of magnetic fields on mammary tumor development induced by 7,12-
dimethylbenz(a)anthracene in rats.
Effects of mobile-phone microwave on dimethylbenz (a) anthracene induced mammary
carcinoma development in rats].
Effects of weak alternating magnetic fields on nocturnal melatonin production and mammary
carcinogenesis in rats.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Evaluation of the potential carcinogenicity of 60 Hz linear sinusoidal continuous-wave magnetic
fields in Fischer F344 rats.
Low-frequency electromagnetic radiation enhances the induction of rat mammary tumors by
nitrosomethyl urea.
Magnetic fields and mammary cancer in rodents: a critical review and evaluation of published
literature.
Male breast tumors in railway engine drivers: investigation of 5 cases].
Microwave absorption by normal and tumor cells.
Modifying effect of light and electromagnetic field on development of mammary tumors induced
by N-nitrosomethyl urea in female rats].
Non dietetic environmental risk factors in prostate cancer].
Occupational exposure to magnetic fields in relation to male breast cancer and testicular cancer:
a Swedish case-control study.
On the role of the interactions of ions with external magnetic fields in physiologic processes and
their importance in chronobiology.
Pulsed magnetic field from video display terminals enhances teratogenic effects of cytosine
arabinoside in mice.
Repeated exposure of C3H/HeJ mice to ultra-wideband electromagnetic pulses: lack of effects on
mammary tumors.
Search for teratogenic risks with the aid of malformation registries.
Significant differences in the effects of magnetic field exposure on 7,12-
dimethylbenz(a)anthracene-induced mammary carcinogenesis in two substrains of Sprague-
Dawley rats.
Study on potential effects of "902-MHz GSM-type Wireless Communication Signals" on
DMBA-induced mammary tumours in Sprague-Dawley rats.
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The effect of low-frequency electromagnetic fields on the development of experimental
mammary tumors].
The influence of electromagnetic radiation generated by a mobile phone on the skeletal system of
rats.
Transferrin receptors and natural killer cell lysis. A study using Colo 205 cells exposed to 60 Hz
electromagnetic fields.
VDT pulse magnetic field enhances teratogenic effect of ara-c in mice].
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FACTOR 12
Theme
–
Skin neoplasms
Key MeSH Headings - Carcinoma, Basal Cell, Carcinoma, Squamous Cell, Skin Neoplasms,
Cocarcinogenesis, Neoplasms, Experimental, Neoplasms, Radiation-Induced, Colonic
Neoplasms
Titles
50-Hz electromagnetic environment and the incidence of childhood tumors in Stockholm
County.
A case-case study of mobile phone use and acoustic neuroma risk in Japan.
A histopathological study on alterations in DMBA-induced mammary carcinogenesis in rats with
50 Hz, 100 muT magnetic field exposure.
A literature review of medical side effects from radio-frequency energy in the human
environment: involving cancer, tumors, and problems of the central nervous system.
A pooled analysis of extremely low-frequency magnetic fields and childhood brain tumors.
A population-based case-control study of radiofrequency exposure in relation to childhood
neoplasm.
A review of in vitro studies: low-frequency electromagnetic fields.
A study on skin tumour formation in mice with 50 Hz magnetic field exposure.
A three-dimensional point process model for the spatial distribution of disease occurrence in
relation to an exposure source.
Acceleration of the development of benzopyrene-induced skin cancer in mice by microwave
radiation.
Acoustic neuroma risk in relation to mobile telephone use: results of the INTERPHONE
international case-control study.
Adverse cutaneous effects of ionizing and non-ionizing electromagnetic radiation.
Alternative functional relationships between ELF field exposure and possible health effects:
report on an expert workshop.
An epidemiological review of mobile telephones and cancer.
Animal carcinogenicity studies on radiofrequency fields related to mobile phones and base
stations.
Application criteria of the precautionary principle].
Assessing the potential carcinogenic activity of magnetic fields using animal models.
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Assessment of cellular telephone and other radio frequency exposure for epidemiologic research.
Association between radiation from mobile phones and tumour risk in adults].
Bcl-2 and p53 immunoprofile in Kaposi's sarcoma.
Bioeffects of electromagnetic fields--safety limits of each frequency band, especially less than
radio one].
Biological effects from electromagnetic field exposure and public exposure standards.
Biological effects of amplitude-modulated radiofrequency radiation.
Biological effects of electromagnetic fields and radiation.
Biological effects of extremely low-frequency electromagnetic fields: in vivo studies.
Biological effects on human health due to radiofrequency/microwave exposure: a synopsis of
cohort studies.
Biological indicators in response to radiofrequency/microwave exposure.
Biological interactions and potential health effects of extremely-low-frequency magnetic fields
from power lines and other common sources.
Biological responses to electromagnetic fields.
Biomarkers of induced electromagnetic field and cancer.
Biophysical estimation of the environmental importance of electromagnetic fields.
Biophysical mechanisms of electromagnetic fields interaction and health effects].
Brain tumor risk in offspring of men occupationally exposed to electric and magnetic fields.
Cancer in radar technicians exposed to radiofrequency/microwave radiation: sentinel episodes.
Cancer incidence among welders: possible effects of exposure to extremely low frequency
electromagnetic radiation (ELF) and to welding fumes.
Cancer incidence and magnetic field exposure in industries using resistance welding in Sweden.
Cancer incidence in California flight attendants (United States).
Cancer incidence vs. FM radio transmitter density.
Cancer morbidity in subjects occupationally exposed to high frequency (radiofrequency and
microwave) electromagnetic radiation.
Cancer promotion in a mouse-skin model by a 60-Hz magnetic field: I. Experimental design and
exposure system.
Cancer promotion in a mouse-skin model by a 60-Hz magnetic field: II. Tumor development and
immune response.
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Cancer risks related to low-level RF/MW exposures, including cell phones.
Cancer versus FM radio polarization types.
Carcinogenic risk of extremely-low-frequency electromagnetic fields: state of the art].
Carcinogenicity study of 217 Hz pulsed 900 MHz electromagnetic fields in Pim1 transgenic
mice.
Carcinogenicity study of GSM and DCS wireless communication signals in B6C3F1 mice.
Carcinogenicity test in B6C3F1 mice after parental and prenatal exposure to 50 Hz magnetic
fields.
Carcinogenicity test of 50 Hz sinusoidal magnetic fields in rats.
Case-control study on uveal melanoma (RIFA): rational and design.
Cell phone radiation exposure on brain and associated biological systems.
Cell phones and cancer: what is the evidence for a connection?
Cellular and cordless telephone use and the association with brain tumors in different age groups.
Childhood cancer and magnetic fields from high-voltage power lines in England and Wales: a
case-control study.
Childhood cancer in relation to distance from high voltage power lines in England and Wales: a
case-control study.
Childhood cancer in relation to indicators of magnetic fields from ground current sources.
Childhood cancer occurrence in relation to power line configurations: a study of potential
selection bias in case-control studies.
Children's health and RF EMF exposure. Views from a risk assessment and risk communication
perspective.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in F344/N
rats.
Chronic, low-level (1.0 W/kg) exposure of mice prone to mammary cancer to 2450 MHz
microwaves.
Comparative health risk assessment of electromagnetic fields.
Concern that "EMF" magnetic fields from power lines cause cancer.
Danger of cellular telephones and their relay stations].
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Delayed biological effect of electromagnetic fields action].
Do cocarcinogenic effects of ELF electromagnetic fields require repeated long-term interaction
with carcinogens? Characteristics of positive studies using the DMBA breast cancer model in
rats.
Do people understand IARC's 2B categorization of RF fields from cell phones?
Ecological study on residences in the vicinity of AM radio broadcasting towers and cancer death:
preliminary observations in Korea.
Effect of 13 week magnetic field exposures on DMBA-initiated mammary gland carcinomas in
female Sprague-Dawley rats.
Effect of 26 week magnetic field exposures in a DMBA initiation-promotion mammary gland
model in Sprague-Dawley rats.
Effect of magnetic field exposure on anchorage-independent growth of a promoter-sensitive
mouse epidermal cell line (JB6).
Effect of radiofrequency radiation exposure on mouse skin tumorigenesis initiated by 7,12-
dimethybenz[alpha]anthracene.
Effects of 2.45-GHz microwave radiation and phorbol ester 12-O-tetradecanoylphorbol-13-
acetate on dimethylhydrazine-induced colon cancer in mice.
Effects of 2450 MHz electromagnetic fields with a wide range of SARs on methylcholanthrene-
induced transformation in C3H10T1/2 cells.
Effects of 900 MHz GSM wireless communication signals on DMBA-induced mammary tumors
in rats.
Effects of GSM-900 microwaves on DMBA-induced mammary gland tumors in female Sprague-
Dawley rats.
Effects of low level microwave radiation on carcinogenesis in Swiss Albino mice.
Effects of mobile phone radiation on UV-induced skin tumourigenesis in ornithine
decarboxylase transgenic and non-transgenic mice.
Electric blanket or mattress cover use and breast cancer incidence in women 50-79 years of age.
Electric Blanket Use and Risk of Thyroid Cancer in the Women's Health Initiative Observational
Cohort.
Electrical field exposure and human health. Risk assessment and problems relative to
bureaucratic procedures and to the role of instituitional organizations in control and prevention].
Electromagnetic fields and cancer risks.
Electromagnetic fields and cancer: the cost of doing nothing.
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Electromagnetic fields and cells.
Electromagnetic fields and female breast cancer.
Electromagnetic fields and health effects--epidemiologic studies of cancer, diseases of the central
nervous system and arrhythmia-related heart disease.
Electromagnetic fields and public health.
Electromagnetic fields at mobile phone frequency induce apoptosis and inactivation of the multi-
chaperone complex in human epidermoid cancer cells.
Electromagnetic fields of mobile telephone systems--thresholds, effects and risks for cochlear
implant patients and healthy people].
Electromagnetic fields--effects on health].
Electromagnetic fields: a cancer promoter?
Electromagnetic radiations and cancer. Cause and prevention.
Electromagnetic-field exposure and cancer.
EMF and current cancer concepts.
EMF and health.
Epidemiologic evidence on mobile phones and tumor risk: a review.
Epidemiological studies of human exposures to radiofrequency radiation. A critical review.
Epidemiological studies of radio frequency exposures and human cancer.
Epidemiological study of power lines and childhood cancer in the UK: further analyses.
Estimates of Environmental Exposure to Radiofrequency Electromagnetic Fields and Risk of
Lymphoma Subtypes.
Estimating exposure in studies of residential magnetic fields and cancer: importance of short-
term variability, time interval between diagnosis and measurement, and distance to power line.
Evaluation of carcinogenic effects of electromagnetic fields (EMF).
Evaluation of potential confounders in planning a study of occupational magnetic field exposure
and female breast cancer.
Evaluation of residential exposure to intermediate frequency magnetic fields.
Evaluation of the effects of electric and magnetic fields in humans].
Evaluation of the potential carcinogenicity of 60 Hz linear sinusoidal continuous-wave magnetic
fields in Fischer F344 rats.
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Evaluation of the potential in vitro antiproliferative effects of millimeter waves at some
therapeutic frequencies on RPMI 7932 human skin malignant melanoma cells.
Evidence for microwave carcinogenesis in vitro.
Experimental data on radiofrequency].
Exposure to low electromagnetic fields and the carcinogenesis process].
Exposure to low-intensive superhigh frequency electromagnetic field as a factor of
carcinogenesis in experimental animals.
Exposure to power-frequency magnetic fields and the risk of childhood cancer. UK Childhood
Cancer Study Investigators.
Exposure to radio-frequency electromagnetic fields from broadcast transmitters and risk of
childhood cancer: a census-based cohort study.
Extremely low frequency electromagnetic fields (EMF) and brain cancer in adults and children:
review and comment.
Extremely low-frequency electromagnetic fields exposure and female breast cancer risk: a meta-
analysis based on 24,338 cases and 60,628 controls.
Follow-up of radio and telegraph operators with exposure to electromagnetic fields and risk of
breast cancer.
Further aspects on cellular and cordless telephones and brain tumours.
Future needs of occupational epidemiology of extremely low frequency electric and magnetic
fields: review and recommendations.
Genetic, carcinogenic and teratogenic effects of radiofrequency fields.
GSM and DCS wireless communication signals: combined chronic toxicity/carcinogenicity study
in the Wistar rat.
Health effects of microwave exposures: a review of the recent (1995-1998) literature.
Health risks from the use of mobile phones.
Health risks of electric and magnetic fields caused by high-voltage systems in Finland.
Health risks of electromagnetic fields. Part I: Evaluation and assessment of electric and magnetic
fields.
Health risks of exposure to non-ionizing radiation--myths or science-based evidence.
Health risks of mobile phones].
Hematopoietic neoplasia in C57BL/6 mice exposed to split-dose ionizing radiation and circularly
polarized 60 Hz magnetic fields.
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High-voltage overhead power lines in epidemiology: patterns of time variations in current load
and magnetic fields.
How dangerous are mobile phones, transmission masts, and electricity pylons?
Human disease resulting from exposure to electromagnetic fields.
Immunotropic effects of electromagnetic fields in the range of radio- and microwave
frequencies].
Improved classification of evidence for EMF health risks.
In vivo exposure of rats to a weak alternating magnetic field increases ornithine decarboxylase
activity in the mammary gland by a similar extent as the carcinogen DMBA.
Incidence of breast cancer in a Norwegian cohort of women with potential workplace exposure
to 50 Hz magnetic fields.
Incorporation of epidemiological findings into radiation protection standards.
Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies.
Indication of cocarcinogenic potential of chronic UMTS-modulated radiofrequency exposure in
an ethylnitrosourea mouse model.
Influence of extremely-low-frequency magnetic field on antioxidative melatonin properties in
AT478 murine squamous cell carcinoma culture.
Invited commentary: electromagnetic fields and cancer in railway workers.
Joint actions of environmental nonionizing electromagnetic fields and chemical pollution in
cancer promotion.
Leukemia, brain tumors, and exposure to extremely low frequency electromagnetic fields in
Swiss railway employees.
Long-term use of cellular phones and brain tumours: increased risk associated with use for > or
=10 years.
Long-term, low-level microwave irradiation of rats.
Lost in laterality: interpreting ''preferred side of the head during mobile phone use and risk of
brain tumour'' associations.
Low frequency electromagnetic fields in the working environment--exposure and health effects.
Elevated risk of cancer, reproductive hazards or other unwanted health effects?].
Low-frequency electromagnetic radiation enhances the induction of rat mammary tumors by
nitrosomethyl urea.
Low-level exposure to radiofrequency electromagnetic fields: health effects and research needs.
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Magnetic fields and breast cancer in Swedish adults residing near high-voltage power lines.
Magnetic fields and childhood cancer--a pooled analysis of two Scandinavian studies.
Magnetic fields and childhood cancer: an epidemiological investigation of the effects of high-
voltage underground cables.
Magnetic fields of high voltage power lines and risk of cancer in Finnish adults: nationwide
cohort study.
Malignant melanoma of the skin - not a sunshine story!
Medical aspects of radiofrequency radiation overexposure.
Medical exposure to ionising radiation and the risk of brain tumours: Interphone study group,
Germany.
Melanoma incidence and frequency modulation (FM) broadcasting.
Melatonin suppression by static and extremely low frequency electromagnetic fields: relationship
to the reported increased incidence of cancer.
Meta-analysis of long-term mobile phone use and the association with brain tumours.
Methods used to calculate exposures in two epidemiological studies of power lines in the UK.
Microwave absorption by normal and tumor cells.
Mobile phone base stations and early childhood cancers: case-control study.
Mobile phone radiation and the risk of cancer; a review.
Mobile phone use and acoustic neuroma risk in Japan.
Mobile phone use and brain tumours in the CERENAT case-control study.
Mobile phone use and risk of parotid gland tumor.
Mobile phone use and the risk of skin cancer: a nationwide cohort study in Denmark.
Mobile phone use, exposure to radiofrequency electromagnetic field, and brain tumour: a case-
control study.
Mobile phones and brain tumours: a review of epidemiological research.
Mobile phones and head tumours. The discrepancies in cause-effect relationships in the
epidemiological studies - how do they arise?
Mobile phones, cordless phones and the risk for brain tumours.
Mobile phones, mobile phone base stations and cancer: a review.
Mortality in workers exposed to electromagnetic fields.
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Mortality indices for hemoblastoses in Rivno Province before and after the accident at the
Chernobyl Atomic Electric Power Station].
Motivation and significance of IARC classification for mobile phone].
Need for a European approach to the effects of extremely low-frequency electromagnetic fields
on cancer. ELF-EMF European Feasibility Study Group.
Non dietetic environmental risk factors in prostate cancer].
Non-ionizing electromagnetic radiation and cancer--is there a relationship?
Non-ionizing electromagnetic radiation: a study of carcinogenic and cancer treatment potential.
Non-ionizing electromagnetic radiations, emitted by a cellular phone, modify cutaneous blood
flow.
Non-thermal bioeffects of static and extremely low frequency electromagnetic fields].
Nonionizing electromagnetic fields and cancer: a review.
Normal doses of visible light can cause mutations in skin].
Occupational exposure to electromagnetic fields and sex-differential risk of uveal melanoma.
Occupational exposure to electromagnetic fields and the occurrence of brain tumors. An analysis
of possible associations.
Occupational exposure to ionizing and non-ionizing radiation and risk of non-Hodgkin
lymphoma.
Occupational exposure to ionizing radiation and electromagnetic fields in relation to the risk of
thyroid cancer in Sweden.
Occupational exposure to non-ionizing radiation and an association with heart disease: an
exploratory study.
Occupational exposure to power frequency magnetic fields and risk of non-Hodgkin lymphoma.
Overview of epidemiologic research on electric and magnetic fields and cancer.
p53 immunoreactivity in cutaneous PUVA tumors is similar to that in other non-melanoma skin
neoplasms.
Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male
reproductive system.
Physical basis of adverse and therapeutic effects of low intensity microwave radiation.
Possible cocarcinogenic effects of ELF electromagnetic fields may require repeated long-term
interaction with known carcinogenic factors.
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Possible health hazards from exposure to power-frequency electric and magnetic fields--a
COMAR Technical Information Statement.
Primary brain cancer in adults and the use of common household appliances: a case-control
study.
Public health and the radio frequency radiation emitted by cellphone technology, smart meters
and WiFi.
Radiation exposure, socioeconomic status, and brain tumor risk in the US Air Force: a nested
case-control study.
Radio and microwave frequency radiation and health--an analysis of the literature].
Radio frequency electromagnetic fields: cancer, mutagenesis, and genotoxicity.
Radio-frequency radiation exposure from AM radio transmitters and childhood leukemia and
brain cancer.
Radiofrequency and microwave radiation in the microelectronics industry.
Radiofrequency electromagnetic fields emitted from base stations of DECT cordless phones and
the risk of glioma and meningioma (Interphone Study Group, Germany).
Radiofrequency exposure and mammalian cell toxicity, genotoxicity, and transformation.
Radiofrequency field exposure and cancer: what do the laboratory studies suggest?
Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering
factor.
Rate of occurrence of transient magnetic field events in U.S. residences.
Reanalysis of risks of childhood leukaemia with distance from overhead power lines in the UK.
Recent advances in research on radiofrequency fields and health: 2001-2003.
Recent advances in research on radiofrequency fields and health: 2004-2007.
Recent data from the literature on the biological and pathologic effects of electromagnetic
radiation, radio waves and stray currents].
Recent experimental data on Extremely Low Frequency (ELF) magnetic field carcinogenic risk:
open questions.
Repeated exposure of C3H/HeJ mice to ultra-wideband electromagnetic pulses: lack of effects on
mammary tumors.
Report of final results regarding brain and heart tumors in Sprague-Dawley rats exposed from
prenatal life until natural death to mobile phone radiofrequency field representative of a 1.8GHz
GSM base station environmental emission.
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Residential and occupational exposure to 50 Hz magnetic fields and malignant melanoma: a
population based study.
Residential mobility of populations near UK power lines and implications for childhood
leukaemia.
Review of possible modulation-dependent biological effects of radiofrequency fields.
Risk of brain tumors from wireless phone use.
Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five
Interphone countries.
Risk of cancer among Danish electricity workers. A cohort study].
Risk of neoplastic diseases in conditions of exposure to radio- and microwave fields--
epidemiologic investigations].
Selection bias from differential residential mobility as an explanation for associations of wire
codes with childhood cancer.
Self-reported electrical appliance use and risk of adult brain tumors.
Short-term exposure to 50 Hz ELF-EMF alters the cisplatin-induced oxidative response in
AT478 murine squamous cell carcinoma cells.
Should the threshold limit value for power frequency (60 Hz) magnetic fields be changed?
Perceptions among scientists and other risk experts.
Significant differences in the effects of magnetic field exposure on 7,12-
dimethylbenz(a)anthracene-induced mammary carcinogenesis in two substrains of Sprague-
Dawley rats.
Socioeconomic status, social mobility and cancer occurrence during working life: a case-control
study among French electricity and gas workers.
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer
344 rats chronically exposed to 836 MHz modulated microwaves.
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer
344 rats exposed to frequency-modulated microwave fields.
Studying the effects of mobile phone use on the auditory system and the central nervous system:
a review of the literature and future directions.
Survival and cancer in laboratory mammals exposed to radiofrequency energy.
Systematic review of wireless phone use and brain cancer and other head tumors.
Testing electromagnetic fields for potential carcinogenic activity: a critical review of animal
models.
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The design, construction and calibration of a carefully controlled source for exposure of
mammalian cells to extremely low-frequency electromagnetic fields.
The effect of 60-Hz magnetic fields on co-promotion of chemically induced skin tumors on
SENCAR mice: a discussion of three studies.
The effect of chronic exposure to 835.62 MHz FDMA or 847.74 MHz CDMA radiofrequency
radiation on the incidence of spontaneous tumors in rats.
The effect of embryonic and fetal exposure to x-ray, microwaves, and ultrasound: counseling the
pregnant and nonpregnant patient about these risks.
The effects of 860 MHz radiofrequency radiation on the induction or promotion of brain tumors
and other neoplasms in rats.
The effects of embryonic and fetal exposure to x-ray, microwaves, and ultrasound.
The effects of ionizing radiation, microwaves, and ultrasound on the developing embryo: clinical
interpretations and applications of the data.
The effects of pulsed 860 MHz radiofrequency radiation on the promotion of neurogenic tumors
in rats.
The epidemiology of electric and magnetic field exposures in the power frequency range and
reproductive outcomes.
The Intracranial Distribution of Gliomas in Relation to Exposure From Mobile Phones: Analyses
From the INTERPHONE Study.
The possible role of contact current in cancer risk associated with residential magnetic fields.
The possible role of radiofrequency radiation in the development of uveal melanoma.
The potential carcinogenic hazards of electromagnetic radiation: a review.
The precautionary principle and electric and magnetic fields.
The probability of developing brain tumours among users of cellular telephones (scientific
information to the decision of the International Agency for Research on Cancer (IARC)
announced on May 31, 2011)].
The problem of hygienic standardization of commercial electric and magnetic fields in Russia
and other countries].
The question of health effects from exposure to electromagnetic fields.
The role of chemical and physical factors in cancer development].
The sensitivity of children to electromagnetic fields.
Time trend in incidence of malignant neoplasms of the central nervous system in relation to
mobile phone use among young people in Japan.
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Use of cellular and cordless telephones and risk of testicular cancer.
Use of cellular telephones and brain tumour risk in urban and rural areas.
Use of cellular telephones and risk of cancer. A Danish cohort study].
Use of cellular telephones and the risk for brain tumours: A case-control study.
Use of mobile phones and cancer risk.
Use of wireless phones and the risk of salivary gland tumours: a case-control study.
Variable E-cadherin expression in a MNU-induced colon tumor model in rats which exposed
with 50 Hz frequency sinusoidal magnetic field.
Variation in cancer risk estimates for exposure to powerline frequency electromagnetic fields: a
meta-analysis comparing EMF measurement methods.
Wire codes, magnetic fields, and childhood cancer.
World Health Organization, radiofrequency radiation and health - a hard nut to crack (Review).
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FACTOR 13
Theme - Leukemia
Key MeSH Headings - Leukemia, Myeloid, Acute, Leukemia, Lymphocytic, Chronic, B-Cell,
Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Leukemia, Myeloid, Leukemia, Multiple
Myeloma, Lymphoma, Leukemia, Radiation-Induced, Acute Disease, Liver Neoplasms,
Experimental, Central Nervous System Neoplasms
Titles
60 Hertz magnetic field exposure assessment for an investigation of leukemia in telephone
lineworkers.
A Bayesian approach to hazard identification. The case of electromagnetic fields and cancer.
A case-control pilot study of traffic exposures and early childhood leukemia using a geographic
information system.
A case-control study of childhood leukemia in southern Ontario, Canada, and exposure to
magnetic fields in residences.
A case-control study of risk of leukaemia in relation to mobile phone use.
A literature review of medical side effects from radio-frequency energy in the human
environment: involving cancer, tumors, and problems of the central nervous system.
A pooled analysis of magnetic fields and childhood leukaemia.
A pooled analysis of magnetic fields, wire codes, and childhood leukemia. Childhood Leukemia-
EMF Study Group.
A population-based case-control study of radiofrequency exposure in relation to childhood
neoplasm.
A precautionary public health protection strategy for the possible risk of childhood leukaemia
from exposure to power frequency magnetic fields.
Acute childhood leukemias and exposure to magnetic fields generated by high voltage overhead
power lines - a risk factor in Iran.
Acute effects of pulsed microwaves and 3-nitropropionic acid on neuronal ultrastructure in the
rat caudate-putamen.
Acute leukaemia in workers exposed to electromagnetic fields.
Acute leukemia in electrical workers: a New Zealand case-control study.
Acute nonlymphocytic leukemia and residential exposure to power frequency magnetic fields.
Acute ocular injuries caused by 60-Ghz millimeter-wave exposure.
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Adult and childhood leukemia near a high-power radio station in Rome, Italy.
Adult mortality from leukemia, brain cancer, amyotrophic lateral sclerosis and magnetic fields
from power lines: a case-control study in Brazil.
Aetiology of childhood leukemia.
Aluminum, calcium ion and radiofrequency synergism in acceleration of lymphomagenesis.
An evaluation of exposure metrics in an epidemiologic study on radio and television broadcast
transmitters and the risk of childhood leukemia.
An examination of underlying physical principles. The interaction of power-line electromagnetic
fields with the human body.
Animal carcinogenicity studies on radiofrequency fields related to mobile phones and base
stations.
Are occupational, hobby, or lifestyle exposures associated with Philadelphia chromosome
positive chronic myeloid leukaemia?
Are the stray 60-Hz electromagnetic fields associated with the distribution and use of electric
power a significant cause of cancer?
Assessment of cellular telephone and other radio frequency exposure for epidemiologic research.
Assessment of selection bias in the Canadian case-control study of residential magnetic field
exposure and childhood leukemia.
Association of childhood cancer with residential traffic density.
Biological effects of environmental electromagnetic fields: molecular mechanisms.
Biophysical mechanisms of electromagnetic fields interaction and health effects].
Can disturbances in the atmospheric electric field created by powerline corona ions disrupt
melatonin production in the pineal gland?
Cancer incidence among welders: possible effects of exposure to extremely low frequency
electromagnetic radiation (ELF) and to welding fumes.
Cancer incidence and magnetic field exposure in industries using resistance welding in Sweden.
Cancer incidence and mortality and proximity to TV towers.
Cancer incidence near radio and television transmitters in Great Britain. I. Sutton Coldfield
transmitter.
Cancer incidence near radio and television transmitters in Great Britain. II. All high power
transmitters.
Carcinogenic risk of extremely-low-frequency electromagnetic fields: state of the art].
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Carcinogenicity test of 50 Hz sinusoidal magnetic fields in rats.
Case-control study of childhood cancer and exposure to 60-Hz magnetic fields.
Case-only study of interactions between DNA repair genes (hMLH1, APEX1, MGMT, XRCC1
and XPD) and low-frequency electromagnetic fields in childhood acute leukemia.
Cell Phones and Risk of brain and acoustic nerve tumours: the French INTERPHONE case-
control study].
Characterization of Children's Exposure to Extremely Low Frequency Magnetic Fields by
Stochastic Modeling.
Childhood cancer and exposure to corona ions from power lines: an epidemiological test.
Childhood cancer and magnetic fields from high-voltage power lines in England and Wales: a
case-control study.
Childhood cancer and residential proximity to power lines. UK Childhood Cancer Study
Investigators.
Childhood cancer in relation to a modified residential wire code.
Childhood cancer in relation to indicators of magnetic fields from ground current sources.
Childhood incidence of acute lymphoblastic leukaemia and exposure to broadcast radiation in
Sydney--a second look.
Childhood leukaemia and distance from power lines in California: a population-based case-
control study.
Childhood leukaemia close to high-voltage power lines--the Geocap study, 2002-2007.
Childhood leukaemia in a residential area with a high-voltage power line: approach according to
the Dutch Community Health Services' guideline 'Cancer Clusters'].
Childhood leukemia and electromagnetic fields: results of a population-based case-control study
in Germany.
Childhood leukemia and magnetic fields in infant incubators.
Childhood leukemia and magnetic fields in Japan: a case-control study of childhood leukemia
and residential power-frequency magnetic fields in Japan.
Childhood leukemia and personal monitoring of residential exposures to electric and magnetic
fields in Ontario, Canada.
Childhood leukemia, electric and magnetic fields, and temporal trends.
Childhood leukemia: electric and magnetic fields as possible risk factors.
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Children's exposure to magnetic fields produced by U.S. television sets used for viewing
programs and playing video games.
Children's health and RF EMF exposure. Views from a risk assessment and risk communication
perspective.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in F344/N
rats.
Cohort and nested case-control studies of hematopoietic cancers and brain cancer among electric
utility workers.
Combined risk estimates for two German population-based case-control studies on residential
magnetic fields and childhood acute leukemia.
Comparative analyses of the studies of magnetic fields and cancer in electric utility workers:
studies from France, Canada, and the United States.
Comparative health risk assessment of electromagnetic fields.
Contact voltage measured in residences: implications to the association between magnetic fields
and childhood leukemia.
Decreased survival for childhood leukemia in proximity to television towers.
Description of a new computer wire coding method and its application to evaluate potential
control selection bias in the Savitz et al. childhood cancer study.
Designs and analyses for exploring the relationship of magnetic fields to childhood leukaemia: a
pilot project for the Danish National Birth Cohort.
Determinants of power-frequency magnetic fields in residences located away from overhead
power lines.
Developing policy in the face of scientific uncertainty: interpreting 0.3 microT or 0.4 microT
cutpoints from EMF epidemiologic studies.
Distance from residence to power line and risk of childhood leukemia: a population-based case-
control study in Denmark.
Distance to high-voltage power lines and risk of childhood leukemia--an analysis of confounding
by and interaction with other potential risk factors.
Do magnetic fields cause increased risk of childhood leukemia via melatonin disruption?
Do naturally occurring magnetic nanoparticles in the human body mediate increased risk of
childhood leukaemia with EMF exposure?
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Do power frequency magnetic fields cause leukemia in children?
Do studies of wire code and childhood leukemia point towards or away from magnetic fields as
the causal agent?
Effect of pulsed magnetic fields on leukemia-prone AKR mice. No-effect on mortality through
five generations.
Effects of centimeter waves on the immune system of mice in endotoxic shock].
Effects of electromagnetic fields on health].
Effects of extremely low-frequency electromagnetic fields (ELF-EMF) exposure on B6C3F1
mice.
Effects of mobile phone type signals on calcium levels within human leukaemic T-cells (Jurkat
cells).
Electric and magnetic fields (EMF): what do we know about the health effects?
Electric and magnetic fields and health outcomes--an overview.
Electric and magnetic fields at power frequencies.
Electrical field exposure and human health. Risk assessment and problems relative to
bureaucratic procedures and to the role of instituitional organizations in control and prevention].
Electrical power lines and childhood leukemia: a study from Greece.
Electromagnetic field exposures and childhood cancers in New Zealand.
Electromagnetic field exposures and childhood leukaemia in New Zealand.
Electromagnetic fields (EMF): do they play a role in children's environmental health (CEH)?
Electromagnetic fields and cancer risks.
Electromagnetic fields from high-voltage installations and cancer in childhood].
Electromagnetic fields--effects on health].
Electromagnetic pollution (electrosmog)--potential hazards of our electromagnetic future].
Electrosmog as a health risk factor: sources of artificial electromagnetic fields, evaluation of
health risk, prevention methods].
EMF and health.
EMFs: cutting through the controversy.
Environmental factors and childhood acute leukemias and lymphomas.
Epidemiologic evidence relevant to radar (microwave) effects.
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Epidemiologic study of residential proximity to transmission lines and childhood cancer in
California: description of design, epidemiologic methods and study population.
Epidemiological appraisal of studies of residential exposure to power frequency magnetic fields
and adult cancers.
Epidemiological study of power lines and childhood cancer in the UK: further analyses.
Epidemiology of health effects of radiofrequency exposure.
Estimates of Environmental Exposure to Radiofrequency Electromagnetic Fields and Risk of
Lymphoma Subtypes.
Estimating exposure in studies of residential magnetic fields and cancer: importance of short-
term variability, time interval between diagnosis and measurement, and distance to power line.
Estimation of population attributable fractions from fitted incidence ratios and exposure survey
data, with an application to electromagnetic fields and childhood leukemia.
Ethical values in the regulation of the exposure to electromagnetic fields].
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Experimental estimation of thermogenic levels of acute microwave exposure for different animal
species].
Exposure of high resolution fetuses in advanced pregnant woman models at different stages of
pregnancy to uniform magnetic fields at the frequency of 50 Hz.
Exposure to 50-Hz electric field and incidence of leukemia, brain tumors, and other cancers
among French electric utility workers.
Exposure to electromagnetic fields and risk of leukemia.
Exposure to electromagnetic fields and the risk of leukemia.
Exposure to low frequency pulsed electromagnetic fields increases interleukin-1 and interleukin-
6 production by human peripheral blood mononuclear cells.
Exposure to low-frequency electromagnetic fields--a health hazard?
Exposure to magnetic fields among electrical workers in relation to leukemia risk in Los Angeles
County.
Exposure to magnetic fields and survival after diagnosis of childhood leukemia: a German cohort
study.
Exposure to power frequency electric fields and the risk of childhood cancer in the UK.
Exposure to power-frequency magnetic fields and the risk of childhood cancer. UK Childhood
Cancer Study Investigators.
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Exposure to radio-frequency electromagnetic fields from broadcast transmitters and risk of
childhood cancer: a census-based cohort study.
Exposure to residential electric and magnetic fields and risk of childhood leukemia.
Extra low frequency electric and magnetic fields in the bedplace of children diagnosed with
leukaemia: a case-control study.
Extremely low frequency electromagnetic fields and cancer: the epidemiologic evidence.
Factors that explain the power line configuration wiring code-childhood leukemia association:
what would they look like?
Geomagnetic field variation in early ontogenesis as a risk factor for oncopathology].
Health effects of electromagnetic fields].
Health effects of low-level electromagnetic fields: phantom or not-so-phantom risk?
Hematopoietic neoplasia in C57BL/6 mice exposed to split-dose ionizing radiation and circularly
polarized 60 Hz magnetic fields.
High incidence of acute leukemia in the proximity of some industrial facilities in El Bierzo,
northwestern Spain.
Hypothesis: the risk of childhood leukemia is related to combinations of power-frequency and
static magnetic fields.
In vitro microwave effects on human neutrophil precursor cells (CFU-C).
Incidence of cancer in the vicinity of Korean AM radio transmitters.
Incidence of leukaemia and brain tumours in some "electrical occupations".
Incorporation of epidemiological findings into radiation protection standards.
Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies.
Increased ornithine decarboxylase activity in cultured cells exposed to low energy modulated
microwave fields and phorbol ester tumor promoters.
Increased risk of childhood acute lymphoblastic leukemia (ALL) by prenatal and postnatal
exposure to high voltage power lines: a case control study in Isfahan, Iran.
Induction of macrophage migration inhibitory factor precedes the onset of acute tonsillitis.
Infantile leukemia and exposure to 50/60 Hz magnetic fields: review of epidemiologic evidence
in 2000].
Influence of 60-Hertz magnetic fields on leukemia.
Investigation of increased incidence in childhood leukemia near radio towers in Hawaii:
preliminary observations.
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Investigation of the sources of residential power frequency magnetic field exposure in the UK
Childhood Cancer Study.
Knowledge and perceptions of the health effects of environmental hazards in the general
population in Italy.
Leukaemia and residence near electricity transmission equipment: a case-control study.
Leukaemia, brain tumours and exposure to extremely low frequency magnetic fields: cohort
study of Swiss railway employees.
Leukemia and lymphoma incidence in rodents exposed to low-frequency magnetic fields.
Leukemia and occupational exposure to electromagnetic fields: review of epidemiologic surveys.
Leukemia following occupational exposure to 60-Hz electric and magnetic fields among Ontario
electric utility workers.
Leukemia in electric utility workers: the evaluation of alternative indices of exposure to 60 Hz
electric and magnetic fields.
Leukemia in telephone linemen.
Leukemia mortality and incidence of infantile leukemia near the Vatican Radio Station of
Rome].
Leukemia risk and occupational electric field exposure in Los Angeles County, California.
Leukemia, brain tumors, and exposure to extremely low frequency electromagnetic fields in
Swiss railway employees.
Living near overhead high voltage transmission power lines as a risk factor for childhood acute
lymphoblastic leukemia: a case-control study.
Lymphoma development in mice chronically exposed to UMTS-modulated radiofrequency
electromagnetic fields.
Lymphoma development of simultaneously combined exposure to two radiofrequency signals in
AKR/J mice.
Lymphoma induced in mice chronically exposed to very strong low-frequency electromagnetic
field.
Magnetic field exposure in relation to leukemia and brain cancer mortality among electric utility
workers.
Magnetic fields and acute leukemia in children with Down syndrome.
Magnetic fields and acute lymphoblastic leukemia in children: a systematic review of case-
control studies.
Magnetic fields and childhood cancer--a pooled analysis of two Scandinavian studies.
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Magnetic fields and leukaemia risks in UK electricity supply workers.
Magnetic fields and leukemia--risk for adults living close to power lines.
Magnetic fields, leukemia, and central nervous system tumors in Swedish adults residing near
high-voltage power lines.
Maternal occupational exposure to electromagnetic fields before, during, and after pregnancy in
relation to risks of childhood cancers: findings from the Oxford Survey of Childhood Cancers,
1953-1981 deaths.
Meta-analysis and its application in epidemiology].
Mortality among workers in the geothermal power plants at Larderello, Italy.
Mortality from brain cancer and leukaemia among electrical workers.
Mortality in workers exposed to electromagnetic fields.
Mortality indices for hemoblastoses in Rivno Province before and after the accident at the
Chernobyl Atomic Electric Power Station].
Mortality of people residing near electric power supply line with voltage of 500 kV].
Mortality of persons resident in the vicinity of electricity transmission facilities.
Myelogenous leukemia and electric blanket use.
Myeloid leukemias and myelodysplastic syndromes: chemical exposure, histologic subtype and
cytogenetics in a case-control study.
Nighttime exposure to electromagnetic fields and childhood leukemia: an extended pooled
analysis.
Occupation and malignant lymphoma: a population based case control study in Germany.
Occupational and residential exposure to electric and magnetic field and its relationship on acute
myeloid leukemia in adults - A Meta-analysis].
Occupational and residential magnetic field exposure and leukemia and central nervous system
tumors.
Occupational electric and magnetic field exposure and brain cancer: a meta-analysis.
Occupational electric and magnetic field exposure and leukemia. A meta-analysis.
Occupational exposure to electromagnetic fields and acute leukaemia: analysis of a case-control
study.
Occupational exposure to electromagnetic fields and its health effects in electric energy
workers].
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Occupational exposure to electromagnetic fields of extremely low frequency (with particular
regard to power plants) and the health status of workers, based on a literature review].
Occupational magnetic field exposure and myocardial infarction incidence.
Occupational risk factors for acute leukaemia: a case-control study.
Occupational risk factors for cancer of the central nervous system: a case-control study on death
certificates from 24 U.S. states.
Overhead electricity power lines and childhood leukemia: a registry-based, case-control study.
Parental occupational exposure to magnetic fields and childhood cancer (Sweden).
Pharmacological correction of the acute effects of microwave irradiation in an experiment].
Pooled analysis of recent studies on magnetic fields and childhood leukaemia.
Potential motion related bias in the worn dosimeter measurements of two childhood leukemia
studies.
Power lines and the geomagnetic field.
Power-frequency electric and magnetic fields and risk of childhood leukemia in Canada.
Probing lymphoma infiltration in spleen of AKR/J mice chronically exposed to electromagnetic
fields for risk assessment--toward noninvasive modeling.
Proximity to overhead power lines and childhood leukaemia: an international pooled analysis.
Radio and microwave frequency radiation and health--an analysis of the literature].
Radio-frequency radiation exposure from AM radio transmitters and childhood leukemia and
brain cancer.
Radiofrequency exposure and mortality from cancer of the brain and lymphatic/hematopoietic
systems.
Reanalysis of risks of childhood leukaemia with distance from overhead power lines in the UK.
Recent data from the literature on the biological and pathologic effects of electromagnetic
radiation, radio waves and stray currents].
Refinements in magnetic field exposure assignment for a case-cohort study of electrical utility
workers.
Remote effects of occupational and non-occupational exposure to electromagnetic fields of
power-line frequency. Epidemiological studies].
Residence close to high-tension electric power lines and its association with leukemia in
children].
Residential electric consumption and childhood cancer in Canada (1971-1986)
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Residential EMF exposure and childhood leukemia: meta-analysis and population attributable
risk.
Residential exposure to 60-Hertz magnetic fields and adult cancers in Taiwan.
Residential exposure to electromagnetic fields and childhood leukaemia: a meta-analysis.
Residential exposure to magnetic fields and risk of canine lymphoma.
Residential magnetic fields and childhood leukemia: a meta-analysis.
Residential magnetic fields as a risk factor for childhood acute leukaemia: results from a German
population-based case-control study.
Residential magnetic fields predicted from wiring configurations: I. Exposure model.
Residential magnetic fields predicted from wiring configurations: II. Relationships To childhood
leukemia.
Residential magnetic fields, contact voltage and their relationship: the effects of distribution
unbalance and residential proximity to a transmission line.
Residential mobility and childhood leukemia.
Residential mobility of populations near UK power lines and implications for childhood
leukaemia.
Residential proximity to electricity transmission and distribution equipment and risk of
childhood leukemia, childhood lymphoma, and childhood nervous system tumors: systematic
review, evaluation, and meta-analysis.
Residential wire codes: reproducibility and relation with measured magnetic fields.
Review of the epidemiologic literature on EMF and Health.
Risk factors for leukemia in Thailand.
Risk for leukaemia and brain and breast cancer among Danish utility workers: a second follow-
up.
Risk of childhood leukemia and environmental exposure to ELF electromagnetic fields].
Risk of childhood leukemia in areas passed by high power lines.
Risk of leukemia in children living near high-voltage transmission lines.
Risk of major lymphoma subtypes and use of mobile phones].
Risk of neoplastic diseases in conditions of exposure to power magnetic fields--epidemiologic
investigations].
Risk of neoplastic diseases in conditions of exposure to radio- and microwave fields--
epidemiologic investigations].
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Risks of leukaemia among residents close to high voltage transmission electric lines.
Selection bias and its implications for case-control studies: a case study of magnetic field
exposure and childhood leukaemia.
Setting prudent public health policy for electromagnetic field exposures.
Should the threshold limit value for power frequency (60 Hz) magnetic fields be changed?
Perceptions among scientists and other risk experts.
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer
344 rats chronically exposed to 836 MHz modulated microwaves.
Study of extremely low frequency electromagnetic fields in infant incubators.
Suggestion of concomitant changes of electric power consumption and childhood leukemia in
Greece.
Synthesis of the epidemiological evidence concerning childhood leukemia in relation to exposure
to 50 Hz. electric and magnetic fields].
Teratogenic effect of broad-band electromagnetic field on neonatal mice (Mus musculus).
The Bernal Lecture 2004 Are low-frequency electromagnetic fields a health hazard?
The determinants of Canadian children's personal exposures to magnetic fields.
The effect of chronic exposure to 835.62 MHz FDMA or 847.74 MHz CDMA radiofrequency
radiation on the incidence of spontaneous tumors in rats.
The effects of low-energy 60-Hz environmental electromagnetic fields upon the growth-related
enzyme ornithine decarboxylase.
The epidemiology of exposure to electromagnetic fields: an overview of the recent literature.
The possible role of contact current in cancer risk associated with residential magnetic fields.
The potential hazard for the development of leukemia from exposure to electromagnetic
radiation (a review of the literature)].
The potential impact of bias in studies of residential exposure to magnetic fields and childhood
leukemia.
The precautionary principle and electric and magnetic fields.
The sensitivity of children to electromagnetic fields.
Time trend in incidence of malignant neoplasms of the central nervous system in relation to
mobile phone use among young people in Japan.
Variation in cancer risk estimates for exposure to powerline frequency electromagnetic fields: a
meta-analysis comparing EMF measurement methods.
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Viral contacts confound studies of childhood leukemia and high-voltage transmission lines.
Wire codes, magnetic fields, and childhood cancer.
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FACTOR 14
Theme
–
Precancerous conditions
Key MeSH Headings - Atrophy, Precancerous Conditions, Hyperplasia, Hypersensitivity,
Delayed, Thymus Gland, Capillary Permeability, Lymphoma
Titles
A histopathological study on alterations in DMBA-induced mammary carcinogenesis in rats with
50 Hz, 100 muT magnetic field exposure.
A study on skin tumour formation in mice with 50 Hz magnetic field exposure.
Aluminum, calcium ion and radiofrequency synergism in acceleration of lymphomagenesis.
Animal carcinogenicity studies on radiofrequency fields related to mobile phones and base
stations.
Calreticulin protects rat microvascular endothelial cells against microwave radiation-induced
injury by attenuating endoplasmic reticulum stress.
Case-control study of childhood cancer and exposure to 60-Hz magnetic fields.
Cerebrovascular permeability to 86Rb in the rat after exposure to pulsed microwaves.
Childhood cancer in relation to a modified residential wire code.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Cohort and nested case-control studies of hematopoietic cancers and brain cancer among electric
utility workers.
Dependence of microwave effect on the secondary structure of DNA on molecular weight of
polynucleotide].
Detrimental effect of electromagnetic pulse exposure on permeability of in vitro blood-brain-
barrier model.
Differential response of the permeability of the rat liver canalicular membrane to sucrose and
mannitol following in vivo acute single and multiple exposures to microwave radiation (2.45
GHz) and radiant-energy thermal stress.
Effect of electromagnetic pulse exposure on brain micro vascular permeability in rats.
Effect of electromagnetic radiation of millimetric wave band on genome of somatic cells].
Effect of extremely high frequency electromagnetic radiation of low intensity on parameters of
humoral immunity in healthy mice].
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Effect of extremely low frequency electromagnetic radiation and ultra-violet radiation on
aggregation of thymocytes and erythrocytes].
Effect of global system for mobile communication (GSM) microwave exposure on blood-brain
barrier permeability in rat.
Effect of global system for mobile communication (gsm)-like radiofrequency fields on vascular
permeability in mouse brain.
Effect of long-term mobile communication microwave exposure on vascular permeability in
mouse brain.
Effect of microwaves on the expression by thymocytes of various surface membrane markers].
Effect of millimeter waves on cyclophosphamide induced suppression of the immune system.
Effect of pulsed magnetic fields on leukemia-prone AKR mice. No-effect on mortality through
five generations.
Effects of electromagnetic pulse on blood-brain barrier permeability and tight junction proteins
in rats].
Effects of extremely high-frequency electromagnetic radiation on the immune system and
systemic regulation of homeostasis].
Effects of GSM-modulated 900 MHz radiofrequency electromagnetic fields on the hematopoietic
potential of mouse bone marrow cells.
Effects of low level microwave radiation on carcinogenesis in Swiss Albino mice.
Effects of low-intensity extremely high frequency electromagnetic radiation on chromatin
structure of lymphoid cells in vivo and in vitro].
Effects of microwave radiation on thymocytes in mice at different power densities].
Electromagnetic fields from high-voltage installations and cancer in childhood].
Environmental factors and childhood acute leukemias and lymphomas.
Estimates of Environmental Exposure to Radiofrequency Electromagnetic Fields and Risk of
Lymphoma Subtypes.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Geomagnetic field variation in early ontogenesis as a risk factor for oncopathology].
Hematopoietic neoplasia in C57BL/6 mice exposed to split-dose ionizing radiation and circularly
polarized 60 Hz magnetic fields.
Immune function and host defense in rodents exposed to 60-Hz magnetic fields.
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Immunomorphologic changes in the testes upon exposure to a microwave electromagnetic field].
Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies.
Increased sensitivity of the non-human primate eye to microwave radiation following ophthalmic
drug pretreatment.
Inhibitory effects of low doses of melatonin on induction of preneoplastic liver lesions in a
medium-term liver bioassay in F344 rats: relation to the influence of electromagnetic near field
exposure.
Japanese encephalitis virus (JEV): potentiation of lethality in mice by microwave radiation.
Leukemia and lymphoma incidence in rodents exposed to low-frequency magnetic fields.
Lymphoma development in mice chronically exposed to UMTS-modulated radiofrequency
electromagnetic fields.
Lymphoma development of simultaneously combined exposure to two radiofrequency signals in
AKR/J mice.
Lymphoma induced in mice chronically exposed to very strong low-frequency electromagnetic
field.
Magnetic fields and childhood cancer--a pooled analysis of two Scandinavian studies.
Melatonin protects rat thymus against oxidative stress caused by exposure to microwaves and
modulates proliferation/apoptosis of thymocytes.
Metabolic and ultrastructural adaptation mechanisms during the primary prophylactic action of
low-intensity electromagnetic radiation under normal and radiation conditions].
Microwave alteration of the blood-brain barrier system of rats.
Microwave irradiation of rats at 2.45 GHz activates pinocytotic-like uptake of tracer by capillary
endothelial cells of cerebral cortex.
Modulation of cell death in the rat thymus. Light and electron microscopic investigations.
Modulation of natural killer cell function after exposure to 60 Hz magnetic fields: confirmation
of the effect in mature B6C3F1 mice.
Mortality in workers exposed to electromagnetic fields.
Mortality indices for hemoblastoses in Rivno Province before and after the accident at the
Chernobyl Atomic Electric Power Station].
Nonlinear determinism in the immune system. In vivo influence of electromagnetic fields on
different functions of murine lymphocyte subpopulations.
Nonlinear dynamical law governs magnetic field induced changes in lymphoid phenotype.
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Occupation and malignant lymphoma: a population based case control study in Germany.
Odontologic survey of referred patients with symptoms allegedly caused by electricity or visual
display units.
Permeability of the blood-brain barrier induced by 915 MHz electromagnetic radiation,
continuous wave and modulated at 8, 16, 50, and 200 Hz.
Prenatal exposure to radiofrequencies: effects of WiFi signals on thymocyte development and
peripheral T cell compartment in an animal model.
Probing lymphoma infiltration in spleen of AKR/J mice chronically exposed to electromagnetic
fields for risk assessment--toward noninvasive modeling.
Radiofrequency exposure and mammalian cell toxicity, genotoxicity, and transformation.
Radiofrequency exposure and mortality from cancer of the brain and lymphatic/hematopoietic
systems.
Residential electric consumption and childhood cancer in Canada (1971-1986)
Residential exposure to magnetic fields and risk of canine lymphoma.
Residential proximity to electricity transmission and distribution equipment and risk of
childhood leukemia, childhood lymphoma, and childhood nervous system tumors: systematic
review, evaluation, and meta-analysis.
Retinal damage experimentally induced by microwave radiation at 55 mW/cm2.
Reversible microwave effects on the blood-brain barrier.
Risk of major lymphoma subtypes and use of mobile phones].
Risk of neoplastic diseases in conditions of exposure to power magnetic fields--epidemiologic
investigations].
Risk of neoplastic diseases in conditions of exposure to radio- and microwave fields--
epidemiologic investigations].
Teratogenic effect of broad-band electromagnetic field on neonatal mice (Mus musculus).
The effect of chronic exposure to 835.62 MHz FDMA or 847.74 MHz CDMA radiofrequency
radiation on the incidence of spontaneous tumors in rats.
The effect of ultrahigh-frequency radiation on adaptation thresholds and the damages to blood
system cells].
The effect on rat thymocytes of the simultaneous in vivo exposure to 50-Hz electric and
magnetic field and to continuous light.
The effects of low-energy 60-Hz environmental electromagnetic fields upon the growth-related
enzyme ornithine decarboxylase.
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The efficiency and direction of thymus changes after whole-body exposure of mice to the weak
electromagnetic field are determined by the initial status of the thymus].
The functional state of thymus cells following microwave exposure of endocrine glands.
The immunological and hormonal effects of combined exposure to a bitemporal ultrahigh-
frequency electrical field and to decimeter waves at different sites].
The immunological mechanism of the modulation of IgE antibody formation during microwave
irradiation of the thymus].
The role of fatty acids in anti-inflammatory effects of low-intensity extremely high-frequency
electromagnetic radiation.
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FACTOR 15
Theme - Circadian Rhythm
Key MeSH Headings - Melatonin, Circadian Rhythm, Pineal Gland
Titles
900-MHz microwave radiation promotes oxidation in rat brain.
A 0.5 G, 60 Hz magnetic field suppresses melatonin production in pinealocytes.
A 50-Hz electromagnetic field impairs sleep.
Acceleration of mammary tumorigenesis by exposure of 7,12-dimethylbenz[a]anthracene-treated
female rats in a 50-Hz, 100-microT magnetic field: replication study.
Acute exposure to 50 Hz magnetic fields with harmonics and transient components: lack of
effects on nighttime hormonal secretion in men.
Age-dependent association of exposure to television screen with children's urinary melatonin
excretion?
Anatomical localization of human detection of weak electromagnetic radiation: experiments with
dowsers.
Anxiogenic effect of chronic exposure to extremely low frequency magnetic field in adult rats.
Biological effects of continuous exposure of embryos and young chickens to electromagnetic
fields emitted by video display units.
Biological effects of extremely low-frequency electromagnetic fields: in vivo studies.
Biological effects of non-ionizing electromagnetic radiation].
Biological effects produced by the influence of low frequency electromagnetic fields on hormone
secretion].
Biological influences of electromagnetic fields].
Biologically based epidemiological studies of electric power and cancer.
Breast cancer and electric power.
Can disturbances in the atmospheric electric field created by powerline corona ions disrupt
melatonin production in the pineal gland?
Cardiac autonomic control mechanisms in power-frequency magnetic fields: a multistudy
analysis.
Cardiovascular diseases and the work environment. A critical review of the epidemiologic
literature on nonchemical factors.
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Chronic exposure to 2.9 mT, 40 Hz magnetic field reduces melatonin concentrations in humans.
Chronic exposure to ELF fields may induce depression.
Chronic exposure to ELF magnetic fields during night sleep with electric sheet: effects on
diurnal melatonin rhythms in men.
Chronotoxicity of 1800 MHz microwave radiation on sex hormones and spermatogenesis in male
mice].
Circadian locomotor activity of Musca flies: recording method and effects of 10 Hz square-wave
electric fields.
Circadian rhythmicity of antioxidant markers in rats exposed to 1.8 GHz radiofrequency fields.
Designing EMF experiments: what is required to characterize "exposure"?
Direct suppressive effects of weak magnetic fields (50 Hz and 16 2/3 Hz) on melatonin synthesis
in the pineal gland of Djungarian hamsters (Phodopus sungorus).
Do magnetic fields cause increased risk of childhood leukemia via melatonin disruption?
Does evening exposure to mobile phone radiation affect subsequent melatonin production?
Earthing: health implications of reconnecting the human body to the Earth's surface electrons.
Effect of occupational EMF exposure from radar at two different frequency bands on plasma
melatonin and serotonin levels.
Effects of 1800-MHz radiofrequency fields on circadian rhythm of plasma melatonin and
testosterone in male rats.
Effects of 60-Hz magnetic field exposure on nocturnal 6-sulfatoxymelatonin, estrogens,
luteinizing hormone, and follicle-stimulating hormone in healthy reproductive-age women:
results of a crossover trial.
Effects of electric and magnetic fields from high-power lines on female urinary excretion of 6-
sulfatoxymelatonin.
Effects of electric and magnetic fields on nocturnal melatonin concentrations in dairy cows.
Effects of electromagnetic fields exposure on plasma hormonal and inflammatory pathway
biomarkers in male workers of a power plant.
Effects of electromagnetic fields on photophasic circulating melatonin levels in American
kestrels.
Effects of electromagnetic radiation from 3G mobile phone on heart rate, blood pressure and
ECG parameters in rats.
Effects of exposure to 16.7 Hz magnetic fields on urinary 6-hydroxymelatonin sulfate excretion
of Swiss railway workers.
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Effects of melatonin on Wi-Fi-induced oxidative stress in lens of rats.
Effects of mobile phone electromagnetic fields at nonthermal SAR values on melatonin and body
weight of Djungarian hamsters (Phodopus sungorus).
Effects of mobile phone radiation on UV-induced skin tumourigenesis in ornithine
decarboxylase transgenic and non-transgenic mice.
Effects of static electromagnetic fields on chick embryo pineal gland development.
Effects of weak alternating magnetic fields on nocturnal melatonin production and mammary
carcinogenesis in rats.
Electric blanket or mattress cover use and breast cancer incidence in women 50-79 years of age.
Electric power, pineal function, and the risk of breast cancer.
Endocrine functions in young men exposed for one night to a 50-Hz magnetic field. A circadian
study of pituitary, thyroid and adrenocortical hormones.
Evaluation in humans of the effects of radiocellular telephones on the circadian patterns of
melatonin secretion, a chronobiological rhythm marker.
Evaluation of the nocturnal levels of urinary biogenic amines in men exposed overnight to 50-Hz
magnetic field.
Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.
Exacerbation of hypertension and disturbances of the geomagnetic field].
Examination of the melatonin hypothesis in women exposed at night to EMF or bright light.
Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial
DNA in primary cultured neurons.
Exposure to electromagnetic fields and suicide among electric utility workers: a nested case-
control study.
Extremely low frequency electromagnetic fields (EMF) and brain cancer in adults and children:
review and comment.
Geomagnetic activity and human melatonin metabolite excretion.
Geomagnetic disturbances are associated with reduced nocturnal excretion of a melatonin
metabolite in humans.
Human melatonin during continuous magnetic field exposure.
Immune markers and ornithine decarboxylase activity among electric utility workers.
Impact of microwave at X-band in the aetiology of male infertility.
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Incidence of micronuclei in human peripheral blood lymphocytes exposed to modulated and
unmodulated 2450 MHz radiofrequency fields.
Increases in geomagnetic activity are associated with increases in thyroxine levels in a single
patient: implications for melatonin levels.
Influence of electromagnetic fields emitted by GSM-900 cellular telephones on the circadian
patterns of gonadal, adrenal and pituitary hormones in men.
Influence of extremely-low-frequency magnetic field on antioxidative melatonin properties in
AT478 murine squamous cell carcinoma culture.
Influence of light and electromagnetic radiation of Sun on circadian rhythms of the total
antioxidant capacity of human saliva in the North].
Inhibitory effects of low doses of melatonin on induction of preneoplastic liver lesions in a
medium-term liver bioassay in F344 rats: relation to the influence of electromagnetic near field
exposure.
Interaction of static and extremely low frequency electric and magnetic fields with living
systems: health effects and research needs.
Is melatonin the hormonal missing link between magnetic field effects and human diseases?
Is newborn melatonin production influenced by magnetic fields produced by incubators?
Is problematic mobile phone use explained by chronotype and personality?
Magnetic fields and pineal function in humans: evaluation of nocturnal acute exposure to
extremely low frequency magnetic fields on serum melatonin and urinary 6-sulfatoxymelatonin
circadian rhythms.
Magnetic storm effect on the circulation of rabbits.
Melatonin and a spin-trap compound block radiofrequency electromagnetic radiation-induced
DNA strand breaks in rat brain cells.
Melatonin and magnetic fields.
Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA
damage and cell cycle arrest in germ cells of male Swiss albino mice.
Melatonin metabolite levels in workers exposed to 60-Hz magnetic fields: work in substations
and with 3-phase conductors.
Melatonin modulates 900 Mhz microwave-induced lipid peroxidation changes in rat brain.
Melatonin protects rat cerebellar granule cells against electromagnetic field-induced increases in
Na(+) currents through intracellular Ca(2+) release.
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Melatonin protects rat thymus against oxidative stress caused by exposure to microwaves and
modulates proliferation/apoptosis of thymocytes.
Melatonin reduces oxidative stress induced by chronic exposure of microwave radiation from
mobile phones in rat brain.
Melatonin suppression by static and extremely low frequency electromagnetic fields: relationship
to the reported increased incidence of cancer.
Mobile phone radiation induces mode-dependent DNA damage in a mouse spermatocyte-derived
cell line: a protective role of melatonin.
Mobile phones and health: a literature overview.
Modifying effect of light and electromagnetic field on development of mammary tumors induced
by N-nitrosomethyl urea in female rats].
Modulation of wireless (2.45 GHz)-induced oxidative toxicity in laryngotracheal mucosa of rat
by melatonin.
Morphometric and structural study of the pineal gland of the Wistar rat subjected to the pulse
action of a 52 Gauss, (50 Hz) magnetic field. Evolutive analysis over 21 days.
Multi-night exposure to 60 Hz magnetic fields: effects on melatonin and its enzymatic
metabolite.
Neuroprotective effects of melatonin and omega-3 on hippocampal cells prenatally exposed to
900 MHz electromagnetic fields.
Nighttime exposure to electromagnetic fields and childhood leukemia: an extended pooled
analysis.
Nocturnal 6-hydroxymelatonin sulfate excretion in female workers exposed to magnetic fields.
Nocturnal excretion of a urinary melatonin metabolite among electric utility workers.
Nocturnal exposure to intermittent 60 Hz magnetic fields alters human cardiac rhythm.
Non-thermal biomarkers of exposure to radiofrequency/microwave radiation.
Nonionizing electromagnetic fields and cancer: a review.
Oxidative stress-mediated skin damage in an experimental mobile phone model can be prevented
by melatonin.
Pathophysiology of microwave radiation: effect on rat brain.
Prevention of mobile phone induced skin tissue changes by melatonin in rat: an experimental
study.
Protective effect of melatonin and vitamin E against prooxidative action of iron ions and static
magnetic field].
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Rapid-onset/offset, variably scheduled 60 Hz electric and magnetic field exposure reduces
nocturnal serum melatonin concentration in nonhuman primates.
Rate of occurrence of transient magnetic field events in U.S. residences.
Reduced excretion of a melatonin metabolite in workers exposed to 60 Hz magnetic fields.
Relationship between amyloid beta protein and melatonin metabolite in a study of electric utility
workers.
Residential magnetic fields and the risk of breast cancer.
Risk factors, health risks, and risk management for aircraft personnel and frequent flyers.
Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca2+ signaling
molecular pathways in breast cancer.
Serum-thyroxine levels in microwave-exposed rats.
Shift work, light at night, and breast cancer on Long Island, New York.
Temporal trends and misclassification in residential 60 Hz magnetic field measurements.
The effect of melatonin on body mass and behaviour of rats during an exposure to microwave
radiation from mobile phone.
The effect of melatonin on the liver of rats exposed to microwave radiation.
The Effects of Electromagnetic Field on the Endocrine System in Children and Adolescents.
The effects of electromagnetic radiation (2450 MHz wireless devices) on the heart and blood
tissue: role of melatonin.
The effects of extremely low-frequency magnetic fields on melatonin and cortisol, two marker
rhythms of the circadian system.
The Effects of Melatonin on Oxidative Stress Parameters and DNA Fragmentation in Testicular
Tissue of Rats Exposed to Microwave Radiation.
The excretion of 6-hydroxymelatonin sulfate in healthy young men exposed to electromagnetic
fields emitted by cellular phone -- an experimental study.
The impact of electromagnetic field at a frequency of 50 Hz and a magnetic induction of 2.5 mT
on viability of pineal cells in vitro.
The influence of long-term exposure of mice to randomly varied power frequency magnetic
fields on their nocturnal melatonin secretion patterns.
The melatonin hypothesis: electric power and breast cancer.
The relationship between electromagnetic field and light exposures to melatonin and breast
cancer risk: a review of the relevant literature.
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The therapeutic effect of a pulsed electromagnetic field on the reproductive patterns of male
Wistar rats exposed to a 2.45-GHz microwave field.
Therapeutic approaches of melatonin in microwave radiations-induced oxidative stress-mediated
toxicity on male fertility pattern of Wistar rats.
Understanding the effects of electromagnetic field emissions from Marine Renewable Energy
Devices (MREDs) on the commercially important edible crab, Cancer pagurus (L.).
Urinary 6-sulphatoxymelatonin excretion is increased in rats after 24 hours of exposure to
vertical 50 Hz, 100 microT magnetic field.
Variations of melatonin and stress hormones under extended shifts and radiofrequency
electromagnetic radiation.
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FACTOR 16
Theme - Eye diseases
Key MeSH Headings - Eye Diseases, Cataract, Vision Disorders, Sensation Disorders, Neurotic
Disorders, Lens, Crystalline, Corneal Diseases, Edema, Hematologic Diseases
Titles
A quantitative study on early changes in rabbit lens capsule epithelium induced by low power
density microwave radiation].
Acute microwave irradiation and cataract formation in rabbits and monkeys.
Acute ocular lesions after exposure to electromagnetic radiation of ultrahigh frequency (an
experimental study)].
Age-Related Modulations of AQP4 and Caveolin-1 in the Hippocampus Predispose the Toxic
Effect of Phoneutria nigriventer Spider Venom.
Ascorbic acid changes in cultured rabbit lenses after microwave irradiation.
Biologic effects and hygienic regulation of electromagnetic fields caused by mobile
communication devices].
Blocking 1800 MHz mobile phone radiation-induced reactive oxygen species production and
DNA damage in lens epithelial cells by noise magnetic fields].
Cataracts induced by microwave and ionizing radiation.
Changes in gap junctional intercellular communication in rabbits lens epithelial cells induced by
low power density microwave radiation.
Combined microwave energy and fixative agent for cataract induction in pig eyes.
Comments on Frey's "Data analysis reveals significant microwave-induced eye damage in
humans".
Data analysis reveals significant microwave-induced eye damage in humans.
Dependence of anti-inflammatory effects of high peak-power pulsed electromagnetic radiation of
extremely high frequency on exposure parameters].
DNA damage and repair induced by acute exposure of microwave from mobile phone on
cultured human lens epithelial cells].
Dosimetric study of microwave cataractogenesis.
Effect of acute exposure to microwave from mobile phone on DNA damage and repair of
cultured human lens epithelial cells in vitro].
Effect of high-power density microwave irradiation on the soluble proteins of the rabbit lens.
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Effect of long-term power frequency electromagnetic field exposure on proliferation and
apoptosis of SRA01/04 cells].
Effect of low-intensity microwave radiation on proliferation of cultured epithelial cells of rabbit
lens].
Effect of superposed electromagnetic noise on DNA damage of lens epithelial cells induced by
microwave radiation.
Effects of different dose microwave radiation on protein components of cultured rabbit lens].
Effects of exposure to microwaves: problems and perspectives.
Effects of Long-Term Exposure to 60 GHz Millimeter-Wavelength Radiation on the
Genotoxicity and Heat Shock Protein (Hsp) Expression of Cells Derived from Human Eye.
Effects of melatonin on Wi-Fi-induced oxidative stress in lens of rats.
Effects of microwave radiation on the eye: the occupational health perspective.
Effects of microwave radiation on the lens epithelium in the rabbit eye.
Effects of mobile phones and radar radiofrequencies on the eye].
Effects of mobile phones on oxidant/antioxidant balance in cornea and lens of rats.
Effects of repeated microwave irradiations to the albino rabbit eye.
Electrical properties of lens material at microwave frequencies.
Electromagnetic noise inhibits radiofrequency radiation-induced DNA damage and reactive
oxygen species increase in human lens epithelial cells.
Epidemiologic studies of the effect of microwaves (neurophysiologic, hematologic and
ophthalmologic aspects)].
Epidemiological studies of human exposures to radiofrequency radiation. A critical review.
Evaluation of lens transparency in persons exposed to electromagnetic radiation of 27--30 MHz
frequency].
Evaluation of possible microwave-induced lens changes in the United States Air Force.
Experimental studies on the influence of millimeter radiation on light transmission through the
lens].
Features of anti-inflammatory effects of modulated extremely high-frequency electromagnetic
radiation.
Glutathione concentration and peptidase activity in the lens after exposure to microwaves.
Hazards of radio frequency magnetic field and their prevention and control].
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Health problems among workers of iron welding machines: an effect of electromagnetic fields.
In vitro studies of microwave-induced cataract. II. Comparison of damage observed for
continuous wave and pulsed microwaves.
In vitro studies of microwave-induced cataract: reciprocity between exposure duration and dose
rate for pulsed microwaves.
Increased occurrence of nuclear cataract in the calf after erection of a mobile phone base station].
Inducing cataract in postmortem pig eyes for cataract surgery training purposes.
Localized effects of microwave radiation on the intact eye lens in culture conditions.
Low power density microwave radiation induced early changes in rabbit lens epithelial cells.
Low power microwave radiation inhibits the proliferation of rabbit lens epithelial cells by
upregulating P27Kip1 expression.
Low-intensity microwave blockes cell cycle and regulate cell cycle related gene expression in
rabbit lens epithelial cells].
Microwave cataract and litigation: a case study.
Microwave cyclodestruction: evaluation on human eyes.
Microwave lens effects in humans. II. Results of five-year survey.
Microwave radiation-induced chromosomal aberrations in corneal epithelium of Chinese
hamsters.
Microwaves and the visual analyzer].
Millimeter wave absorption in the nonhuman primate eye at 35 GHz and 94 GHz.
Mobile Phone Radiation: Physiological & Pathophysiologcal Considerations.
Neurotic disturbances, depression and anxiety disorders in the population living in the vicinity of
overhead high-voltage transmission line 400 kV. Epidemiological pilot study].
Non-thermal cellular effects of lowpower microwave radiation on the lens and lens epithelial
cells.
Observation of microwave-induced eye lens surface motion in vitro.
Ocular effects of radiofrequency energy.
Odontologic survey of referred patients with symptoms allegedly caused by electricity or visual
display units.
On the microwave exposure.
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Phantom vibration and phantom ringing among mobile phone users: A systematic review of
literature.
Post-mortem histologic evaluation of microwave lesions after epicardial pulmonary vein
isolation for atrial fibrillation.
Prevalence of nuclear cataract in Swiss veal calves and its possible association with mobile
telephone antenna base stations.
Proteomic analysis of human lens epithelial cells exposed to microwaves.
Radiofrequency and microwave radiation in the microelectronics industry.
Some ocular symptoms and sensations experienced by long term users of mobile phones.
Some ocular symptoms experienced by users of mobile phones.
State of peripheral blood of technical personnel exposed to constant magnetic fields].
The effect of extremely low frequency magnetic field on the conjunctiva and goblet cells.
The effects of cell phone use on peripheral vision.
The effects of ionizing radiation, microwaves, and ultrasound on the developing embryo: clinical
interpretations and applications of the data.
The ocular effects of microwaves on hypothermic rabbits: a study of microwave cataractogenic
mechanisms.
Thermal cataract formation in rabbits.
Thresholds for lenticular damage in the rabbit eye due to single exposure to CW microwave
radiation: an analysis of the experimental information at a frequency of 2.45 GHz.
Ultrastructural change of rabbit lens epithelial cells induced by low power level microwave
radiation].
Ultrastructural changes in the rabbit lens induced by microwave radiation.
Video display terminals: risk of electromagnetic radiation.
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FACTOR 17
Theme - Electromagnetic interference in implanted electronic devices
Key MeSH Headings - Tachycardia, Ventricular, Ventricular Fibrillation, Death, Sudden,
Cardiac, Arrhythmias, Cardiac
Titles
AANA Journal Course: update for nurse anesthetists. Arrhythmia management devices and
electromagnetic interference.
Accidental deaths caused by electricity in Sweden, 1975-2000.
Are patients with cardiac implants protected against electromagnetic interference in daily life and
occupational environment?
Avoidance behaviors in patients with implantable cardioverter defibrillators.
Cardiac autonomic control mechanisms in power-frequency magnetic fields: a multistudy
analysis.
Deaths associated with implantable cardioverter defibrillator failure and deactivation reported in
the United States Food and Drug Administration Manufacturer and User Facility Device
Experience Database.
Detection of refrigerator-associated 60 Hz alternating current as ventricular fibrillation by an
implantable defibrillator.
Disturbances in the function of cardiac pacemaker caused by short wave and microwave
diathermies and pulsed high frequency current.
Do airport metal detectors interfere with implantable pacemakers or cardioverter-defibrillators?
Do media players cause interference with pacemakers?
Do mobile telephones have adverse effects on the functions of implantable cardioverter
defibrillators?].
ECG changes caused by the effect of static magnetic fields of nuclear magnetic resonance
tomography using magnets with a field power of 0.5 to 4.0 Telsa].
Effects of 900 MHz electromagnetic field emitted by cellular phones on electrocardiograms of
guinea pigs.
Electromagnetic fields and health effects--epidemiologic studies of cancer, diseases of the central
nervous system and arrhythmia-related heart disease.
Electromagnetic Interference (EMI) and arrhythmic events in ICD patients undergoing
gastrointestinal procedures.
Electromagnetic interference in cardiac rhythm management devices.
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Electromagnetic interference in implantable cardioverter defibrillators: present but rare.
Electromagnetic interference of cardiac rhythmic monitoring devices to radio frequency
identification: analytical analysis and mitigation methodology.
Electromagnetic interference with cardiac pacemakers and implantable cardioverter-defibrillators
from low-frequency electromagnetic fields in vivo.
Electromagnetic interference with implantable cardioverter-defibrillators at power frequency: an
in vivo study.
Fine structural alterations in radiofrequency energy-induced lesions in dog hearts: possible basis
for reduced arrhythmic complications.
Implantable cardioverter defibrillators and cellular telephones: is there any interference?
Implanted devices and electromagnetic interference: case presentations and review.
Induction ovens and electromagnetic interference: what is the risk for patients with implantable
cardioverter defibrillators?
Induction ovens and electromagnetic interference: what is the risk for patients with implanted
pacemakers?
Influence of 50 Hz electric and magnetic fields on the human heart.
Influence of digital and analogue cellular telephones on implanted pacemakers.
Interference of electrical dental equipment with implantable cardioverter-defibrillators.
Interference with cardiac pacemakers by cellular telephones.
Interference with cardiac pacing.
Is there any risk interaction between electromagnetic field generated by mobile phones and
artificial pacemakers].
Magnetic field exposure and arrythmic risk: evaluation in railway drivers.
Magnetism and cardiac arrhythmias.
Microwave effects on isolated chick embryo hearts.
Modifications in ventricular fibrillation and capture capacity induced by a linear radiofrequency
lesion.
Risk of severe cardiac arrhythmia in male utility workers: a nationwide danish cohort study.
Selective interference with pacemaker activity by electrical dental devices.
Studies on microwaves in medicine and biology: from snails to humans.
The effect of power frequency high intensity electric fields on implanted cardiac pacemakers.
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Ventricular fibrillation induced by radiofrequency energy delivery for premature ventricular
contractions arising from the right ventricular outflow tract: is
implantablecardioverterdefibrillator indicated?
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FACTOR 18
Theme
–
Liver Neoplasms
Key MeSH Headings - Liver Neoplasms, Carcinoma, Hepatocellular, Neoplasm Recurrence,
Local, Lymphatic Metastasis
Titles
40 GHz RF biosensor based on microwave coplanar waveguide transmission line for cancer cells
(HepG2) dielectric characterization.
A case of hepatocellular carcinoma rupturing after angiography.
A case of recurring hepatocellular carcinoma with a solitary Virchow's lymph node metastasis.
A case report of primary hepatic carcinoid with lymph node metastasis--treatment of hepatic
arterial infusion to post-reoperative liver and radiation to metastasis of para-aortic lymph nodes].
Construction and clinical significance of a predictive system for prognosis of hepatocellular
carcinoma.
Effects of extremely low-frequency electromagnetic fields (ELF-EMF) exposure on B6C3F1
mice.
Geomagnetic field variation in early ontogenesis as a risk factor for oncopathology].
Inhibitory effects of low doses of melatonin on induction of preneoplastic liver lesions in a
medium-term liver bioassay in F344 rats: relation to the influence of electromagnetic near field
exposure.
Lymphoma development of simultaneously combined exposure to two radiofrequency signals in
AKR/J mice.
Mobile phone radiation alters proliferation of hepatocarcinoma cells.
MoS2 nanosheets encapsulated in sodium alginate microcapsules as microwave embolization
agents for large orthotopic transplantation tumor therapy.
Multimodal treatment of hepatocellular carcinoma.
Non-resection approaches for colorectal liver metastases.
Rat liver foci study on coexposure with 50 Hz magnetic fields and known carcinogens.
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FACTOR 19
Theme
–
Symptoms of discomfort
Key MeSH Headings - Headache, Dizziness, Fatigue, Depression, Anxiety, Tremor, Sleep Wake
Disorders, Neurotic Disorders, Stress, Psychological, Anxiety Disorders, Nervous System
Diseases
Titles
A 50-Hz electromagnetic field impairs sleep.
A literature review of medical side effects from radio-frequency energy in the human
environment: involving cancer, tumors, and problems of the central nervous system.
A study on the biological effects of exposure mobile-phone frequency EMF].
A survey study on some neurological symptoms and sensations experienced by long term users
of mobile phones.
Altered cortical excitability in subjectively electrosensitive patients: results of a pilot study.
An analysis of the impact of cell phone use on depressive symptoms among Japanese elders.
Anxiety-like behavioural effects of extremely low-frequency electromagnetic field in rats.
Anxiogenic effect of chronic exposure to extremely low frequency magnetic field in adult rats.
Are media reports able to cause somatic symptoms attributed to WiFi radiation? An experimental
test of the negative expectation hypothesis.
Association between Excessive Use of Mobile Phone and Insomnia and Depression among
Japanese Adolescents.
Association between exposure to radiofrequency electromagnetic fields assessed by dosimetry
and acute symptoms in children and adolescents: a population based cross-sectional study.
Association between mobile phone use and depressed mood in Japanese adolescents: a cross-
sectional study.
Association between overuse of mobile phones on quality of sleep and general health among
occupational health and safety students.
Association between problematic cellular phone use and suicide: the moderating effect of family
function and depression.
Association of low job control with a decrease in memory (CD4+ CD45RO+) T lymphocytes in
Japanese middle-aged male workers in an electric power plant.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep
disturbance in Saudi population.
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Association of tinnitus and electromagnetic hypersensitivity: hints for a shared pathophysiology?
Associations between problematic mobile phone use and psychological parameters in young
adults.
Avoidance behaviors in patients with implantable cardioverter defibrillators.
Bedtime mobile phone use and sleep in adults.
Behavior and memory evaluation of Wistar rats exposed to 1.8 GHz radiofrequency
electromagnetic radiation.
Can exposure to a terrestrial trunked radio (TETRA)-like signal cause symptoms? A randomised
double-blind provocation study.
Cancer incidence and magnetic field exposure in industries using resistance welding in Sweden.
Cell phones: modern man's nemesis?
Cellular phones for reducing battlefield stress: rationale and a preliminary research.
Cerebral radiofrequency exposures during adolescence: Impact on astrocytes and brain functions
in healthy and pathologic rat models.
Chronic exposure to an extremely low-frequency magnetic field induces depression-like
behavior and corticosterone secretion without enhancement of the hypothalamic-pituitary-
adrenal axis in mice.
Chronic exposure to ELF fields may induce depression.
Clinical features of headache associated with mobile phone use: a cross-sectional study in
university students.
Cohort study on the effects of everyday life radio frequency electromagnetic field exposure on
non-specific symptoms and tinnitus.
Contribution of physical factors to the complex anthropogenic load in an industrial town].
Coping and self-image in patients with visual display terminal-related skin symptoms and
perceived hypersensitivity to electricity.
Correction of microcirculatory disturbances with terahertz electromagnetic radiation at nitric
oxide frequencies in albino rats under conditions of acute stress.
Delayed biological effect of electromagnetic fields action].
Depression in high voltage power line workers.
Determinants and stability over time of perception of health risks related to mobile phone base
stations.
Development of a problematic mobile phone use scale for Turkish adolescents.
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Do mobile phone base stations affect sleep of residents? Results from an experimental double-
blind sham-controlled field study.
Does short-term exposure to mobile phone base station signals increase symptoms in individuals
who report sensitivity to electromagnetic fields? A double-blind randomized provocation study.
Effect of hypokinetic stress and low intensity electromagnetic field of extremely high frequency
on changes of cytokine concentration in rat blood].
Effect of short-term 50 Hz electromagnetic field exposure on the behavior of rats.
Effect of stress and intesity of mobile phone using on the health and subjective symptoms in
GSM workers].
Effective methods of protection from technogenic electromagnetic irradiation and information-
wave diagnostic means].
Effects of acute exposure to ultrahigh radiofrequency radiation on three antenna engineers.
Effects of chronic exposure of power frequency magnetic field on neurobehavior in rats].
Effects of electromagnetic fields from mobile phones on depression and anxiety after titanium
mesh cranioplasty among patients with traumatic brain injury.
Effects of exposure to microwaves: problems and perspectives.
Effects of extremely low frequency electromagnetic fields (100muT) on behaviors in rats.
Effects of GSM-900 microwaves on the experimental allergic encephalomyelitis (EAE) rat
model of multiple sclerosis.
Effects of GSM-Frequency Electromagnetic Radiation on Some Physiological and Biochemical
Parameters in Rats.
Effects of information and 50 Hz magnetic fields on cognitive performance and reported
symptoms.
Effects of mobile phone radiation (900 MHz radiofrequency) on structure and functions of rat
brain.
Effects of Sleep Quality on the Association between Problematic Mobile Phone Use and Mental
Health Symptoms in Chinese College Students.
Electromagnetic field effect or simply stress? Effects of UMTS exposure on hippocampal
longterm plasticity in the context of procedure related hormone release.
Electromagnetic fields and health outcomes.
Electromagnetic fields at a mobile phone frequency (900 MHz) trigger the onset of general stress
response along with DNA modifications in Eisenia fetida earthworms.
Electromagnetic fields hypersensitivity].
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Electromagnetic fields: damage to health due to the nocebo effect].
Electromagnetic hypersensitivity (EHS) and subjective health complaints associated with
electromagnetic fields of mobile phone communication--a literature review published between
2000 and 2004.
Electromagnetic hypersensitivity: evidence for a novel neurological syndrome.
Endocrine mechanism of placental circulatory disturbances induced by microwave in pregnant
rats].
Enhancement of allergic skin wheal responses in patients with atopic eczema/dermatitis
syndrome by playing video games or by a frequently ringing mobile phone.
Environmental illness: fatigue and cholinesterase activity in patients reporting hypersensitivity to
electricity.
Enzymatic activity of some tissues and blood serum from animals and humans exposed to
microwaves and hypothesis on the possible role of free radical processes in the nonlinear effects
and modification of emotional behavior of animals].
Epidemiologic studies of the effect of microwaves (neurophysiologic, hematologic and
ophthalmologic aspects)].
Epidemiological risk assessment of pathology development in occupational exposure to
radiofrequency electromagnetic fields].
EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
Exposure to electromagnetic fields and suicide among electric utility workers: a nested case-
control study.
Exposure to mobile phone electromagnetic field radiation, ringtone and vibration affects anxiety-
like behaviour and oxidative stress biomarkers in albino wistar rats.
Exposure to radio-frequency radiation from an aircraft radar unit.
Expression of the immediate early gene, c-fos, in mouse brain after acute global system for
mobile communication microwave exposure.
Follow up study on the immune response to low frequency electromagnetic fields in men and
women working in a museum.
Frequent cellular phone use modifies hypothalamic-pituitary-adrenal axis response to a cellular
phone call after mental stress in healthy children and adolescents: A pilot study.
Functional changes in human peripheral neutrophils in workers with different exposure to
noxious agents.
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Health Effects of Electromagnetic Fields on Reproductive-Age Female Operators of Plastic
Welding Machines in Fuzhou, China.
Health effects of living near mobile phone base transceiver station (BTS) antennae: a report from
Isfahan, Iran.
Health of workers exposed to electric fields.
Health response of two communities to military antennae in Cyprus.
Health status of the workers exposed to strong, constant magnetic fields].
Hypersensitivity to electricity: working definition and additional characterization of the
syndrome.
Individual subject sensitivity to extremely low frequency magnetic field.
Individual variation in temporal relationships between exposure to radiofrequency
electromagnetic fields and non-specific physical symptoms: A new approach in studying
'electrosensitivity'.
Influence of electromagnetic fields on the emotional behaviour of rats].
Influence of microwave exposure on chlordiazepoxide effects in the mouse staircase test.
Interference with cardiac pacemakers by cellular telephones.
Investigation of sleep disorders in the vicinity of high frequency transmitters].
Is There a Connection Between Electrosensitivity and Electrosensibility? A Replication Study.
Life styles, anxiety, expertise: the perception of risk from electromagnetic fields.
Low-frequency pulsed electromagnetic field therapy in fibromyalgia: a randomized, double-
blind, sham-controlled clinical study.
Low-level microwave irradiation and central cholinergic systems.
Magnetic fields of transmission lines and depression.
Magnetic fields of video display terminals and spontaneous abortion.
MEMO--a mobile phone depression prevention intervention for adolescents: development
process and postprogram findings on acceptability from a randomized controlled trial.
Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric
effects including depression.
Microwave sickness: a reappraisal.
Mobile communication and health of population: estimation of danger, social and ethical
problems].
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Mobile communication: radiobiology problems and evaluation of danger].
Mobile phone base stations and adverse health effects: phase 1 of a population-based, cross-
sectional study in Germany.
Mobile phone base stations and adverse health effects: phase 2 of a cross-sectional study with
measured radio frequency electromagnetic fields.
Mobile phone headache: a double blind, sham-controlled provocation study.
Mobile phone use and stress, sleep disturbances, and symptoms of depression among young
adults--a prospective cohort study.
Mobile phone use and subjective symptoms. Comparison of symptoms experienced by users of
analogue and digital mobile phones.
Mobile Phone Use and The Risk of Headache: A Systematic Review and Meta-analysis of Cross-
sectional Studies.
Mobile phone use, school electromagnetic field levels and related symptoms: a cross-sectional
survey among 2150 high school students in Izmir.
Motor activity of rabbits in conditions of chronic low-intensity pulse microwave irradiation].
Natural very-low-frequency sferics and headache.
Neurobehavioral effects among inhabitants around mobile phone base stations.
Neurodegenerative diseases, suicide and depressive symptoms in relation to EMF.
Neurological changes induced by a mobile phone.
Neurophysiological effects of flickering light in patients with perceived electrical
hypersensitivity.
Neurotic disturbances, depression and anxiety disorders in the population living in the vicinity of
overhead high-voltage transmission line 400 kV. Epidemiological pilot study].
Non-contact determination of parasympathetic activation induced by a full stomach using
microwave radar.
Non-specific physical symptoms and electromagnetic field exposure in the general population:
can we get more specific? A systematic review.
Occupational electromagnetic field exposures associated with sleep quality: a cross-sectional
study.
Occupational factors of anxiety and depressive disorders in the French National Electricity and
Gas Company. The Anxiety-Depression Group.
Odontologic survey of referred patients with symptoms allegedly caused by electricity or visual
display units.
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Phantom vibration and phantom ringing among mobile phone users: A systematic review of
literature.
Physical factors and stress].
Physicians appeals on the dangers of mobile communication--what is the evidence? Assessment
of public health data.
Polluted places or polluted minds? An experimental sham-exposure study on background
psychological factors of symptom formation in 'Idiophatic Environmental Intolerance attributed
to electromagnetic fields'.
Preliminary report: symptoms associated with mobile phone use.
Prevalence of annoyance attributed to electrical equipment and smells in a Swedish population,
and relationship with subjective health and daily functioning.
Prevalence of depression among electrical workers.
Prevalence of headache among handheld cellular telephone users in Singapore: a community
study.
Provocation with stress and electricity of patients with "sensitivity to electricity".
Psychologic aspects of patients with symptoms presumed to be caused by electricity or visual
display units.
Psychological factors associated with self-reported sensitivity to mobile phones.
Psychological symptoms and intermittent hypertension following acute microwave exposure.
Quantitative analysis of lesion parameters in radiofrequency trigeminal rhizotomy.
Radio and microwave frequency radiation and health--an analysis of the literature].
Recent data from the literature on the biological and pathologic effects of electromagnetic
radiation, radio waves and stray currents].
Review of the epidemiologic literature on EMF and Health.
Risk factors, health risks, and risk management for aircraft personnel and frequent flyers.
Self-reported depression and anxiety symptoms and usage of computers and mobile phones
among working-age Finns.
Self-reporting of symptom development from exposure to radiofrequency fields of wireless
smart meters in victoria, australia: a case series.
Specific patterns of weak (1 microTesla) transcerebral complex magnetic fields differentially
affect depression, fatigue, and confusion in normal volunteers.
Speculations on the influence of electromagnetism on genomic and associated structures.
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Stress-related endocrinological and psychopathological effects of short- and long-term 50Hz
electromagnetic field exposure in rats.
Study of human neurovegetative and hematologic effects of environmental low-frequency (50-
Hz) electromagnetic fields produced by transformers.
Subjective symptoms related to mobile phone use--a pilot study].
Subjective symptoms, sleeping problems, and cognitive performance in subjects living near
mobile phone base stations.
Sympathetic Resonance Technology: scientific foundation and summary of biologic and clinical
studies.
Symptom prevalence and worry about high voltage transmission lines.
Symptoms experienced by people in vicinity of base stations: II/ Incidences of age, duration of
exposure, location of subjects in relation to the antennas and other electromagnetic factors].
Symptoms of ill health ascribed to electromagnetic field exposure--a questionnaire survey.
Symptoms of problematic cellular phone use, functional impairment and its association with
depression among adolescents in Southern Taiwan.
Symptoms reported by mobile cellular telephone users].
Symptoms, personality traits, and stress in people with mobile phone-related symptoms and
electromagnetic hypersensitivity.
The association between use of mobile phones after lights out and sleep disturbances among
Japanese adolescents: a nationwide cross-sectional survey.
The effect of chronic exposure to extremely low-frequency electromagnetic fields on sleep
quality, stress, depression and anxiety.
The effect of electromagnetic radiation in the mobile phone range on the behaviour of the rat.
The effects of 884 MHz GSM wireless communication signals on headache and other symptoms:
an experimental provocation study.
The effects of multivitamin supplementation on mood and general well-being in healthy young
adults. A laboratory and at-home mobile phone assessment.
The immune response of women with prolonged exposure to electromagnetic fields produced by
radiotelevision broadcasting stations.
The influence of occupational environment and professional factors on the risk of cardiovascular
disease].
The prevalence of symptoms attributed to electromagnetic field exposure: a cross-sectional
representative survey in Switzerland.
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The relationship between adolescents' well-being and their wireless phone use: a cross-sectional
study.
The risk of subjective symptoms in mobile phone users in Poland--an epidemiological study.
The role of anxiety in the perception of technological hazards - a cross-sectional study on cell
phones and masts.
The role of electromagnetic fields in neurological disorders.
Time-dependent hematological changes in workers exposed to electromagnetic fields.
Use of terahertz electromagnetic radiation at nitric oxide frequencies for the correction of thyroid
functional state during stress].
Work environment and cardiovascular diseases. A short review of the literature.
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FACTOR 20
Theme - Neoplasms
Key MeSH Headings - Lung Neoplasms, Ovarian Neoplasms, Pituitary Neoplasms, Lymphoma,
Prostatic Neoplasms, Colonic Neoplasms, Carcinoma, Breast Neoplasms, Hematologic
Neoplasms, Neoplasms, Liver Neoplasms, Cell Transformation, Neoplastic, Nervous System
Neoplasms
Titles
2-GHz band CW and W-CDMA modulated radiofrequency fields have no significant effect on
cell proliferation and gene expression profile in human cells.
40 GHz RF biosensor based on microwave coplanar waveguide transmission line for cancer cells
(HepG2) dielectric characterization.
50 Hz extremely low frequency electromagnetic fields enhance protein carbonyl groups content
in cancer cells: effects on proteasomal systems.
50-Hz electromagnetic environment and the incidence of childhood tumors in Stockholm
County.
A case of hepatocellular carcinoma rupturing after angiography.
A case of recurring hepatocellular carcinoma with a solitary Virchow's lymph node metastasis.
A case report of primary hepatic carcinoid with lymph node metastasis--treatment of hepatic
arterial infusion to post-reoperative liver and radiation to metastasis of para-aortic lymph nodes].
A large-scale study of the ultrawideband microwave dielectric properties of normal, benign and
malignant breast tissues obtained from cancer surgeries.
A meta-analysis of epidemiologic studies of electric and magnetic fields and breast cancer in
women and men.
A microwave radiometric method for the study of the semiconductor properties of living tissue:
its potential application to tumour location.
A mortality study of electrical utility workers in Quebec.
A new electromagnetic exposure metric: high frequency voltage transients associated with
increased cancer incidence in teachers in a California school.
A review of cancer induction by extremely low frequency electromagnetic fields. Is there a
plausible mechanism?
A review of epidemiological studies on the relationship of residential electromagnetic exposure
to cancer].
A unified approach to the analysis of case-distribution (case-only) studies.
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Activation of Signaling Cascades by Weak Extremely Low Frequency Electromagnetic Fields.
Adult cancers near high-voltage overhead power lines.
Age diseases depending on geomagnetic field activity inside the womb period].
Alternate indices of electric and magnetic field exposures among Ontario electrical utility
workers.
Aluminum, calcium ion and radiofrequency synergism in acceleration of lymphomagenesis.
An alternate hypothesis for the association between electrical wiring configurations and cancer.
An apparently incongruous exposure-response relationship resulting from the use of job
description to assess magnetic field exposure.
An epidemiological study of cancer morbidity and mortality among the population living in areas
close to thermal and atomic electric power stations].
An evaluation of the existing evidence on the carcinogenic potential of extremely low frequency
magnetic fields.
An evaluation of the mutagenic, carcinogenic and teratogenic potential of microwaves.
Animal carcinogenicity studies on radiofrequency fields related to mobile phones and base
stations.
Annals of conflicting results: looking back on electromagnetic field research.
Are mobile phones harmful?
Are the stray 60-Hz electromagnetic fields associated with the distribution and use of electric
power a significant cause of cancer?
Assessment of occupational exposure patterns by frequency-domain analysis of time series data.
Association between exposure to pulsed electromagnetic fields and cancer in electric utility
workers in Quebec, Canada, and France.
Association of childhood cancer with residential traffic density.
Bioelectromagnetic field effects on cancer cells and mice tumors.
Biologic effects and health consequences of low and high (radio) frequency electromagnetic
fields.
Biological and health effects on electric and magnetic fields at extremely low frequencies].
Biological effects and mechanisms of shortwave radiation: a review.
Biological effects of electromagnetic fields and recently updated safety guidelines for strong
static magnetic fields.
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Biological effects of electromagnetic fields].
Biological effects of low frequency electromagnetic fields.
Biological effects of non-ionizing electromagnetic fields: Two sides of a coin.
Biological effects of power-frequency fields as they relate to carcinogenesis.
Biological influences of electromagnetic fields].
Biological mechanisms and health effects of emf in view of requirements of reports on the
impact of various installations on the environment].
Biologically based epidemiological studies of electric power and cancer.
Biophysical cancer transformation pathway.
Breast cancer and electric power.
Breast cancer and electromagnetic fields--a review.
Cancer cluster among young Indian adults living near power transmission lines in Bom Jesus do
Tocantins, Para, brazil.
Cancer from exposure to 50/60 Hz electric and magnetic fields--a major scientific debate.
Cancer in Korean war navy technicians: mortality survey after 40 years.
Cancer in the electric power industry.
Cancer incidence among Norwegian airline pilots.
Cancer incidence among welders: possible effects of exposure to extremely low frequency
electromagnetic radiation (ELF) and to welding fumes.
Cancer incidence and mortality and proximity to TV towers.
Cancer incidence in California flight attendants (United States).
Cancer incidence near radio and television transmitters in Great Britain. I. Sutton Coldfield
transmitter.
Cancer incidence near radio and television transmitters in Great Britain. II. All high power
transmitters.
Cancer mortality among electricity utility workers in a the state of Sao Paulo, Brazil].
Cancer mortality and residence near electricity transmission equipment: a retrospective cohort
study.
Carcinogenesis and initiation of cell cycling by charge-induced membrane clusters may be due to
mitogen receptors and Na+/H+ antiports.
Carcinogenic risk of extremely-low-frequency electromagnetic fields: state of the art].
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Case-control study of childhood cancer and exposure to 60-Hz magnetic fields.
Cell phones and tumor: still in no man's land.
Cell phones: modern man's nemesis?
Cellular neoplastic transformation induced by 916 MHz microwave radiation.
Cellular phones and public health].
Chicken embryo fibroblasts exposed to weak, time-varying magnetic fields share cell
proliferation, adenosine deaminase activity, and membrane characteristics of transformed cells.
Childhood cancer and magnetic fields from high-voltage power lines in England and Wales: a
case-control study.
Childhood cancer and residential proximity to power lines. UK Childhood Cancer Study
Investigators.
Childhood cancer in relation to a modified residential wire code.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Cohort and nested case-control studies of hematopoietic cancers and brain cancer among electric
utility workers.
Combined biological effect of electromagnetic fields and chemical substances (toxic)].
Construction and clinical significance of a predictive system for prognosis of hepatocellular
carcinoma.
Current Understanding of the Health Effects of Electromagnetic Fields.
Delayed biological effect of electromagnetic fields action].
Description of a new computer wire coding method and its application to evaluate potential
control selection bias in the Savitz et al. childhood cancer study.
Determining health policy for sensible mobile phone use--current world status].
Developing policy in the face of scientific uncertainty: interpreting 0.3 microT or 0.4 microT
cutpoints from EMF epidemiologic studies.
Dielectric Properties for Differentiating Normal and Malignant Thyroid Tissues.
Dielectric properties for non-invasive detection of normal, benign, and malignant breast tissues
using microwave theories.
Dirty electricity": what, where, and should we care?
Do extremely low frequency magnetic fields enhance the effects of environmental carcinogens?
A meta-analysis of experimental studies.
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Does our electricity distribution system pose a serious risk to public health?
Effect of electromagnetic field exposure on chemically induced differentiation of friend
erythroleukemia cells.
Effect of lesion morphology on microwave signature in 2-D ultra-wideband breast imaging.
Effect of magnetic field exposure on anchorage-independent growth of a promoter-sensitive
mouse epidermal cell line (JB6).
Effect of millimeter waves on cyclophosphamide induced NF-kappaB.
Effect of pulsed electromagnetic field with different frequencies on the proliferation, apoptosis
and migration of human ovarian cancer cells].
Effects of 2.45-GHz microwave radiation and phorbol ester 12-O-tetradecanoylphorbol-13-
acetate on dimethylhydrazine-induced colon cancer in mice.
Effects of 2450 MHz electromagnetic fields with a wide range of SARs on methylcholanthrene-
induced transformation in C3H10T1/2 cells.
Effects of 60-Hz fields, estradiol and xenoestrogens on human breast cancer cells.
Effects of ELF magnetic fields on protein expression profile of human breast cancer cell MCF7.
Effects of extremely low-frequency electromagnetic fields (ELF-EMF) exposure on B6C3F1
mice.
Effects of extremely low-frequency pulsed electromagnetic fields on morphological and
biochemical properties of human breast carcinoma cells (T47D).
Effects of Mobile Phones on Children's and Adolescents' Health: A Commentary.
Electric and magnetic fields (EMF): what do we know about the health effects?
Electric and magnetic fields and health outcomes--an overview.
Electric blanket or mattress cover use and breast cancer incidence in women 50-79 years of age.
Electric blanket use and breast cancer in the Nurses' Health Study.
Electric blanket use and breast cancer on Long Island.
Electric blanket use and breast cancer risk among younger women.
Electric power, pineal function, and the risk of breast cancer.
Electromagnetic field exposure and cancer: a review of epidemiologic evidence.
Electromagnetic field exposures and childhood cancers in New Zealand.
Electromagnetic fields and breast cancer on Long Island: a case-control study.
Electromagnetic fields and cancer in children residing near Norwegian high-voltage power lines.
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Electromagnetic fields and cancer risks.
Electromagnetic fields and female breast cancer.
Electromagnetic fields and health outcomes.
Electromagnetic fields and male breast cancer.
Electromagnetic fields and people's health].
Electromagnetic fields from high-voltage installations and cancer in childhood].
Electromagnetic fields, polychlorinated biphenyls, and prostate cancer mortality in electric utility
workers.
Electromagnetic fields: is there any probability of the risk of cancer?].
Electromagnetic fields: low dose exposure, current update.
Electromagnetic residential fields and childhood cancers: state of epidemiological research].
ELF magnetic fields in a city environment.
EMF and current cancer concepts.
EMF-cancer link: the ferritin hypothesis.
Enhancement of efficacy of neoadjuvant polychemotherapy in combined treatment of lung
cancer].
Environment and cancer risk].
Environmental exposure to electromagnetic fields and the risk of cancer].
Environmental factors and breast cancer.
Environmental factors and childhood acute leukemias and lymphomas.
Environmental risk factors and female breast cancer.
Epidemiologic studies of electric and magnetic fields and cancer: a case study of distortions by
the media.
Epidemiologic studies of electric and magnetic fields and cancer: strategies for extending
knowledge.
Epidemiologic study of residential proximity to transmission lines and childhood cancer in
California: description of design, epidemiologic methods and study population.
Epidemiological appraisal of studies of residential exposure to power frequency magnetic fields
and adult cancers.
Epidemiological risk assessment of mobile phones and cancer: where can we improve?
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Estimates of Environmental Exposure to Radiofrequency Electromagnetic Fields and Risk of
Lymphoma Subtypes.
EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Evaluation of potential confounders in planning a study of occupational magnetic field exposure
and female breast cancer.
Evidence for microwave carcinogenesis in vitro.
Examination of the melatonin hypothesis in women exposed at night to EMF or bright light.
Exposure assessment for power frequency electric and magnetic fields (EMF) and its application
to epidemiologic studies.
Exposure from occupational versus other sources.
Exposure to 50-Hz electric field and incidence of leukemia, brain tumors, and other cancers
among French electric utility workers.
Exposure to electromagnetic fields and the risk of leukemia.
Exposure to electromagnetic fields from use of electric blankets and other in-home electrical
appliances and breast cancer risk.
Exposure to extremely low frequency electromagnetic fields and the risk of malignant diseases--
an evaluation of epidemiological and experimental findings.
Exposure to low-frequency electromagnetic fields--a health hazard?
Exposure to power frequency electric fields and the risk of childhood cancer in the UK.
Extremely low frequency electromagnetic fields (EMF) and brain cancer in adults and children:
review and comment.
Extremely low frequency electromagnetic fields and cancer: the epidemiologic evidence.
Extremely low-frequency electromagnetic fields exposure and female breast cancer risk: a meta-
analysis based on 24,338 cases and 60,628 controls.
Fields and currents in the organs of the human body when exposed to power lines and VLF
transmitters.
Follow-up of radio and telegraph operators with exposure to electromagnetic fields and risk of
breast cancer.
Genetic damage in human cells exposed to non-ionizing radiofrequency fields: a meta-analysis
of the data from 88 publications (1990-2011).
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Genetic damage in mammalian somatic cells exposed to extremely low frequency electro-
magnetic fields: a meta-analysis of data from 87 publications (1990-2007).
Genetic damage in mammalian somatic cells exposed to radiofrequency radiation: a meta-
analysis of data from 63 publications (1990-2005).
Genotoxicity of radiofrequency radiation. DNA/Genetox Expert Panel.
Geomagnetic field variation in early ontogenesis as a risk factor for oncopathology].
Health disorders caused by radiation].
Hematopoietic neoplasia in C57BL/6 mice exposed to split-dose ionizing radiation and circularly
polarized 60 Hz magnetic fields.
How to approach complex mixtures: lessons from the epidemiology of electromagnetic fields.
Human cancer from environmental pollutants: the epidemiological evidence.
Human health consequences of environmentally-modulated gene expression: potential roles of
ELF-EMF induced epigenetic versus mutagenic mechanisms of disease.
Hypothesis on a casual link between EMF and an evolutionary class of cancer and spontaneous
abortion.
Incidence of breast cancer in a Norwegian cohort of women with potential workplace exposure
to 50 Hz magnetic fields.
Incidence of cancer among workers in Norwegian hydroelectric power companies.
Incidence of cancer in Norwegian workers potentially exposed to electromagnetic fields.
Incidence of cancer in persons with occupational exposure to electromagnetic fields in Denmark.
Increased incidence of cancer in a cohort of office workers exposed to strong magnetic fields.
Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies.
Induction of neoplastic transformation in C3H/10T1/2 cells by 2.45-GHz microwaves and
phorbol ester.
Induction of tamoxifen resistance in breast cancer cells by ELF electromagnetic fields.
Influence of power frequency electric and magnetic fields on human health.
Inhibitory effects of low doses of melatonin on induction of preneoplastic liver lesions in a
medium-term liver bioassay in F344 rats: relation to the influence of electromagnetic near field
exposure.
Interaction of static and extremely low frequency electric and magnetic fields with living
systems: health effects and research needs.
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Joint actions of environmental nonionizing electromagnetic fields and chemical pollution in
cancer promotion.
Knowledge and perceptions of the health effects of environmental hazards in the general
population in Italy.
Leukemia and lymphoma incidence in rodents exposed to low-frequency magnetic fields.
Limitations of interview-based risk assessment of RF exposure from appliances.
Long-term exposure to microwave radiation provokes cancer growth: evidences from radars and
mobile communication systems.
Low intensity and frequency pulsed electromagnetic fields selectively impair breast cancer cell
viability.
Low-frequency magnetic fields and cancer. What you should know and what to tell your
patients.
Lymphoma development in mice chronically exposed to UMTS-modulated radiofrequency
electromagnetic fields.
Lymphoma development of simultaneously combined exposure to two radiofrequency signals in
AKR/J mice.
Lymphoma induced in mice chronically exposed to very strong low-frequency electromagnetic
field.
Magnetic field exposure related to cancer subtypes.
Magnetic fields and breast cancer in Swedish adults residing near high-voltage power lines.
Magnetic fields and cancer in children residing near Swedish high-voltage power lines.
Magnetic fields and childhood cancer--a pooled analysis of two Scandinavian studies.
Magnetic fields and mammary cancer in rodents: a critical review and evaluation of published
literature.
Magnetic fields of high voltage power lines and risk of cancer in Finnish adults: nationwide
cohort study.
Magnetic resonance imaging of the chest. Where we stand.
Maternal occupational exposure to electromagnetic fields before, during, and after pregnancy in
relation to risks of childhood cancers: findings from the Oxford Survey of Childhood Cancers,
1953-1981 deaths.
Measurement of DNA damage and apoptosis in Molt-4 cells after in vitro exposure to
radiofrequency radiation.
Melatonin and magnetic fields.
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Meta-analysis of extremely low frequency electromagnetic fields and cancer risk: a pooled
analysis of epidemiologic studies.
Micronucleus induction in Syrian hamster embryo cells following exposure to 50 Hz magnetic
fields, benzo(a)pyrene, and TPA in vitro.
Microwave absorption by normal and tumor cells.
Microwave antigen retrieval blocks endogenous peroxidase activity in immunohistochemistry.
Microwave induces apoptosis in A549 human lung carcinoma cell line.
Mobile phone radiation alters proliferation of hepatocarcinoma cells.
Mobile phone use and risk of brain neoplasms and other cancers: prospective study.
Mobile phone use and risk of tumors: a meta-analysis.
Mobile phones, heat shock proteins and cancer.
Mobile telecommunications and health: report of an investigation into an alleged cancer cluster
in Sandwell, West Midlands.
Mobile telephones and cancer--a review of epidemiological evidence.
Modeling of noninvasive microwave characterization of breast tumors.
Modification of the 1979 "Denver wire code" for different wire or plumbing types.
Morbidity experience in populations residentially exposed to 50 hz magnetic fields: methodology
and preliminary findings of a cohort study.
Mortality among workers in the geothermal power plants at Larderello, Italy.
Mortality by neoplasia and cellular telephone base stations in the Belo Horizonte municipality,
Minas Gerais state, Brazil.
Mortality in workers exposed to electromagnetic fields.
Mortality indices for hemoblastoses in Rivno Province before and after the accident at the
Chernobyl Atomic Electric Power Station].
Mortality of persons resident in the vicinity of electricity transmission facilities.
Mortality of plastic-ware workers exposed to radiofrequencies.
MoS2 nanosheets encapsulated in sodium alginate microcapsules as microwave embolization
agents for large orthotopic transplantation tumor therapy.
Multi-physics modeling to study the influence of tissue compression and cold stress on
enhancing breast tumor detection using microwave radiometry.
Multimodal treatment of hepatocellular carcinoma.
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Mutagenic, carcinogenic and teratogenic effects induced by radiofrequency electromagnetic field
of mobile phone].
Neoplastic transformation in C3H 10T(1/2) cells after exposure to 835.62 MHz FDMA and
847.74 MHz CDMA radiations.
Neoplastic transformation of C3H/10T1/2 cells following exposure to 120-Hz modulated 2.45-
GHz microwaves and phorbol ester tumor promoter.
News in occupational cancers].
Non dietetic environmental risk factors in prostate cancer].
Non-ionizing electromagnetic radiation: a study of carcinogenic and cancer treatment potential.
Non-resection approaches for colorectal liver metastases.
Occupation and malignant lymphoma: a population based case control study in Germany.
Occupational and residential magnetic field exposure and breast cancer in females.
Occupational exposure to electromagnetic field and breast cancer risk in a large, population-
based, case-control study in the United States.
Occupational exposures associated with male breast cancer.
Occupational exposures to extremely low frequency magnetic fields and postmenopausal breast
cancer.
Occupational magnetic field exposure and site-specific cancer incidence: a Swedish cohort study.
Occupational magnetic fields and female breast cancer: a case-control study using Swedish
population registers and new exposure data.
Occupational risk factors for lung cancer in the French electricity and gas industry: a case-
control survey nested in a cohort of active employees.
Parental occupational exposure to extremely low frequency magnetic fields and childhood
cancer: a German case-control study.
Parental occupational exposure to magnetic fields and childhood cancer (Sweden).
Paternal occupational exposure to electro-magnetic fields as a risk factor for cancer in children
and young adults: a case-control study from the North of England.
Paternal work in the power industry: effects on children at delivery.
Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male
reproductive system.
Perspectives on health effects of electric and magnetic fields.
Pituitary tumor risk in relation to mobile phone use: A case-control study.
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Population-based case-control study of occupational exposure to electromagnetic fields and
breast cancer.
Power frequency electromagnetic fields and health. Where's the evidence?
Preliminary study of cause-specific mortality of a population exposed to 50 Hz magnetic fields,
in a district of Rome municipality].
Probing lymphoma infiltration in spleen of AKR/J mice chronically exposed to electromagnetic
fields for risk assessment--toward noninvasive modeling.
Prostate cancer in relation to the use of electric blanket or heated water bed.
Radiation from mobile phone and the health].
Radio and microwave frequency radiation and health--an analysis of the literature].
Radio frequency radiation-related cancer: assessing causation in the occupational/military
setting.
Radiofrequency exposure and mammalian cell toxicity, genotoxicity, and transformation.
Radiofrequency exposure and mortality from cancer of the brain and lymphatic/hematopoietic
systems.
Rat liver foci study on coexposure with 50 Hz magnetic fields and known carcinogens.
Rate of occurrence of transient magnetic field events in U.S. residences.
Recent advances in research on radiofrequency fields and health.
Recent data from the literature on the biological and pathologic effects of electromagnetic
radiation, radio waves and stray currents].
Relationship between exposure to extremely low-frequency electromagnetic fields and breast
cancer risk: a meta-analysis.
Remote effects of occupational and non-occupational exposure to electromagnetic fields of
power-line frequency. Epidemiological studies].
Residence near high voltage facilities and risk of cancer in children.
Residential and occupational exposure to 50 Hz magnetic fields and hematological cancers in
Norway.
Residential and occupational exposures to 50-Hz magnetic fields and breast cancer in women: a
population-based study.
Residential electric consumption and childhood cancer in Canada (1971-1986)
Residential exposure to 60-Hertz magnetic fields and adult cancers in Taiwan.
Residential exposure to magnetic fields and risk of canine lymphoma.
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Residential exposure to magnetic fields generated by 110-400 kV power lines in Finland.
Residential magnetic field exposure and breast cancer risk: a nested case-control study from a
multiethnic cohort in Los Angeles County, California.
Residential magnetic fields and the risk of breast cancer.
Residential proximity to electricity transmission and distribution equipment and risk of
childhood leukemia, childhood lymphoma, and childhood nervous system tumors: systematic
review, evaluation, and meta-analysis.
Residential proximity to high-voltage power lines and risk of childhood hematological
malignancies.
Results of lifespan exposure to continuous and intermittent extremely low frequency
electromagnetic fields (ELFEMF) administered alone to Sprague Dawley rats.
Review of the epidemiologic literature on EMF and Health.
Risk for leukaemia and brain and breast cancer among Danish utility workers: a second follow-
up.
Risk of cancer among Danish electricity workers. A cohort study].
Risk of cancer among Danish utility workers--a nationwide cohort study.
Risk of cancer in Finnish children living close to power lines.
Risk of hematological malignancies associated with magnetic fields exposure from power lines:
a case-control study in two municipalities of northern Italy.
Risk of major lymphoma subtypes and use of mobile phones].
Risk of neoplastic diseases in conditions of exposure to power magnetic fields--epidemiologic
investigations].
Risk of neoplastic diseases in conditions of exposure to radio- and microwave fields--
epidemiologic investigations].
Risk of pituitary tumors in cellular phone users: a case-control study.
Risk of premenopausal breast cancer and use of electric blankets.
Risk perception of the general public of cell phone towers and cancer: trend and associated
factors, 2005-2010].
Risks of carcinogenesis from electromagnetic radiation of mobile telephony devices.
Rodent cell transformation and immediate early gene expression following 60-Hz magnetic field
exposure.
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Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca2+ signaling
molecular pathways in breast cancer.
Role of radical pairs and feedback in weak radio frequency field effects on biological systems.
Scaling Relationship of In Vivo Muscle Contraction Strength of Rabbits Exposed to High-
Frequency Nanosecond Pulse Bursts.
Searching for the perfect wave: the effect of radiofrequency electromagnetic fields on cells.
Selenium reduces mobile phone (900 MHz)-induced oxidative stress, mitochondrial function,
and apoptosis in breast cancer cells.
Shift work, light at night, and breast cancer on Long Island, New York.
Socioeconomic status, social mobility and cancer occurrence during working life: a case-control
study among French electricity and gas workers.
Some characteristics of the glutathione cycle revealed by ionising and non-ionising
electromagnetic radiation.
Speculations on the influence of electromagnetism on genomic and associated structures.
Studies on microwaves in medicine and biology: from snails to humans.
Studying the protein expression in human B lymphoblastoid cells exposed to 1.8-GHz (GSM)
radiofrequency radiation (RFR) with protein microarray.
Teratogenic effect of broad-band electromagnetic field on neonatal mice (Mus musculus).
Testing electromagnetic fields for potential carcinogenic activity: a critical review of animal
models.
The effects of 860 MHz radiofrequency radiation on the induction or promotion of brain tumors
and other neoplasms in rats.
The effects of ionizing radiation, microwaves, and ultrasound on the developing embryo: clinical
interpretations and applications of the data.
The effects of low-energy 60-Hz environmental electromagnetic fields upon the growth-related
enzyme ornithine decarboxylase.
The effects of recall errors and of selection bias in epidemiologic studies of mobile phone use
and cancer risk.
The electromagnetic spectrum: current and future applications in oncology.
The enhanced lethality of cells in suspension during simultaneous exposure to pulsed electrical
and shock-wave acoustic fields].
The epidemiology of exposure to electromagnetic fields: an overview of the recent literature.
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The INTERPHONE study: design, epidemiological methods, and description of the study
population.
The measured electrical properties of normal and malignant human tissues from 50 to 900 MHz.
The melatonin hypothesis: electric power and breast cancer.
The relationship between electromagnetic field and light exposures to melatonin and breast
cancer risk: a review of the relevant literature.
The relative merits of contemporary measurements and historical calculated fields in the Swedish
childhood cancer study.
The residential case-specular method to study wire codes, magnetic fields, and disease.
The role of chemical and physical factors in cancer development].
The role of household electromagnetic fields in the development of mammary tumors in women:
clinical case-record observations.
The use of cell phone and insight into its potential human health impacts.
Towards 5G communication systems: Are there health implications?
Transmission electron microscopy study of the effects produced by wide-band low-power
millimeter waves on MCF-7 human breast cancer cells in culture.
Use of cellular telephones and risk of cancer. A Danish cohort study].
Use of electric bedding devices and risk of breast cancer in African-American women.
Use of electric blankets and risk of postmenopausal breast cancer.
Validation of self-reported cellular phone use.
Variable E-cadherin expression in a MNU-induced colon tumor model in rats which exposed
with 50 Hz frequency sinusoidal magnetic field.
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Appendix 4
–
Hierarchical Text Clustering Taxonomy of Adverse EMF Effects Database
A4-A. Cluster Themes
A query to retrieve Medline records showing adverse health effects of wireless radiation
was generated. The query was entered into the Medline search engine, and ~15,000 records were
retrieved. Filtering was applied to the retrieval to remove records not associated with adverse
health effects of wireless radiation, and 5311 records remained. Further filtering was not done,
and more records showing no adverse effects, examining ELF frequencies, and exceeding the
FCC exposure limits, were included compared to the filtered database in Appendix 2. The
partially filtered records were imported into the CLUTO software, and a 48-cluster hierarchical
text clustering of titles/abstracts was performed.
The following tables (A4-1,
A4-2)
show the categories in the taxonomy. The first table
shows hierarchical Levels 2 and 4, and the second table shows Level 4 and its associated leaf
(lowest level) clusters. For each cluster in both tables, the number of associated records is shown
in parentheses, followed by the cluster theme. Following the tables, each leaf cluster is shown,
including numbers of records, theme, and associated record titles. The Level 4 clusters in the
second table are hyperlinked to their positions in the list of titles. Because of the filtering
process limitations, most, but not all, records are associated with adverse effects of wireless
radiation. To access the full record, insert the titles of interest into Pubmed or other Medline
search engine.
Main adverse effects identified at the cluster theme level include cancer, brain tumors,
mammary cancer, childhood cancer, childhood leukemia, breast cancer, acoustic neuromas,
neurodegenerative diseases, cognitive function, neural function, oxidative stress, genotoxic,
DNA damage, chromosome damage, gene expression alterations, implanted electronic device
malfunction, sleep, melatonin secretion, embryos, cataracts, hearing, electrohypersensitivity.
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Table A4-1 - CLUTO-Based Text Clustering Taxonomy
–
Top Levels
SECOND LEVEL
Cluster 92 (2561)
–
Adverse effects of
wireless radiation at
cellular level,
including radiation
absorption at
different
frequencies
Cluster 93 (2750)
–
Adverse health
effects of EMF on
humans, especially
cancer and
neurodegenerative
diseases, and on
implanted
electronic devices
FOURTH LEVEL
Cluster 78 (912)
–
Adverse impacts of wireless radiation, especially
on cataracts, cells, and cognitive functions
Cluster 79 (428)
–
Microwave radiation absorption at different
frequencies
Cluster 82 (529)
–
Adverse effects of mobile phone radiation,
especially oxidative stress
Cluster 84 (692)
–
Genotoxic effects of radiofrequency radiation
Cluster 81 (673)
–
Adverse impacts of power-line EMF
Cluster 85 (540)
–
Adverse impacts of low-frequency EMF,
emphasizing cancer and neurodegenerative diseases
Cluster 83 (668)
–
Adverse effects of mobile phone use, especially
brain tumors, and brain and neural function
Cluster 89 (869)
–
Human health risks from electromagnetic radiation,
including adverse effects on implanted electronic devices, and
possible protections
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Table A4-2. CLUTO-Based Text Clustering Taxonomy - Bottom Levels
FOURTH LEVEL
Cluster 78 (912)
–
Adverse impacts of
wireless radiation,
especially on
cataracts, cells, and
cognitive functions
LEAF (LOWEST) LEVEL
Cluster 46 (331)
–
Adverse effects of microwave radiation, mainly on
rats
Cluster 3 (39)
–
Adverse impact of wireless radiation on eye lens
Cluster 35 (107)
–
Adverse impacts of microwave radiation on cells
and cognitive functions
Cluster 39 (211)
–
Adverse effects from microwave radiation
Cluster 29 (94)
–
Adverse effects of microwave radiation, especially
pulsed microwave
Cluster 31 (130)
–
Adverse effects of microwave exposures on rats,
especially at WiFi frequencies
Cluster 10 (75)
–
Dielectric properties of tissue at different microwave
frequencies
Cluster 23 (88)
–
Specific absorption rate in human body models
Cluster 21 (63)
–
Adverse effects of millimeter-wave exposures on
biological systems
Cluster 44 (95)
–
Adverse effects of microwave resonances in
biological systems
Cluster 47 (107)
–
Adverse biological effects of decimeter waves
Cluster 22 (127)
–
Effects of radiofrequency radiation, especially from
mobile phones, on rats
Cluster 26 (129) - Oxidative stress effects from mobile phone
radiofrequency radiation
Cluster 37 (140)
–
Effect of radiofrequency exposure, especially
prenatal exposure, on rats
Cluster 38 (133)
–
Effect of radiofrequency radiation on rat brain
Cluster 20 (126)
–
DNA damage after microwave radiation
Cluster 28 (100)
–
Chromosome damage in lymphocytes exposed to
radiofrequency radiation
Cluster 45 (179)
–
Adverse effects of low-frequency EMF on cells
Cluster 24 (111)
–
Gene expression alterations following
radiofrequency exposure
Cluster 11 (51)
–
Adverse impacts of radiofrequency fields on sleep
Cluster 41 (125)
–
Adverse effects of radiofrequency fields on cells
Cluster 9 (43)
–
Adverse effects of ELF magnetic field exposures
Cluster 17 (55)
–
Adverse impacts of EMF on mammary cancer
development
Cluster 6 (67)
–
Adverse health effects of magnetic fields associated
with magnetic resonance imaging
Cluster 32 (139)
–
Health risks of power-line electromagnetic fields on
humans
Cluster 34 (188)
–
Adverse effects of low-frequency electromagnetic
fields on humans
379
Cluster 79 (428)
–
Microwave radiation
absorption at
different frequencies
Cluster 82 (529)
–
Adverse effects of
mobile phone
radiation, especially
oxidative stress
Cluster 84 (692)
–
Genotoxic effects of
radiofrequency
radiation
Cluster 81 (673)
–
Adverse impacts of
power-line EMF
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Cluster 40 (116)
–
Adverse effects of low-frequency magnetic fields on
rodents
Cluster 2 (27)
–
Effects of electromagnetic fields on chicken embryos
Cluster 12 (38)
–
Impact of static and low-frequency magnetic fields on
melatonin secretion
Cluster 85 (540)
–
Cluster 4 (97)
–
Exposure to power lines and risk of childhood cancer
Adverse impacts of
Cluster 15 (131)
–
Residential magnetic fields and childhood leukemia
low-frequency EMF, Cluster 13 (113)
–
Electromagnetic fields and cancer, especially breast
emphasizing cancer cancer
and
Cluster 18 (62)
–
Mortality studies of electrical utility workers,
neurodegenerative
focusing on electromagnetic field exposures
diseases
Cluster 27 (137)
–
Occupational exposure to electromagnetic fields,
emphasizing neurodegenerative disease and cancer
Cluster 83 (668)
–
Cluster 30 (321)
–
Adverse health symptoms from mobile phone use
Adverse effects of
Cluster 1 (36)
–
Effects of mobile phones on brain and neural function
mobile phone use,
Cluster 25 (68)
–
Effects of cell phone radiation on cognitive function
especially brain
and hearing
tumors, and brain
Cluster 14 (93)
–
Myriad adverse health effects from cellphones
and neural function
Cluster 7 (44)
–
Risks from cell phone use, especially brain tumors
Cluster 8 (106)
–
Risk of brain tumors/acoustic neuromas from mobile
phone use
Cluster 89 (869)
–
Cluster 0 (63)
–
Electromagnetic interference with cardiac pacemakers
Human health risks
Cluster 16 (103)
–
Electromagnetic interference on implanted cardiac
from
devices
electromagnetic
Cluster 5 (120)
–
Health risks from mobile phone base stations
radiation, including
Cluster 19 (84)
–
Electromagnetic hypersensitivity
adverse effects on
Cluster 43 (202)
–
Health risks from low-frequency electromagnetic
implanted electronic fields
devices, and
Cluster 33 (91)
–
Health risks to workers in different occupations
possible protections Cluster 36 (84)
–
Precautionary measures to reduce potential EMF
health risks
Cluster 42 (122) - Regulatory protections against electromagnetic
fields
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A4-B. Cluster Record Titles
Fourth Level Cluster 78 (912)
Theme - Adverse impacts of wireless radiation, especially on cataracts, cells, and cognitive
functions
--Leaf Cluster 46 (331)
Theme - Adverse effects of microwave radiation, mainly on rats
Titles
Recent advances in the effects of microwave radiation on brains.
Microwave radiation absorption: behavioral effects.
Behavioral thermoregulation with microwave radiation of albino rats.
[Effect of microwave irradiation on biological systems].
[Microwave radiation sources requiring periodic or sporadic hygienic control].
Microwave radiation (2.45 GHz)-induced oxidative stress: Whole-body exposure effect on
histopathology of Wistar rats.
Low intensity microwave radiation induced oxidative stress, inflammatory response and DNA
damage in rat brain.
Mechanism of low-level microwave radiation effect on nervous system.
Apoptosis of Lewis Lung Carcinoma Cells Induced by Microwave via p53 and Proapoptotic
Proteins In vivo.
Studies on the interaction of microwave radiation with cholinesterase.
A system for studying effects of microwaves on cells in culture.
Enzymatic alterations in developing rat brain cells exposed to a low-intensity 16.5 GHz
microwave radiation.
Bioeffects of microwave--a brief review.
Behavioral effects of chlorpromazine and diazepam combined with low-level microwaves.
Microwave radiation induced oxidative stress, cognitive impairment and inflammation in brain
of Fischer rats.
Interaction of microwave radiation with turkey sperm.
Effect of Low Level Subchronic Microwave Radiation on Rat Brain.
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Acceleration of the development of benzopyrene-induced skin cancer in mice by microwave
radiation.
Effect of 2.45 GHz microwave radiation on the fertility pattern in male mice.
Alterations in activity at auditory nuclei of the rat induced by exposure to microwave radiation:
autoradiographic evidence using [14C]2-deoxy-D-glucose.
[Effect of microwave radiation on the rat hematopoietic system].
The effect of exposure of acetylcholinesterase to 2,450-MHz microwave radiation.
[The impact of electromagnetic radiation at microwave frequency (9.8 HhZ)on the embryonic
and postembryonic development of the tick Hyalomma asiaticum (Acarina, Ixodidae)].
[Structural and metabolic analysis of the reaction of the central nervous system to the combined
action of microwave and ionizing radiations].
[Mechanism of the effect of nonionizing radiation on animals at the level of sensory systems].
Effects of microwaves on membranes of hematopoietic cells in their structural and functional
organization.
Microwave radiation and chlordiazepoxide: synergistic effects on fixed-interval behavior.
Behavioral effects of microwaves.
[Long-term exposure to low intensity microwave radiation affects male reproductivity].
[Effect of microwave radiation on cellular immunity indices in conditions of chronic exposure].
[Long-term microwave radiation affects male reproduction in rats].
Results of our 15-year study into the biological effects of microwave exposure.
Effect of whole-body 1800MHz GSM-like microwave exposure on testicular steroidogenesis and
histology in mice.
Genotoxic Effects in Human Fibroblasts Exposed to Microwave Radiation.
[The effect of microwave radiation on the levels of MDA and the activity of SOD of
nasopharyngeal carcinoma cells].
The effects of low-level radiofrequency and microwave radiation on brain tissue and animal
behaviour.
Physiological changes in rats after exposure to low levels of microwaves.
The influence of prenatal 10 GHz microwave radiation exposure on a developing mice brain.
[The phenomenon of adaptive immunity in exposure to nonionizing microwave radiation].
Non-thermal effects of 500MHz - 900MHz microwave radiation on enzyme kinetics.
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Activation of TLR signalling regulates microwave radiation-mediated impairment of
spermatogenesis in rat testis.
Effect of 2.45 GHz microwave radiation on permeability of unilamellar liposomes to 5(6)-
carboxyfluorescein. Evidence of non-thermal leakage.
Spatial memory and learning performance and its relationship to protein synthesis of Swiss
albino mice exposed to 10 GHz microwaves.
[Effects of the microwave radiation from the cellular phones on humans and animals].
Cognitive impairment and neurogenotoxic effects in rats exposed to low-intensity microwave
radiation.
Microwave hearing: evidence for thermoacoustic auditory stimulation by pulsed microwaves.
Effects of 2.45 GHz microwave radiation and heat on mouse spermatogenic epithelium.
Studies of the induction of dominant lethals and translocations in male mice after chronic
exposure to microwave radiation.
Effect of Low-Intensity Microwave Radiation on Monoamine Neurotransmitters and Their Key
Regulating Enzymes in Rat Brain.
Fluorescence depolarization studies of red cell membrane fluidity. The effect of exposure to 1.0-
GHz microwave radiation.
[Effects of microwave radiation on the content of five elements in mice bone tissue].
Research on the neurological effects of nonionizing radiation at the University of Washington.
Cellular neoplastic transformation induced by 916 MHz microwave radiation.
Radiofrequency and microwave radiation in the microelectronics industry.
Reduced exposure to microwave radiation by rats: frequency specific effects.
[Reaction of the brain receptor system to the effect of low intensity microwaves].
Ten gigahertz microwave radiation impairs spatial memory, enzymes activity, and
histopathology of developing mice brain.
Cytogenetic effects of 18.0 and 16.5 GHz microwave radiation on human lymphocytes in vitro.
Influence of microwave exposure on fertility of male rats.
Health aspects of radio and microwave radiation.
Japanese encephalitis virus (JEV): potentiation of lethality in mice by microwave radiation.
Microwave exposure induces Hsp70 and confers protection against hypoxia in chick embryos.
Potentially hazardous microwave radiation source--a review.
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Behavioral effects of microwave reinforcement schedules and variations in microwave intensity
on albino rats.
[Metabolic changes in cells under electromagnetic radiation of mobile communication systems].
Effect of microwave radiation on inactivation of Clostridium sporogenes (PA 3679) spores.
A circular dichroism study of human erythrocyte ghost proteins during exposure to 2450 MHz
microwave radiation.
[Evaluation of bone density in rats after hydrocortisone and microwave radiation].
[Chronotoxicity of 1800 MHz microwave radiation on sex hormones and spermatogenesis in
male mice].
Radiation hazard assessment of pulsed microwave radars.
Results of a United States and Soviet Union joint project on nervous system effects of
microwave radiation.
Non-thermal microwave effects on protein dynamics? An X-ray diffraction study on tetragonal
lysozyme crystals.
Effect of microwave radiation on permeability of liposomes. Evidence against non-thermal
leakage.
Assessment of cytogenetic damage and oxidative stress in personnel occupationally exposed to
the pulsed microwave radiation of marine radar equipment.
[Modification of the effects of microwave irradiation on biochemical processes by using foreign
protein].
Some behavioral effects of short-term exposure of rats to 2.45 GHz microwave radiation.
[5-HT contents change in peripheral blood of workers exposed to microwave and high frequency
radiation].
Microwave radiation effects on the thermally driven oxidase of erythrocytes.
Effects of microwave radiation (340 and 900 MHz) on different structural levels of erythrocyte
membranes.
Environmental radiation hazards.
[Radiation protection and possible mechanisms for low intensity microwave].
Effects of low level microwave radiation on carcinogenesis in Swiss Albino mice.
Effects of pulsed 2.856 GHz microwave exposure on BM-MSCs isolated from C57BL/6 mice.
[Effect of pulse electromagnetic radiation on erythrocyte ghosts].
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[Experimental modeling of autoimmune reactions as affected by nonionizing microwave
radiation].
Biologic effects of microwave exposure. II. Studies on the mechanisms controlling susceptibility
to microwave-induced increases in complement receptor-positive spleen cells.
Hearing of microwave pulses by humans and animals: effects, mechanism, and thresholds.
Individual responsiveness to induction of micronuclei in human lymphocytes after exposure in
vitro to 1800-MHz microwave radiation.
Immunologic and hematopoietic alterations by 2,450-MHz electromagnetic radiation.
Exposure of cultured astroglial and microglial brain cells to 900 MHz microwave radiation.
Influence of microwave exposure on chlordiazepoxide effects in the mouse staircase test.
Activation of endoplasmic reticulum stress in rat brain following low-intensity microwave
exposure.
Non-thermal effects of microwaves on proteins: thermophilic enzymes as model system.
[Morinda officialis how extract improves microwave-induced reproductive impairment in male
rats].
Reception of microwaves by the brain.
Interaction of radiofrequency and microwave radiation with living systems. A review of
mechanisms.
Effect on the immune system of mice exposed chronically to 50 Hz amplitude-modulated 2.45
GHz microwaves.
Selective changes in locomotor activity in mice due to low-intensity microwaves amplitude
modulated in the EEG spectral domain.
Physical basis of adverse and therapeutic effects of low intensity microwave radiation.
Resonance effect of microwaves on the genome conformational state of E. coli cells.
Induction of micronuclei in human lymphocytes exposed in vitro to microwave radiation.
Biological effects of electromagnetic fields--mechanisms for the effects of pulsed microwave
radiation on protein conformation.
The influence of microwave radiation on transdermal delivery systems.
Parametric mechanism of excitation of the electroencephalographic rhythms by modulated
microwave radiation.
[Cytogenetic changes induced by low-intensity microwaves in the species Triticum aestivum].
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High-frequency electromagnetic radiation injury to the upper extremity: local and systemic
effects.
Effect of chronic microwave radiation on T cell-mediated immunity in the rabbit.
Prenatal microwave exposure and behavior.
[The state of receptor-dependent signal pathways in the agranulocytes from the peripheral blood
of the reconvalescent patients following community-acquired pneumonia under the influence of
microwave radiation].
Effects of 2.45 GHz microwaves on meiotic chromosomes of male CBA/CAY mice.
Inhibitory Effects of Microwave Radiation on LPS-Induced NFkappaB Expression in THP-1
Monocytes.
The relation of dose rate of microwave radiation to the time of death and total absorbed dose in
the mouse.
Differential damage in bacterial cells by microwave radiation on the basis of cell wall structure.
Effect of 7, 14 and 21 Hz modulated 450 MHz microwave radiation on human
electroencephalographic rhythms.
Immunotropic influence of 900 MHz microwave GSM signal on human blood immune cells
activated in vitro.
[Are microwaves a co-teratogen? Experimental model concept and its verification].
Studies on microwaves in medicine and biology: from snails to humans.
Changes in human EEG caused by low level modulated microwave stimulation.
Electromagnetic radiations and cancer. Cause and prevention.
Microwave elution of red cell antibodies.
Influence of low intensity 2,450 MHz microwave radiation upon the growth of various micro-
organisms and their sensitivity towards chemical inactivation.
Low power microwave interaction with phospholipase C and D signal transduction pathways in
myogenic cells.
[Antagonistic effect of microwave on hematopoietic damage of mice induced by gamma-ray
irradiation].
Acid resistance and verocytotoxin productivity of enterohemorrhagic Escherichia coli O157:H7
exposed to microwave.
The relationship between colony-forming ability, chromosome aberrations and incidence of
micronuclei in V79 Chinese hamster cells exposed to microwave radiation.
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Effects of differently polarized microwave radiation on the microscopic structure of the nuclei in
human fibroblasts.
The correlation between the frequency of micronuclei and specific chromosome aberrations in
human lymphocytes exposed to microwave radiation in vitro.
A search for nonthermal effects of 434 MHz microwave radiation on whole human blood.
Review of the specific effects of microwave radiation on bacterial cells.
Microwave dissociation of antigen-antibody complexes: a new elution technique to permit
phenotyping of antibody-coated red cells.
[Nature of the changes in the morphofunctional and cytochemical indices of blood leukocytes as
affected by low-intensity microwaves].
Effects of 2.45-GHz microwave radiation and phorbol ester 12-O-tetradecanoylphorbol-13-
acetate on dimethylhydrazine-induced colon cancer in mice.
Effects of X-band microwave exposure on rabbit erythrocytes.
Transgenic nematodes as biomonitors of microwave-induced stress.
The effects of microwave radiation on avian dominance behavior.
Dominant lethal studies in male mice after exposure to 2.45 GHz microwave radiation.
[Action of UHF microwaves on the germ and somatic cells of mammals].
Sperm count and sperm abnormality in male mice after exposure to 2.45 GHz microwave
radiation.
Effect of microwaves (2450-MHz) on the immune system in mice: studies of nucleic acid and
protein synthesis.
The influence of differently polarised microwave radiation on chromatin in human cells.
Effects of 10-GHz microwaves on hematological parameters in Swiss albino mice and their
modulation by Prunus avium.
Effects of fetal microwave radiation exposure on offspring behavior in mice.
Ibuprofen effects on behavioral thermoregulation with microwave radiation in albino rats.
Microwave and man: the direct and indirect hazards, and the precautions.
Biomarkers in volunteers exposed to mobile phone radiation.
Effects of 900-MHz microwave radiation on gamma-ray-induced damage to mouse
hematopoietic system.
Detection of probable effects of microwave exposure of blood parameters of RBC, PCV and Hb
in rat.
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Effects of microwaves on the colony-forming capacity of haemopoietic stem cells in mice.
2.45-GHz microwave irradiation adversely affects reproductive function in male mouse, Mus
musculus by inducing oxidative and nitrosative stress.
Adaptation of human brain bioelectrical activity to low-level microwave.
Biochemical changes in rat brain exposed to low intensity 9.9 GHz microwave radiation.
Effect of microwave radiation on the permeability of carbonic anhydrase loaded unilamellar
liposomes.
Effects on the nervous system by exposure to electromagnetic fields: experimental and clinical
studies.
Microwave effect on diffusion: a possible mechanism for non-thermal effect.
Teratology, survival, and reversal learning after fetal irradiation of mice by 2450-MHz
microwave energy.
[Changes in drug pharmacokinetics and pharmacodynamics under the influence of microwaves
of different ranges].
Increase in the frequency of Fc receptor (FcR) bearing cells in the mouse spleen following a
single exposure of mice to 2450 MHz microwaves.
Modification of membrane fluidity in melanin-containing cells by low-level microwave
radiation.
Effects of low level microwave radiation on the digestive transit of the rat.
Microwave-stimulated drug release from liposomes.
[Changes in immunobiological reactivity under the combined action of microwave, infrasonic
and gamma irradiation].
Behavioral and cognitive effects of microwave exposure.
The effect of microwave radiation on the cell genome.
Neurological effects of microwave exposure related to mobile communication.
Microwave effects on plasmid DNA.
Differential response of the permeability of the rat liver canalicular membrane to sucrose and
mannitol following in vivo acute single and multiple exposures to microwave radiation (2.45
GHz) and radiant-energy thermal stress.
Effects of microwave radiation and strychnine on cerebral biopotentials in narcotized rats.
[Some biochemical indexes in white rabbit's blood affected by acute high intensity microwave].
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Long-term exposure to microwave radiation provokes cancer growth: evidences from radars and
mobile communication systems.
Effect of low power microwave on the mouse genome: a direct DNA analysis.
Fluorescence depolarization studies of the phase transition in multilamellar phospholipid vesicles
exposed to 1.0-GHz microwave radiation.
Effect of low frequency modulated microwave exposure on human EEG: individual sensitivity.
A negative test for mutagenic action of microwave radiation in Drosophila melanogaster.
[Non-thermal microwave effect on nerve fiber function].
Influence of microwaves on different types of receptors and the role of peroxidation of lipids on
receptor-protein shedding.
[Effect of nonionizing microwave radiation on autoimmune reactions and antigenic structure of
serum proteins].
Effects of 9.4 GHz microwave exposure on meiosis in mice.
[Two-step exposure of biological objects to infrared laser and microwave radiation].
Influence of in vitro microwave radiation on the fertilizing capacity of turkey sperm.
Measure of enzymatic activity coincident with 2450 MHz microwave exposure.
Effect of microwave radiation on redissolving precipitated matter in fluorouracil injection.
[Germ reduction by microwaves--microwave specific effects].
Effects of microwave (2.45 GHz) irradiation on some biological characters of Salmonella
typhimurium.
The relation of sex, age, and weight of mice to microwave radiation sensitivity.
The origins of U.S. safety standards for microwave radiation.
Pathophysiology of microwave radiation: effect on rat brain.
Influence of CW microwave radiation on in vitro release of enzymes from retinol- treated hepatic
lysosomes.
Cytological effects of microwave radiation in Chinese hamster cells in vitro.
Ouabain inhibition of kidney ATPase is altered by 9.14 GHz radiation.
Cytogenetic investigations on microwaves emitted by a 455.7 MHz car phone.
[The reaction of the tick Hyalomma asiaticum (Acarina, Ixodidae) to 1- to 4-GHz microwaves].
Microwave effects on the central nervous system--a study of radar mechanics.
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[The characteristics of the reactions of excitable tissue to combined exposure to microwaves and
low-intensity ultrasound].
[Cumulated biological effects of microwaves and their reflection in behavior, work capacity,
growth of body mass and state of brain neurons].
[Quantitative patterns in the cytogenetic action of microwaves].
[The action of microwave radiation on potassium ion transport and oxygen consumption in the
perfused rat liver].
The effects of low level microwaves on the fluidity of photoreceptor cell membrane.
Insensitivity of cardiovascular function to low power cm-/mm-microwaves.
[Ultracytochemical changes in the brain and liver in exposure to low-intensity nonionizing
microwave radiation].
Microwave effect on camphor binding to rat olfactory epithelium.
In vitro effects of microwave radiation on rat liver mitochondria.
Induction of neoplastic transformation in C3H/10T1/2 cells by 2.45-GHz microwaves and
phorbol ester.
Evidence for microwave carcinogenesis in vitro.
Microwave radiation injury.
Effect of microwave radiation on human EEG at two different levels of exposure.
Effects of noinionizing radiation on the central nervous system, behavior, and blood: a progress
report.
Brain enzyme histochemistry following stabilization by microwave irradiation.
Poly ADP ribosylation as a possible mechanism of microwave--biointeraction.
Investigation of an acute microwave-oven hand injury.
Rat lymphocytes in cell culture exposed to 2450 MHz (CW) microwave radiation.
Effect of electromagnetic microwave radiation on the growth of Ehrlich ascites carcinoma.
Effects of 36.6 GHz and static magnetic field on degree of endoreduplication in Drosophila
melanogaster polytene chromosomes.
Extremely low-level microwaves attenuate immune imbalance induced by inhalation exposure to
low-level toluene in mice.
[The effect of microwaves on the neuronal activity of the hyperstriatum in chick embryos at the
critical developmental period].
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Psychological symptoms and intermittent hypertension following acute microwave exposure.
Very new waves in very old meridians: quantum medical physics of the living.
[The effect of various occupational exposures to microwave radiation on the concentrations of
immunoglobulins and T lymphocyte subsets].
Microwave effect upon chlorpromazine-inhibited kidney ATPase.
Evidence for genetic control of microwave-induced augmentation of complement receptor-
bearing B lymphocytes.
[The combined action of microwave radiation and hydrogen peroxide on the viability and
ultrastructure of Pseudomonas aeruginosa cells].
A demonstration of athermal effects of continuous microwave irradiation on the growth and
antibiotic sensitivity of Pseudomonas aeruginosa PAO1.
Influence of low power cm-/mm-microwaves on cardiovascular function.
Local cerebral blood flow after microwave exposure.
The properties of bird feathers as converse piezoelectric transducers and as receptors of
microwave radiation. II. Bird feathers as dielectric receptors of microwave radiation.
Different methods for evaluating the effects of microwave radiation exposure on the nervous
system.
Microwave cell death: Immunohistochemical and enzyme histochemical evaluation.
Study of nonionizing microwave radiation effects upon the central nervous system and behavior
reactions.
[Cellular effects of microwaves of thermal intensity].
Microwave induced stimulation of 32Pi incorporation into phosphoinositides of rat brain
synaptosomes.
Laser doppler flowmetry as a method for evaluating the microwave radiation effect on cutaneous
microcirculation.
Microwave effects on acetylcholine-induced channels in cultured chick myotubes.
[The participation of thyroid hormones in modifying the mutagenic effect of microwaves].
Investigation of the effects of continuous-wave, pulse- and amplitude-modulated microwaves on
single excitable cells of Chara corallina.
Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric
effects including depression.
[Effect of centimeter microwaves on the antibody production in mice].
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[Effect of electromagnetic SHF-radiation on the morphofunctional status of early mouse
embryos].
The effect of acute far field exposure at 2.45 GHz on the mouse testis.
[Pharmacological correction of the acute effects of microwave irradiation in an experiment].
Effects of exposure to microwaves: problems and perspectives.
Semen analysis of military personnel associated with military duty assignments.
Setting exposure limits for radiofrequency radiation and microwaves in China.
Effect of exposure to operant-controlled microwaves on certain blood and immunological
parameters in the young chick.
In vitro cytogenetic effects of 2450 MHz waves on human peripheral blood lymphocytes.
[Microwaves and blood-brain barrier].
Microwave radiation: an epidemiologic assessment.
[The dynamics of the immunobiological effects in transcerebral microwave exposures].
Microwave absorption by normal and tumor cells.
Microwaves induce an increase in the frequency of complement receptor-bearing lymphoid
spleen cells in mice.
Microwave radiation-induced calcium ion efflux from human neuroblastoma cells in culture.
Studies on possible genetic effects of microwaves in procaryotic and eucaryotic cells.
Middle-ear structures contribute little to auditory perception of microwaves.
[Effect of long wave pre-illumination on the kinetic characteristics of microwave
photoconductivity signals in Chlorella cells and the Emerson effect].
Non-thermal effects of 2.45 GHz microwaves on spindle assembly, mitotic cells and viability of
Chinese hamster V-79 cells.
Microwave diathermy: the invisible healer.
[Biological effects of microwave radiation of low nonthermal intensity (regarding the maximal
admissible values)].
[Effect of electromagnetic radiation of radio frequency (340 and 800 MHz) on liposomes from
dimyristoyl lecithin].
[A comparative analysis of the biological action of microwaves and laser radiation].
[Studies on the microwave leakage of the interphone].
Effect of microwave radiation on the stability of frozen cefoxitin sodium solution in plastic bags.
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[The role of TLR4 receptor in the stress response of lymphocytes].
Febrile convulsions induced by microwaves and the alteration in behavior of albino mouse OF1.
[Immunobiological effect of bitemporal exposure of rabbits to microwaves].
Thermal effects of 2450 MHz microwave exposure near a titanium alloy plate implanted in
rabbit limbs.
[The role of protein kinase SAPK/JNK in cell responses to low-intensity nonionizing radiation].
[Activity of cytochromes P-450p and P-450h in liver microsomes and blood corticosteroid levels
in experimental animals under the action of physical factors].
The effect of high intensity microwave exposure on enucleation of murine erythroid cells in
vitro.
Microwave-evoked brainstem potentials in cats.
Tight junctional changes upon microwave and x-ray irradiation.
The analysis of animal bioelectric brain activity influenced by microwaves or by the introduction
of strychnine.
[The characteristics of the effect of centimeter-range microwaves on drug pharmacokinetics in
the body of experimental animals].
[Effect of centimeter microwaves and the combined magnetic field on the tumor necrosis factor
production in cells of mice with experimental tumors].
[Enzymatic activity of some tissues and blood serum from animals and humans exposed to
microwaves and hypothesis on the possible role of free radical processes in the nonlinear effects
and modification of emotional behavior of animals].
Non-thermal effects in the microwave induced unfolding of proteins observed by chaperone
binding.
[Study of bioeffects of ship-borne microwave navigation radar in chronic experiments].
[Combined effect of microwaves and gamma-rays on the imprinting of chickens, irradiated in
early embryogenesis].
Effects of nonionizing radiation on birds.
[The effect of electromagnetic radiation on the membranes of the sarcoplasmic reticulum].
[The combined action of microwave irradiation and hypoxia on the biogenic amine content of the
blood in guinea pigs in anaphylactic shock].
Possible humoral mechanism of 2450-MHz microwave-induced increase in complement receptor
positive cells.
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[Synaptic transmission in the frog spinal cord exposed to intensive microwave radiation].
Microwave-enhanced folding and denaturation of globular proteins.
[Hematologic changes in workers exposed to radio wave radiation].
[The reaction of glia in visual centers during the whole body effect of combined microwaves and
x-rays].
Elimination of microwave effects on the vitality of nerves after blockage of active transport.
Low frequency amplitude modulated microwave fields change calcium efflux rates from
synaptosomes.
Study of effects of low level microwave field by method of face masking.
Association of microwaves and ionizing radiation: potentiation of teratogenic effects in the rat.
[The use of microwave for immunohistochemical technology in forensic pathology].
[The effect of microwaves on the bioelectric brain activity].
MoS2 nanosheets encapsulated in sodium alginate microcapsules as microwave embolization
agents for large orthotopic transplantation tumor therapy.
Microwave drying of microorganisms: I. Influence of the microwave energy and of the sample
thickness on the drying of yeast.
Effect of non-ionising radiation on body weight and growth of the gastro-intestinal tract in
broilers.
[The role of the thyroid hormones in regulating chromosomal resistance to microwave exposure].
[Analysis of ECG on the staffs exposed to microwave in the radio calling signal station].
Cochlear microphonics generated by microwave pulses.
Holographic assessment of a hypothesized microwave hearing mechanism.
Enhancement of allergic skin wheal responses by microwave radiation from mobile phones in
patients with atopic eczema/dermatitis syndrome.
Microwave antigen retrieval blocks endogenous peroxidase activity in immunohistochemistry.
[Increase in the immunogenicity of cancer cells exposed to microwaves].
Aspirin (acetylsalicylic acid) effects on behavioral thermoregulation with microwave radiation.
[The effect of microwaves on lipid peroxidation and on lipid and mineral metabolism in warm-
blooded animals (experimental research)].
Effects of microwave radiation on house dust mites, Dermatophagoides pteronyssinus and
Dermatophagoides farinae (Astigmata: Pyroglyphidae).
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The effect of non ionising electromagnetic radiation on RAAF personnel during World War II.
[Action of millimeter-range electromagnetic radiation on the Ca pump of sarcoplasmic
reticulum].
After-effect induced by microwave radiation in human electroencephalographic signal: a
feasibility study.
Superconductivity--a possible mechanism for non-thermal biological effects of microwaves.
Microwaving for double indirect immunofluorescence with primary antibodies from the same
species and for staining of mouse tissues with mouse monoclonal antibodies.
[Accelerated decalcification using microwaves].
Influence of chopper and mixer speeds and microwave power level during the high-shear
granulation process on the final granule characteristics.
[Effects of prolonged low-intensity radiofrequency radiation in cm-range on the development of
subcutaneously grafted Ehrlich's adenocarcinoma].
The effects of irradiation intensity on the microwave-enhanced advanced oxidation process.
The role of coherence time in the effect of microwaves on ornithine decarboxylase activity.
[Effect of microwaves over Staphylococcus aureus and Salmonella spp. inoculated into frozen
minced meat].
Microwave decalcification of human temporal bones.
An EM radiation safety controller.
Electrosmog and autoimmune disease.
Capability of Thai Mission grass (Pennisetum polystachyon) as a new weedy lignocellulosic
feedstock for production of monomeric sugar.
A novel autonomic activation measurement method for stress monitoring: non-contact
measurement of heart rate variability using a compact microwave radar.
Late heat damage in normal swine rectum: a comparison of thermosensitivity of rectum and
oesophagus.
[Effect of UHF and ionizing radiation on the Na-K-ATPase activity of Ehrlich ascitic carcinoma
cells].
Acute multiple mononeuropathy after accidental exposure to oven microwaves.
Microwave enhanced ion exchange of cationic and anionic clays.
[New mechanisms of biological effects of electromagnetic fields].
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Non-contact determination of parasympathetic activation induced by a full stomach using
microwave radar.
Immunohistochemistry and microwave decalcification of human temporal bones.
Monitoring of lung edema by microwave reflectometry during lung ischemia-reperfusion injury
in vivo.
Joint effects of microwave and chromium trioxide on root tip cells of Vicia faba.
An alternative approach to the treatment of mammary duct fistulas: a combination of microwave
and ultrasound.
[Body's reaction to weakened geomagnetic field (the effect of magnetic deprivation)].
Influence of radar radiation on breeding biology of tits (Parus sp.).
[Effect of short-term exposure to ash from electric power plants on histochemical reactions of
succinate dehydrogenase and lactate dehydrogenase in the lungs of experimental animals].
--Leaf Cluster 3 (39)
Theme - Adverse impact of wireless radiation on eye lens
Titles
[Effect of low-intensity microwave radiation on proliferation of cultured epithelial cells of rabbit
lens].
Localized effects of microwave radiation on the intact eye lens in culture conditions.
[Effects of different dose microwave radiation on protein components of cultured rabbit lens].
Non-thermal electromagnetic radiation damage to lens epithelium.
Non-thermal cellular effects of lowpower microwave radiation on the lens and lens epithelial
cells.
[A quantitative study on early changes in rabbit lens capsule epithelium induced by low power
density microwave radiation].
[Ultrastructural change of rabbit lens epithelial cells induced by low power level microwave
radiation].
Cataracts induced by microwave and ionizing radiation.
Ultrastructural changes in the rabbit lens induced by microwave radiation.
Low power density microwave radiation induced early changes in rabbit lens epithelial cells.
Effects of microwave radiation on the eye: the occupational health perspective.
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[Experimental studies on the influence of millimeter radiation on light transmission through the
lens].
Glutathione concentration and peptidase activity in the lens after exposure to microwaves.
Low power microwave radiation inhibits the proliferation of rabbit lens epithelial cells by
upregulating P27Kip1 expression.
Microwave lens effects in humans. II. Results of five-year survey.
Changes in gap junctional intercellular communication in rabbits lens epithelial cells induced by
low power density microwave radiation.
Combined microwave energy and fixative agent for cataract induction in pig eyes.
[Evaluation of lens transparency in persons exposed to electromagnetic radiation of 27--30 MHz
frequency].
[Low-intensity microwave blockes cell cycle and regulate cell cycle related gene expression in
rabbit lens epithelial cells].
Thermal cataract formation in rabbits.
Effects of microwave radiation on the lens epithelium in the rabbit eye.
On the microwave exposure.
Observation of microwave-induced eye lens surface motion in vitro.
Data analysis reveals significant microwave-induced eye damage in humans.
Microwave irradiation and soft contact lens parameters.
Inducing cataract in postmortem pig eyes for cataract surgery training purposes.
Dosimetric study of microwave cataractogenesis.
Evaluation of possible microwave-induced lens changes in the United States Air Force.
[Acute ocular lesions after exposure to electromagnetic radiation of ultrahigh frequency (an
experimental study)].
Microwave radiation-induced chromosomal aberrations in corneal epithelium of Chinese
hamsters.
The ocular effects of microwaves on hypothermic rabbits: a study of microwave cataractogenic
mechanisms.
Microwave cataract and litigation: a case study.
[Biologic effects and hygienic regulation of electromagnetic fields caused by mobile
communication devices].
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Comments on Frey's "Data analysis reveals significant microwave-induced eye damage in
humans".
Microwave-induced retinal destruction with sparing of sclera and choriocapillaris.
[The effect of chronic irradiation with intermittent unmodulated microwaves on the functional
status of the rabbit].
[Hazardous health effects of microwaves and radio waves].
Microwave cyclodestruction: evaluation on human eyes.
Effects of radiofrequency radiation on rabbit kidney: a morphological and immunological study.
--Leaf Cluster 35 (107)
Theme - Adverse impacts of microwave radiation on cells and cognitive functions
Titles
[A aquaporin 4 expression and effects in rat hippocampus after microwave radiation].
Impairment of long-term potentiation induction is essential for the disruption of spatial memory
after microwave exposure.
[Changes of apoptosis, mitochondrion membrane potential and Ca2+ of hypothalamic neurons
induced by high power microwave].
Upregulation of HIF-1alpha via activation of ERK and PI3K pathway mediated protective
response to microwave-induced mitochondrial injury in neuron-like cells.
[Microwave radiation induces injury to GC-2spd cells].
The relationship between NMDA receptors and microwave-induced learning and memory
impairment: a long-term observation on Wistar rats.
Apoptosis induced by microwave radiation in pancreatic cancer JF305 cells.
[The cardiac injury effect of microwave radiation on rabbit and its mechanism].
[The injury effects of microwave exposure on visual performance and retinal ganglion cells
(RGCs) in rats].
[Inhibitory effect of microwave radiation on proliferation of human pancreatic cancer JF305 cells
and its mechanism].
Study on dose-dependent, frequency-dependent, and accumulative effects of 1.5 GHz and 2.856
GHz microwave on cognitive functions in Wistar rats.
Microwave induces apoptosis in A549 human lung carcinoma cell line.
Acute effects of pulsed microwaves and 3-nitropropionic acid on neuronal ultrastructure in the
rat caudate-putamen.
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[Influence of microwave radiation on synaptic structure and function of hippocampus in Wistar
rats].
Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling.
Identification of a Novel Rat NR2B Subunit Gene Promoter Region Variant and Its Association
with Microwave-Induced Neuron Impairment.
Microwave exposure impairs synaptic plasticity in the rat hippocampus and PC12 cells through
over-activation of the NMDA receptor signaling pathway.
iTRAQ quantitatively proteomic analysis of the hippocampus in a rat model of accumulative
microwave-induced cognitive impairment.
The apoptotic effect and the plausible mechanism of microwave radiation on rat myocardial
cells.
Neural cell apoptosis induced by microwave exposure through mitochondria-dependent caspase-
3 pathway.
The effect of 2450 MHz microwave radiation on the ultrastructure of snail neurons.
Relationship between cognition function and hippocampus structure after long-term microwave
exposure.
2.45 GHz Microwave Radiation Impairs Learning and Spatial Memory via Oxidative/Nitrosative
Stress Induced p53-Dependent/Independent Hippocampal Apoptosis: Molecular Basis and
Underlying Mechanism.
Real-time Microwave Exposure Induces Calcium Efflux in Primary Hippocampal Neurons and
Primary Cardiomyocytes.
AduoLa Fuzhenglin down-regulates microwave-induced expression of beta1-adrenergic receptor
and muscarinic type 2 acetylcholine receptor in myocardial cells of rats.
Alterations of cognitive function and 5-HT system in rats after long term microwave exposure.
Extracellular calcium and microwave enhancement of membrane conductance in snail neurons.
[Effect of handportable mobiletelephone microwave radiation on rat central neuron apoptosis].
[Effect of electromagnetic radiation in a decimeter wave-length range on the calcium current of
molluscan neurons].
[Effects of microwave radiation on thymocytes in mice at different power densities].
Long term impairment of cognitive functions and alterations of NMDAR subunits after
continuous microwave exposure.
Reduction of phosphorylated synapsin I (ser-553) leads to spatial memory impairment by
attenuating GABA release after microwave exposure in Wistar rats.
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Retinal damage experimentally induced by microwave radiation at 55 mW/cm2.
[Microwave radiation decreases the expressions of occludin and JAM-1 in rats].
[Changes of the expression of beta1-adrenergic receptor and M2-muscarinic acetylcholine
receptor in rat hearts after high power microwave radiation].
[Effect of qindan fuzheng capsule on ultrastructure of microwave radiation injured
cardiomyocytes and hepatocytes in rats].
From the Cover: 2.45-GHz Microwave Radiation Impairs Hippocampal Learning and Spatial
Memory: Involvement of Local Stress Mechanism-Induced Suppression of iGluR/ERK/CREB
Signaling.
[Influence of microwave radiation on synapsin I expression in PC12 cells and its mechanism].
[Effect of vitamin E on morphological variation of retinal ganglion cells after microwave
radiation].
[Effect of microwave radiation on primary cultured Sertoli cells].
Chronic exposure to GSM 1800-MHz microwaves reduces excitatory synaptic activity in
cultured hippocampal neurons.
Microwave radiation leading to shrinkage of dendritic spines in hippocampal neurons mediated
by SNK-SPAR pathway.
Activation of VEGF/Flk-1-ERK Pathway Induced Blood-Brain Barrier Injury After Microwave
Exposure.
The study of retinal ganglion cell apoptosis induced by different intensities of microwave
irradiation.
The effects of high-power microwaves on the ultrastructure of Bacillus subtilis.
The effect of microwave radiation on passive membrane properties of snail neurons.
[Effect of 900MHz electromagnetic fields on energy metabolism of cerebral cortical neurons in
postnatal rat].
Effects of GSM 1800 MHz on dendritic development of cultured hippocampal neurons.
Low intensity microwave radiation effects on the ultrastructure of Chang liver cells.
[Effect of 900Mhz electromagnetic fields on energy metabolism in postnatal rat cerebral cortical
neurons].
Real-time Assessment of Cytosolic, Mitochondrial, and Nuclear Calcium Levels Change in Rat
Pheochromocytoma Cells during Pulsed Microwave Exposure Using a Genetically Encoded
Calcium Indicator.
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Protective Role of NMDAR for Microwave-Induced Synaptic Plasticity Injuries in Primary
Hippocampal Neurons.
Abnormality of synaptic vesicular associated proteins in cerebral cortex and hippocampus after
microwave exposure.
RKIP Regulates Neural Cell Apoptosis Induced by Exposure to Microwave Radiation Partly
Through the MEK/ERK/CREB Pathway.
[The protective effects of Aduola Fuzhenglin on the heart injury induced by microwave exposure
in rats].
Differentiation of murine erythroleukemic cells during exposure to microwave radiation.
Cytokines produced by microwave-radiated Sertoli cells interfere with spermatogenesis in rat
testis.
[Effect of 900 MHz electromagnetic fields on the expression of GABA receptor of cerebral
cortical neurons in postnatal rats].
[Effects of high power microwave exposure on cholinergic neurotrophic factors protein in rabbit
retina].
[Neuroeffects of prolonged exposure to microwaves: systemic, neuronal and electron microscope
study].
Microwave enhancement of membrane conductance: calmodulin hypothesis.
[Influence of electromagnetic radiation on raf kinase inhibitor protein and its related proteins of
hippocampus].
2.45 GHz microwave radiation induced oxidative and nitrosative stress mediated testicular
apoptosis: Involvement of a p53 dependent bax-caspase-3 mediated pathway.
Microwave effects on input resistance and action potential firing of snail neurons.
MicroRNAs: Novel Mechanism Involved in the Pathogenesis of Microwave Exposure on Rats'
Hippocampus.
The Screening of Genes Sensitive to Long-Term, Low-Level Microwave Exposure and
Bioinformatic Analysis of Potential Correlations to Learning and Memory.
[Pathological study of testicular injury induced by high power microwave radiation in rats].
Noise-modulated-microwave-induced response in snail neurons.
[Early ultrastructural reactions in various parts of the visual analyzer in guinea pigs after
thermogenic microwave irradiation].
[Changes of rat testicular germ cell apoptosis after high power microwave radiation].
The transmission of reflexes in the spinal cord of cats during direct irradiation with microwaves.
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[Lipid peroxide damage in retinal ganglion cells induced by microwave].
Calreticulin attenuated microwave radiation-induced human microvascular endothelial cell injury
through promoting actin acetylation and polymerization.
[Reaction of the ultrastructure of the rat spinal ganglion to exposure to a pulsed electromagnetic
field].
Specific electromagnetic effects of microwave radiation on Escherichia coli.
Microwave enhancement of membrane conductance: effects of EDTA, caffeine and tetracaine.
[Effect of Qidan Granule on PMC Derived Peptide Content and Structure of Hippocampal CA1
Region in Microwave Radiated Rats].
[The microarray study on the stress gene transcription profile in human retina pigment epithelial
cells exposed to microwave radiation].
[The electroporation effects of high power pulse microwave and electromagnetic pulse
irradiation on the membranes of cardiomyocyte cells and the mechanism therein involved].
Non-thermal effects of continuous 2.45 GHz microwaves on Fas-induced apoptosis in human
Jurkat T-cell line.
[Zinc protective effects on pig retinal pigment epithelial cell damage of lipid peroxide induced
by 2450 MHz microwave].
Pathological changes in the sinoatrial node tissues of rats caused by pulsed microwave exposure.
[High power microwave radiation damages blood-testis barrier in rats].
[Experimental analysis of biological effects of microwaves: their systemic, ultrastructural and
neuronal mechanisms].
[Relationship between activation of microglia and Jaks phosphorylation induced by microwave
irradiation].
Ultrastructural changes following treatment with a microwave pulse in the oocyst of Eimeria
magna Perard, 1925.
The functional state of thymus cells following microwave exposure of endocrine glands.
Non-thermal effects of electromagnetic fields at mobile phone frequency on the refolding of an
intracellular protein: myoglobin.
[Effect of microwaves on the expression by thymocytes of various surface membrane markers].
[Dynamics of morphological changes in the spinal cord following exposure to non-ionizing
microwave radiation].
Immunoreactivity of normal rabbit serum with epinephrine (E) cells of the rat adrenal medulla
after microwave antigen retrieval.
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[Changes in response of neurons in visual area of cerebral cortex of rabbits to flashes of light
under the influence of low-intensity physical factors of non-ionizing nature].
Ultrastructural studies of alterations induced by microwaves in Toxocara canis eggs:
prophylactic interest.
Morphological changes in the liver after microwave destruction.
Studies of childhood brain tumors using immunohistochemistry and microwave technology:
methodological considerations.
Cell attachment and viability on micro-arc-oxidation (MAO) microwave/hydrothermal treated
titanium surface.
The role of the NF-kappaB, SAPK/JNK, and TLR4 signalling pathways in the responses of
RAW 264.7 cells to extremely low-intensity microwaves.
Calreticulin stabilizes F-actin by acetylating actin and protects microvascular endothelial cells
against microwave radiation.
Dual effects of microwaves on single Ca(2+)-activated K+ channels in cultured kidney cells
Vero.
Microwave antigen retrieval of beta-amyloid precursor protein immunoreactivity.
Nerve agent exposure elicits site-specific changes in protein phosphorylation in mouse brain.
Cyclic AMP-dependent signaling system is a primary metabolic target for non-thermal effect of
microwaves on heart muscle hydration.
[Microwaves and the visual analyzer].
Evaluation of immunohistochemical staining of human duodenal endocrine cells after microwave
antigen retrieval.
[Quantitative histologic changes of the glioneuronal complex in the central and intermediate
parts of the visual analyzer exposed to microwaves of thermogenic intensity].
Study of interlaboratory reliability and reproducibility of estrogen and progesterone receptor
assays in Europe. Documentation of poor reliability and identification of insufficient microwave
antigen retrieval time as a major contributory element of unreliable assays.
Structural changes in abdominal aorta and vena cava inferior after experimental microwave
destruction.
--Leaf Cluster 39 (211)
Theme - Adverse effects from microwave radiation
Titles
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[Effect of quinacrine on inflammatory reaction of blood system induced by microwave
irradiation].
Cumulative effect in microwave irradiation.
[Protective effects of Genistein on human renal tubular epithelial cells damage of microwave
radiation].
[Effects of occupational microwave irradiation on heat shock protein 70 expressions in rat
hippocampus].
Effects of radiation on frozen lactate dehydrogenase.
Effect of microwave energy on the metabolism of Enterobacteriaceae.
[Analysis of pulsed bioelectric activity of rabbit cerebral cortex in response to low-intensity
microwave radiation].
[Pro- and antioxidant effect of electromagnetic fields of extremely high frequency (460 MHz) on
brain tissues in experiment].
[Pulse flows of neuronal populations of the cerebral cortex exposed to low intensity
microwaves].
[Recovery responses in the bodies of rats following irradiation with microwaves (2400 MHz)].
Microwave irradiation induces neurite outgrowth in PC12m3 cells via the p38 mitogen-activated
protein kinase pathway.
Application of high-powered microwave irradiation for acetylcholine analysis in mouse brain.
Effect of microwave irradiation on brain tissue structure and catecholamine distribution.
[Effect of microwave irradiation on neurocyte mitochondrial ultrastructure and mtTFA mRNA
expression in rats cerebral cortex and hippocampus].
[Development of the Chlamydomonas actinochloris culture after microwave irradiation].
Reduced weight in mice offspring after in utero exposure to 2450-MHz (CW) microwaves.
[Changes in body weight of rats during irradiation with microwaves of nonthermal intensity].
[Dependence of changes in summary bioelectric activity of the brain on low-intensity microwave
irradiation from density of flow energy].
Microwave facilitation of domperidone antagonism of apomorphine-induced stereotypic
climbing in mice.
[Experimental data on reaction of neurons of the brain to low-intensity package-pulsing
microwave irradiation].
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Growth and development of mice offspring after irradiation in utero with 2,450-MHz
microwaves.
[Traumatic ulcer following microwave irradiation and local anesthesia].
Behavioral evaluation of microwave irradiation.
[Survival and physical development of progeny of Swiss mice after 2450 Mhz microwave
irradiation during pregnancy].
[Effects of injurying and restoring the body of mice with microwave (2400 MHz) irradiation].
Effect of microwave irradiation on monoamine metabolism in dissected rat brain.
Effects of microwave irradiation on rat hepatic tissue evaluated by enzyme histochemistry for
acid phosphatase.
The effects of microwave radiation from mobile telephones on humans and animals.
Increase of brain ammonia after microwave irradiation and its mechanism.
[Behavioral effects of the combined chronic action of 9375 and 1765 MHz microwaves].
[Effect of the agents of general anesthesia on mice after microwave irradiation].
[Effects of microwave irradiation and electrostatic field on the survival, growth and reproduction
of Moina mongolica Daday].
Incidence of low-level microwave irradiation on intestinal myoelectrical activity in the rat.
Multinucleated giant cell appearance after whole body microwave irradiation of rats.
[The pathogenesis of central nervous system functional disordersafter exposure to microwave
radiation].
Comparison of native and microwave irradiated DNA.
Effect of high-power density microwave irradiation on the soluble proteins of the rabbit lens.
Microwave radiation (2450-MHz) potentiates the lethal effect of endotoxin in mice.
Pulse activity of populations of cortical neurons under microwave exposures of different
intensity.
Changes in the blood count of growing rats irradiated with a microwave pulse field.
[Effect of continuous low-intensity microwave irradiation on the behavior of albino rats].
Microwave irradiation and cross-linking of collagen.
[Combined effect of microwave and ionizing radiation].
Reproduction of Japanese quail after microwave irradiation (2.45 GHz CW) during embryogeny.
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Psychoactive-drug response is affected by acute low-level microwave irradiation.
Microwaves and cellular immunity. I. Effect of whole body microwave irradiation on tumor
necrosis factor production in mouse cells.
Radio and microwave radiation and experimental atherosclerosis.
Biosynthesis of acetylcholine in different brain regions in vivo following alternative methods of
sacrifice by microwave irradiation.
Microwaves and cellular immunity. II. Immunostimulating effects of microwaves and naturally
occurring antioxidant nutrients.
Effects of microwave irradiation on blood flow in the dog hindlimb.
Tissue structure of rat brain after microwave irradiation using maximum magnetic field
component.
[Experimental study of the effects of acute uneven microwave irradiation].
Microwave accelerated transglycosylation of rutin by cyclodextrin glucanotransferase from
Bacillus sp. SK13.002.
The effect of 2.45 GHz microwave irradiation on human peripheral lymphocytes.
[Motor activity of rabbits in conditions of chronic low-intensity pulse microwave irradiation].
Autoradiographic analysis of protein synthesis and measurements of nuclear volume in WISH
cell cultures irradiated with 3 GHz electromagnetic radiation.
Leukocyte numbers during the humoral and cell-mediated immune response of Japanese quail
after microwave irradiation in ovo.
The respiratory response to microwaves.
Aversion/attraction of blue jays to microwave irradiation.
Low-level microwave irradiation attenuates naloxone-induced withdrawal syndrome in
morphine-dependent rats.
Response of Aspergillus nidulans and Physarum polycephalum to microwave irradiation.
[Combined action of gamma and UHF radiation on conditioned reflex behavior of rats].
Ethanol-induced hypothermia and ethanol consumption in the rat are affected by low-level
microwave irradiation.
Inhibitory action of microwave radiation on gamma-glutamyl transpeptidase activity in liver of
rats treated with hydrocortisone.
Effect of low-level microwave irradiation on the duodenal electrical activity of the
unanesthetized rat.
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Behavioral sensitivity to microwave irradiation.
In vitro microwave effects on human neutrophil precursor cells (CFU-C).
The effect of microwave irradiation on vasopressin in plasma and hypothalamo-
neurohypophyseal system.
Karyometric observations of WISH cell cultures irradiated with 3 GHz microwaves.
[Effects of injurying and restoring the body of rats with microwave (2400 MHz) irradiation].
[Spontaneous electrical activity of the rat cerebral cortex during microwave irradiation].
[The immune and hormonal effects of the local action of microwaves of different intensities].
[Effects of microwave irradiation on ATPase activity and voltage dependent ion channel of rat
hippocampus cell membrane].
Assessment of immune function development in mice irradiated in utero with 2450-MHz
microwaves.
[Response of neurons of the sensomotor region of the cerebral cortex to low-intensity pulsed
ultra-high frequency irradiation].
Effects of modulated microwave and X-ray irradiation on the activity and distribution of Ca(2+)-
ATPase in small intestine epithelial cells.
[Cross-correlation analysis of the interconnection in neuronal pulses in living sections of the
neocortex under the effect of microwave irradiation].
[Total bioelectric activity of various structures of the brain in low-intensity microwave
irradiation].
Effects of microwave irradiation on some membrane-related processes in bacteria.
Effects of modulated and continuous microwave irradiation on the morphology and cell surface
negative charge of 3T3 fibroblasts.
Microwave facilitation of methylatropine antagonism of central cholinomimetic drug effects.
[Effects of microwave acute irradiation on biomechanic properties of rabbit tissues].
Search for millimeter microwave effects on enzyme or protein functions.
[The effect of microwave irradiation on the status of the thyroid gland].
Study of the use of the microwave magnetic field for the rapid inactivation of brain enzymes.
Serum enzymes in hemorrhaged Japanese quail after microwave irradiation during embryogeny.
[Effect of acute exposure to microwave from mobile phone on DNA damage and repair of
cultured human lens epithelial cells in vitro].
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[An effect of delayed behavioral activation during a single exposure to microwaves].
[The status of the higher nervous activity in animals exposed to microwaves in conditions
simulating the intermittent work of radiolocators].
[Effect of microwave irradiation on expression of heat shock proteins family in primary cultured
rat hippocampal neurons].
Cytogenetic consequences of microwave irradiation on mammalian cells incubated in vitro.
[Pulse flows of populations of cortical neurons under microwave radiation: the number of burst
activity].
Photic cuing of escape by rats from an intense microwave field.
Effect of microwaves on the activity of murine macrophages in vitro.
Determination of a thermal equivalent of millimeter microwaves in living cells.
Ascorbic acid changes in cultured rabbit lenses after microwave irradiation.
The response of the 22A strain of scrapie agent to microwave irradiation compared with boiling.
[Tactical behavior of rats when choosing among negative stimuli: pain or exposure to an
electromagnetic field].
[Pulse flows of populations of cortical neurons under low-intensity pulsed microwave: interspike
intervals].
[Pulse flows of cortical neuron populations exposed to microwaves: interspike intervals].
[Changes in the activity and conditioned-reflex behavior of white rats during and after chronic
microwave irradiation].
Analysis of the effects of microwave energy on enzymatic activity of lactate dehydrogenase
(LDH).
Changes of amino acid gradients in brain tissues induced by microwave irradiation and other
means.
Plasma and red cell volumes of microwave irradiated mice tissues.
A comparison between microwave irradiation and decapitation: basal levels of dynorphin and
enkephalin and the effect of chronic morphine treatment on dynorphin peptides.
Microwaves (2,450 MHz) suppress murine natural killer cell activity.
[Effect of impulse-intermittent ultrahigh frequency irradiation on synthesis of nucleic acids in
tumor cells].
The effect of microwave irradiation on the vitality of various dermatophytes.
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Focused microwave irradiation of the brain preserves in vivo protein phosphorylation:
comparison with other methods of sacrifice and analysis of multiple phosphoproteins.
Brain regional levels of adenosine and adenosine nucleotides in rats killed by high-energy
focused microwave irradiation.
The effect of 2450 MHz microwave radiation on histamine secretion by rat peritoneal mast cells.
Microwave-induced hearing: some preliminary theoretical observations.
[Effect of microwave radiation on regional blood flow and tissue oxygenation in the brain].
The effect of electromagnetic radiation on the hematopoietic stem cells of mice.
Reversible irritative effect of acute 2.45GHz microwave exposure on rabbit eyes--a preliminary
evaluation.
Acute microwave irradiation and cataract formation in rabbits and monkeys.
Chronic non-thermal exposure of modulated 2450 MHz microwave radiation alters thyroid
hormones and behavior of male rats.
Microwave-mediated enzymatic modifications of DNA.
Excellent acceleration of the Diels-Alder reaction by microwave irradiation for the synthesis of
new fluorine-substituted ligands of NMDA receptor.
[Effect of 2450 MHz microwaves on the fertility of Swiss female mice].
[Myelokaryocyte mitotic activity during microwave irradiation (2375 MHz)].
Anesthesia as an effective agent against the production of congenital anomalies in mouse fetuses
exposed to electromagnetic radiation.
[Stimulation of production of tumor necrosis factor by murine macrophages when exposed in vio
and in vitro to weak electromagnetic waves in the centimeter range].
[Evaluation of changes in electrophysiological and hormonal parameters in rabbits resulting from
short-term low-intensity ultra-high-frequency irradiation].
[The effect of millimeter-range electromagnetic and of ionizing radiation on the body and
thymocytes of mice and rats].
Effect of microwave irradiation on the blow fly Chrysomya megacephala (F.) (Diptera:
Calliphoridae).
Leukocyte numbers in hemorrhaged Japanese quail after microwave irradiation in ovo.
The effect of repeated microwave irradiation on the frequency of sex-linked recessive lethal
mutations in Drosophila melanogaster.
[The epididymal adipose tissue of mice after nanosecond pulse-periodic microwave irradiation].
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A method for dissection of discrete regions of rat brain following microwave irradiation.
Effect of microwave irradiation (2450 MHz) on murine cytotoxic lymphocyte and natural killer
(NK) cells.
Dynamics of Metabolic Parameters in Rats during Repeated Exposure to Modulated Low-
Intensity UHF Radiation.
[The effect of superhigh-frequency electromagnetic radiation on the course of Helicobacter
pylori-associated peptic ulcer].
Effect of microwave electromagnetic field on skeletal muscle fibre activity.
[Effects of microwaves on the cellular immune response of Swiss mice].
[The effect of ultrahigh-frequency electromagnetic radiation on learning and memory processes].
Does microwave irradiation have other than thermal effects on glutaraldehyde crosslinking of
collagen?
The tissue content of cyclic AMP in rats after microwave irradiation in vivo.
[Effects of microwave irradiation on NMDA receptor subunits mRNA expressions in rat
hippocampus].
Plasma corticosterone in hemorrhaged Japanese quail after microwave irradiation in ovo.
[Electron microscopic analysis of the effect of modulated microwave radiation on isolated rat
olfactory mucosa].
Animal study on electromagnetic field biological potency.
[The effect of low-intensity prolonged impulse electromagnetic irradiation in the UHF range on
the testes and the appendages of the testis in rats].
Germ cell degeneration in normal and microwave-irradiated rats: potential sperm production
rates at different developmental steps in spermatogenesis.
[Experimental research on the biological action of the pulse-modulated microwave radiation
created by shipboard radar stations].
Cell-density dependent effects of low-dose ionizing radiation on E. coli cells.
[Effects of electromagnetic irradiation on glucocorticoid in serum and its receptor expression in
rat hippocampus].
[The effect of microwave irradiation on the peroxide modification of low density lipoproteins in
human blood serum].
[Stimulation of murine natural killer cells by weak electromagnetic waves in the centimeter
range].
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Use of 300-msec microwave irradiation for enzyme inactivation: a study of effects of sodium
pentobarbital on acetylcholine concentration in mouse brain regions.
[Studies on the screening high yield acid protease producing strain L336 by combining
microwave irradiation with chemical inducing].
[Effect of super-high electromagnetic radiation and hormones on the osmotic resistance of mouse
erythrocytes].
Effects of 2.45 GHz microwave exposures on the peroxidation status in Wistar rats.
[Effect of electromagnetic waves in the centimeter range on the production of tumor necrosis
factor and interleukin-3 in immunized mice].
Radiation-induced lung toxicity in mice irradiated in a strong magnetic field.
Nonthermal effect of microwave irradiation in nonaqueous enzymatic esterification.
[Role of the thyroid gland in developing the genetic effects of microwaves of nonthermal
intensity].
Regional levels of cyclic AMP in rat brain: pitfalls of microwave inactivation.
[Effect of electromagnetic radiation on discharge activity of neurons in the hippocampus CA1 in
rats].
Effects of repeated microwave irradiations to the albino rabbit eye.
Inactivation of kallikrein and kininases and stabilization of whole rat brain kinin levels following
focused microwave irradiation.
Fragmentation of genomic DNA using microwave irradiation.
[Modifying effect of low-intensive electromagnetic radiation on the irradiated cells].
Intraoperative peritoneal washing cytology with the rapid immunoperoxidase method using
microwave irradiation.
[Effect of SHF-radiation on spontaneous impulse activity of cerebral cortex slices in vitro].
[The effect of millimeter-band radiation of nonthermal intensity on sensitivity of Staphylococcus
to various antibiotics].
[Infrared spectra of erythrocyte shadows in the region of the amide I and amide II bands
following microwave irradiation].
[The immunological mechanism of the modulation of IgE antibody formation during microwave
irradiation of the thymus].
Microwave irradiation influences on the state of human cell nuclei.
Acetylcholine: oscillation of levels in mouse brain following electroshock.
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[The inhibiting action of superhigh-frequency millimeter waves on adenovirus (author's transl)].
Slow potentials and spike unit activity of the cerebral cortex of rabbits exposed to microwaves.
[The immunostimulating properties of erythrocytes subjected to the action of ultraviolet
irradiation and electromagnetic radiation during vibration exposure].
GSM 900 MHz microwave radiation affects embryo development of Japanese quails.
[Immunomodulating effect of electromagnetic waves on production of tumor necrosis factor in
mice with various rates of neoplasm growth].
[Clinical significance of tonsillar provocation test in diagnosis of tonsillar focal infection--by
indirect irradiation of ultra-micro waves].
[The immunomodulating action of microwaves in the induction of an immune response to Vi
antigen].
[A comparison of conditioned avoidance reflex in rabbits formed under the influence of
permanent magnetic fields, ultra-high-frequency irradiation, light and sound].
Physiological measurements during radio-frequency irradiation.
Microwave-induced formation of oligomeric amyloid aggregates.
[Biological oxidation in cells exposed to microwaves in the millimeter range].
Brain amino acid concentrations in rats killed by decapitation and microwave irradiation.
[The effect of electromagnetic waves of very high frequency of molecular spectra of radiation
and absorption of nitric oxide on the functional activity of platelets].
Exposure to low-intensive superhigh frequency electromagnetic field as a factor of
carcinogenesis in experimental animals.
[Effects of centimeter waves on the immune system of mice in endotoxic shock].
Effect of continuous irradiation with terahertz electromagnetic waves of the NO frequency range
on behavioral reactions of male albino rats under stress conditions.
[The effect of electromagnetic radiation with extremely high frequency and low intensity on
cytotoxic activity of human natural killer cells].
Exocytosis sensitivity to growth hormone-releasing hormone in subsets of GH cells in rats under
different corticosterone conditions. Ultrastructural study using microwave irradiation for fixation
and immunocytochemistry.
[Effect of extremely high frequency electromagnetic radiation of low intensity on parameters of
humoral immunity in healthy mice].
[The electrical activity of symmetrical areas of the rat cerebral cortex during the use of a low-
intensity UHF field].
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[Effect of local SHF-irradiation of the rat foot on impulse activity in the tibial nerve].
[Effect of radiofrequency of electromagnetic radiation on yeast sensitivity to fungicide
antibiotics].
Effects of acute and chronic ethanol administration on thromboxane and prostacyclin levels and
release in rat brain cortex.
[Effect of microwave on the dentin of root canal wall].
[Constant direct action of the magnetic field on the brain fabric].
[Functional activity and metabolism of blood neutrophils exposed to low-intensity microwaves].
[Effect of weak electromagnetic radiation on regeneration of the pharynx in Dugesia tigrina
planaria].
[Effects of hypogeomagnetic fields on the structural-functional activity of rat cerebral cortex].
[Effect of microwaves of nonthermal intensity on the number of aberrant hepatocytes in rats].
[Stimulation of the defenses of trypanosomic mice by a combination of magnetic field and
electromagnetic wave radiation].
Visual abnormalities associated with high-energy microwave exposure.
[Changes in the proteinase-inhibitor system of rats with hyperlipoproteinemia during
transcerebral exposures to a 100-Hz-frequency pulse current and to an ultrahigh-frequency field].
Hypothalamic cholinergic and noradrenergic neurons in hyperglycemia induced by 2-
deoxyglucose.
[A mathematical modelling study of the respiratory system during exposure to a low-intensity
UHF field].
[Heterogeneity of neurocytes of different brain regions to repeated superhigh-frequency
irradiation].
Effects of electro-acupuncture and physical exercise on regional concentrations of neuropeptides
in rat brain.
Continuous microwave enhances the healing process of septic and aseptic wounds in rabbits.
[Effect of weak electromagnetic radiation on larva development and metamorphosis of grain
beetle Tenebrio molitor].
[Effects of low-intensity EHF-radiation on peripheral sections of the nervous system].
[The influence of electromagnetic field on active avoidance reaction, biogenic amines and amino
acids in brain of rats in spite of backround of food-stuff addition seratonus].
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Visualization of in vivo metabolic flows reveals accelerated utilization of glucose and lactate in
penumbra of ischemic heart.
--Leaf Cluster 29 (94)
Theme - Adverse effects of microwave radiation, especially pulsed microwave
Titles
Physiological effects of 2.8 GHz radio-frequency radiation: a comparison of pulsed and
continuous-wave radiation.
Abnormal cardiovascular responses induced by localized high power microwave exposure.
Thermoregulatory responses of rats exposed to 9.3-GHz radiofrequency radiation.
Microwave alteration of the blood-brain barrier system of rats.
Blood-brain barrier permeation in the rat during exposure to low-power 1.7-GHz microwave
radiation.
Low-level microwave irradiations affect central cholinergic activity in the rat.
Cerebrovascular permeability to 86Rb in the rat after exposure to pulsed microwaves.
Effects of pulsed microwave radiation on the contractile rate of isolated frog hearts.
High-peak-power microwave pulses: effects on heart rate and blood pressure in unanesthetized
rats.
Microwave-induced lethal heat stress: effects of phentolamine, prazosin and metoprolol.
Low-level microwave irradiation and central cholinergic activity: a dose-response study.
Cardiorespiratory changes during microwave-induced lethal heat stress and beta-adrenergic
blockade.
Tolazoline decreases survival time during microwave-induced lethal heat stress in anesthetized
rats.
Studies on blood-brain barrier permeability after microwave-radiation.
Low-level microwave irradiation and central cholinergic systems.
Heart rate changes due to 5.6-GHz radiofrequency radiation: relation to average power density.
Effects of 2.8-GHz microwaves on restrained and ketamine-anesthetized rats.
Effect of 2450 MHz microwave energy on the blood-brain barrier to hydrophilic molecules. C.
Effect on the permeability to [14C]sucrose.
Increased sensitivity of the non-human primate eye to microwave radiation following ophthalmic
drug pretreatment.
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Circulating antibody response of mice exposed to 9-GHz pulsed microwave radiation.
Immediate post-exposure effects of high-peak-power microwave pulses on operant behavior of
Wistar rats.
Permeability of the blood-brain barrier to mannitol in the rat following 2450 MHz microwave
irradiation.
Effects of esmolol on 35 GHz microwave-induced lethal heat stress.
Studies on microwave and blood-brain barrier interaction.
Effects of 2.45-GHz microwaves on primate corneal endothelium.
Corticotropin-releasing factor antagonist blocks microwave-induced decreases in high-affinity
choline uptake in the rat brain.
Cardiovascular and thermal effects of microwave irradiation at 1 and/or 10 GHz in anesthetized
rats.
Effect of 2450 MHz microwave energy on the blood-brain barrier to hydrophilic molecules. B.
Effect on the permeability to HRP.
Microwave influence on the isolated heart function: II. Combined effect of radiation and some
drugs.
Acute low-level microwave exposure and central cholinergic activity: studies on irradiation
parameters.
Microwave irradiation of rats at 2.45 GHz activates pinocytotic-like uptake of tracer by capillary
endothelial cells of cerebral cortex.
Microwave influence on the isolated heart function: I. Effect of modulation.
Permeability of the blood-brain barrier induced by 915 MHz electromagnetic radiation,
continuous wave and modulated at 8, 16, 50, and 200 Hz.
Rhesus monkey behavior during exposure to high-peak-power 5.62-GHz microwave pulses.
The insensitivity of frog heart rate to pulse modulated microwave energy.
Effects of low-level microwave irradiation on hippocampal and frontal cortical choline uptake
are classically conditionable.
[Comparative estimation of the effects of continuous and intermittent cyclical microwave
radiation on the behavior of rats in the extraordinary situation].
In vitro studies of microwave-induced cataract: reciprocity between exposure duration and dose
rate for pulsed microwaves.
Effect of 2450 MHz microwave energy on the blood-brain barrier to hydrophilic molecules. A.
Effect on the permeability to sodium fluorescein.
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Absorption of microwave radiation by the anesthetized rat: electromagnetic and thermal hotspots
in body and tail.
Opioid receptor subtypes that mediate a microwave-induced decrease in central cholinergic
activity in the rat.
Cardiovascular changes in unanesthetized and ketamine-anesthetized Sprague-Dawley rats
exposed to 2.8-GHz radiofrequency radiation.
Auditory unit responses to single-pulse and twin-pulse microwave stimuli.
Naltrexone pretreatment blocks microwave-induced changes in central cholinergic receptors.
Microwave effects on isolated chick embryo hearts.
Comparative effects of extremely high power microwave pulses and a brief CW irradiation on
pacemaker function in isolated frog heart slices.
Temporal bisection in rats: the effects of high-peak-power pulsed microwave irradiation.
[Effects of 2375 MHz pulse-modulated microwave radiation on ATPase activity of the rat
muscle actomyosin].
Influence of microwaves on the beating rate of isolated rat hearts.
Microwave radiation and heart-beat rate of rabbits.
Effects of continuous-wave, pulsed, and sinusoidal-amplitude-modulated microwaves on brain
energy metabolism.
In vitro studies of microwave-induced cataract. II. Comparison of damage observed for
continuous wave and pulsed microwaves.
Antibody responses of mice exposed to low-power microwaves under combined, pulse-and-
amplitude modulation.
[Proposed exposure levels of pulse-modulated electromagnetic fields].
Characteristics of microwave evoked body movements in mice.
The effect of pulsed microwaves on passive electrical properties and interspike intervals of snail
neurons.
[Effect of low-intensity pulse-modulated microwave on human blood aspartate aminotransferase
activity].
Effect of global system for mobile communication (GSM) microwave exposure on blood-brain
barrier permeability in rat.
Slow and rapid responses to CW and pulsed microwave radiation by individual Aplysia
pacemakers.
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Effects of continuous and pulsed 2450-MHz radiation on spontaneous lymphoblastoid
transformation of human lymphocytes in vitro.
Effects of high power microwave pulses on synaptic transmission and long term potentiation in
hippocampus.
Bursting responses of Lymnea neurons to microwave radiation.
Influence of acute microwave radiation on cardiac function in normal and myocardial ischemic
cats.
NF-kappaB DNA-binding activity after high peak power pulsed microwave (8.2 GHz) exposure
of normal human monocytes.
Measurement of blood-brain barrier permeation in rats during exposure to 2450-MHz
microwaves.
Single vs. repeated microwave exposure: effects on benzodiazepine receptors in the brain of the
rat.
In vitro study of microwave effects on calcium efflux in rat brain tissue.
Thermoregulatory responses of rats exposed to 9.3-GHz microwaves: a comparison of E and H
orientation.
Modification of acoustic startle by microwave pulses in the rat: a preliminary report.
Effects of high peak power microwaves on the retina of the rhesus monkey.
Alteration of circulating antibody response of mice exposed to 9-GHz pulsed microwaves.
Effect of 9.6-GHz pulsed microwaves on the orb web spinning ability of the cross spider
(Araneus diadematus).
Environmental-health aspects of pulse-modulated microwaves.
[The effect of pulsed cyclical microware radiation on the conditioned behavior of rats].
[Effects of electromagnetic radiation of various modes on heart activity (in experiments)].
Modification of acoustic and tactile startle by single microwave pulses.
Effect of short electromagnetic pulses on brain acetylcholine content and spontaneous motor
activity of mice.
Microwave auditory effect- a comparison of some possible transduction mechanisms.
Increased susceptibility to radiofrequency radiation due to pharmacological agents.
Microwave irradiation affects radial-arm maze performance in the rat.
[Changes in serum alkaline phosphatase activity during in vitro exposure to amplitude-
modulated electromagnetic field of ultrahigh frequency (2375 MHz) in guinea pigs].
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Reversible microwave effects on the blood-brain barrier.
Effect of microwave radiation on the beating rate of isolated frog hearts.
Amino acid concentrations in hypothalamic and caudate nuclei during microwave-induced
thermal stress: analysis by microdialysis.
Character of the effect of microwave on conduction velocity of frog ventricular muscle.
Inter-beat intervals of cardiac-cell aggregates during exposure to 2.45 GHz CW, pulsed, and
square-wave-modulated microwaves.
[The efficiency and direction of thymus changes after whole-body exposure of mice to the weak
electromagnetic field are determined by the initial status of the thymus].
Alterations in alpha-adrenergic and muscarinic cholinergic receptor binding in rat brain
following nonionizing radiation.
[Dependence of microwave effect on the secondary structure of DNA on molecular weight of
polynucleotide].
Effects of weak amplitude-modulated microwave fields on calcium efflux from awake cat
cerebral cortex.
In vivo exposure of rats to GSM-modulated microwaves: flow cytometry analysis of lymphocyte
subpopulations and of mitogen stimulation.
[Microwave method of determining cerebral blood flow].
[Effects of unmodulated electromagnetic radiation of decimetric diapason on the morphogenesis
of Drosophila].
Pulsed magnetic field induced "analgesia" in the land snail, Cepaea nemoralis, and the effects of
mu, delta, and kappa opioid receptor agonists/antagonists.
--Leaf Cluster 31 (130)
Theme - Adverse effects of microwave exposures on rats, especially at WiFi frequencies
Titles
Behavioral effects of chronic exposure to 0.5 mW/cm2 of 2,450-MHz microwaves.
Effects of 2.45 GHz CW microwave radiation on embryofetal development in mice.
Decreased body weight in fetal rats after irradiation with 2450-MHz (CW) microwaves.
Observations of rat fetuses after irradiation with 2450-MHz (CW) microwaves.
Teratogenic, biochemical, and histological studies with mice prenatally exposed to 2.45-GHz
microwave radiation.
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Intermittent exposure of rats to 2450 MHz microwaves at 2.5 mW cm2: behavioral and
physiological effects.
Behavioral and physiological effects of chronic 2,450-MHz microwave irradiation of the rat at
0.5 mW/cm2.
Effect of nonionizing radiation on the Purkinje cells of the rat cerebellum.
Physiological and behavioral effects of prolonged exposure to 915 MHz microwaves.
Physiological and behavioral effects of chronic exposure to 2450-MHz microwaves.
Behavioral thermoregulation in the squirrel monkey: adaptation processes during prolonged
microwave exposure.
Microwave radiation (2450 MHz) alters the endotoxin-induced hypothermic response of rats.
Cardiovascular, hematologic, and biochemical effects of acute ventral exposure of conscious rats
to 2450-MHz (CW) microwave radiation.
Tests of mutagenesis and reproduction in male rats exposed to 2,450-MHz (CW) microwaves.
Observations of Syrian hamster fetuses after exposure to 2450-MHz microwaves.
Nonthermal effects of mobile-phone frequency microwaves on uteroplacental functions in
pregnant rats.
Serum-thyroxine levels in microwave-exposed rats.
Blood-forming system in rats after whole-body microwave exposure; reference to the
lymphocytes.
The in vivo effects of 2.45 GHz microwave radiation of rabbit serum components and sleeping
times.
Hematologic and immunologic effects of pulsed microwaves in mice.
Microwave-induced increase of water and conductivity in submaxillary salivary gland of rats.
Effects of whole body microwave exposure on the rat brain contents of biogenic amines.
Effects of microwave exposure in utero on embryonal, fetal and postnatal development of mice.
Effect of continuous-wave and amplitude-modulated 2.45 GHz microwave radiation on the liver
and brain aminoacyl-transfer RNA synthetases of in utero exposed mice.
Influence of 2.45-GHz CW microwave radiation on spontaneously beating rat atria.
Alteration of life span of mice chronically exposed to 2.45 GHz CW microwaves.
Studies on the hematologic effects of long-term, low-dose microwave exposure.
[Development of murine embryos and fetuses after irradiation with 2450 MHz microwaves].
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Thermoregulatory adjustments in squirrel monkeys exposed to microwaves at high power
densities.
[Effects of microwave radiation on lipid peroxidation and the content of neurotransmitters in
mice].
An evaluation of the teratogenic potential of protracted exposure of pregnant rats to 2450-MHz
microwave radiation: I. Morphologic analysis at term.
[Effects of microwave radiation on conditioned behavior of rats].
Increased serum enzyme activity in microwave-exposed rats.
Long-term, low-level microwave irradiation of rats.
Microwaves modify thermoregulatory behavior in squirrel monkey.
Testicular function of rats following exposure to microwave radiation.
Uteroplacental circulatory disturbance mediated by prostaglandin f2alpha in rats exposed to
microwaves. [email protected].
Effects of microwaves on three different strains of rats.
The effect of melatonin on body mass and behaviour of rats during an exposure to microwave
radiation from mobile phone.
Thermoregulatory, metabolic, and cardiovascular response of rats to microwaves.
Modification of the repeated acquisition of response sequences in rats by low-level microwave
exposure.
Preliminary investigations of the effects of low-level microwave radiation on spontaneous motor
activity in rats.
Delineating acute neuroendocrine responses in microwave-exposed rats.
Acute exposure to pulsed 2450-MHz microwaves affects water-maze performance of rats.
Quantitative changes in potassium, sodium, and calcium in the submaxillary salivary gland and
blood serum of rats exposed to 2880-MHz microwave radiation.
Effects of hypophysectomy and dexamethasone on rat adrenal response to microwaves.
Simultaneous response of brain electrical activity (EEG) and cerebral circulation (REG) to
microwave exposure in rats.
[Effects of whole-body microwave exposure on the plasma adrenocorticotropic hormone,
thyroid-stimulating hormone and thyroid hormones in rats].
An evaluation of the teratogenic potential of protracted exposure of pregnant rats to 2450-MHz
microwave radiation. II. Postnatal psychophysiologic analysis.
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Effects of 2.45-GHz microwave radiation on embryonic quail hearts.
Chronic exposure of rabbits to 0.5 and 5 mW/cm2 2450-MHz CW microwave radiation.
Effect of 2,450 MHz microwave radiation on the development of the rat brain.
In utero exposure to microwave radiation and rat brain development.
Thermoregulatory responses of the immature rat following repeated postnatal exposures to
2,450-MHz microwaves.
Studies of the teratogenic potential of exposure of rats to 6000-MHz microwave radiation. I.
Morphologic analysis at term.
Effects of acute low-level microwaves on pentobarbital-induced hypothermia depend on
exposure orientation.
Adjustments in metabolic heat production by squirrel monkeys exposed to microwaves.
Effect of 2450 MHz microwave radiation on hematopoiesis of pregnant mice.
Natural killer cell activity reduced by microwave exposure during pregnancy is mediated by
opioid systems.
Interaction of microwaves and a temporally incoherent magnetic field on spatial learning in the
rat.
Effects of exposure to microwaves on cellular immunity and placental steroids in pregnant rats.
Acute, whole-body microwave exposure and testicular function of rats.
Reproduction in male Japanese quail exposed to microwave radiation during embryogeny.
Repeated exposure to low-level extremely low frequency-modulated microwaves affects baseline
and scopolamine-modified electroencephalograms in freely moving rats.
Microwaves: effect on thermoregulatory behavior in rats.
Effects of microwaves on the adrenal cortex.
[Effects of whole-body microwave exposure on the plasma corticosterone, glucose, uric acid and
allantoin levels in rats].
Effects of microwave exposure on the hamster immune system. IV. Spleen cell IgM hemolytic
plaque formation.
Microwave irradiation and instrumental behavior in rats: unitized irradiation and behavioral
evaluation facility.
Cytogenetic effects of microwave irradiation on male germ cells of the mouse.
Effect of microwave irradiation (2.45 GHz, CW) on egg weight loss, egg hatchability, and
hatchling growth of the Coturnix quail.
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Microwave effects on energy metabolism of rat brain.
[Experimental estimation of thermogenic levels of acute microwave exposure for different
animal species].
Lethality in mice and rats exposed to 2450 MHz circularly polarized microwaves as a function of
exposure duration and environmental factors.
Heat-dissipation rate of mice after microwave irradiation.
Studies of the teratogenic potential of exposure of rats to 6000-MHz microwave radiation. II.
Postnatal psychophysiologic evaluations.
Effects of 2450 MHz microwave radiation during the gestational period on the postnatal
hematology of rats.
Effects of 2.45 GHz microwave radiation on the development of Japanese quail cerebellum.
Repeated exposure to low-level extremely low frequency-modulated microwaves affects cortex-
hypothalamus interplay in freely moving rats: EEG study.
Comparative effects of pulsed and continuous-wave 2.8-GHz microwaves on temporally defined
behavior.
[Endocrine mechanism of placental circulatory disturbances induced by microwave in pregnant
rats].
Response of Japanese quail to hemorrhagic stress after exposure to microwave radiation during
embryogeny.
Exposure of fertile chicken eggs to microwave radiation (2.45 GHz, CW) during incubation:
technique and evaluation.
B16 melanoma development in black mice exposed to low-level microwave radiation.
Complement receptor positive spleen cells in microwave (2450-MHz)-irradiated mice.
Prolonged microwave irradiation of rats: effects on concurrent operant behavior.
Effects of microwave exposure on the hamster immune system. II. Peritoneal macrophage
function.
Space efficient system for small animal, whole body microwave exposure at 1.6 GHz.
[Animal death after exposure to ultra-high frequency waves in the dependence of power flux
density and specific absorption rate].
Effects of microwave exposure on the hamster immune system. I. Natural killer cell activity.
Influence of pre- and postnatal exposure of rats to 2.45-GHz microwave radiation on
neurobehavioral function.
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Morphological changes in cerebellum of neonatal rats exposed to 2.45 GHz microwaves.
Effect of nonionizing radiation on the Purkinje cells of the uvula in squirrel monkey cerebellum.
Pulse modulated and continuous wave microwave radiation yield equivalent changes in operant
behavior of rodents.
Effects of postnatal microwave exposure on thyrotropin level in the adult male rat.
The effects of single and repeated exposure to 2.45 GHz radiofrequency fields on c-Fos protein
expression in the paraventricular nucleus of rat hypothalamus.
Miniature anechoic chamber for chronic exposure of small animals to plane-wave microwave
fields.
Microwaves induce peripheral vasodilation squirrel monkeys.
Some effects of exposure of the Japanese quail embryo to 2.45-GHz microwave radiation.
Protein kinase C activity in developing rat brain cells exposed to 2.45 GHz radiation.
Longevity and food consumption of microwave-treated (2.45 GHz CW) honeybees in the
laboratory.
Age-dependent effect of long-term microwave radiation on postnatal neurogenesis in rats:
morphological and behavioral study.
Radial arm maze performance of rats following repeated low level microwave radiation
exposure.
Microwave radiation enhances teratogenic effect of cytosine arabinoside in mice.
Effects of microwaves (900 MHz) on the cochlear receptor: exposure systems and preliminary
results.
Effects of GSM-900 microwaves on the experimental allergic encephalomyelitis (EAE) rat
model of multiple sclerosis.
Transbilayer movement of 24Na in sonicated phosphatidylcholine vesicles exposed to frequency-
modulated microwave radiation.
Antipruritic effect of millimeter waves in mice: evidence for opioid involvement.
Effects on energy absorption of orientation and size of animals exposed to 2.45-GHz microwave
radiation.
Biological studies with continuous-wave radiofrequency (28 MHz) radiation.
Flight, orientation, and homing abilities of honeybees following exposure to 2.45-GHz CW
microwaves.
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Age-related changes in the noradrenergic pattern and receptor responses of the rat cardiovascular
system after repeated microwave exposure.
Failure of rats to escape from a potentially lethal microwave field.
Humoral and cell-mediated immune function in adult Japanese Quail following exposure to 2.45-
GHz microwave radiation during embryogeny.
[Which neurophysiologic effects at low level 2.45 GHz RF exposure?].
[Effects of 2450 MHz microwave on long-term potentiation of hippocampus and lipofuscin
contents in rat brain].
The effect of microwave radiation on the primary IgM response to sheep red blood cells in mice.
[Effects of electromagnetic field of thermal intensity on the hypophysis-thyroid unit of the
neuroendocrine system].
[Action of a UHF field on GABA-ergic and acetylcholinergic systems in synaptic transmission].
Noradrenergic innervation and receptor responses of cardiovascular tissues from young and aged
rats after acute microwave exposure.
Effects of weak microwave fields amplitude modulated at ELF on EEG of symmetric brain areas
in rats.
Erythropoietic dynamic equilibrium in rats maintained after microwave irradiation.
Glucose administration attenuates spatial memory deficits induced by chronic low-power-density
microwave exposure.
Behavioral Abnormality along with NMDAR-related CREB Suppression in Rat Hippocampus
after Shortwave Exposure.
Effects of microwave exposure on the hamster immune system. III. Macrophage resistance to
vesicular stomatitis virus infection.
Retrograde amnesia: effects of handling and microwave radiation.
[Effect of high frequency electromagnetic fields on the processes of transamination in the liver
and small intestine tissues of rats].
Influence of postnatal exposition to microwaves on brain and hypothalamo-pituitary
monoamines in the adult male rat.
Electric power induction through an isolated intestinal pouch.
[Effect of microwaves on the spike activity of cerebellar Purkinje cells in the cat].
Fourth Level Cluster 79 (428)
Theme - Microwave radiation absorption at different frequencies
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--Leaf Cluster 10 (75)
Theme - Dielectric properties of tissue at different microwave frequencies
Titles
The UHF and microwave dielectric properties of normal and tumour tissues: variation in
dielectric properties with tissue water content.
Changes in the dielectric properties of rat tissue as a function of age at microwave frequencies.
Dielectric properties of muscle and liver from 500 MHz-40 GHz.
Dielectric properties of tissues; variation with age and their relevance in exposure of children to
electromagnetic fields; state of knowledge.
A large-scale study of the ultrawideband microwave dielectric properties of normal, benign and
malignant breast tissues obtained from cancer surgeries.
A quick accurate method for measuring the microwave dielectric properties of small tissue
samples.
A method for in vivo detection of abnormal subepidermal tissues based on dielectric properties.
Microwave method for determing dielectric parameters of living biological objects I.
Microwave dielectric studies on proteins, tissues, and heterogeneous suspensions.
Dielectric properties of porcine brain tissue in the transition from life to death at frequencies
from 800 to 1900 MHz.
A large-scale study of the ultrawideband microwave dielectric properties of normal breast tissue
obtained from reduction surgeries.
Dielectric property measurement of ocular tissues up to 110 GHz using 1 mm coaxial sensor.
Radio-frequency and microwave dielectric properties of insects.
Dielectric properties of Co-gamma-irradiated and microwave-heated rat tumour and skin
measured in vivo between 0.2 and 2.4 GHz.
Microwave dielectric relaxation in muscle. A second look.
Dielectric properties of animal tissues in vivo at radio and microwave frequencies: comparison
between species.
Dielectric properties of rat embryo and foetus as a function of gestation.
Dielectric properties of porcine cerebrospinal tissues at microwave frequencies: in vivo, in vitro
and systematic variation with age.
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Dielectric properties of insect tissues.
Development of anatomically realistic numerical breast phantoms with accurate dielectric
properties for modeling microwave interactions with the human breast.
Dielectric properties at microwave frequencies studied in partially filled cylindrical TE011
cavities.
Dielectric properties of human brain tissue measured less than 10 h postmortem at frequencies
from 800 to 2450 MHz.
[Dielectric properties of human sweat fluid in the microwave range].
Dielectric behavior of DNA solution at radio and microwave frequencies (at 20 degrees C).
A heterogeneous breast phantom for microwave breast imaging.
Dielectric properties of supersaturated alpha-D-glucose aqueous solutions at 2450 MHz.
Variation of the dielectric properties of tissues with age: the effect on the values of SAR in
children when exposed to walkie-talkie devices.
Microwave dielectric properties of tissue. Some comments on the rotational mobility of tissue
water.
Monitoring water content of rat lung tissue in vivo using microwave reflectometry.
Microwave dielectric properties and thermochemical characteristics of the mixtures of walnut
shell and manganese ore.
Microwave-induced thermal imaging of tissue dielectric properties.
Dielectrical model of cellular structures in radio frequency and microwave spectrum. Electrically
interacting versus noninteracting cells.
Average dielectric property analysis of complex breast tissue with microwave transmission
measurements.
Modeling of the dielectric properties of trabecular bone samples at microwave frequency.
Dielectric properties for non-invasive detection of normal, benign, and malignant breast tissues
using microwave theories.
Microwave dielectric measurements (0.8-70 GHz) on Artemia cysts at variable water content.
An evaluation of the mutagenic, carcinogenic and teratogenic potential of microwaves.
Microwave dielectric analysis of human stratum corneum in vivo.
Dielectric properties of human ovary follicular fluid at 9.2 GHz.
A macroscopic model of lungs and a material simulating their properties at radio and microwave
frequencies.
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Microwave dielectric measurements and tissue characteristics of the human brain: potential in
localizing intracranial tissues.
Theoretical evaluation of dielectric absorption of microwave energy at the scale of nucleic acids.
40 GHz RF biosensor based on microwave coplanar waveguide transmission line for cancer cells
(HepG2) dielectric characterization.
Modeling of noninvasive microwave characterization of breast tumors.
Cole-Cole parameters for the dielectric properties of porcine tissues as a function of age at
microwave frequencies.
The dielectric properties of normal and tumour mouse tissue between 50 MHz and 10 GHz.
Dielectric Properties for Differentiating Normal and Malignant Thyroid Tissues.
The dielectric properties of the cerebellum, cerebrum and brain stem of mouse brain at
radiowave and microwave frequencies.
Effect of ultraviolet light on the dielectric behavior of bone at microwave frequencies.
Microwave dielectric measurements of erythrocyte suspensions.
Electrical properties of lens material at microwave frequencies.
A semi-automatic method for developing an anthropomorphic numerical model of dielectric
anatomy by MRI.
Microwave absorption in aqueous solutions of DNA.
The measured electrical properties of normal and malignant human tissues from 50 to 900 MHz.
Numerical assessment of the reduction of specific absorption rate by adding high dielectric
materials for fetus MRI at 3 T.
Non-invasive and continuous monitoring of the sol-gel phase transition of supramolecular gels
using a fast (open-ended coaxial) microwave sensor.
Carbon-coated CoFe-CoFe2O4 composite particles with high and dual-band electromagnetic
wave absorbing properties.
A microwave radiometric method for the study of the semiconductor properties of living tissue:
its potential application to tumour location.
Theoretical evaluation of the distributed power dissipation in biological cells exposed to electric
fields.
[Mechanism of microwave radiation absorption by biological membranes].
A generalized model for the interaction of microwave radiation with bound water in biological
material.
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Understanding physical mechanism of low-level microwave radiation effect.
Analytical approximations in multiple scattering of electromagnetic waves by aligned dielectric
spheroids.
A novel discrete particle swarm optimization algorithm for estimating dielectric constants of
tissue.
Multi-physics modeling to study the influence of tissue compression and cold stress on
enhancing breast tumor detection using microwave radiometry.
Microwave facilities for welding thermoplastic composites and preliminary results.
Biological effects of low-level environmental agents.
Multifunctional composites: optimizing microstructures for simultaneous transport of heat and
electricity.
The properties of bird feathers as converse piezoelectric transducers and as receptors of
microwave radiation. I. Bird feathers as converse piezoelectric transducers.
Brain banks and non nervous tissues.
Characterization of three iron ferredoxins by microwave power saturation.
[Possible mechanisms of aftereffects of GSM electromagnetic radiation on air-dry seeds].
Microwave grafted, composite and coprocessed materials: drug delivery applications.
Production of a Novel Mineral-based Sun Lotion for Protecting the Skin from Biohazards of
Electromagnetic Radiation in the UV Region.
Microwave drying remediation of petroleum-contaminated drill cuttings.
--Leaf Cluster 23 (88)
Theme - Specific absorption rate in human body models
Titles
Body effects on SAR distributions for microwave exposures in a realistic model of the human
head.
Analysis of SAR distribution in human head of antenna used in wireless power transform based
on magnetic resonance.
FDTD chiral brain tissue model for specific absorption rate determination under radiation from
mobile phones at 900 and 1800 MHz.
FDTD calculations of specific energy absorption rate in a seated voxel model of the human body
from 10 MHz to 3 GHz.
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Development of a rat head exposure system for simulating human exposure to RF fields from
handheld wireless telephones.
Radio frequency electromagnetic exposure: tutorial review on experimental dosimetry.
SAR calculations in an anatomically realistic model of the head for mobile communication
transceivers at 900 MHz and 1.8 GHz.
Specific absorption rate (SAR) in models of the human head exposed to hand-held UHF portable
radios.
Initial analysis of SAR from a cell phone inside a vehicle by numerical computation.
Dosimetry associated with exposure to non-ionizing radiation: very low frequency to
microwaves.
SAR versus S(inc): What is the appropriate RF exposure metric in the range 1-10 GHz? Part I:
Using planar body models.
Whole-body and local dosimetry in rats exposed to 2.45-GHz microwave radiation.
Specific absorption rate in rats exposed to 2,450-MHz microwaves under seven exposure
conditions.
Electromagnetic fields: human safety issues.
Microwave radiation absorption in the rat: frequency-dependent SAR distribution in body and
tail.
Observing-responses of rats exposed to 1.28- and 5.62-GHz microwaves.
Multibody effects on microwave power absorption by multilayered cylindrical models of man.
Numerical compliance testing of human exposure to electromagnetic radiation from smart-
watches.
A simulation for effects of RF electromagnetic radiation from a mobile handset on eyes model
using the finite-difference time-domain method.
Outdoor measurement of SAR in a full-sized human model exposed to 29.9 MHz in the near
field.
Effects of frequency, irradiation geometry and polarisation on computation of SAR in human
brain.
SAR in a child voxel phantom from exposure to wireless computer networks (Wi-Fi).
Preliminary studies: far-field microwave dosimetric measurements of a full-scale model of man.
Numerical simulation of pressure waves in the cochlea induced by a microwave pulse.
The effects of RF absorbers on exposure levels at 100 MHz.
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Comparison of numerical and experimental methods for determination of SAR and radiation
patterns of handheld wireless telephones.
Dominant factors influencing whole-body average SAR due to far-field exposure in whole-body
resonance frequency and GHz regions.
Numerical evaluation of human exposure to WiMax patch antenna in tablet or laptop.
Far-field microwave dosimetry in a rhesus monkey model.
A method for safety testing of radiofrequency/microwave-emitting devices using MRI.
Local exposure system for rats head using a figure-8 loop antenna in 1500-MHz band.
Analytic SAR computation in a multilayer elliptic cylinder for bioelectromagnetic applications.
Computation of high-resolution SAR distributions in a head due to a radiating dipole antenna
representing a hand-held mobile phone.
Thermal mapping on male genital and skin tissues of laptop thermal sources and electromagnetic
interaction.
Acute dosimetry and estimation of threshold-inducing behavioral signs of thermal stress in
rabbits at 2.45-GHz microwave exposure.
Comparison of Thermal Response for RF Exposure in Human and Rat Models.
Systems for exposing mice to 2,450-MHz electromagnetic fields.
A suggested limit for population exposure to radiofrequency radiation.
SAR distribution in a bio-medium in close proximity with dual segment cylindrical dielectric
resonator antenna.
A comparative study of the PIFA and printed monopole antenna EM absorption.
Compact shielded exposure system for the simultaneous long-term UHF irradiation of forty
small mammals. II. Dosimetry.
Thermal effects of radiation from cellular telephones.
SAR in rats exposed in 2,450-MHz circularly polarized waveguides.
A formula for human average whole-body SARwb under diffuse fields exposure in the GHz
region.
Scaling the physiological effects of exposure to radiofrequency electromagnetic radiation:
consequences of body size.
Radiofrequency dosimetry in subjects implanted with metallic straight wires: a numerical study.
Further studies of human whole-body radiofrequency absorption rates.
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Estimation of whole-body SAR from electromagnetic fields using personal exposure meters.
Numerical modelling of thermal effects in rats due to high-field magnetic resonance imaging
(0.5-1 GHZ).
Dosimetry for a study of effects of 2.45-GHz microwaves on mouse testis.
SAR exposure from UHF RFID reader in adult, child, pregnant woman, and fetus anatomical
models.
Head and neck resonance in a rhesus monkey--a comparison with results from a human model.
On the averaging area for incident power density for human exposure limits at frequencies over 6
GHz.
Dosimetric study on eye's exposure to wide band radio frequency electromagnetic fields:
variability by the ocular axial length.
Absorption of microwave energy by muscle models and by birds of differing mass and geometry.
Influence of electromagnetic polarization on the whole-body averaged SAR in children for
plane-wave exposures.
Thermal effects of MR imaging: worst-case studies on sheep.
Comparison of dose dependences for bioeffects of continuous-wave and high-peak power
microwave emissions using gel-suspended cell cultures.
An attempt at quantitative specification of SAR distribution homogeneity.
A new method of SAR determination in animals exposed to microwave/radiofrequency radiation
(MW/RFR).
Metabolic and vasomotor responses of rhesus monkeys exposed to 225-MHz radiofrequency
energy.
Exposure assessment of one-year-old child to 3G tablet in uplink mode and to 3G femtocell in
downlink mode using polynomial chaos decomposition.
Harmful effects of 41 and 202 MHz radiations on some body parts and tissues.
Whole-body new-born and young rats' exposure assessment in a reverberating chamber operating
at 2.4 GHz.
A 3-D hp finite/infinite element method to calculate power deposition in the human head.
Ocular effects of radiofrequency energy.
The development of biomedical approaches and concepts in radiofrequency radiation protection.
Absorbed energy distribution from radiofrequency electromagnetic radiation in a mammalian
cell model: effect of membrane-bound water.
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Statistical analysis of whole-body absorption depending on anatomical human characteristics at a
frequency of 2.1 GHz.
Computational human model VHP-FEMALE derived from datasets of the national library of
medicine.
Modeling the detectability of vesicoureteral reflux using microwave radiometry.
Radio-wave exposure of the human head: analytical study based on a versatile eccentric spheres
model including a brain core and a pair of eyeballs.
Millimeter-wave absorption by cutaneous blood vessels: a computational study.
Simple method to measure power density entering a plane biological sample at millimeter
wavelengths.
Exposure of Insects to Radio-Frequency Electromagnetic Fields from 2 to 120 GHz.
[Use of dose parameters of UHF irradiation in the interpretation of lethal effects in laboratory
animals].
Noninvasive measurement of current in the human body for electromagnetic dosimetry.
Exposure to non-ionizing radiation provokes changes in rat thyroid morphology and expression
of HSP-90.
Induced EM fields inside human bodies irradiated by EM waves of up to 500 MHz.
A dual vial waveguide exposure facility for examining microwave effects in vitro.
[Estimation of the restricted area related to the limitation of exposure of the general public to
electromagnetic fields in the vicinity of microwave relay antenna systems].
FDTD simulation of electromagnetic wave scattering from retina cells.
Effect of metal-framed spectacles on microwave radiation hazards to the eye of humans.
Effect of insertion depth on helical antenna performance in a muscle-equivalent phantom.
A survey of the urban radiofrequency (RF) environment.
[The evaluation of the consequences of electromagnetic irradiation of hands in operators of high-
frequency welding devices].
Dosimetry considerations in far field microwave exposure of mammalian cells.
[Changes of neurocytes in CNS under general exposure to UHF field with local protection
applied].
--Leaf Cluster 21 (63)
Theme - Adverse effects of millimeter-wave exposures on biological systems
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Titles
[Effects of millimeter wave irradiation with different frequency and power density on their
offsprings in mice].
[Relationship between millimeter wave irradiation in pregnant mice and c-Fos protein expression
in hippocampus and learning and memory functions in their offsprings].
Gene expression changes in the skin of rats induced by prolonged 35 GHz millimeter-wave
exposure.
[Effect of low intensity of electromagnetic radiation in the centimeter and millimeter range on
proliferative and cytotoxic activity of murine spleen lymphocytes].
[Effects of millimeter wave on gene expression in human keratinocytes].
Current state and implications of research on biological effects of millimeter waves: a review of
the literature.
Acute ocular injuries caused by 60-Ghz millimeter-wave exposure.
A non-thermal effect of millimeter wave radiation on the puffing of giant chromosomes.
Effects of millimeter waves on ionic currents of Lymnaea neurons.
Evaluation of the potential in vitro antiproliferative effects of millimeter waves at some
therapeutic frequencies on RPMI 7932 human skin malignant melanoma cells.
[Acoustic detection of absorption of millimeter-band electromagnetic waves in biological
objects].
Reception of low-intensity millimeter-wave electromagnetic radiation by the electroreceptors in
skates.
Effect of cyclophosphamide and 61.22 GHz millimeter waves on T-cell, B-cell, and macrophage
functions.
Frequency and irradiation time-dependant antiproliferative effect of low-power millimeter waves
on RPMI 7932 human melanoma cell line.
Hypothalamic effects of millimeter wave irradiation depend on location of exposed acupuncture
zones in unanesthetized rabbits.
Some basic properties of biological tissues for potential biomedical applications of millimeter
waves.
[The electrical activity of the hypothalamus in exposure to millimeter-wave radiation at
biologically active points].
Electromagnetic millimeter wave induced hypoalgesia: frequency dependence and involvement
of endogenous opioids.
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Comparison of blood pressure and thermal responses in rats exposed to millimeter wave energy
or environmental heat.
Modulation of neuronal activity and plasma membrane properties with low-power millimeter
waves in organotypic cortical slices.
Thermal modeling of millimeter wave damage to the primate cornea at 35 GHz and 94 GHz.
Thermal response of tissues to millimeter waves: implications for setting exposure guidelines.
[Activity of natural killer cells of the spleen of mice exposed to low-intensity of extremely high
frequency electromagnetic radiation].
Study of narrow band millimeter-wave potential interactions with endoplasmic reticulum stress
sensor genes.
Effect of millimeter waves on natural killer cell activation.
Transmission electron microscopy study of the effects produced by wide-band low-power
millimeter waves on MCF-7 human breast cancer cells in culture.
Morphological changes in skin nerves caused by electromagnetic radiation of the millimeter
range.
The use of millimeter wavelength electromagnetic waves in cardiology.
Millimeter wave exposure reverses TPA suppression of gap junction intercellular communication
in HaCaT human keratinocytes.
Millimeter wave induced reversible externalization of phosphatidylserine molecules in cells
exposed in vitro.
[The simulation of the cooperative effect of development in a culture of early mouse embryos
after irradiation with electromagnetic waves in the millimeter range].
Effects of Millimeter-Wave Electromagnetic Radiation on the Experimental Model of Migraine.
Effect of 99 GHz continuous millimeter wave electro-magnetic radiation on E. coli viability and
metabolic activity.
Effect of low-intensity millimeter wave electromagnetic radiation on regeneration of the sciatic
nerve in rats.
Millimeter waves thermally alter the firing rate of the Lymnaea pacemaker neuron.
Numerical model of heat transfer in the rabbit eye exposed to 60-GHz millimeter wave radiation.
[Power density analysis on millimeter waves irradiated into cell monolayers in culture dishes].
Effect of millimeter waves on cyclophosphamide induced suppression of the immune system.
Immunomodulating action of low intensity millimeter waves on primed neutrophils.
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Suppression of pain sensation caused by millimeter waves: a double-blinded, cross-over,
prospective human volunteer study.
[The effect of continuous millimeter low-intensity radiation on the Na+ ion transport in the frog
skin].
[Effects of millimeter wave on gap junctional intercellular communication in human
keratinocytes].
[The effect of electromagnetic radiation in the millimeter-wave range on the immune status of
peptic ulcer patients].
Effect of millimeter waves on cyclophosphamide induced suppression of T cell functions.
Millimeter-wave effects on electric activity of crayfish stretch receptors.
Reflection and penetration depth of millimeter waves in murine skin.
Search for frequency-specific effects of millimeter-wave radiation on isolated nerve function.
Millimeter wave-induced modulation of calcium dynamics in an engineered skin co-culture
model: role of secreted ATP on calcium spiking.
Millimeter wave absorption in the nonhuman primate eye at 35 GHz and 94 GHz.
[Effect of extremely high-frequency electromagnetic radiation on the function of skin sensory
endings].
Induced movements of giant vesicles by millimeter wave radiation.
Sustained 35-GHz radiofrequency irradiation induces circulatory failure.
[The effects of electromagnetic radiation of extremely high frequency and low intensity on the
growth rate of bacteria Escherichia coli and the role of medium pH].
[Effect of coherent extremely high-frequency and low-intensity electromagnetic radiation on the
activity of membrane systems in Escherichia coli].
Effect of millimeter waves on cyclophosphamide induced NF-kappaB.
[Resonance effect of coherent millimeter-band electromagnetic waves on living organisms].
Large Metasurface Aperture for Millimeter Wave Computational Imaging at the Human-Scale.
[The effect of millimeter-range electromagnetic radiation on the evoked potentials from the
vestibular cortical area of the cerebral hemispheres (an experimental study)].
Long-lasting (fatiguing) activity of isolated muscle fibres influenced by microwave
electromagnetic field.
The mechanisms of athermal microwave biological effects.
[Experimental study on possibility of corneal injury by electromagnetic wave].
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Multi-center feasibility study of microwave radiometry thermometry for non-invasive
differential diagnosis of arterial disease in diabetic patients with suspected critical limb ischemia.
Tagging frogs with passive integrated transponders causes disruption of the cutaneous bacterial
community and proliferation of opportunistic fungi.
--Leaf Cluster 44 (95)
Theme
–
Adverse effects of microwave resonances in biological systems
Titles
Thermal Response of Human Skin to Microwave Energy: A Critical Review.
Tissue models for RF exposure evaluation at frequencies above 6 GHz.
Thermal models for microwave hazards and their role in standards development.
A thermal model for human thresholds of microwave-evoked warmth sensations.
Modeling thermal responses in human subjects following extended exposure to radiofrequency
energy.
Physiological interaction processes and radio-frequency energy absorption.
Human exposure at two radio frequencies (450 and 2450 MHz): similarities and differences in
physiological response.
Vibrational resonances in biological systems at microwave frequencies.
Thermoregulatory physiologic responses in the human body exposed to microwave radiation.
[Dosimetric aspects in studying the biological action of nonionizing electromagnetic radiation].
High-resolution simulations of the thermophysiological effects of human exposure to 100 MHz
RF energy.
Thermal Modeling for the Next Generation of Radiofrequency Exposure Limits: Commentary.
Microwave-induced pressure waves in a model of muscle tissue.
Radiofrequency energy on cortical bone and soft tissue: a pilot study.
[Role of polarization and resonance in assessing the biological effects of electromagnetic
radiation].
Microwave challenges to the thermoregulatory system.
Physiologic regulation in electromagnetic fields.
Thermal Response of In Vivo Human Skin to Fractional Radiofrequency Microneedle Device.
Impact of monopolar radiofrequency energy on subchondral bone viability.
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A comparative study of human sensory thresholds: 2450-MHz microwaves vs far-infrared
radiation.
Energy deposition processes in biological tissue: nonthermal biohazards seem unlikely in the
ultra-high frequency range.
Generalized model of the microwave auditory effect.
Thermophysiological responses of human volunteers during controlled whole-body radio
frequency exposure at 450 MHz.
Mechanical and biochemical effect of monopolar radiofrequency energy on human articular
cartilage: an in vitro study.
The influence of radiofrequency/microwave energy absorption on physiological regulation.
Considerations for human exposure standards for fast-rise-time high-peak-power electromagnetic
pulses.
[Mechanisms of biophysical effects of microwaves].
Effects of electromagnetic radiation on the Q of quartz resonators.
Energy issues in microwave food processing: A review of developments and the enabling
potentials of solid-state power delivery.
Biophysical limits on athermal effects of RF and microwave radiation.
Auditory response to pulsed radiofrequency energy.
Thresholds for lenticular damage in the rabbit eye due to single exposure to CW microwave
radiation: an analysis of the experimental information at a frequency of 2.45 GHz.
A Closer Look at the Thresholds of Thermal Damage: Workshop Report by an ICNIRP Task
Group.
Theory of the anomalous resonant absorption of DNA at microwave frequencies.
Intrinsic and roughness-induced absorption of electromagnetic radiation incident on optical
surfaces.
Ultrawide-band electromagnetic pulses induced hypotension in rats.
Ultrawide-band electromagnetic pulses induced hypotension in rats.
2D plasmon excitation and nonthermal effects of microwaves on biological membranes.
Thresholds of microwave-evoked warmth sensations in human skin.
The effect of radiofrequency energy on the ultrastructure of joint capsular collagen.
[Resonance interactions of surface charged lipid vesicles with the microwave electromagnetic
field].
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Synchronization in a mechanical resonator array coupled quadratically to a common
electromagnetic field mode.
Ovicidal levels of 2.45 GHz electromagnetic energy for the southern corn rootworm.
On the possibility of nonthermal biological effects of pulsed electromagnetic radiation.
Fine structural alterations in radiofrequency energy-induced lesions in dog hearts: possible basis
for reduced arrhythmic complications.
Microwave and RF hazard standard considerations.
A model of the electric field of the brain at EEG and microwave frequencies.
[The peculiarities of the microwave in the frequency range of 51-52 GHz spectrum effects on E.
coli cells].
[Electromagnetic radiation in the radiofrequency range: radiation safety].
Ultrashort microwave signals: a didactic discussion.
A cooperative model for Ca(++) efflux windowing from cell membranes exposed to
electromagnetic radiation.
Electromagnetic-field exposure and cancer.
Monte Carlo simulations of electromagnetic wave scattering from a random rough surface with
three-dimensional penetrable buried object: mine detection application using the steepest-descent
fast multipole method.
Microwave absorption by magnetite: a possible mechanism for coupling nonthermal levels of
radiation to biological systems.
Nonlinear changes in brain electrical activity due to cell phone radiation.
Thermoregulatory responses of febrile monkeys during microwave exposure.
[Experiment with the local effect of superhigh-frequency electromagnetic energy on biologically
active points].
Monte Carlo simulations for scattering of electromagnetic waves from perfectly conductive
random rough surfaces.
[Electromagnetic radiofrequency radiation (microwaves): principles and criteria of
standardization, threshold dose levels].
Development of a hybrid microwave-optical tissue oxygenation probe to measure thermal
response in the deep tissue.
[Dependence of anti-inflammatory effects of high peak-power pulsed electromagnetic radiation
of extremely high frequency on exposure parameters].
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Electrical discontinuity of tissue substitute models at 27.12 MHz.
Analysis of strain-induced EPR-line shapes and anisotropic spin-lattice relaxation in a [2Fe-2S]
ferredoxin.
The human skin as a sub-THz receiver - Does 5G pose a danger to it or not?
Effects of microwave radiation on living tissues.
Monitoring variations of biological impedances using microwave Doppler radar.
Scaling Relationship of In Vivo Muscle Contraction Strength of Rabbits Exposed to High-
Frequency Nanosecond Pulse Bursts.
Biophysical injury mechanisms in electrical shock trauma.
Dynamic nuclear polarisation of biological matter.
Microwave imaging using the finite-element method and a sensitivity analysis approach.
[An evaluation of absorbed doses of high energy electromagnetic radiation in radiotherapy of
laryngeal cancer].
[The effects of pulsed low-level EM fields on memory processes].
Ultrawideband radiation and pentylenetetrazol-induced convulsions in rats.
Multi-Center Pilot Study to Evaluate the Safety Profile of High Energy Fractionated
Radiofrequency With Insulated Microneedles to Multiple Levels of the Dermis.
Propagation of an electromagnetic wave in an absorbing anisotropic medium and infrared
transmission of liquid crystals: comparison with experiments.
Microwave medical imaging based on sparsity and an iterative method with adaptive
thresholding.
Microwave-field-driven acoustic modes in DNA.
Long-term study of 435 MHz radio-frequency radiation on blood-borne end points in cannulated
rats. Part I: Engineering considerations.
Comment I on "Generation of focused, nonspherically decaying pulses of electromagnetic
radiation"
Moisture Monitoring in Fluid-Bed Granulation by Multi-Resonance Microwave Sensor:
Applicability on Crystal-Water Containing Donepezil Granules.
[Immunotropic effects of electromagnetic fields in the range of radio- and microwave
frequencies].
Multiple scattering of electromagnetic waves by an array of parallel gyrotropic rods.
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Human leukocyte functions and the U.S. safety standard for exposure to radio-frequency
radiation.
[Biological and ecological aspects of the effects combined electromagnetic rays on farm
animals].
A model of cell electromagnetic susceptibility associated with the membrane electric field.
An algorithm to derive the fraction of photosynthetically active radiation absorbed by
photosynthetic elements of the canopy (FAPAR(ps)) from eddy covariance flux tower data.
Transfer of light-induced electron-spin polarization from the intermediary acceptor to the
prereduced primary acceptor in the reaction center of photosynthetic bacteria.
A signal-to-noise standard for pulsed EPR.
[Effect of decimeter polarized electromagnetic radiation on germinating capacity of seeds].
Multifrequency electron paramagnetic resonance study on deproteinized human bone.
Measurement of heart rate variability and stress evaluation by using microwave reflectometric
vital signal sensing.
Frequency selective solutions for an efficient non-ionising radiation protection in the
radiofrequency and microwave ranges.
How might spatial nonuniformity of dose in a homogeneous biological system affect its total
response?
EM-field effect upon properties of NADPH-cytochrome P-450 reductase with model substrates.
Comment II on "Generation of focused, nonspherically decaying pulses of electromagnetic
radiation"
--Leaf Cluster 47 (107)
Theme - Adverse biological effects of decimeter waves
Titles
[Energy and plastic metabolism of the heart muscle in rabbits undergoing thyroid irradiation with
decimeter waves].
[The action of decimeter waves and merkazolil on myocardial metabolism in the rabbit and its
hormonal regulation].
[The immunological and hormonal effects of combined exposure to a bitemporal ultrahigh-
frequency electrical field and to decimeter waves at different sites].
[Effect of electromagnetic radiation of the decimetric wave range on myocardium cell
membranes].
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[Role of ultrasonic dopplerography in monitoring the effectiveness of treatment of patients who
have sustained a stroke with decimeter-range electromagnetic waves].
[Dynamic ultrastructural shifts in the cardiomyocytes during the irradiation of the cardiac area
with decimeter electromagnetic waves].
[Myocardial energy metabolism in decimeter-wave exposures].
Modulation of a compressional electromagnetic wave in a magnetized electron-positron quantum
plasma.
Interference of electromagnetic waves in dynamic metabolism.
Electromagnetic wave scattering from a rough interface above a chiral medium: generalized field
transforms.
[Ultrastructure of the cerebral cortex in the rat after the effect of electromagnetic impulse].
Information transfer by electromagnetic waves in cortex layers.
Levy noise improves the electrical activity in a neuron under electromagnetic radiation.
Response of Electrical Activity in an Improved Neuron Model under Electromagnetic Radiation
and Noise.
Possible microwave mechanisms of the mammalian nervous system.
[The effect of decimeter waves on the metabolism of the myocardium and its hormonal
regulation in rabbits with experimental ischemia].
[Ultrastructure of cells of the lateral field of the hypothalamus of the cat after exposure to
electromagnetic radiation].
[Morphological changes in the thyroid and adrenals under the bitemporal action of a UHF
electrical field and decimeter waves (experimental research)].
Some neurotropic effects of low-intensity electromagnetic waves in rats with different
typological characteristics of higher nervous activity.
[Systematic analysis of the state of man exposed to radio wave irradiation for a long time].
Poly(dimethylsilylene)diacetylene-Guided ZIF-Based Heterostructures for Full Ku-Band
Electromagnetic Wave Absorption.
[The brain function of animals exposed to the action of centimeter electromagnetic waves].
Modulation of coherence of vectorial electromagnetic waves in the Young interferometer.
[Effect of electromagnetic waves with 59-63 GHz frequency on myocardial infarct patients in the
subacute stage].
Reflection and transmission of electromagnetic waves at a temporal boundary.
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Effect of low-intensity millimeter-range electromagnetic irradiation on the recovery of function
in lesioned sciatic nerves in rats.
[Changes in physico-chemical parameters of homeopathic remedies ferrum metallicum CH6 and
ferrum metallicum CH30 after exposure to high frequency electromagnetic radiation of low
intensity].
Multi-functional coding metasurface for dual-band independent electromagnetic wave control.
[Changes in intracellular regeneration and the indices of endocrine function and cardiac
microcirculation in exposure to decimeter waves].
Multiple scattering of electromagnetic waves by an aggregate of uniaxial anisotropic spheres.
Low power radio-frequency and microwave effects on human electroencephalogram and
behavior.
Electrophysiological effects of non-invasive Radio Electric Asymmetric Conveyor (REAC) on
thalamocortical neural activities and perturbed experimental conditions.
[Electromagnetic radiation of non-thermal intensity and short exposition as a sub-threshold
irritant for the central nervous system].
[The effects of influence of electromagnetic irradiation of millimeter wavelength on background
impulse activity of supraoptic nucleus' neurons of rats' hypothalamus].
Current problems of nonionizing radiation.
MOF-Derived Porous Co/C Nanocomposites with Excellent Electromagnetic Wave Absorption
Properties.
Hierarchical neuronal modeling of cognitive functions: from synaptic transmission to the Tower
of London.
Electromagnetic wave absorbing properties of amorphous carbon nanotubes.
[Electromagnetic radiation damage to the retina (author's transl)].
Prediction and measurement of the electromagnetic environment of high-power medium-wave
and short-wave broadcast antennas in far field.
Hierarchical neuronal modeling of cognitive functions: from synaptic transmission to the Tower
of London.
Out of time: a possible link between mirror neurons, autism and electromagnetic radiation.
About the biological effects of high and extremely high frequency electromagnetic fields.
Exact description of free electromagnetic wave fields in terms of rays.
[Health disorders caused by radiation].
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Nanometer-scale surface modification of epoxy with carbon black and electromagnetic waves.
The histologic effects of pulsed and continuous radiofrequency lesions at 42 degrees C to rat
dorsal root ganglion and sciatic nerve.
[Effect of low intensity and ultra high frequency electromagnetic irradiation on memory
functions].
[The enhanced lethality of cells in suspension during simultaneous exposure to pulsed electrical
and shock-wave acoustic fields].
Food collection and response to pheromones in an ant species exposed to electromagnetic
radiation.
Morphology-Control Synthesis of a Core-Shell Structured NiCu Alloy with Tunable
Electromagnetic-Wave Absorption Capabilities.
[Degranulation of skin mast cells caused by high frequency electromagnetic irradiation of low
intensity].
[The general patterns in the development of the ultrastructural reactions under the action of
electromagnetic radiations].
Controlling Energy Radiations of Electromagnetic Waves via Frequency Coding Metamaterials.
Intensity statistics and the finesse of electromagnetic radiation in random structures.
Effects of the action of microwave-frequency electromagnetic radiation on the spike activity of
neurons in the supraoptic nucleus of the hypothalamus in rats.
[Immunosuppressive effect of the decimeter-band electromagnetic field].
A Route to Chaotic Behavior of Single Neuron Exposed to External Electromagnetic Radiation.
[Radiosensitivity of morphoenzymological structural elements of the jejunum mucous membrane
in chronodynamics of the impact of electromagnetic fields impulses].
Radiofrequency neurolysis in a clinical model. Neuropathological correlation.
[Experimental research on the electromagnetic radiation immunity of a kind of portable
monitor].
Possible physical substrates for the interaction of electromagnetic fields with biologic
membranes.
Modifications in ventricular fibrillation and capture capacity induced by a linear radiofrequency
lesion.
Evaluation of the maximum permissible level of low-intensity electromagnetic radiation at
mobile connection frequency (1 GHz) by changes in motor activity of Spirostomum Ambiguum.
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Post-mortem histologic evaluation of microwave lesions after epicardial pulmonary vein
isolation for atrial fibrillation.
Modulation of surface electromagnetic waves.
[Adaptive changes in the body upon exposure to electromagnetic radiation].
[Effect of impulse extrabroad-band electromagnetic radiation on electroencephalogram and sleep
in laboratory animals].
[Influence of ultra-high electromagnetic irradiation on the electrophoretic mobility of
erythrocytes].
Nanocomposite synthesis by absorption of nanoparticles into macroporous hydrogels. Building a
chemomechanical actuator driven by electromagnetic radiation.
Spontaneous bodily rotations and direction of locomotion at different times after radio frequency
lesions at sites in and near the substantia nigra.
Effect of lesion morphology on microwave signature in 2-D ultra-wideband breast imaging.
[The evaluation of the body response of experimental animals to exposure to the magnetic
component of electromagnetic radiation for setting a hygiene standard].
Quantitative analysis of lesion parameters in radiofrequency trigeminal rhizotomy.
Features of electromagnetic radiation time-and-frequency fluctuation intensity distributions from
human brain structures.
[The effects of space flight factors on the central nervous system. Structural-functional aspects of
radio-modifying action].
[Dissipative functions of processes of electromagnetic radiation interaction with biological
objects].
[Specific and non-specific electromagnetic irradiation effects on biological objects].
[Changes in gastric electric activity and serum catecholamine level under the influence of
electromagnetic microwaves (experimental studies)].
[Features of control of electromagnetic radiation emitted by personal computers].
[Phenomenology and genesis of changes in the total bioelectrical activity of the brain in response
to electromagnetic radiation].
Nano sulfur particles decorated bi-lamella composites for superior electromagnetic wave
absorption.
Meridian is a three-dimensional network from bio-electromagnetic radiation interference: an
interference hypothesis of meridian.
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Modulational instability of electromagnetic waves in birefringent fibers with periodic and
random dispersion.
[Effect of extremely low frequency electromagnetic radiation and ultra-violet radiation on
aggregation of thymocytes and erythrocytes].
Numerical study of electromagnetic waves interacting with negative index materials.
[The structural dynamics of the afferent flow in the action on the receptor field of a low-intensity
stimulant].
General description of electromagnetic radiation processes based on instantaneous charge
acceleration in "endpoints".
[Behavior of the human skin under the influence of electromagnetic radiation in the visible and
near infrared region (author's transl)].
Physical modalities other than stretch in spastic hypertonia.
[Ultrastructure of skeletal muscle tissue of microwave damaged chick embryos].
Response to pulsed and continuous radiofrequency lesioning of the dorsal root ganglion and
segmental nerves in patients with chronic lumbar radicular pain.
The biological effectiveness of solar electromagnetic radiation in space.
[Myocardial damage after high tension electricity injury in rabbits].
Bacterial transformation using micro-shock waves.
[Effect of electromagnetic irradiation of the millimetric range on hemodynamics in patients with
arterial hypertension].
The biological effects of solar activity.
Mode of action of Phoneutria nigriventer spider venom at the isolated phrenic nerve-diaphragm
of the rat.
GSM 900 MHz radiation inhibits ants' association between food sites and encountered cues.
Extending human perception of electromagnetic radiation to the UV region through biologically
inspired photochromic fuzzy logic (BIPFUL) systems.
[Ecological and hygienic studies of electromagnetic irradiation of navigation safety system in
Eastern area of the Finnish Gulf].
Failure of chronic exposure to nonthermal FM radio waves to mutate Drosophila.
[Normal doses of visible light can cause mutations in skin].
Effect of cyclooxygenase blockade on blood flow through well-developed coronary collateral
vessels.
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Long-wavelength red light emission from TV and photosensitive siezures.
The aversive effect of electromagnetic radiation on foraging bats: a possible means of
discouraging bats from approaching wind turbines.
Bilateral symmetry of local inflammatory activation in human carotid atherosclerotic plaques.
Fourth Level Cluster 82 (529)
Theme - Adverse effects of mobile phone radiation, especially oxidative stress
--Leaf Cluster 22 (127)
Theme - Effects of radiofrequency radiation, especially from mobile phones, on rats
Titles
Effects of electromagnetic field produced by mobile phones on the oxidant and antioxidant status
of rats.
Nanometer-scale elongation rate fluctuations in the Myriophyllum aquaticum (Parrot feather)
stem were altered by radio-frequency electromagnetic radiation.
Nanometer-scale elongation rate fluctuations in the Myriophyllum aquaticum (Parrot feather)
stem were altered by radio-frequency electromagnetic radiation.
The effect of electromagnetic radiation in the mobile phone range on the behaviour of the rat.
Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones
induces oxidative stress and reduces sperm motility in rats.
The effects of radiofrequency electromagnetic radiation on sperm function.
Effects of folic acid on rat kidney exposed to 900 MHz electromagnetic radiation.
[Experimental justification of possible mechanisms of action of low intensity electromagnetic
radiation (EMR) on animals' behavior].
Modulation of mammalian immunity by electromagnetic radiation.
Recent reports of Wi-Fi and mobile phone-induced radiation on oxidative stress and reproductive
signaling pathways in females and males.
The radioprotective effects of Moringa oleifera against mobile phone electromagnetic radiation-
induced infertility in rats.
Protective Effects of Zinc on 2.45 GHz Electromagnetic Radiation-Induced Oxidative Stress and
Apoptosis in HEK293 Cells.
Long-term exposure to 4G smartphone radiofrequency electromagnetic radiation diminished
male reproductive potential by directly disrupting Spock3-MMP2-BTB axis in the testes of adult
rats.
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The effect of pulsed electromagnetic radiation from mobile phone on the levels of monoamine
neurotransmitters in four different areas of rat brain.
Long-term exposure of 2450MHz electromagnetic radiation induces stress and anxiety like
behavior in rats.
The impact of electromagnetic radiation (2.45 GHz, Wi-Fi) on the female reproductive system:
The role of vitamin C.
Electromagnetic radiation influence on nonlinear charge and energy transport in biosystems.
900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat
endometrium: protection by vitamins E and C.
Probing the Origins of 1,800 MHz Radio Frequency Electromagnetic Radiation Induced Damage
in Mouse Immortalized Germ Cells and Spermatozoa in vitro.
Effects of the exposure to mobile phones on male reproduction: a review of the literature.
Neurobiological effects of microwave exposure: a review focused on morphological findings in
experimental animals.
Impact of 2.45 GHz microwave radiation on the testicular inflammatory pathway biomarkers in
young rats: The role of gallic acid.
Liver antioxidant stores protect the brain from electromagnetic radiation (900 and 1800 MHz)-
induced oxidative stress in rats during pregnancy and the development of offspring.
Effects of electromagnetic radiation from a cellular telephone on epidermal Merkel cells.
Effects of electromagnetic radiation from a cellular telephone on the oxidant and antioxidant
levels in rabbits.
Electromagnetic radiation 2450 MHz exposure causes cognition deficit with mitochondrial
dysfunction and activation of intrinsic pathway of apoptosis in rats.
Protective effects of beta-glucan against oxidative injury induced by 2.45-GHz electromagnetic
radiation in the skin tissue of rats.
[Possible modification of radiation injury using radio frequency electromagnetic radiation].
[Role of phospholipase A2 and epoxygenase in inhibition of respiration burst in neutrophils by
low intensity radiation of extremely high frequency].
Effects of acute and chronic exposure to both 900 MHz and 2100 MHz electromagnetic radiation
on glutamate receptor signaling pathway.
Behavior and memory evaluation of Wistar rats exposed to 1.8 GHz radiofrequency
electromagnetic radiation.
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[Biological effects of electromagnetic radiation of extremely high frequencies combined with
physiologically active compounds].
Non-ionizing electromagnetic radiation and cancer--is there a relationship?
Benefits and hazards of electromagnetic waves, telecommunication, physical and biomedical: a
review.
[Suppression of nonspecific resistance of the body under the effect of extremely high frequency
electromagnetic radiation of low intensity].
The impact of exposure of diabetic rats to 900 MHz electromagnetic radiation emitted from
mobile phone antenna on hepatic oxidative stress.
Analysis of emotionality and locomotion in radio-frequency electromagnetic radiation exposed
rats.
[Effects of extremely high-frequency electromagnetic radiation on the immune system and
systemic regulation of homeostasis].
Challenging cell phone impact on reproduction: a review.
Radiofrequency electromagnetic radiation-induced behavioral changes and their possible basis.
Selenium reduces mobile phone (900 MHz)-induced oxidative stress, mitochondrial function,
and apoptosis in breast cancer cells.
[Electromagnetic radiations from computer video terminals and their effect on health].
Mobile phone radiation induces reactive oxygen species production and DNA damage in human
spermatozoa in vitro.
[FEATURES OF MODIFYING EFFECT OF LOW-INTENSITY ELECTROMAGNETIC
RADIATION OF NATURAL AND TECHNOGENIC ORIGIN ON VIABILITY AND
FUNCTIONAL STATUS OF NEUTROPHILIC GRANULOCYTES].
Effects of electromagnetic radiation from a cellular phone on human sperm motility: an in vitro
study.
[Intracellular regeneration of adrenocorticocytes in response to the prophylactic application of
low-intensity electromagnetic radiation under the conditions of radiation (an experimental
study)].
Electromagnetic radiation--parameters for risk assessment.
Effect of 1.8 GHz radiofrequency electromagnetic radiation on novel object associative
recognition memory in mice.
[Epidemiologic studies of the effect of microwaves (neurophysiologic, hematologic and
ophthalmologic aspects)].
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[The activity of prooxidant-antioxidant system in loach embryos under the action of microwave
radiation].
The effects of electromagnetic radiation (2450 MHz wireless devices) on the heart and blood
tissue: role of melatonin.
Immune responses of a wall lizard to whole-body exposure to radiofrequency electromagnetic
radiation.
Features of anti-inflammatory effects of modulated extremely high-frequency electromagnetic
radiation.
Effect of exposure and withdrawal of 900-MHz-electromagnetic waves on brain, kidney and
liver oxidative stress and some biochemical parameters in male rats.
Overproduction of free radical species in embryonal cells exposed to low intensity
radiofrequency radiation.
Possible cause for altered spatial cognition of prepubescent rats exposed to chronic
radiofrequency electromagnetic radiation.
Polarization: A Key Difference between Man-made and Natural Electromagnetic Fields, in
regard to Biological Activity.
Exposure to acute electromagnetic radiation of mobile phone exposure range alters transiently
skin homeostasis of a model of pigmented reconstructed epidermis.
Structural and ultrastructural study of rat liver influenced by electromagnetic radiation.
[Effects of low-intensity electromagnetic radiation of extremely high frequency on the animal
body within the framework of total low-dose x-ray irradiation].
[Metabolic and ultrastructural adaptation mechanisms during the primary prophylactic action of
low-intensity electromagnetic radiation under normal and radiation conditions].
Exposure of tumor-bearing mice to extremely high-frequency electromagnetic radiation modifies
the composition of fatty acids in thymocytes and tumor tissue.
The antioxidant effect of Green Tea Mega EGCG against electromagnetic radiation-induced
oxidative stress in the hippocampus and striatum of rats.
The chronic effect of pulsed 1800 MHz electromagnetic radiation on amino acid
neurotransmitters in three different areas of juvenile and young adult rat brain.
[Decrease in the intensity of the cellular immune response and nonspecific inflammation upon
exposure to extremely high frequency electromagnetic radiation].
Electromagnetic radiation at 900 MHz induces sperm apoptosis through bcl-2, bax and caspase-3
signaling pathways in rats.
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Model analysis of nonlinear modification of neutrophil calcium homeostasis under the influence
of modulated electromagnetic radiation of extremely high frequencies.
Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice
to GSM 1800 MHz mobile phone radiation: An exploratory study.
[The specific features of the development of metabolic and regenerative processes under the
action of low-intensity electromagnetic radiation in radiation exposure conditions (an
experimental study)].
Impact of electromagnetic radiation emitted by monitors on changes in the cellular membrane
structure and protective antioxidant effect of vitamin A - In vitro study.
Mobile Phone Radiation: Physiological & Pathophysiologcal Considerations.
Fatty Acid Content and Tumor Growth Changes in Mice After Exposure to Extremely High-
Frequency Electromagnetic Radiation and Consumption of N-3 Fatty Acids.
Disordered redox metabolism of brain cells in rats exposed to low doses of ionizing radiation or
UHF electromagnetic radiation.
[Modulated extremely high frequency electromagnetic radiation of low intensity activates or
inhibits respiratory burst in neutrophils depending on modulation frequency].
The role of fatty acids in anti-inflammatory effects of low-intensity extremely high-frequency
electromagnetic radiation.
[Effect of low intensity pulse-modulated electromagnetic radiation on activity of alkaline
phosphatase in blood serum].
The effect of electromagnetic radiation on the rat brain: an experimental study.
[Protective action of electromagnetic radiation (40.68 MHz) on Saccharomyces cerevisiae UCM
Y-517].
Radiofrequency electromagnetic radiation exposure effects on amygdala morphology, place
preference behavior and brain caspase-3 activity in rats.
[Influence of electromagnetic fields on the emotional behaviour of rats].
Testicular apoptosis and histopathological changes induced by a 2.45 GHz electromagnetic field.
[The application of low-intensity electromagnetic radiation under immobilization stress
conditions (an experimental study)].
Extremely high-frequency electromagnetic radiation enhances neutrophil response to particulate
agonists.
Inhibition by Egb761 of the effect of cellphone radiation on the male reproductive system.
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Variations in amino acid neurotransmitters in some brain areas of adult and young male albino
rats due to exposure to mobile phone radiation.
[Effect of radio-frequency electromagnetic radiation on physiological features of Saccharomyces
cerevisiae strain UCM Y-517].
Variations of melatonin and stress hormones under extended shifts and radiofrequency
electromagnetic radiation.
[Effect of radiofrequency range electromagnetic radiation on chemoreceptor structure].
Effects of intensive cell phone (Philips Genic 900) use on the rat kidney tissue.
Effects of prenatal and postnatal exposure of Wi-Fi on development of teeth and changes in teeth
element concentration in rats. [corrected].
Changes in mitochondrial functioning with electromagnetic radiation of ultra high frequency as
revealed by electron paramagnetic resonance methods.
Effect of electromagnetic waves on human reproduction.
Effects of short-duration electromagnetic radiation on early postnatal neurogenesis in rats: Fos
and NADPH-d histochemical studies.
[The effect of electromagnetic radiation on the monoamine oxidase A activity in the rat brain].
[Changes in the immune status under the influence of high-frequency electromagnetic radiation].
The effect of low frequency electromagnetic radiation on the morphology of dental and
periodontal tissues (experimental investigation).
Structural and ultrastructural study of rat testes influenced by electromagnetic radiation.
[The combined action of drinking mineral water and low-intensity electromagnetic radiation
under the immobilization stress conditions (an experimental study)].
Effects of low-intensity ultrahigh frequency electromagnetic radiation on inflammatory
processes.
[Effect of Low-Intensity 900 MHz Frequency Electromagnetic Radiation on Rat Brain Enzyme
Activities Linked to Energy Metabolism].
Adverse cutaneous effects of ionizing and non-ionizing electromagnetic radiation.
[The influence of electromagnetic radiation of industrial frequency on Daphnia magna (Straus)].
Effects of electromagnetic radiation from 3G mobile phone on heart rate, blood pressure and
ECG parameters in rats.
[Mechanism of radiobiological effects of low intensity nonionizing electromagnetic radiation].
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Transdermal patches loaded with L-cysteine HCL as a strategy for protection from mobile phone
emitting electromagnetic radiation hazards.
Effect of delta-rhythm-modulated extremely high frequency electromagnetic radiation on rats.
[Effect of hypokinetic stress and low intensity electromagnetic field of extremely high frequency
on changes of cytokine concentration in rat blood].
Non-ionizing electromagnetic radiations, emitted by a cellular phone, modify cutaneous blood
flow.
Low frequency electromagnetic waves increase human sperm motility - A pilot study revealing
the potent effect of 43 kHz radiation.
Biological effects of electromagnetic fields and radiation.
[Status quo of the researches on the biological effect of electromagnetic radiation on the testis
and epididymal sperm].
[Effect of low intensity electromagnetic waves from cell phones on human health].
[Impact of cell phone radiation on male reproduction].
Mobile phones electromagnetic radiation and NAD(+)-dependent isocitrate dehydrogenase as a
mitochondrial marker in asthenozoospermia.
Electromagnetic radiation emitted from video computer terminals.
[Effect of low intensity and very high frequency electromagnetic radiation on occupationally
exposed personnel].
[Effects of electromagnetic radiation in metropolis environment on teenagers' electrocardiogram
and blood cells].
Influence of electromagnetic radiation produced by mobile phone on some biophysical blood
properties in rats.
[Influence of light and electromagnetic radiation of Sun on circadian rhythms of the total
antioxidant capacity of human saliva in the North].
[Radar radiation damages sperm quality].
[Influence of electromagnetic radiation on toxicity of Vipera lebetina obtusa venom].
[On prevention of a combined impact of electromagnetic radiation and climatic/weather factors
on worker's organism].
Propagation of electromagnetic radiation in mitochondria?
The effect of low level radiofrequency electromagnetic radiation on the excretion rates of stress
hormones in operators during 24-hour shifts.
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[Physical factors and stress].
[Effect of weak electromagnetic radiation on learning in the grain beetle Tenebrio monitor].
[Disturbances of glucose tolerance in workers exposed to electromagnetic radiation].
--Leaf Cluster 26 (129)
Theme - Oxidative stress effects from mobile phone radiofrequency radiation
Titles
Ginkgo biloba prevents mobile phone-induced oxidative stress in rat brain.
Mobile phone radiation-induced free radical damage in the liver is inhibited by the antioxidants
N-acetyl cysteine and epigallocatechin-gallate.
The link between radiofrequencies emitted from wireless technologies and oxidative stress.
The protective effects of N-acetyl-L-cysteine and epigallocatechin-3-gallate on electric field-
induced hepatic oxidative stress.
Modulation of wireless (2.45 GHz)-induced oxidative toxicity in laryngotracheal mucosa of rat
by melatonin.
Effect of 900 MHz radiofrequency radiation on oxidative stress in rat brain and serum.
The protective effect of caffeic acid phenethyl ester (CAPE) on oxidative stress in rat liver
exposed to the 900 MHz electromagnetic field.
Exposure to radiofrequency radiation induces oxidative stress in duckweed Lemna minor L.
The prophylactic effect of vitamin C on oxidative stress indexes in rat eyes following exposure
to radiofrequency wave generated by a BTS antenna model.
Vitamin C protects rat cerebellum and encephalon from oxidative stress following exposure to
radiofrequency wave generated by a BTS antenna model.
Effects of Electromagnetic Radiation Use on Oxidant/Antioxidant Status and DNA Turn-over
Enzyme Activities in Erythrocytes and Heart, Kidney, Liver, and Ovary Tissues From Rats:
Possible Protective Role of Vitamin C.
Long-term exposure to electromagnetic radiation from mobile phones and Wi-Fi devices
decreases plasma prolactin, progesterone, and estrogen levels but increases uterine oxidative
stress in pregnant rats and their offspring.
Oxidative stress and prevention of the adaptive response to chronic iron overload in the brain of
young adult rats exposed to a 150 kilohertz electromagnetic field.
Effect of 900-, 1800-, and 2100-MHz radiofrequency radiation on DNA and oxidative stress in
brain.
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Melatonin reduces oxidative stress induced by chronic exposure of microwave radiation from
mobile phones in rat brain.
Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the
HEK293 cells.
Therapeutic approaches of melatonin in microwave radiations-induced oxidative stress-mediated
toxicity on male fertility pattern of Wistar rats.
Effects of mobile phones on oxidant/antioxidant balance in cornea and lens of rats.
Effects of acute exposure to the radiofrequency fields of cellular phones on plasma lipid peroxide
and antioxidase activities in human erythrocytes.
Exposure to static magnetic field of pregnant rats induces hepatic GSH elevation but not
oxidative DNA damage in liver and kidney.
Effects of 837 and 1950 MHz radiofrequency radiation exposure alone or combined on oxidative
stress in MCF10A cells.
Oxidative stress effects on the central nervous system of rats after acute exposure to ultra high
frequency electromagnetic fields.
A cross-sectional study on oxidative stress in workers exposed to extremely low frequency
electromagnetic fields.
Effects of melatonin on Wi-Fi-induced oxidative stress in lens of rats.
The effect of melatonin on the liver of rats exposed to microwave radiation.
Oxidative stress-mediated alterations on sperm parameters in male Wistar rats exposed to 3G
mobile phone radiation.
Wi-Fi (2.45 GHz)- and mobile phone (900 and 1800 MHz)-induced risks on oxidative stress and
elements in kidney and testis of rats during pregnancy and the development of offspring.
Effects of Low-Frequency Electromagnetic Field on Oxidative Stress in Selected Structures of
the Central Nervous System.
Effect of low level microwave radiation exposure on cognitive function and oxidative stress in
rats.
900 MHz pulse-modulated radiofrequency radiation induces oxidative stress on heart, lung, testis
and liver tissues.
Exposure to mobile phone (900-1800 MHz) during pregnancy: tissue oxidative stress after
childbirth.
The Effects of Melatonin on Oxidative Stress Parameters and DNA Fragmentation in Testicular
Tissue of Rats Exposed to Microwave Radiation.
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Exposure to cell phone induce oxidative stress in mice preantral follicles during in vitro
cultivation: An experimental study.
[Effect of American Ginseng Capsule on the liver oxidative injury and the Nrf2 protein
expression in rats exposed by electromagnetic radiation of frequency of cell phone].
Effects of acute electromagnetic field exposure and movement restraint on antioxidant system in
liver, heart, kidney and plasma of Wistar rats: a preliminary report.
Effect of mobile phone exposure on apoptotic glial cells and status of oxidative stress in rat
brain.
Effects of third generation mobile phone-emitted electromagnetic radiation on oxidative stress
parameters in eye tissue and blood of rats.
Pathological Findings Observed in the Kidneys of Postnatal Male Rats Exposed to the 2100 MHz
Electromagnetic Field.
Effects of exposure to 50 Hz electric field at different strengths on oxidative stress and
antioxidant enzyme activities in the brain tissue of guinea pigs.
Melatonin modulates 900 Mhz microwave-induced lipid peroxidation changes in rat brain.
Biochemical modifications and neuronal damage in brain of young and adult rats after long-term
exposure to mobile phone radiations.
The preventive effect of lotus seedpod procyanidins on cognitive impairment and oxidative
damage induced by extremely low frequency electromagnetic field exposure.
900-MHz microwave radiation promotes oxidation in rat brain.
Influence of extremely-low-frequency magnetic field on antioxidative melatonin properties in
AT478 murine squamous cell carcinoma culture.
2.45 GHz microwave irradiation-induced oxidative stress affects implantation or pregnancy in
mice, Mus musculus.
In vitro free radical scavenging activities and effect of synthetic oligosaccharides on antioxidant
enzymes and lipid peroxidation in aged mice.
The physiopathological effects of quercetin on oxidative stress in radiation of 4.5 g mobile phone
exposed liver tissue of rat.
Assessment of oxidant/antioxidant status in saliva of cell phone users.
Effects of 900-MHz electromagnetic field emitted from cellular phone on brain oxidative stress
and some vitamin levels of guinea pigs.
Chronic exposure to 50Hz magnetic fields causes a significant weakening of antioxidant defence
systems in aged rat brain.
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Effects of static magnetic field and cadmium on oxidative stress and DNA damage in rat cortex
brain and hippocampus.
Melatonin protects rat thymus against oxidative stress caused by exposure to microwaves and
modulates proliferation/apoptosis of thymocytes.
Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation.
The effects of N-acetylcysteine and epigallocatechin-3-gallate on liver tissue protein oxidation
and antioxidant enzyme levels after the exposure to radiofrequency radiation.
Oxidative stress-mediated skin damage in an experimental mobile phone model can be prevented
by melatonin.
Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis,
mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root
ganglion of rats.
Impacts of exposure to 900 MHz mobile phone radiation on liver function in rats.
Static magnetic field affects oxidative stress in mouse cochlea.
Effects of cell phone radiation on lipid peroxidation, glutathione and nitric oxide levels in mouse
brain during epileptic seizure.
The effect of electromagnetic radiation emitted by display screens on cell oxygen metabolism -
in vitro studies.
Effects of electromagnetic radiation produced by 3G mobile phones on rat brains: magnetic
resonance spectroscopy, biochemical, and histopathological evaluation.
Role of Mitochondria in the Oxidative Stress Induced by Electromagnetic Fields: Focus on
Reproductive Systems.
Effect of selenium pre-treatment on plasma antioxidant vitamins A (retinol) and E (alpha-
tocopherol) in static magnetic field-exposed rats.
Effect of cell phone use on salivary total protein, enzymes and oxidative stress markers in young
adults: a pilot study.
Radiofrequency radiation emitted from Wi-Fi (2.4 GHz) causes impaired insulin secretion and
increased oxidative stress in rat pancreatic islets.
[Corrective effects of electromagnetic radiation in a millimeter wavelength range on the
parameters of oxidative stress after standard anti-helicobacterial therapy in patients with ulcer
disease].
Oxidative effects of extremely low frequency magnetic field and radio frequency radiation on
testes tissues of diabetic and healthy rats.
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Investigation of the effects of distance from sources on apoptosis, oxidative stress and cytosolic
calcium accumulation via TRPV1 channels induced by mobile phones and Wi-Fi in breast cancer
cells.
Radiofrequency electromagnetic radiation from cell phone causes defective testicular function in
male Wistar rats.
Effect of 950 MHz UHF electromagnetic radiation on biomarkers of oxidative damage,
metabolism of UFA and antioxidants in the livers of young rats of different ages.
The influence of microwave radiation from cellular phone on fetal rat brain.
Effects of chronic exposure to 950 MHz ultra-high-frequency electromagnetic radiation on
reactive oxygen species metabolism in the right and left cerebral cortex of young rats of different
ages.
Effects of radiofrequency electromagnetic wave exposure from cellular phones on the
reproductive pattern in male Wistar rats.
Radiations and male fertility.
Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through
activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats.
Immunohistopathologic demonstration of deleterious effects on growing rat testes of
radiofrequency waves emitted from conventional Wi-Fi devices.
[Effect of electromagnetic field produced by mobile phones on the activity of superoxide
dismutase (SOD-1) and the level of malonyldialdehyde (MDA)--in vitro study].
[Effects of extremely low frequency electromagnetic field and its combination with lead on the
antioxidant system in mouse].
Mobile phone (1800MHz) radiation impairs female reproduction in mice, Mus musculus,
through stress induced inhibition of ovarian and uterine activity.
[Interference of vitamin E on the brain tissue damage by electromagnetic radiation of cell phone
in pregnant and fetal rats].
Evaluation of genotoxic effects in male Wistar rats following microwave exposure.
1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53
dependent Bax mediated testicular apoptosis in mice, Mus musculus.
The 2100MHz radiofrequency radiation of a 3G-mobile phone and the DNA oxidative damage in
brain.
[On the mechanism of cytogenetic effect of electromagnetic radiation: a role of oxidation
homeostasis].
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Neuroprotective effects of dietary supplement Kang-fu-ling against high-power microwave
through antioxidant action.
Effect of extremely low frequency magnetic field on antioxidant activity in plasma and red blood
cells in spot welders.
Antioxidants alleviate electric field-induced effects on lung tissue based on assays of heme
oxygenase-1, protein carbonyl content, malondialdehyde, nitric oxide, and hydroxyproline.
Cell phone electromagnetic field radiations affect rhizogenesis through impairment of
biochemical processes.
GSM base station electromagnetic radiation and oxidative stress in rats.
The Effects of Cell Phone Waves (900 MHz-GSM Band) on Sperm Parameters and Total
Antioxidant Capacity in Rats.
Extremely low frequency electromagnetic field reduces oxidative stress during the rehabilitation
of post-acute stroke patients.
Evaluation of selected biochemical parameters in the saliva of young males using mobile phones.
Protein oxidation under extremely low frequency electric field in guinea pigs. Effect of N-acetyl-
L-cysteine treatment.
Selenium supplementation ameliorates static magnetic field-induced disorders in antioxidant
status in rat tissues.
In vitro effects of 50 Hz magnetic fields on oxidatively damaged rabbit red blood cells.
[Protective effect of Liuweidihuang Pills against cellphone electromagnetic radiation-induced
histomorphological abnormality, oxidative injury, and cell apoptosis in rat testes].
The impact of electromagnetic radiation of different parameters on platelet oxygen metabolism -
in vitro studies.
Melatonin attenuates radiofrequency radiation (900 MHz)-induced oxidative stress, DNA
damage and cell cycle arrest in germ cells of male Swiss albino mice.
The effect of 50 hz magnetic field of different shape on oxygen metabolism in blood platelets: in
vitro studies.
[Protective effect of melatonin and vitamin E against prooxidative action of iron ions and static
magnetic field].
The role of zinc supplementation in the inhibition of tissue damage caused by exposure to
electromagnetic field in rat lung and liver tissues.
The influence of 1800 MHz GSM-like signals on hepatic oxidative DNA and lipid damage in
nonpregnant, pregnant, and newly born rabbits.
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Effect of rosmarinic acid on sertoli cells apoptosis and serum antioxidant levels in rats after
exposure to electromagnetic fields.
Effects of electromagnetic radiation exposure on bone mineral density, thyroid, and oxidative
stress index in electrical workers.
[Electromagnetic radiation of the terahertz range at the nitric oxide frequency in correction and
prophylaxis of functional activity disorders in thrombocytes of white rats under long-term
stress].
Wi-Fi is an important threat to human health.
The influence of 1800 MHz GSM-like signals on blood chemistry and oxidative stress in non-
pregnant and pregnant rabbits.
[Effect of electromagnetic field produced by mobile phones on the activity of superoxide
dismutase (SOD-1)--in vitro researches].
[Effects of nano-selenium on cognition performance of mice exposed in 1800 MHz
radiofrequency fields].
Mobile phone usage and male infertility in Wistar rats.
Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.
[Use of terahertz electromagnetic radiation at nitric oxide frequencies for the correction of
thyroid functional state during stress].
Correction of microcirculatory disturbances with terahertz electromagnetic radiation at nitric
oxide frequencies in albino rats under conditions of acute stress.
The effect of Wi-Fi electromagnetic waves on neuronal response properties in rat barrel cortex.
Electromagnetic wave emitting products and "Kikoh" potentiate human leukocyte functions.
[Influence of 900 MHz frequency electromagnetic radiation on some blood indices].
Effects of electromagnetic waves emitted from 3G+wi-fi modems on human semen analysis.
Reactive oxygen species elevation and recovery in Drosophila bodies and ovaries following
short-term and long-term exposure to DECT base EMF.
[PARAMETERS OF SPERMATOGENESIS IN MEN EXPOSED TO DIFFICULT
ENVIRONMENTS].
Metal, EMF, and brain energy metabolism.
[Changes in the functional state of rat liver and kidney mitochondria under the effect of
electromagnetic fields].
[Effect of low-intensity 900 MHz frequency electromagnetic radiation on rat liver and blood
serum enzyme activities].
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Ultra-wideband pulses increase nitric oxide production by RAW 264.7 macrophages incubated in
nitrate.
[Some regularities of morphological changes in liver tissue exposed to electricity].
Microwave effects on immobilized peroxidase chemiluminescence.
Sympathetic Resonance Technology: scientific foundation and summary of biologic and clinical
studies.
Examination of electric field effects on tissues by using back propagation neural network.
A novel method to estimate changes in stress-induced salivary alpha-amylase using heart rate
variability and respiratory rate, as measured in a non-contact manner using a single radar
attached to the back of a chair.
Effects of new Phoneutria spider toxins on glutamate release and [Ca2+]i in rat cortical
synaptosomes.
--Leaf Cluster 37 (140)
Theme - Effect of radiofrequency exposure, especially prenatal exposure, on rats
Titles
Maternal exposure to a continuous 900-MHz electromagnetic field provokes neuronal loss and
pathological changes in cerebellum of 32-day-old female rat offspring.
The effects of prenatal exposure to a 900-MHz electromagnetic field on the 21-day-old male rat
heart.
The effects of exposure to electromagnetic field on rat myocardium.
900 MHz electromagnetic field exposure affects qualitative and quantitative features of
hippocampal pyramidal cells in the adult female rat.
The effect of prenatal exposure to 1800 MHz electromagnetic field on calcineurin and bone
development in rats.
Exposure to a 900 MHz electromagnetic field for 1 hour a day over 30 days does change the
histopathology and biochemistry of the rat testis.
Effects of a unique electromagnetic field system on the fertility of rats.
Protective effects of luteolin on rat testis following exposure to 900 MHz electromagnetic field.
Evaluation of testicular degeneration induced by low-frequency electromagnetic fields.
Maternal mobile phone exposure alters intrinsic electrophysiological properties of CA1
pyramidal neurons in rat offspring.
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Electromagnetic fields promote severe and unique vascular calcification in an animal model of
ectopic calcification.
Effects of exposure to electromagnetic field (1.8/0.9 GHz) on testicular function and structure in
growing rats.
The effects of prenatal long-duration exposure to 900-MHz electromagnetic field on the 21-day-
old newborn male rat liver.
Common behaviors alterations after extremely low-frequency electromagnetic field exposure in
rat animal model.
Pathological effects of prenatal exposure to a 900 MHz electromagnetic field on the 21-day-old
male rat kidney.
Deleterious impacts of a 900-MHz electromagnetic field on hippocampal pyramidal neurons of
8-week-old Sprague Dawley male rats.
Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout
adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-
day-old Sprague Dawley male rats.
The effect of exposure of rats during prenatal period to radiation spreading from mobile phones
on renal development.
Effects of extremely low frequency electromagnetic fields (100muT) on behaviors in rats.
Biological and morphological effects on the reproductive organ of rats after exposure to
electromagnetic field.
An evaluation of the effects of long-term cell phone use on the testes via light and electron
microscope analysis.
Effects of 900-MHz electromagnetic fields exposure throughout middle/late adolescence on the
kidney morphology and biochemistry of the female rat.
Effects of electromagnetic field (1.8/0.9 GHz) exposure on growth plate in growing rats.
Effects of low-intensity electromagnetic fields on behavioral activity of rats.
Anxiety-like behavioural effects of extremely low-frequency electromagnetic field in rats.
Biochemical and pathological changes in the male rat kidney and bladder following exposure to
continuous 900-MHz electromagnetic field on postnatal days 22-59.
The effects of an electromagnetic field on the boundary tissue of the seminiferous tubules of the
rat: A light and transmission electron microscope study.
The effect of prenatal exposure to 900-MHz electromagnetic field on the 21-old-day rat testicle.
Testicular development evaluation in rats exposed to 60 Hz and 1 mT electromagnetic field.
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Effect of electromagnetic irradiation produced by 3G mobile phone on male rat reproductive
system in a simulated scenario.
Lasting hepatotoxic effects of prenatal mobile phone exposure.
Nonthermal effects of lifelong high-frequency electromagnetic field exposure on social memory
performance in rats.
Effects of prenatal 900 MHz electromagnetic field exposures on the histology of rat kidney.
Neuroprotective effects of melatonin and omega-3 on hippocampal cells prenatally exposed to
900 MHz electromagnetic fields.
Microwave exposure affecting reproductive system in male rats.
Morphological and antioxidant impairments in the spinal cord of male offspring rats following
exposure to a continuous 900MHz electromagnetic field during early and mid-adolescence.
Whole-body microwave exposure emitted by cellular phones and testicular function of rats.
Purkinje cell number decreases in the adult female rat cerebellum following exposure to 900
MHz electromagnetic field.
Effect of electromagnetic waves from mobile phone on immune status of male rats: possible
protective role of vitamin D.
Changes in antioxidant capacity of blood due to mutual action of electromagnetic field (1800
MHz) and opioid drug (tramadol) in animal model of persistent inflammatory state.
Evaluation of hormonal change, biochemical parameters, and histopathological status of uterus
in rats exposed to 50-Hz electromagnetic field.
Stress-related endocrinological and psychopathological effects of short- and long-term 50Hz
electromagnetic field exposure in rats.
Impact of microwave at X-band in the aetiology of male infertility.
The effect on rat thymocytes of the simultaneous in vivo exposure to 50-Hz electric and
magnetic field and to continuous light.
Effects on rat testis of 1.95-GHz W-CDMA for IMT-2000 cellular phones.
Disruption of the ovarian follicle reservoir of prepubertal rats following prenatal exposure to a
continuous 900-MHz electromagnetic field.
Influence of electromagnetic field (1800 MHz) on lipid peroxidation in brain, blood, liver and
kidney in rats.
[Effect of Guilingji Capsule on the fertility, liver functions, and serum LDH of male SD rats
exposed by 900 mhz cell phone].
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Zinc supplementation ameliorates electromagnetic field-induced lipid peroxidation in the rat
brain.
A histopathological and biochemical evaluation of oxidative injury in the sciatic nerves of male
rats exposed to a continuous 900-megahertz electromagnetic field throughout all periods of
adolescence.
Effects of short-term exposure to powerline-frequency electromagnetic field on the electrical
activity of the heart.
Altered operant behavior of adult rats after perinatal exposure to a 60-Hz electromagnetic field.
[Autoimmune processes after long-term low-level exposure to electromagnetic fields (the results
of an experiment). Part 5. Impact of the blood serum from rats exposed to low-level
electromagnetic fields on pregnancy, foetus and offspring development of intact female rats].
The effects of long-term exposure to a 2450 MHz electromagnetic field on growth and pubertal
development in female Wistar rats.
Effects of mobile phone radiation on serum testosterone in Wistar albino rats.
Effects of exposure to 2100MHz GSM-like radiofrequency electromagnetic field on auditory
system of rats.
Maternal mobile phone exposure adversely affects the electrophysiological properties of Purkinje
neurons in rat offspring.
[Female genital toxicities of high-frequency electromagnetic field on rats].
Effects of exposure to electromagnetic field from mobile phone on serum hepcidin and iron
status in male albino rats.
[State of the reproductive systemin in male rats of 1st generation obtained from irradiated parents
and exposed to electromagnetic radiation (897 MHz) during embryogenesis and postnatal
development].
The effects of microwave emitted by cellular phones on ovarian follicles in rats.
Effects of prenatal exposure to a 900 MHz electromagnetic field on the dentate gyrus of rats: a
stereological and histopathological study.
Effect of Modified Wuzi Yanzong Pill () on Tip60-Mediated Apoptosis in Testis of Male Rats
after Microwave Radiation.
Influence of electromagnetic fields on reproductive system of male rats.
Effect of 910-MHz electromagnetic field on rat bone marrow.
Effects of electromagnetic radiation exposure on stress-related behaviors and stress hormones in
male wistar rats.
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Chronic prenatal exposure to the 900 megahertz electromagnetic field induces pyramidal cell
loss in the hippocampus of newborn rats.
Effect of short duration electromagnetic field exposures on rat mass.
Hypospermatogenesis and spermatozoa maturation arrest in rats induced by mobile phone
radiation.
[The delayed effects of modulated and non-modulated electromagnetic field on epileptiformic
activity in rats].
Effect of extremely low frequency electromagnetic field on brain histopathology of Caspian Sea
Cyprinus carpio.
Effects of chronic exposure to electromagnetic waves on the auditory system.
Influence of a 60 Hz, 3 microT, electromagnetic field on the somatic maturation of wistar rat
offspring fed a regional basic diet during pregnancy.
The effect of extremely low-frequency electromagnetic fields on skin and thyroid amine- and
peptide-containing cells in rats: an immunohistochemical and morphometrical study.
Effects of the electromagnetic field, 60 Hz, 3 microT, on the hormonal and metabolic regulation
of undernourished pregnant rats.
[Early and Delayed Effects of Radio Frequency Electromagnetic Fields on the Reproductive
Function and Functional Status of the Offspring of Experimental Animals].
The effects of electromagnetic waves emitted by the cell phones on the testicular tissue.
2.1 GHz electromagnetic field does not change contractility and intracellular Ca2+ transients but
decreases beta-adrenergic responsiveness through nitric oxide signaling in rat ventricular
myocytes.
The influence of electromagnetic radiation generated by a mobile phone on the skeletal system of
rats.
Inhibitory effects of low doses of melatonin on induction of preneoplastic liver lesions in a
medium-term liver bioassay in F344 rats: relation to the influence of electromagnetic near field
exposure.
Effects of cellular phone emissions on sperm motility in rats.
[The physiological mechanisms of the regulation of zoosocial behavior in rats exposed to low-
frequency electromagnetic fields].
The therapeutic effect of a pulsed electromagnetic field on the reproductive patterns of male
Wistar rats exposed to a 2.45-GHz microwave field.
Postnatal development and behavior effects of in-utero exposure of rats to radiofrequency waves
emitted from conventional WiFi devices.
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Effects of prenatal exposure to WIFI signal (2.45GHz) on postnatal development and behavior in
rat: Influence of maternal restraint.
Effect of Electromagnetic Waves from Mobile Phones on Spermatogenesis in the Era of 4G-
LTE.
Exposure to radio-frequency electromagnetic waves alters acetylcholinesterase gene expression,
exploratory and motor coordination-linked behaviour in male rats.
Post-continuous whole body exposure of rabbits to 650 MHz electromagnetic fields: effects on
liver, spleen, and brain.
Effect of low-intensity extremely high frequency radiation on reproductive function in wistar
rats.
[The neurotropic effects of low-intensity electromagnetic waves in rats with different typological
characteristics of higher nervous activity].
[The progeny of male rats subjected to chronic exposure to a permanent magnetic field].
The influence of electric field exposure on bone growth and fracture repair in rats.
Effects of pulsed and sinusoidal electromagnetic fields on MMP-2, MMP-9, collagen type IV
and E-cadherin expression levels in the rat kidney: an immunohistochemical study.
[Study on effects of bioelectric parameters of rats in electromagnetic radiation of HV
transmission line].
Effect of chronic exposure to cellular telephone electromagnetic fields on hearing in rats.
[Bioeffects of chronic exposure to radiofrequency electromagnetic fields of low intensity
(standardization strategy)].
[cts of prenatal exposure of 850-1900MHz mobile phone on the expression of PCNA and DCX
in dentate gyrus of offspring rats].
Short-Term Exposure to Electromagnetic Fields Generated by Mobile Phone Jammers Decreases
the Fasting Blood Sugar in Adult Male Rats.
Learning ability of young rats is unaffected by repeated exposure to a static electromagnetic field
in early life.
Effects of exposure to electromagnetic field radiation (EMFR) generated by activated mobile
phones on fasting blood glucose.
Histological characteristics of cutaneous and thyroid mast cell populations in male rats exposed
to power-frequency electromagnetic fields.
Neural and behavioral teratological evaluation of rats exposed to ultra-wideband electromagnetic
fields.
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Effect of 50-Hz electromagnetic field on the retention of toxic radionuclides in rat tissues.
Influence of electromagnetic fields on bone mass and growth in developing rats: a morphometric,
densitometric, and histomorphometric study.
[Cellphone electromagnetic radiation damages the testicular ultrastructure of male rats].
Effect of the pulsed electromagnetic field on the release of inflammatory mediators from
adipose-derived stem cells (ADSCs) in rats.
Prevention of mobile phone induced skin tissue changes by melatonin in rat: an experimental
study.
[The effects of extremely low frequency electromagnetic field exposure on the pH of the adult
male semen and the motoricity parameters of spermatozoa in vitro].
Congenital anomalies in the offspring of rats after exposure of the testis to an electrostatic field.
Effect of a 1800 MHz electromagnetic field emitted during embryogenesis on chick development
and hatchability.
[Systemic effects of the interaction of an organism and microwaves].
Prenatal exposure to non-ionizing radiation: effects of WiFi signals on pregnancy outcome,
peripheral B-cell compartment and antibody production.
[Morphological structure of rat epiphysis exposed to electromagnetic radiation from
communication devices].
The effects of microwave frequency electromagnetic fields on the development of Drosophila
melanogaster.
Effects of low level electromagnetic field exposure at 2.45 GHz on rat cornea.
[Reaction of Reproductive System and Epididymal Spermatozoa .of Rats to Electromagnetic
Radiation from Mobile Phone (1745 MHz) of Various Duration].
Excretion and tissue distribution of selenium following treatment of male F344 rats with
benzylselenocyanate or sodium selenite.
[Immunomorphologic changes in the testes upon exposure to a microwave electromagnetic
field].
Effects of 900 MHz electromagnetic field emitted by cellular phones on electrocardiograms of
guinea pigs.
Effect of whole-body exposure to high-frequency electromagnetic field on the brain electrogeny
in neurodefective and healthy mice.
Effect of Electromagnetic Wave on Bone Healing in Fixed and Unfixed Conditions.
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Some immunological responses of common carp (Cyprinus carpio) fingerling to acute extremely
low-frequency electromagnetic fields (50 Hz).
Effects of 60 Hz electromagnetic fields on early growth in three plant species and a replication of
previous results.
Influence of 400, 900, and 1900 MHz electromagnetic fields on Lemna minor growth and
peroxidase activity.
[Effect of fluctuating electromagnetic fields on the processes of growth and blastomogenesis].
Effects of broad band electromagnetic fields on HSP70 expression and ischemia-reperfusion in
rat hearts.
[The effect of electromagnetic radiation in the millimeter range on the development of disorders
in the liver induced by ether anesthesia (experimental research)].
Cell Phone Radiation Effect on Bone-to-Implant Osseointegration: A Preliminary Histologic
Evaluation in Rabbits.
The Effects of Electromagnetic Fields Generated from 1800 MHz Cell Phones on Erythrocyte
Rheological Parameters and Zinc Level in Rats.
[The biological activity of a decameter-range electromagnetic field with a frequency of 24 MHz].
[Effect of discontinuous short-wave electromagnetic field irradiation on the state of the
endocrine glands].
Effects of microwaves (950 MHZ mobile phone) on morphometric and apoptotic changes of
rabbit epididymis.
Effect of high frequency electromagnetic wave stimulation on muscle injury in a rat model.
[Respondence to electricity in the muscles of rat's jaw].
Hematological and toxicogenomic effects of ferromagnetic screening of natural electromagnetic
fields.
The effects of 910-MHz electromagnetic field on rat cranial arachnoid and dura mater collagen.
The axial periodicity of collagen fibrils.
Effect of electromagnetic radiation modulated by biostructures on the course of alloxan-induced
diabetes mellitus in rats.
[The interaction of changes in the genitalia in the pathogenesis of sterility in men].
[Evaluation of magnesium, zinc, copper and calcium levels in workers exposed to organic
solvents, hydrogen cyanide and harmful physical factors].
Induction of macrophage migration inhibitory factor precedes the onset of acute tonsillitis.
--Leaf Cluster 38 (133)
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Theme - Effect of radiofrequency radiation on rat brain
Titles
Effects of early-onset radiofrequency electromagnetic field exposure (GSM 900 MHz) on
behavior and memory in rats.
Mobile phone radiation and the developing brain: behavioral and morphological effects in
juvenile rats.
GFAP expression in the rat brain following sub-chronic exposure to a 900 MHz electromagnetic
field signal.
Blood-brain barrier permeability and nerve cell damage in rat brain 14 and 28 days after
exposure to microwaves from GSM mobile phones.
Effect of a chronic GSM 900 MHz exposure on glia in the rat brain.
Effect of mobile telephony on blood-brain barrier permeability in the fetal mouse brain.
Biochemical and histological studies on adverse effects of mobile phone radiation on rat's brain.
Blood-brain barrier and electromagnetic fields: effects of scopolamine methylbromide on
working memory after whole-body exposure to 2.45 GHz microwaves in rats.
Effects of GSM modulated radio-frequency electromagnetic radiation on permeability of blood-
brain barrier in male & female rats.
Effect of 900 MHz radio frequency radiation on beta amyloid protein, protein carbonyl, and
malondialdehyde in the brain.
Histopathological examinations of rat brains after long-term exposure to GSM-900 mobile phone
radiation.
Effects of GSM and UMTS mobile telephony signals on neuron degeneration and blood-brain
barrier permeation in the rat brain.
Cognitive impairment in rats after long-term exposure to GSM-900 mobile phone radiation.
Genotoxic potential of 1.6 GHz wireless communication signal: in vivo two-year bioassay.
One-year, simultaneous combined exposure of CDMA and WCDMA radiofrequency
electromagnetic fields to rats.
A confirmation study of Russian and Ukrainian data on effects of 2450 MHz microwave
exposure on immunological processes and teratology in rats.
Long term and excessive use of 900 MHz radiofrequency radiation alter microRNA expression
in brain.
Radio frequency radiation effects on protein kinase C activity in rats' brain.
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Confirmation studies of Soviet research on immunological effects of microwaves: Russian
immunology results.
Long-term effects of 900 MHz radiofrequency radiation emitted from mobile phone on testicular
tissue and epididymal semen quality.
Nerve cell damage in mammalian brain after exposure to microwaves from GSM mobile phones.
Biological and morphological effects on the brain after exposure of rats to a 1439 MHz TDMA
field.
Report of final results regarding brain and heart tumors in Sprague-Dawley rats exposed from
prenatal life until natural death to mobile phone radiofrequency field representative of a 1.8GHz
GSM base station environmental emission.
8-Oxo-7, 8-dihydro-2'-deoxyguanosine as a biomarker of DNA damage by mobile phone
radiation.
Glial markers and emotional memory in rats following acute cerebral radiofrequency exposures.
Histological and cytological examination of rat reproductive tissue after short-time intermittent
radiofrequency exposure.
Acute exposure to GSM 900-MHz electromagnetic fields induces glial reactivity and
biochemical modifications in the rat brain.
[Autoimmune processes after long-term low-level exposure to electromagnetic fields (the results
of an experiment). Part 3. The effect of the long-term non-thermal RF EMF exposure on
complement-fixation antibodies against homologenous tissue].
Effects of 2.4 GHz radiofrequency radiation emitted from Wi-Fi equipment on microRNA
expression in brain tissue.
Blood-brain barrier disruption by continuous-wave radio frequency radiation.
Effect of long-term (2 years) exposure of mouse brains to global system for mobile
communication (GSM) radiofrequency fields on astrocytic immunoreactivity.
Effect of long-term mobile communication microwave exposure on vascular permeability in
mouse brain.
The effects of pulsed 860 MHz radiofrequency radiation on the promotion of neurogenic tumors
in rats.
Micronucleus frequency in erythrocytes of mice after long-term exposure to radiofrequency
radiation.
Fifty-gigahertz microwave exposure effect of radiations on rat brain.
The effect of chronic exposure to 835.62 MHz FDMA or 847.74 MHz CDMA radiofrequency
radiation on the incidence of spontaneous tumors in rats.
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Effect of an acute 900MHz GSM exposure on glia in the rat brain: a time-dependent study.
Does prolonged radiofrequency radiation emitted from Wi-Fi devices induce DNA damage in
various tissues of rats?
The effect of radiofrequency radiation generated by a Global System for Mobile
Communications source on cochlear development in a rat model.
Mutagenic response of 2.45 GHz radiation exposure on rat brain.
Effect of GSM-900 and -1800 signals on the skin of hairless rats. I: 2-hour acute exposures.
Long-term study of 435 MHz radio-frequency radiation on blood-borne end points in cannulated
rats. Part II: methods, results, and summary.
Exposure to GSM 900 MHz electromagnetic fields affects cerebral cytochrome c oxidase
activity.
GSM and DCS wireless communication signals: combined chronic toxicity/carcinogenicity study
in the Wistar rat.
Evidence for mobile phone radiation exposure effects on reproductive pattern of male rats: role
of ROS.
Microglial activation as a measure of stress in mouse brains exposed acutely (60 minutes) and
long-term (2 years) to mobile telephone radiofrequency fields.
DNA damage in rat brain cells after in vivo exposure to 2450 MHz electromagnetic radiation and
various methods of euthanasia.
Commentary on the utility of the National Toxicology Program study on cell phone
radiofrequency radiation data for assessing human health risks despite unfounded criticisms
aimed at minimizing the findings of adverse health effects.
Effect of in utero wi-fi exposure on the pre- and postnatal development of rats.
Cerebral radiofrequency exposures during adolescence: Impact on astrocytes and brain functions
in healthy and pathologic rat models.
The effect of 2100 MHz radiofrequency radiation of a 3G mobile phone on the parotid gland of
rats.
Expression of the water channel protein, aquaporin-4, in mouse brains exposed to mobile
telephone radiofrequency fields.
Effects of mobile phone radiation (900 MHz radiofrequency) on structure and functions of rat
brain.
Effects of 900 MHz radiofrequency on corticosterone, emotional memory and
neuroinflammation in middle-aged rats.
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Circadian rhythmicity of antioxidant markers in rats exposed to 1.8 GHz radiofrequency fields.
[Effects of electromagnetic pulse on blood-brain barrier permeability and tight junction proteins
in rats].
Effects of head-only exposure of rats to GSM-900 on blood-brain barrier permeability and
neuronal degeneration.
Effects of 900 MHz radiofrequency radiation on skin hydroxyproline contents.
Effects of gestational exposure to 1.95-GHz W-CDMA signals for IMT-2000 cellular phones:
Lack of embryotoxicity and teratogenicity in rats.
In utero and early-life exposure of rats to a Wi-Fi signal: screening of immune markers in sera
and gestational outcome.
The effect of radiofrequency radiation on DNA and lipid damage in female and male infant
rabbits.
Effect of global system for mobile communication (gsm)-like radiofrequency fields on vascular
permeability in mouse brain.
Does head-only exposure to GSM-900 electromagnetic fields affect the performance of rats in
spatial learning tasks?
The effects of mobile phones on apoptosis in cerebral tissue: an experimental study on rats.
Survival and cancer in laboratory mammals exposed to radiofrequency energy.
The effects of simultaneous combined exposure to CDMA and WCDMA electromagnetic fields
on rat testicular function.
Teratogenic effects of 27.12 MHz radiofrequency radiation in rats.
The effects of 860 MHz radiofrequency radiation on the induction or promotion of brain tumors
and other neoplasms in rats.
Effect of long-term exposure of 2.4 GHz radiofrequency radiation emitted from Wi-Fi equipment
on testes functions.
Effects of continuous low-level exposure to radiofrequency radiation on intrauterine
development in rats.
Electromagnetic fields and the blood-brain barrier.
Effects of 20-MHz radiofrequency radiation on rat hematology, splenic function, and serum
chemistry.
Effects of GSM-like radiofrequency irradiation during the oogenesis and spermiogenesis of
Xenopus laevis.
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Effects of mobile phone electromagnetic fields at nonthermal SAR values on melatonin and body
weight of Djungarian hamsters (Phodopus sungorus).
Expression of the immediate early gene, c-fos, in fetal brain after whole of gestation exposure of
pregnant mice to global system for mobile communication microwaves.
Electromagnetic field effect or simply stress? Effects of UMTS exposure on hippocampal
longterm plasticity in the context of procedure related hormone release.
Effect of GSM-900 and -1800 signals on the skin of hairless rats. II: 12-week chronic exposures.
Exposure to cell phone radiofrequency changes corticotrophin hormone levels and histology of
the brain and adrenal glands in male Wistar rat.
Neurodegenerative changes and apoptosis induced by intrauterine and extrauterine exposure of
radiofrequency radiation.
Rat fertility and embryo fetal development: influence of exposure to the Wi-Fi signal.
Effects of prenatal and postnatal exposure to GSM-like radiofrequency on blood chemistry and
oxidative stress in infant rabbits, an experimental study.
Heat shock protein induction in fetal mouse brain as a measure of stress after whole of gestation
exposure to mobile telephony radiofrequency fields.
Micronucleus induction after whole-body microwave irradiation of rats.
Effects of GSM-Frequency Electromagnetic Radiation on Some Physiological and Biochemical
Parameters in Rats.
Effects of simultaneous combined exposure to CDMA and WCDMA electromagnetic fields on
serum hormone levels in rats.
The differential effects of 200, 591, and 2,450 MHz radiation on rat brain energy metabolism.
RAPD Profiling, DNA Fragmentation, and Histomorphometric Examination in Brains of Wistar
Rats Exposed to Indoor 2.5 Ghz Wi-Fi Devices Radiation.
[Autoimmune processes after long-term low-level exposure to electromagnetic fields (the results
of an experiment). Part 4. Manifestation of oxidative intracellular stress-reaction after long-term
non-thermal EMF exposure of rats].
Exposure to an 890-MHz mobile phone-like signal and serum levels of S100B and transthyretin
in volunteers.
Effects of electromagnetic radiation on spatial memory and synapses in rat hippocampal CA1.
Developmental toxicity interactions of salicylic acid and radiofrequency radiation or 2-
methoxyethanol in rats.
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The effect of radiofrequency radiation on DNA and lipid damage in non-pregnant and pregnant
rabbits and their newborns.
Effect of Short-term 900 MHz low level electromagnetic radiation exposure on blood serotonin
and glutamate levels.
Effect of electromagnetic pulse exposure on brain micro vascular permeability in rats.
Alteration of adaptive behaviors of progeny after maternal mobile phone exposure.
Survivability and long-term stress reactivity levels following repeated exposure to nuclear
magnetic resonance imaging procedures in rats.
[Autoimmune processes after long-term low-level exposure to electromagnetic fields (the results
of an experiment). Part 2. General scheme and conditions of the experiment. Development of RF
exposure conditions complying with experimental tasks. Animal's status during the long-term
exposure].
Multigenerational effects of whole body exposure to 2.14 GHz W-CDMA cellular phone signals
on brain function in rats.
Detrimental effect of electromagnetic pulse exposure on permeability of in vitro blood-brain-
barrier model.
Effects of exposure to electromagnetic field from 915 MHz radiofrequency identification system
on circulating blood cells in the healthy adult rat.
[Effects of 2000 muW/cm2; electromagnetic radiation on expression of immunoreactive protein
and mRNA of NMDA receptor 2A subunit in rats hippocampus].
Effects of 1800-MHz radiofrequency fields on circadian rhythm of plasma melatonin and
testosterone in male rats.
Effects of exposure of the ear to GSM microwaves: in vivo and in vitro experimental studies.
Age-Related Modulations of AQP4 and Caveolin-1 in the Hippocampus Predispose the Toxic
Effect of Phoneutria nigriventer Spider Venom.
GSM radiation triggers seizures and increases cerebral c-Fos positivity in rats pretreated with
subconvulsive doses of picrotoxin.
[Studies on the injury effects of hippocampus induced by high power microwave radiation in
rat].
GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant
rabbits.
Exposure to GSM 900-MHz mobile radiation impaired inhibitory avoidance memory
consolidation in rat: Involvements of opioidergic and nitrergic systems.
Electromagnetic pulse exposure induces overexpression of beta amyloid protein in rats.
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Effects of intrauterine and extrauterine exposure to GSM-like radiofrequency on distortion
product otoacoustic emissions in infant male rabbits.
Effects of whole-body exposure to 915 MHz RFID on secretory functions of the thyroid system
in rats.
[The assessment of modulated radiofrequence electromagnetic radiation on cognitive function in
rats of different ages].
Life-Time Dosimetric Assessment for Mice and Rats Exposed in Reverberation Chambers of the
2-Year NTP Cancer Bioassay Study on Cell Phone Radiation.
Exposure setup to study potential adverse effects at GSM 1800 and UMTS frequencies on the
auditory systems of rats.
The effects of 2100-MHz radiofrequency radiation on nasal mucosa and mucociliary clearance in
rats.
[A comparative histochemical study of cytochrome oxidase activity in the somatosensory and
auditory brain centers in the normal rat and after exposure to superhigh-frequency
electromagnetic fields].
Estimates of absorption of radiofrequency radiation by the embryo and fetus during pregnancy.
MRI gradient fields increase brain mannitol space.
The identification of an intensity 'window' on the bioeffects of mobile telephony radiation.
Effects of 7 Hz-modulated 450 MHz electromagnetic radiation on human performance in visual
memory tasks.
Dataset on significant role of Candesartan on cognitive functions in rats having memory
impairment induced by electromagnetic waves.
Effects of electromagnetic radiation on morphology and TGF-beta3 expression in mouse
testicular tissue.
Effects of radiofrequency exposure on the GABAergic system in the rat cerebellum: clues from
semi-quantitative immunohistochemistry.
Metabolomic study of urinary polyamines in rat exposed to 915 MHz radiofrequency
identification signal.
An international project to confirm Soviet-era results on immunological and teratological effects
of RF field exposure in Wistar rats and comments on Grigoriev et al. [2010].
Radiotelemetry and wildlife: Highlighting a gap in the knowledge on radiofrequency radiation
effects.
Non-thermal continuous and modulated electromagnetic radiation fields effects on sleep EEG of
rats.
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The Radiofrequency Radiation Dosimetry Handbook: reminiscences.
Effects of acute exposure to ultrahigh radiofrequency radiation on three antenna engineers.
Bioeffects of mobile telephony radiation in relation to its intensity or distance from the antenna.
Mediastinal fibrosis and radiofrequency radiation exposure: is there an association?
Effects of GSM-like radiofrequency on distortion product otoacoustic emissions in pregnant
adult rabbits.
[The biological action of physical factors in the critical periods of embryogenesis].
Fourth Level Cluster 84 (692)
Theme - Genotoxic effects of radiofrequency radiation
--Leaf Cluster 20 (126)
Theme - DNA damage after microwave radiation
Titles
Evaluation of basal DNA damage and oxidative stress in Wistar rat leukocytes after exposure to
microwave radiation.
The effect of electromagnetic field exposure on the formation of DNA single strand breaks in
human cells.
Measurement of DNA damage after exposure to 2450 MHz electromagnetic radiation.
Human fibroblasts and 900 MHz radiofrequency radiation: evaluation of DNA damage after
exposure and co-exposure to 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5h)-furanone (MX).
Electromagnetic noise inhibits radiofrequency radiation-induced DNA damage and reactive
oxygen species increase in human lens epithelial cells.
Influence of 1.8-GHz (GSM) radiofrequency radiation (RFR) on DNA damage and repair
induced by X-rays in human leukocytes in vitro.
DNA Damage of Lymphocytes in Volunteers after 4 hours Use of Mobile Phone.
Studying the synergistic damage effects induced by 1.8 GHz radiofrequency field radiation
(RFR) with four chemical mutagens on human lymphocyte DNA using comet assay in vitro.
Effect of superposed electromagnetic noise on DNA damage of lens epithelial cells induced by
microwave radiation.
[DNA damage and repair induced by acute exposure of microwave from mobile phone on
cultured human lens epithelial cells].
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Intermittent extremely low frequency electromagnetic fields cause DNA damage in a dose-
dependent way.
50-Hertz electromagnetic fields induce gammaH2AX foci formation in mouse preimplantation
embryos in vitro.
Measurement of DNA damage after acute exposure to pulsed-wave 2450 MHz microwaves in rat
brain cells by two alkaline comet assay methods.
Single- and double-strand DNA breaks in rat brain cells after acute exposure to radiofrequency
electromagnetic radiation.
Exposure to 1800 MHz radiofrequency electromagnetic radiation induces oxidative DNA base
damage in a mouse spermatocyte-derived cell line.
Measurements of alkali-labile DNA damage and protein-DNA crosslinks after 2450 MHz
microwave and low-dose gamma irradiation in vitro.
Electromagnetic fields and the induction of DNA strand breaks.
Age-related effects on induction of DNA strand breaks by intermittent exposure to
electromagnetic fields.
[Influence of 1.8 GHz microwave on DNA damage induced by ultraviolet C ray].
Non-thermal DNA breakage by mobile-phone radiation (1800 MHz) in human fibroblasts and in
transformed GFSH-R17 rat granulosa cells in vitro.
DNA and chromosomal damage in response to intermittent extremely low-frequency magnetic
fields.
The toxic effects of mobile phone radiofrequency (940 MHz) on the structure of calf thymus
DNA.
Melatonin and a spin-trap compound block radiofrequency electromagnetic radiation-induced
DNA strand breaks in rat brain cells.
Effects of in vitro exposure to power frequency magnetic fields on UV-induced DNA damage of
rat lymphocytes.
Evaluating the combinative effects on human lymphocyte DNA damage induced by ultraviolet
ray C plus 1.8 GHz microwaves using comet assay in vitro.
[Influence of 1.8 GHz microwave on DNA damage induced by 4 chemical mutagens].
Induction of DNA strand breaks by intermittent exposure to extremely-low-frequency
electromagnetic fields in human diploid fibroblasts.
60 Hz magnetic field exposure induces DNA crosslinks in rat brain cells.
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Combined effects of 872 MHz radiofrequency radiation and ferrous chloride on reactive oxygen
species production and DNA damage in human SH-SY5Y neuroblastoma cells.
8-oxoG DNA glycosylase-1 inhibition sensitizes Neuro-2a cells to oxidative DNA base damage
induced by 900 MHz radiofrequency electromagnetic radiation.
Evaluation of the genotoxicity of cell phone radiofrequency radiation in male and female rats and
mice following subchronic exposure.
Radioprotective effects of honeybee venom (Apis mellifera) against 915-MHz microwave
radiation-induced DNA damage in wistar rat lymphocytes: in vitro study.
Assessment of DNA sensitivity in peripheral blood leukocytes after occupational exposure to
microwave radiation: the alkaline comet assay and chromatid breakage assay.
Assessment of genetic damage in peripheral blood of human volunteers exposed (whole-body) to
a 200 muT, 60 Hz magnetic field.
Acute exposure to a 60 Hz magnetic field increases DNA strand breaks in rat brain cells.
Influence of a static magnetic field (250 mT) on the antioxidant response and DNA integrity in
THP1 cells.
Investigation of co-genotoxic effects of radiofrequency electromagnetic fields in vivo.
Evaluation of genotoxic effects in human leukocytes after in vitro exposure to 1950 MHz UMTS
radiofrequency field.
Adaptive response in mouse bone-marrow stromal cells exposed to 900-MHz radiofrequency
fields: Gamma-radiation-induced DNA strand breaks and repair.
Short-term exposure to 50 Hz ELF-EMF alters the cisplatin-induced oxidative response in
AT478 murine squamous cell carcinoma cells.
Measurement of DNA damage and apoptosis in Molt-4 cells after in vitro exposure to
radiofrequency radiation.
Electromagnetic fields and health: DNA-based dosimetry.
Combinative exposure effect of radio frequency signals from CDMA mobile phones and
aphidicolin on DNA integrity.
Magnetic-field-induced DNA strand breaks in brain cells of the rat.
Genotoxicity of radiofrequency signals. I. Investigation of DNA damage and micronuclei
induction in cultured human blood cells.
DNA repair after gamma irradiation in lymphocytes exposed to low-frequency pulsed
electromagnetic fields.
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Epinephrine, DNA integrity and oxidative stress in workers exposed to extremely low-frequency
electromagnetic fields (ELF-EMFs) at 132 kV substations.
Measurement of DNA damage after exposure to electromagnetic radiation in the cellular phone
communication frequency band (835.62 and 847.74 MHz).
Effect of Radiofrequency Radiation on Human Hematopoietic Stem Cells.
Mobile phone signal exposure triggers a hormesis-like effect in Atm(+/+) and Atm(-/-) mouse
embryonic fibroblasts.
Evaluation of genotoxic effects in human fibroblasts after intermittent exposure to 50 Hz
electromagnetic fields: a confirmatory study.
Single strand DNA breaks in rat brain cells exposed to microwave radiation.
DNA damage, cell kinetics and ODC activities studied in CBA mice exposed to electromagnetic
fields generated by transmission lines.
Acute low-intensity microwave exposure increases DNA single-strand breaks in rat brain cells.
The effect of electromagnetic field exposure on the formation of DNA lesions.
Single-strand DNA breaks in human hair root cells exposed to mobile phone radiation.
Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic
radiation will increase in lipopolysaccharide-induced inflammation in vitro model.
Oxidative DNA damage in rats exposed to extremely low frequency electro magnetic fields.
Ataxia telangiectasia mutated deficiency does not result in genetic susceptibility to 50 Hz
magnetic fields exposure in mouse embryonic fibroblasts.
[Effects of 2,450 MHz microwave on DNA damage induced by three chemical mutagens in
vitro].
In vitro assessment of clastogenicity of mobile-phone radiation (835 MHz) using the alkaline
comet assay and chromosomal aberration test.
Effects of pulsed electric fields on DNA of human lymphocytes.
[Blocking 1800 MHz mobile phone radiation-induced reactive oxygen species production and
DNA damage in lens epithelial cells by noise magnetic fields].
Adaptive response in mice exposed to 900 MHz radiofrequency fields: primary DNA damage.
Exposure of mammalian cells to 60-Hz magnetic or electric fields: analysis for DNA single-
strand breaks.
Impact of radio frequency electromagnetic radiation on DNA integrity in the male germline.
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Effect of GSTM1 and GSTT1 Polymorphisms on Genetic Damage in Humans Populations
Exposed to Radiation From Mobile Towers.
DNA damage induced in brain cells of CBA mice exposed to magnetic fields.
[Effects of GSM 1800 MHz radiofrequency electromagnetic fields on DNA damage in Chinese
hamster lung cells].
Loss of transforming activity of plasmid DNA (pBR322) in E. coli caused by singlet molecular
oxygen.
Decreased DNA repair rates and protection from heat induced apoptosis mediated by
electromagnetic field exposure.
Cytotoxic and genotoxic effect in RTG-2 cell line exposed to selected biocides used in the
disinfection of cooling towers.
Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide
excision repair in serum-deprived human glioblastoma cells.
Adaptive response in mice exposed to 900 MHZ radiofrequency fields: bleomycin-induced DNA
and oxidative damage/repair.
14.6 mT ELF magnetic field exposure yields no DNA breaks in model system Salmonella, but
provides evidence of heat stress protection.
Effect of Radiofrequency Radiation Emitted from 2G and 3G Cell Phone on Developing Liver of
Chick Embryo - A Comparative Study.
Cell type-specific genotoxic effects of intermittent extremely low-frequency electromagnetic
fields.
Biological effects of non-ionizing electromagnetic fields: Two sides of a coin.
Radiofrequency exposure and mammalian cell toxicity, genotoxicity, and transformation.
Studying the protein expression in human B lymphoblastoid cells exposed to 1.8-GHz (GSM)
radiofrequency radiation (RFR) with protein microarray.
Mobile phone radiation induces mode-dependent DNA damage in a mouse spermatocyte-derived
cell line: a protective role of melatonin.
An evaluation of genotoxicity in human neuronal-type cells subjected to oxidative stress under
an extremely low frequency pulsed magnetic field.
Exposure of rat brain to 915 MHz GSM microwaves induces changes in gene expression but not
double stranded DNA breaks or effects on chromatin conformation.
Radiofrequency (microwave) radiation exposure of mammalian cells during UV-induced DNA
repair synthesis.
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[Effect of low-intensity microwave of on mitomycin C-induced genotoxicity in vitro].
Effects of 1800 MHz RF-EMF exposure on DNA damage and cellular functions in primary
cultured neurogenic cells.
Importance of DNA fragmentation in apoptosis with regard to TUNEL specificity.
Oxidative changes and apoptosis induced by 1800-MHz electromagnetic radiation in NIH/3T3
cells.
The genomic effects of cell phone exposure on the reproductive system.
Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial
DNA in primary cultured neurons.
Mitochondrial DNA damage and oxidative damage in HL-60 cells exposed to 900MHz
radiofrequency fields.
Microwave miniprep of total genomic DNA from fungi, plants, protists and animals for PCR.
Exposure to 915 MHz radiation induces micronuclei in Vicia faba root tips.
[Pulse-modulated Electromagnetic Radiation of Extremely High Frequencies Protects Cellular
DNA against Damaging Effect of Physico-Chemical Factors in vitro].
GSM 900 MHz cellular phone radiation can either stimulate or depress early embryogenesis in
Japanese quails depending on the duration of exposure.
Microwaves from UMTS/GSM mobile phones induce long-lasting inhibition of 53BP1/gamma-
H2AX DNA repair foci in human lymphocytes.
915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci
in human lymphocytes from hypersensitive and healthy persons.
Synergism between electricity and ionizing radiation.
[Mechanisms of electromagnetic radiation damaging male reproduction].
Comments on "Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic
effects in vitro in human fibroblasts but not in lymphocytes" by Schwarz et al. (Int Arch Occup
Environ Health 2008: doi: 10.1007/s00420-008-0305-5).
Genotoxic effects of exposure to radiofrequency electromagnetic fields (RF-EMF) in HL-60
cells are not reproducible.
[Changes in the chromatin structure of lymphoid cells under the influence of low-intensity
extremely high-frequency electromagnetic radiation against the background of inflammatory
process].
Effect of 7 mT static magnetic field and iron ions on rat lymphocytes: apoptosis, necrosis and
free radical processes.
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[Cytophotometry of myelokaryocyte DNA following a single exposure to low-intensity UHF
irradiation].
Genotoxicity of radiofrequency radiation. DNA/Genetox Expert Panel.
Effect of Mobile Phone Radiation on Cardiovascular Development of Chick Embryo.
Effects of gamma rays, ultraviolet radiation, sunlight, microwaves and electromagnetic fields on
gene expression mediated by human immunodeficiency virus promoter.
Radiofrequency radiation (900 MHz)-induced DNA damage and cell cycle arrest in testicular
germ cells in swiss albino mice.
Effect of exposure to 900 MHz radiofrequency radiation on intrachromosomal recombination in
pKZ1 mice.
Evaluation of DNA damage in spinal cord and mutagenic effect of a Phalpha1beta recombinant
toxin with analgesic properties from the Phoneutria nigriventer spider.
Microwaves from GSM mobile telephones affect 53BP1 and gamma-H2AX foci in human
lymphocytes from hypersensitive and healthy persons.
Effects of co-exposure to extremely low frequency (ELF) magnetic fields and benzene or
benzene metabolites determined in vitro by the alkaline comet assay.
Study of low-intensity 2450-MHz microwave exposure enhancing the genotoxic effects of
mitomycin C using micronucleus test and comet assay in vitro.
Effects of radiofrequency electromagnetic waves (RF-EMW) from cellular phones on human
ejaculated semen: an in vitro pilot study.
Oxidative and mutagenic effects of low intensity GSM 1800 MHz microwave radiation.
Effects of Long-Term Exposure to 60 GHz Millimeter-Wavelength Radiation on the
Genotoxicity and Heat Shock Protein (Hsp) Expression of Cells Derived from Human Eye.
Investigation of potential genotoxic effects of low frequency electromagnetic fields on
Escherichia coli.
[Impact of mobile phone radiation on the quality and DNA methylation of human sperm in
vitro].
[Effects of low-intensity extremely high frequency electromagnetic radiation on chromatin
structure of lymphoid cells in vivo and in vitro].
Characterisation of transcriptionally active and inactive chromatin domains in neurons.
Effect of microwave exposure on the ovarian development of Drosophila melanogaster.
Exposure to non-ionizing electromagnetic radiation of public risk prevention instruments
threatens the quality of spermatozoids.
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The biological effects of radiofrequency radiation: a critical review and recommendations.
Increase in the mitotic recombination frequency in Drosophila melanogaster by magnetic field
exposure and its suppression by vitamin E supplement.
[Mechanisms of the combined effect of SHF electromagnetic radiation and hydrogen peroxide on
the viability of microorganisms].
RNA-dependent DNA polymerase (reverse transcriptase) from avian myeloblastosis virus: a zinc
metalloenzyme.
--Leaf Cluster 28 (100)
Theme - Chromosome damage in lymphocytes exposed to radiofrequency radiation
Titles
Chromosome damage and micronucleus formation in human blood lymphocytes exposed in vitro
to radiofrequency radiation at a cellular telephone frequency (847.74 MHz, CDMA).
Cytogenetic studies in human blood lymphocytes exposed in vitro to 2.45 GHz or 8.2 GHz
radiofrequency radiation.
Cytogenetic studies in human blood lymphocytes exposed in vitro to radiofrequency radiation at
a cellular telephone frequency (835.62 MHz, FDMA).
Effects of modulated microwave radiation at cellular telephone frequency (1.95 GHz) on X-ray-
induced chromosome aberrations in human lymphocytes in vitro.
Influence of radiofrequency radiation on chromosome aberrations in CHO cells and its
interaction with DNA-damaging agents.
Increased levels of numerical chromosome aberrations after in vitro exposure of human
peripheral blood lymphocytes to radiofrequency electromagnetic fields for 72 hours.
Comparison of chromosome aberrations in peripheral blood lymphocytes from people
occupationally exposed to ionizing and radiofrequency radiation.
935 MHz cellular phone radiation. An in vitro study of genotoxicity in human lymphocytes.
Evaluation of genotoxic effects in human peripheral blood leukocytes following an acute in vitro
exposure to 900 MHz radiofrequency fields.
Genetic damage in mammalian somatic cells exposed to radiofrequency radiation: a meta-
analysis of data from 63 publications (1990-2005).
Mutagenic and morphologic impacts of 1.8GHz radiofrequency radiation on human peripheral
blood lymphocytes (hPBLs) and possible protective role of pre-treatment with Ginkgo biloba
(EGb 761).
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Effects of 1-week and 6-week exposure to GSM/DCS radiofrequency radiation on micronucleus
formation in B6C3F1 mice.
Influence of GSM signals on human peripheral lymphocytes: study of genotoxicity.
The repair of gamma-ray-induced chromosomal damage in human lymphocytes after exposure to
extremely low frequency electromagnetic fields.
Exposure of human peripheral blood lymphocytes to electromagnetic fields associated with
cellular phones leads to chromosomal instability.
Genetic damage in human cells exposed to non-ionizing radiofrequency fields: a meta-analysis
of the data from 88 publications (1990-2011).
Incidence of micronuclei in human peripheral blood lymphocytes exposed to modulated and
unmodulated 2450 MHz radiofrequency fields.
Effects of in vivo exposure to GSM-modulated 900 MHz radiation on mouse peripheral
lymphocytes.
Clastogenic effects in human lymphocytes of power frequency electric fields: in vivo and in vitro
studies.
Frequency of micronuclei in the blood and bone marrow cells of mice exposed to ultra-wideband
electromagnetic radiation.
Micronucleus assay and lymphocyte mitotic activity in risk assessment of occupational exposure
to microwave radiation.
Effect of nuclear magnetic resonance on chromosomes of mouse bone marrow cells.
In vitro lymphocyte proliferation induced by radio-frequency electromagnetic radiation under
isothermal conditions.
Induction of adaptive response in human blood lymphocytes exposed to 900 MHz
radiofrequency fields: influence of cell cycle.
Lymphocytes and low-frequency electromagnetic fields.
Chromosomal effects in lymphocytes of 400 kV-substation workers.
Effects of high-frequency electromagnetic fields on human lymphocytes in vitro.
Assessment of genotoxicity and genomic instability in rat primary astrocytes exposed to 872
MHz radiofrequency radiation and chemicals.
Increased chromatid-type chromosomal aberrations in mouse m5S cells exposed to power-line
frequency magnetic fields.
Cytogenetic studies in human cells exposed in vitro to GSM-900 MHz radiofrequency radiation
using R-banded karyotyping.
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Genotoxic effects of 3 T magnetic resonance imaging in cultured human lymphocytes.
Age-dependent effects of in vitro radiofrequency exposure (mobile phone) on CD95+ T helper
human lymphocytes.
Micronuclei in peripheral blood and bone marrow cells of mice exposed to 42 GHz
electromagnetic millimeter waves.
Cytogenetic effects of 900 MHz (GSM) microwaves on human lymphocytes.
Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic effects in vitro in
human fibroblasts but not in lymphocytes.
Elevated sister chromatid exchange frequencies in dividing human peripheral blood lymphocytes
exposed to 50 Hz magnetic fields.
Chromosomal damage in human diploid fibroblasts by intermittent exposure to extremely low-
frequency electromagnetic fields.
Micronuclei in the blood and bone marrow cells of mice exposed to specific complex time-
varying pulsed magnetic fields.
Enhanced cytotoxic and genotoxic effects of gadolinium following ELF-EMF irradiation in
human lymphocytes.
[Effects of electromagnetic radiation on health and immune function of operators].
[Chromosome abnormalities caused by computer video display monitors' radiation].
Effect of low-level pulsed electromagnetic fields on human chromosomes in vitro: analysis of
chromosomal aberrations.
Effect of high-frequency electromagnetic fields with a wide range of SARs on chromosomal
aberrations in murine m5S cells.
Cytogenetic effects of 935.2-MHz (GSM) microwaves alone and in combination with mitomycin
C.
Effect of 900 MHz Electromagnetic Radiation on the Induction of ROS in Human Peripheral
Blood Mononuclear Cells.
Analysis of chromosomal aberrations, sister chromatid exchanges and micronuclei among power
linesmen with long-term exposure to 50-Hz electromagnetic fields.
A chromosomal study of workers with long-term exposure to radio-frequency radiation.
Induction of adaptive response in mice exposed to 900MHz radiofrequency fields: application of
micronucleus assay.
Genetic damage in subjects exposed to radiofrequency radiation.
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Investigation of the genotoxic effect of microwave irradiation in rat bone marrow cells: in vivo
exposure.
[Effect of electromagnetic radiation on T-lymphocyte subpopulations and immunoglobulin level
in human blood serum after occupational exposure].
Effects of low frequency electromagnetic fields on expression of lymphocyte subsets and
production of cytokines of men and women employed in a museum.
Terahertz radiation increases genomic instability in human lymphocytes.
Cytogenetic damage in human lymphocytes following GMSK phase modulated microwave
exposure.
Aneuploidy studies in human cells exposed in vitro to GSM-900 MHz radiofrequency radiation
using FISH.
X-rays, microwaves and vinyl chloride monomer: their clastogenic and aneugenic activity, using
the micronucleus assay on human lymphocytes.
[The effect of ultrahigh-frequency radiation on adaptation thresholds and the damages to blood
system cells].
Erythropoietic changes in rats after 2.45 GJz nonthermal irradiation.
Cytogenetic observations in human peripheral blood leukocytes following in vitro exposure to
THz radiation: a pilot study.
Effect of long-term 50 Hz magnetic field exposure on the micronucleated polychromatic
erythrocytes of mice.
Interactive developmental toxicity of radiofrequency radiation and 2-methoxyethanol in rats.
Proflavin and microwave radiation: absence of a mutagenic interaction.
Effects of GSM-modulated 900 MHz radiofrequency electromagnetic fields on the hematopoietic
potential of mouse bone marrow cells.
Follow up study on the immune response to low frequency electromagnetic fields in men and
women working in a museum.
Adverse and beneficial effects in Chinese hamster lung fibroblast cells following radiofrequency
exposure.
Cytogenetic effects of extremely low frequency magnetic field on Wistar rat bone marrow.
[Chromosome studies of personnel exposed to electromagnetic radiation at radar centers].
Evaluation of the cytogenotoxic damage in immature and mature rats exposed to 900 MHz
radiofrequency electromagnetic fields.
Clastogenicity and aneuploidy in newborn and adult mice exposed to 50 Hz magnetic fields.
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Effects of electromagnetic fields on the immune systems of occupationally exposed humans and
mice.
954 MHz microwaves enhance the mutagenic properties of mitomycin C.
[Comparative effectiveness of different tests to determine the mutagenicity of certain factors in
mammals. II. Frequency of anomalous sperm head in mice exposed to different factors].
Cytotoxic and genotoxic effects of high-frequency electromagnetic fields (GSM 1800 MHz) on
immature and mature rats.
Interactions of radiofrequency radiation on 2-methoxyethanol teratogenicity in rats.
[The cytogenetic action of electromagnetic fields in the short-wave range].
In vitro fertilization of mouse ova by spermatozoa exposed isothermally to radio-frequency
radiation.
Effect of Exposure to 900 MHz GSM Mobile Phone Radiofrequency Radiation on Estrogen
Receptor Methylation Status in Colon Cells of Male Sprague Dawley Rats.
Adaptive response in mouse bone marrow stromal cells exposed to 900MHz radiofrequency
fields: Impact of poly (ADP-ribose) polymerase (PARP).
Effects of electromagnetic fields produced by radiotelevision broadcasting stations on the
immune system of women.
Assessment of radio-frequency electromagnetic radiation by the micronucleus test in bovine
peripheral erythrocytes.
[Levels of immunoglobulin and subpopulations of T lymphocytes and NK cells in men
occupationally exposed to microwave radiation in frequencies of 6-12 GHz].
Association of low job control with a decrease in memory (CD4+ CD45RO+) T lymphocytes in
Japanese middle-aged male workers in an electric power plant.
Effects of extremely low-frequency electromagnetic fields on delayed chromosomal instability
induced by bleomycin in normal human fibroblast cells.
[Proliferation of bone marrow cells upon exposure to constant magnetic fields of ultra-high
strength].
The immune response of women with prolonged exposure to electromagnetic fields produced by
radiotelevision broadcasting stations.
Acute exposure to 930 MHz CW electromagnetic radiation in vitro affects reactive oxygen
species level in rat lymphocytes treated by iron ions.
The process of myelopoiesis in guinea pigs under conditions of a static magnetic field.
[Effect of electromagnetic radiation of millimetric wave band on genome of somatic cells].
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Suppression of T-lymphocyte cytotoxicity following exposure to 60-Hz sinusoidal electric fields.
Reactive oxygen species formation and apoptosis in human peripheral blood mononuclear cell
induced by 900 MHz mobile phone radiation.
Occupational exposure to high frequency electromagnetic fields and its effect on human immune
parameters.
Does radio frequency radiation induce micronuclei frequency in exfoliated bladder cells of
diabetic rats?
Radiofrequency radiation and the immune system. Part 3. In vitro effects on human
immunoglobin and on murine T- and B-lymphocytes.
Leukocyte trafficking in response to magnetic resonance imaging.
Combined effects of traffic and electromagnetic fields on the immune system of fertile atopic
women.
Developmental toxicity interactions of methanol and radiofrequency radiation or 2-
methoxyethanol in rats.
Neoplastic transformation in C3H 10T(1/2) cells after exposure to 835.62 MHz FDMA and
847.74 MHz CDMA radiations.
Adaptive response in animals exposed to non-ionizing radiofrequency fields: some underlying
mechanisms.
Probing lymphoma infiltration in spleen of AKR/J mice chronically exposed to electromagnetic
fields for risk assessment--toward noninvasive modeling.
Combined exposure of ELF magnetic fields and x-rays increased mutant yields compared with x-
rays alone in pTN89 plasmids.
--Leaf Cluster 45 (179)
Theme - Adverse effects of low-frequency EMF on cells
Titles
Extremely low frequency variable electromagnetic fields affect cancer and noncancerous cells in
vitro differently: Preliminary study.
Effect of electromagnetic field exposure on chemically induced differentiation of friend
erythroleukemia cells.
Extremely low-frequency electromagnetic fields cause G1 phase arrest through the activation of
the ATM-Chk2-p21 pathway.
Extremely low frequency electromagnetic field exposure promotes differentiation of pituitary
corticotrope-derived AtT20 D16V cells.
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Effect of extremely low-frequency electromagnetic fields on antioxidant activity in the human
keratinocyte cell line NCTC 2544.
Electromagnetic fields with frequencies of 5, 60 and 120 Hz affect the cell cycle and viability of
human fibroblast BJ in vitro.
Bidirectional frequency-dependent effect of extremely low-frequency electromagnetic field on E.
coli K-12.
Melatonin protects rat cerebellar granule cells against electromagnetic field-induced increases in
Na(+) currents through intracellular Ca(2+) release.
Neuroprotective effects of lotus seedpod procyanidins on extremely low frequency
electromagnetic field-induced neurotoxicity in primary cultured hippocampal neurons.
Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in
Doxorubicin-treated Mouse Osteosarcoma Cells.
Effects of low frequency electromagnetic field on proliferation of human epidermal stem cells:
An in vitro study.
Extremely low-frequency electromagnetic field exposure enhances inflammatory response and
inhibits effect of antioxidant in RAW 264.7 cells.
[Effects of extremely low frequency pulsed electromagnetic field on different-derived osteoblast-
like cells].
Impact of extremely low frequency electromagnetic fields on CD4 expression in peripheral blood
mononuclear cells.
[Effect of long-term power frequency electromagnetic field exposure on proliferation and
apoptosis of SRA01/04 cells].
[Effect of pulsed electromagnetic field with different frequencies on the proliferation, apoptosis
and migration of human ovarian cancer cells].
Extremely low frequency electromagnetic fields affect proliferation and mitochondrial activity of
human cancer cell lines.
Effects of extremely low-frequency pulsed electromagnetic fields on morphological and
biochemical properties of human breast carcinoma cells (T47D).
Correlation between pulsed electromagnetic fields exposure time and cell proliferation increase
in human osteosarcoma cell lines and human normal osteoblast cells in vitro.
Influence of extremely low frequency electromagnetic fields on the swimming behavior of
ciliates.
Suppression of a differentiation response in MC-3T3-E1 osteoblast-like cells by sustained, low-
level, 30 Hz magnetic-field exposure.
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Exposure of rats to extremely low-frequency electromagnetic fields (ELF-EMF) alters cytokines
production.
Exposure to extremely low frequency electromagnetic fields alters the calcium dynamics of
cultured entorhinal cortex neurons.
Effects of electromagnetic fields on molecules and cells.
Effect of intermittent and continuous exposure to electromagnetic fields on cultured hippocampal
cells.
The impact of electromagnetic field at a frequency of 50 Hz and a magnetic induction of 2.5 mT
on viability of pineal cells in vitro.
Induction of apoptotic cell death in human leukemic cell line, HL-60, by extremely low
frequency electric magnetic fields: analysis of the possible mechanisms in vitro.
Acute effects of low-frequency electromagnetic fields on leukocyte-endothelial interactions in
vivo.
Effects of 50 Hz pulsed electromagnetic fields on the growth and cell cycle arrest of
mesenchymal stem cells: an in vitro study.
Haemopoietic cell proliferation in murine bone marrow cells exposed to extreme low frequency
(ELF) electromagnetic fields.
Extremely low frequency electromagnetic field exposure affects fertilization outcome in swine
animal model.
Effects of extremely low frequency electromagnetic fields on human fetal scleral fibroblasts.
Action of a 50 Hz magnetic field on proliferation of cells in culture.
In vitro evaluation of teratogenic effects by time-varying MR gradient fields on fetal human
fibroblasts.
Chronic electromagnetic field exposure decreases HSP70 levels and lowers cytoprotection.
Effect of exposure to an extremely low frequency-electromagnetic field on the cellular collagen
with respect to signaling pathways in osteoblast-like cells.
Effect of puerarin on matrix metalloproteinase-2 in human fetal scleral fibroblasts treated with
low frequency electromagnetic fields.
Effects of extremely low frequency electromagnetic fields on intracellular calcium transients in
cardiomyocytes.
[Biological effects of non-ionizing electromagnetic radiation].
Effects of 60 Hz extremely low frequency magnetic fields (EMF) on radiation- and chemical-
induced mutagenesis in mammalian cells.
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Exposure to ELF-pulse modulated X band microwaves increases in vitro human astrocytoma cell
proliferation.
Bioelectromagnetic field effects on cancer cells and mice tumors.
A 700 MHz 1H-NMR study reveals apoptosis-like behavior in human K562 erythroleukemic
cells exposed to a 50 Hz sinusoidal magnetic field.
Low intensity and frequency pulsed electromagnetic fields selectively impair breast cancer cell
viability.
Cellular effects of electromagnetic fields.
50 Hz extremely low frequency electromagnetic fields enhance protein carbonyl groups content
in cancer cells: effects on proteasomal systems.
Pulsed electromagnetic fields accelerate apoptotic rate in osteoclasts.
A short-term extremely low frequency electromagnetic field exposure increases circulating
leukocyte numbers and affects HPA-axis signaling in mice.
Delineation of electric and magnetic field effects of extremely low frequency electromagnetic
radiation on transcription.
Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signaling
pathway in mouse spermatogenic cells in vitro and thus may affect male fertility.
Power-frequency electromagnetic fields and the capacitative calcium entry system in SV40-
transformed Swiss 3T3 cells.
Transferrin receptors and natural killer cell lysis. A study using Colo 205 cells exposed to 60 Hz
electromagnetic fields.
Electromagnetic fields and cells.
Calcium protects differentiating neuroblastoma cells during 50 Hz electromagnetic radiation.
A review of in vitro studies: low-frequency electromagnetic fields.
Electric and/or magnetic field effects on DNA structure and function in cultured human cells.
Effects of long-term 50Hz power-line frequency electromagnetic field on cell behavior in Balb/c
3T3 cells.
Low-intensity electromagnetic fields induce human cryptochrome to modulate intracellular
reactive oxygen species.
Effect of extremely low frequency (ELF) magnetic field exposure on morphological and
biophysical properties of human lymphoid cell line (Raji).
Effect of 0.2 T static magnetic field on human neurons: remodeling and inhibition of signal
transduction without genome instability.
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Exposure to 1.8 GHz electromagnetic fields affects morphology, DNA-related Raman spectra
and mitochondrial functions in human lympho-monocytes.
Effects of 60-Hz fields, estradiol and xenoestrogens on human breast cancer cells.
Influence of a 50 hz extra low frequency electromagnetic field on spermatozoa motility and
fertilization rates in rabbits.
Semi-quantitative proteomics of mammalian cells upon short-term exposure to non-ionizing
electromagnetic fields.
[Experimental data on extremely low frequency (ELF) electromagnetic fields].
[Effect of static magnetic field on development toxicity of rat embryonic midbrain neurons
cells].
[Flow cytometric analysis of the effects of 50 Hz magnetic fields on mouse spermatogenesis].
Dose dependence of acetylcholinesterase activity in neuroblastoma cells exposed to modulated
radio-frequency electromagnetic radiation.
Increased apoptosis, changes in intracellular Ca2+, and functional alterations in lymphocytes and
macrophages after in vitro exposure to static magnetic field.
Biomarkers of induced electromagnetic field and cancer.
IGF-II receptor number is increased in TE-85 osteosarcoma cells by combined magnetic fields.
Nonlinear cell response to strong electric fields.
Mechanisms underlying spontaneous calcium spiking in aequorin-loaded ROS 17/2.8 cells.
The effects of low-energy 60-Hz environmental electromagnetic fields upon the growth-related
enzyme ornithine decarboxylase.
Effects of extremely low frequency electromagnetic fields on turkeys.
The Bioeffects Resulting from Prokaryotic Cells and Yeast Being Exposed to an 18 GHz
Electromagnetic Field.
The effect of electromagnetic field on reactive oxygen species production in human neutrophils
in vitro.
[Effect of low-frequency electromagnetic fields on the individual functional systems of the
body].
[Modeling of the effect of modulated electromagnetic radiation on animal cells].
2.45-Gz wireless devices induce oxidative stress and proliferation through cytosolic Ca(2)(+)
influx in human leukemia cancer cells.
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[Influence of electromagnetic radiation of different ranges on the transmembrane transport of
Na+, K+, and Ca2+ ions in normal and tumor cells].
Reactive oxygen species levels and DNA fragmentation on astrocytes in primary culture after
acute exposure to low intensity microwave electromagnetic field.
Analysis of the effect of a 60 Hz AC field on histamine release by rat peritoneal mast cells.
Intramembrane protein distribution in cell cultures is affected by 50 Hz pulsed magnetic fields.
Calcium homeostasis of isolated heart muscle cells exposed to pulsed high-frequency
electromagnetic fields.
Do electromagnetic fields interact directly with DNA?
Extremely low frequency 7 Hz 100 microT electromagnetic radiation promotes differentiation in
the human epithelial cell line HaCaT.
Effects of 60 Hz electromagnetic field exposure on testicular germ cell apoptosis in mice.
Antiproliferative effect of millimeter radiation on human erythromyeloid leukemia cell line
K562 in culture: ultrastructural- and metabolic-induced changes.
A 3 milliTesla 60 Hz magnetic field is neither mutagenic nor co-mutagenic in the presence of
menadione and MNU in a transgenic rat cell line.
Exposure to low frequency pulsed electromagnetic fields increases interleukin-1 and interleukin-
6 production by human peripheral blood mononuclear cells.
Enhanced proliferation caused by a low frequency weak magnetic field in chick embryo
fibroblasts is suppressed by radical scavengers.
The interaction between electromagnetic fields at megahertz, gigahertz and terahertz frequencies
with cells, tissues and organisms: risks and potential.
In vitro evaluation of magnetic resonance imaging at 3.0 tesla on clonogenic ability,
proliferation, and cell cycle in human embryonic lung fibroblasts.
Increased ornithine decarboxylase activity in cultured cells exposed to low energy modulated
microwave fields and phorbol ester tumor promoters.
Subchronic effects on leukocyte-endothelial interactions in mice by whole body exposure to
extremely low frequency electromagnetic fields.
Acute and chronic effects of exposure to a 1-mT magnetic field on the cytoskeleton, stress
proteins, and proliferation of astroglial cells in culture.
Effects of weak environmental magnetic fields on the spontaneous bioelectrical activity of snail
neurons.
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Long-term effects of repetitive exposure to a static magnetic field (1.5 T) on proliferation of
human fetal lung fibroblasts.
Modification of electrokinetic properties of nuclei in human buccal epithelial cells by electric
fields.
Bioeffects induced by exposure to microwaves are mitigated by superposition of ELF noise.
Electromagnetic fields (UHF) increase voltage sensitivity of membrane ion channels; possible
indication of cell phone effect on living cells.
Synaptosomal acetylcholinesterase activity variation pattern in the presence of electromagnetic
fields.
Chicken embryo fibroblasts exposed to weak, time-varying magnetic fields share cell
proliferation, adenosine deaminase activity, and membrane characteristics of transformed cells.
Low-frequency electromagnetic fields alter the replication cycle of MS2 bacteriophage.
Effects of exposure to electromagnetic radiation at 835 MHz on growth, morphology and
secretory characteristics of a mast cell analogue, RBL-2H3.
Cell membrane lipid molecular dynamics in a solenoid versus a magnetically shielded room.
Studies on the possible biological effects of 50 Hz electric and/or magnetic fields: evaluation of
some glycolytic enzymes, glycolytic flux, energy and oxido-reductive potentials in human
erythrocytes exposed in vitro to power frequency fields.
Modelling the internal field distribution in human erythrocytes exposed to MW radiation.
Nonlinear dynamical law governs magnetic field induced changes in lymphoid phenotype.
Extremely low frequency electromagnetic fields and heat shock can increase microvesicle
motility in astrocytes.
[Extremely low frequency electromagnetic radiation enhanced energy metabolism and induced
oxidative stress in Caenorhabditis elegans].
Exposure to low-frequency pulsed electromagnetic fields increases mitogen-induced lymphocyte
proliferation in Down's syndrome.
Injury by electrical forces: pathophysiology, manifestations, and therapy.
Joint actions of environmental nonionizing electromagnetic fields and chemical pollution in
cancer promotion.
Cellular communication in clone 9 cells exposed to magnetic fields.
Spindle disturbances in human-hamster hybrid (A(L) ) cells induced by the electrical component
of the mobile communication frequency range signal.
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Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6:
microwaves act through voltage-gated calcium channel activation to induce biological impacts at
non-thermal levels, supporting a paradigm shift for microwave/lower frequency electromagnetic
field action.
Neoplastic transformation of C3H/10T1/2 cells following exposure to 120-Hz modulated 2.45-
GHz microwaves and phorbol ester tumor promoter.
Effects of 50 Hz electromagnetic fields on rat cortical synaptosomes.
Effect of pulsed electromagnetic field exposure on adenosine receptors in rat brain.
[Effect of sinusoidal electricity magnetic fields on the proliferation and differentiation of
osteoblasts in vitro].
A study of the electric field distribution in erythrocyte and rod shape cells from direct RF
exposure.
Carcinogenesis and initiation of cell cycling by charge-induced membrane clusters may be due to
mitogen receptors and Na+/H+ antiports.
The effect of a high frequency electromagnetic field in the microwave range on red blood cells.
[A static magnetic field loading system for in vitro cultured cells].
Mobile phones modulate response patterns of human brain activity.
Cytokine profile of human peripheral blood mononuclear cells exposed to 50 Hz EMF.
Low-Frequency Electromagnetic Field Exposure Enhances Extracellular Trap Formation by
Human Neutrophils through the NADPH Pathway.
Alterations in protein kinase activity following exposure of cultured human lymphocytes to
modulated microwave fields.
Offset of the vacuolar potential of Characean cells in response to electromagnetic radiation over
the range 250 Hz-250 kHz.
Effect of 935-MHz phone-simulating electromagnetic radiation on endometrial glandular cells
during mouse embryo implantation.
Human standing balance is affected by exposure to pulsed ELF magnetic fields: light intensity-
dependent effects.
Effects of ELF (1-120 Hz) and modulated (50 Hz) RF fields on the efflux of calcium ions from
brain tissue in vitro.
Influence of extremely low frequency magnetic fields on Ca2+ signaling and NMDA receptor
functions in rat hippocampus.
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A 50 Hz sinusoidal magnetic field does not damage MG-63 three-dimensional tumor spheroids
but induces changes in their invasive properties.
A mechanism for action of oscillating electric fields on cells.
Electromagnetic fields (1.8 GHz) increase the permeability to sucrose of the blood-brain barrier
in vitro.
ELF magnetic fields increase amino acid uptake into Vicia faba L. roots and alter ion movement
across the plasma membrane.
Nonlinear determinism in the immune system. In vivo influence of electromagnetic fields on
different functions of murine lymphocyte subpopulations.
Modulation of cell death in the rat thymus. Light and electron microscopic investigations.
Spindle disturbances in human-hamster hybrid (AL) cells induced by mobile communication
frequency range signals.
Occupational exposure to static, ELF, VF and VLF magnetic fields and immune parameters.
Role of radical pairs and feedback in weak radio frequency field effects on biological systems.
Vacuolar hyperpolarizing offsets in characean cells exposed to mono- and bichromatic CW and
to squarewave-modulated electromagnetic radiation in the band 200-1,000 MHz.
Evaluations of Acute and Sub-Acute Biological Effects of Narrowband and Moderate-Band High
Power Electromagnetic Waves on Cellular Spheroids.
A 0.5 G, 60 Hz magnetic field suppresses melatonin production in pinealocytes.
Response of the seminiferous epithelium of the mouse exposed to low dose high energy (HZE)
and electromagnetic radiation.
Initial studies on the effects of combined 60 Hz electric and magnetic field exposure on the
immune system of nonhuman primates.
Induction of stress proteins by electromagnetic fields in cultured HL-60 cells.
Electromagnetic fields may act via calcineurin inhibition to suppress immunity, thereby
increasing risk for opportunistic infection: Conceivable mechanisms of action.
The vacuolar potential of Characean cells subjected to electromagnetic radiation in the range
200-8,200 MHz.
Radiation and brain calcium: a review and critique.
Effects of a moderate-intensity static magnetic field on VEGF-A stimulated endothelial capillary
tubule formation in vitro.
Low-amplitude, high-frequency electromagnetic field exposure causes delayed and reduced
growth in Rosa hybrida.
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[The laboratory detection of intra-cellular factors of anti-viral defense under community-
acquired pneumonia in evaluation of effects of low-intensity microwave radiation].
Induced mitogenic activity in AML-12 mouse hepatocytes exposed to low-dose ultra-wideband
electromagnetic radiation.
Are there modulated electromagnetic field effects on human conscious perception during
attentional blink test?
Effects of electromagnetic radiation in the range 20-300 MHz on the vacuolar potential of
characean cells.
Frohlich electromagnetic radiation from human leukocytes: implications for leukocyte adherence
inhibition test.
Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance
of processes driven by the calcium ion signal.
Diacetyl and 2,3-pentanedione exposure of human cultured airway epithelial cells: Ion transport
effects and metabolism of butter flavoring agents.
[Mechanism of the biological impact of weak electromagnetic fields and in vitro effects of
degassing of blood].
Effects of 45-Hz magnetic fields on the functional state of the human brain.
Some characteristics of the glutathione cycle revealed by ionising and non-ionising
electromagnetic radiation.
Magnetic Field Reference Levels for Arbitrary Periodic Waveforms for Prevention of Peripheral
Nerve Stimulation.
Magnetism and cardiac arrhythmias.
Aluminum, calcium ion and radiofrequency synergism in acceleration of lymphomagenesis.
Low-frequency electromagnetic fields induce a stress effect upon higher plants, as evident by the
universal stress signal, alanine.
Electromagnetic Fields and Stem Cell Fate: When Physics Meets Biology.
Inhibition of neuronal high-voltage activated calcium channels by the omega-phoneutria
nigriventer Tx3-3 peptide toxin.
Effect of pulsed high frequency electromagnetic radiation on embryonic mouse palate in vitro.
[The physical mechanism of the effect of low-intensity electromagnetic radiation on biological
cells].
[Changes in the acaricidal properties of organophosphorus compounds under the influence of
magnetic resonance treatment].
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Functional changes in human peripheral neutrophils in workers with different exposure to
noxious agents.
Relationship between the Contents of Cyclins, Cyclin-Dependent Kinases, and Their Inhibitors
in Whole Blood Mononuclear Leukocytes during the Postclinical Stage of Community-Acquired
Pneumonia under the Influence of 1-GHz Microwaves.
Circadian locomotor activity of Musca flies: recording method and effects of 10 Hz square-wave
electric fields.
The spark of life: electricity and regeneration.
Sensitive model with which to detect athermal effects of non-ionizing electromagnetic radiation.
--Leaf Cluster 24 (111)
Theme - Gene expression alterations following radiofrequency exposure
Titles
2.45 GHz radiofrequency fields alter gene expression in cultured human cells.
Whole-genome expression analysis in primary human keratinocyte cell cultures exposed to 60
GHz radiation.
Analysis of gene expression in a human-derived glial cell line exposed to 2.45 GHz continuous
radiofrequency electromagnetic fields.
Analysis of gene expression in mouse brain regions after exposure to 1.9 GHz radiofrequency
fields.
Analysis of proto-oncogene and heat-shock protein gene expression in human derived cell-lines
exposed in vitro to an intermittent 1.9 GHz pulse-modulated radiofrequency field.
Characterization of biological effect of 1763 MHz radiofrequency exposure on auditory hair
cells.
Using model organism Saccharomyces cerevisiae to evaluate the effects of ELF-MF and RF-
EMF exposure on global gene expression.
Expression of cancer-related genes in human cells exposed to 60 Hz magnetic fields.
Effects on protein kinase C and gene expression in a human mast cell line, HMC-1, following
microwave exposure.
Gene expression analysis of a human lymphoblastoma cell line exposed in vitro to an
intermittent 1.9 GHz pulse-modulated radiofrequency field.
Mobile phone radiation causes changes in gene and protein expression in human endothelial cell
lines and the response seems to be genome- and proteome-dependent.
Gene expression changes in human cells after exposure to mobile phone microwaves.
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Gene expression profiles in white blood cells of volunteers exposed to a 50 Hz electromagnetic
field.
Gene Expression Analysis in Human Peripheral Blood Cells after 900 MHz RF-EMF Short-
Term Exposure.
In vitro study of the effects of ELF electric fields on gene expression in human epidermal cells.
Analysis of gene expression in two human-derived cell lines exposed in vitro to a 1.9 GHz pulse-
modulated radiofrequency field.
[Global gene response to GSM 1800 MHz radiofrequency electromagnetic field in MCF-7 cells].
Biological effects of EMF exposure on Ets genes.
Evaluation of HSP70 expression and DNA damage in cells of a human trophoblast cell line
exposed to 1.8 GHz amplitude-modulated radiofrequency fields.
Effects of the exposure to intermittent 1.8 GHz radio frequency electromagnetic fields on HSP70
expression and MAPK signaling pathways in PC12 cells.
2-GHz band CW and W-CDMA modulated radiofrequency fields have no significant effect on
cell proliferation and gene expression profile in human cells.
Mobile phone radiation might alter protein expression in human skin.
Radiofrequency radiation (900 MHz) induces Egr-1 gene expression and affects cell-cycle
control in human neuroblastoma cells.
Evaluation of bax, bcl-2, p21 and p53 genes expression variations on cerebellum of BALB/c
mice before and after birth under mobile phone radiation exposure.
HSP70 expression in human trophoblast cells exposed to different 1.8 Ghz mobile phone signals.
Effects of exposure to a 1950 MHz radio frequency field on expression of Hsp70 and Hsp27 in
human glioma cells.
Analysis of Gene Expression in Mice Testes Exposed to 1.765 GHz Microwave in Utero.
Modulation of heat shock protein response in SH-SY5Y by mobile phone microwaves.
Gene expression in human breast epithelial cells exposed to 60 Hz magnetic fields.
Gene and protein expression following exposure to radiofrequency fields from mobile phones.
Influence of high-frequency electromagnetic fields on different modes of cell death and gene
expression.
Biological stress responses to radio frequency electromagnetic radiation: are mobile phones
really so (heat) shocking?
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A Genome-Wide mRNA Expression Profile in Caenorhabditis elegans under Prolonged
Exposure to 1750MHz Radiofrequency Fields.
Impact of 60-GHz millimeter waves on stress and pain-related protein expression in
differentiating neuron-like cells.
[Effects of GSM 1800 MHz radiofrequency electromagnetic fields on protein expression profile
of human breast cancer cell MCF-7].
Gene expression and reproductive abilities of male Drosophila melanogaster subjected to ELF-
EMF exposure.
Biological monitoring of non-thermal effects of mobile phone radiation: recent approaches and
challenges.
Mobile-phone radiation-induced perturbation of gene-expression profiling, redox equilibrium
and sporadic-apoptosis control in the ovary of Drosophila melanogaster.
The genotoxic effect of radiofrequency waves on mouse brain.
Connection between Cell Phone use, p53 Gene Expression in Different Zones of Glioblastoma
Multiforme and Survival Prognoses.
Exposure to cell phone radiation up-regulates apoptosis genes in primary cultures of neurons and
astrocytes.
In vivo modulation of ETS genes induced by electromagnetic fields.
Human health consequences of environmentally-modulated gene expression: potential roles of
ELF-EMF induced epigenetic versus mutagenic mechanisms of disease.
Exposure to 2.45 GHz electromagnetic fields induces hsp70 at a high SAR of more than 20 W/kg
but not at 5W/kg in human glioma MO54 cells.
Hsp70 is an independent stress marker among frequent users of mobile phones.
Study of p53 expression and post-transcriptional modifications after GSM-900 radiofrequency
exposure of human amniotic cells.
Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in
human endothelial cells: molecular mechanism for cancer- and blood-brain barrier-related
effects.
Exposure to global system for mobile communication (GSM) cellular phone radiofrequency
alters gene expression, proliferation, and morphology of human skin fibroblasts.
Expression analysis of human HL60 cells exposed to 60 Hz square- or sine-wave magnetic
fields.
p53, Rb and bcl-2 expression during the cell cycle: a study in phytohaemagglutinin stimulated
lymphocytes and microwave irradiated lymphoid tissue sections.
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Human skin cell stress response to GSM-900 mobile phone signals. In vitro study on isolated
primary cells and reconstructed epidermis.
In vitro study of the stress response of human skin cells to GSM-1800 mobile phone signals
compared to UVB radiation and heat shock.
Proteomic analysis on the alteration of protein expression in the early-stage placental villous
tissue of electromagnetic fields associated with cell phone exposure.
Activity and expression of acetylcholinesterase in PC12 cells exposed to intermittent 1.8 GHz
217-GSM mobile phone signal.
Effect of 900 MHz electromagnetic fields on nonthermal induction of heat-shock proteins in
human leukocytes.
In vitro effect of cell phone radiation on motility, DNA fragmentation and clusterin gene
expression in human sperm.
Electromagnetic fields at a mobile phone frequency (900 MHz) trigger the onset of general stress
response along with DNA modifications in Eisenia fetida earthworms.
Effects of a 2450 MHz high-frequency electromagnetic field with a wide range of SARs on the
induction of heat-shock proteins in A172 cells.
Effect of GSM-900 and -1800 signals on the skin of hairless rats. III: Expression of heat shock
proteins.
Analysis of the cellular stress response in MCF10A cells exposed to combined radio frequency
radiation.
The Effect of Radiation Emitted by Cell Phone on The Gelatinolytic Activity of Matrix
Metalloproteinase-2 and -9 of Mouse Pre-Antral Follicles during In Vitro Culture.
Effect of 3G cell phone exposure with computer controlled 2-D stepper motor on non-thermal
activation of the hsp27/p38MAPK stress pathway in rat brain.
[Responses of thymocytes and splenocytes to low-intensity extremely high-frequency
electromagnetic radiation in normal mice and in mice with systemic inflammation].
Analysis of proteome response to the mobile phone radiation in two types of human primary
endothelial cells.
Mobile phone electromagnetic radiation activates MAPK signaling and regulates viability in
Drosophila.
Novel electric power-driven hydrodynamic injection system for gene delivery: safety and
efficacy of human factor IX delivery in rats.
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Proto-oncogene mRNA levels and activities of multiple transcription factors in C3H 10T 1/2
murine embryonic fibroblasts exposed to 835.62 and 847.74 MHz cellular phone communication
frequency radiation.
Effect of cell phone-like electromagnetic radiation on primary human thyroid cells.
Expression of the immediate early gene, c-fos, in mouse brain after acute global system for
mobile communication microwave exposure.
[Effects of high power microwave on the expressions of Bcl-2 and C-myc proteins in the rat
testis].
[The Impact of Electroacupuncture Intervention on Expression of 5-HTR 1 B/2 C Genes in Mice
under Radiation Stimulation from Mobile Phone].
Cell phone use and parotid salivary gland alterations: no molecular evidence.
Electromagnetic fields may act directly on DNA.
Stimulation of ubiquitin-proteasome pathway through the expression of amidohydrolase for N-
terminal asparagine (Ntan1) in cultured rat hippocampal neurons exposed to static magnetism.
Proteomic analysis of human lens epithelial cells exposed to microwaves.
[Effects of electromagnetic pulses on apoptosis and TGF-beta3 expression of mouse testis
tissue].
[Changes in Ca(2+)concentration and caspase-3 expression and their relationship in Raji cells
exposed to electromagnetic radiation].
Effects of pulsed electromagnetic fields on cartilage apoptosis signalling pathways in
ovariectomised rats.
Upregulation of specific mRNA levels in rat brain after cell phone exposure.
Meta-proteomic analysis of protein expression distinctive to electricity-generating biofilm
communities in air-cathode microbial fuel cells.
Response of Caenorhabditis elegans to wireless devices radiation exposure.
[The role of heat shock proteins HSP90 in the response of immune cells to centimeter
microwaves].
Mechanism of short-term ERK activation by electromagnetic fields at mobile phone frequencies.
[Effects of electromagnetic radiation on RAF/MEK/ERK signaling pathway in rats
hippocampus].
Electromagnetic-pulse-induced activation of p38 MAPK pathway and disruption of blood-retinal
barrier.
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Electromagnetic fields at mobile phone frequency induce apoptosis and inactivation of the multi-
chaperone complex in human epidermoid cancer cells.
Electromagnetic wave irradiation promotes osteoblastic cell proliferation and up-regulates
growth factors via activation of the ERK1/2 and p38 MAPK pathways.
Millimeter-wave exposure promotes the differentiation of bone marrow stromal cells into cells
with a neural phenotype.
Electromagnetic pulse activated brain microglia via the p38 MAPK pathway.
Cytotoxicity of temozolomide on human glioblastoma cells is enhanced by the concomitant
exposure to an extremely low-frequency electromagnetic field (100Hz, 100G).
Exposure to 50 Hz electromagnetic radiation promote early maturation and differentiation in
newborn rat cerebellar granule neurons.
Analysis of the novel excretory cell expressed ECP-1 protein and its proposed ECP-1/IFC-2
fusion protein EXC-2 in the nematode Caenorhabditis elegans.
Microwave induced alteration in the neuron specific enolase gene expression.
Cytosolic calreticulin inhibits microwave radiation-induced microvascular endothelial cell injury
through the integrin-focal adhesion kinase pathway.
Experimental study of millimeter wave-induced differentiation of bone marrow mesenchymal
stem cells into chondrocytes.
Effect of 72 Hz pulsed magnetic field exposure on ras p21 expression in CCRF-CEM cells.
Bcl-2 and p53 immunoprofile in Kaposi's sarcoma.
The amelioration of phagocytic ability in microglial cells by curcumin through the inhibition of
EMF-induced pro-inflammatory responses.
Cell phone use is associated with an inflammatory cytokine profile of parotid gland saliva.
Calreticulin protects rat microvascular endothelial cells against microwave radiation-induced
injury by attenuating endoplasmic reticulum stress.
Qualitative effect on mRNAs of injury-associated proteins by cell phone like radiation in rat
facial nerves.
p53 immunoreactivity in cutaneous PUVA tumors is similar to that in other non-melanoma skin
neoplasms.
Effects of 2.45 GHz electromagnetic fields with a wide range of SARs on bacterial and HPRT
gene mutations.
Microglia M1/M2 polarization contributes to electromagnetic pulse-induced brain injury.
900-MHz microwave radiation enhances gamma-ray adverse effects on SHG44 cells.
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[The role of RKIP mediated ERK pathway in hippocampus neurons injured by electromagnetic
radiation].
Isoflurane preconditioning ameliorates electromagnetic pulse-induced neural damage by shifting
microglia polarization toward anti-inflammatory phenotype via upregulation of SOCS1.
Effects of prolonged exposure to moderate static magnetic field and its synergistic effects with
alkaline pH on Enterococcus faecalis.
Abnormal physical architecture of the lipophilic domains of human sperm membrane in
oligospermia: a logical cause for low fertility profiles.
[Ecological and biological characteristics of Drosophila melanogaster features depending on the
dose of electromagnetic radiation of various types].
Construction and clinical significance of a predictive system for prognosis of hepatocellular
carcinoma.
--Leaf Cluster 11 (51)
Theme - Adverse impacts of radiofrequency fields on sleep
Titles
Stimulation of the brain with radiofrequency electromagnetic field pulses affects sleep-dependent
performance improvement.
Exposure to radiofrequency electromagnetic fields and sleep quality: a prospective cohort study.
Effects of mobile phone exposure (GSM 900 and WCDMA/UMTS) on polysomnography based
sleep quality: An intra- and inter-individual perspective.
Environmental Radiofrequency Electromagnetic Fields Exposure at Home, Mobile and Cordless
Phone Use, and Sleep Problems in 7-Year-Old Children.
Radio frequency electromagnetic field exposure in humans: Estimation of SAR distribution in
the brain, effects on sleep and heart rate.
Wireless communication fields and non-specific symptoms of ill health: a literature review.
Cohort study on the effects of everyday life radio frequency electromagnetic field exposure on
non-specific symptoms and tinnitus.
Memory performance, wireless communication and exposure to radiofrequency electromagnetic
fields: A prospective cohort study in adolescents.
Exposure to pulse-modulated radio frequency electromagnetic fields affects regional cerebral
blood flow.
Symptoms and the use of wireless communication devices: A prospective cohort study in Swiss
adolescents.
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Sleep after mobile phone exposure in subjects with mobile phone-related symptoms.
Cognitive performance measures in bioelectromagnetic research--critical evaluation and
recommendations.
Sleep duration, quality, and timing and their associations with age in a community without
electricity in Haiti.
Radiofrequency electromagnetic field exposure and non-specific symptoms of ill health: a
systematic review.
Children's health and RF EMF exposure. Views from a risk assessment and risk communication
perspective.
Human sleep under the influence of pulsed radiofrequency electromagnetic fields: a
polysomnographic study using standardized conditions.
Conduct of a personal radiofrequency electromagnetic field measurement study: proposed study
protocol.
Effects of electromagnetic fields emitted from W-CDMA-like mobile phones on sleep in
humans.
International policy and advisory response regarding children's exposure to radio frequency
electromagnetic fields (RF-EMF).
Effects of short- and long-term pulsed radiofrequency electromagnetic fields on night sleep and
cognitive functions in healthy subjects.
Electromagnetic fields, such as those from mobile phones, alter regional cerebral blood flow and
sleep and waking EEG.
Effects of electromagnetic fields emitted by mobile phones (GSM 900 and WCDMA/UMTS) on
the macrostructure of sleep.
Individual variation in temporal relationships between exposure to radiofrequency
electromagnetic fields and non-specific physical symptoms: A new approach in studying
'electrosensitivity'.
Mobile phone use, behavioural problems and concentration capacity in adolescents: A
prospective study.
Towards 5G communication systems: Are there health implications?
Acute effects of electromagnetic fields emitted by GSM mobile phones on subjective well-being
and physiological reactions: a meta-analysis.
A Prospective Cohort Study of Adolescents' Memory Performance and Individual Brain Dose of
Microwave Radiation from Wireless Communication.
[Investigation of sleep disorders in the vicinity of high frequency transmitters].
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Effect of a single 30 min UMTS mobile phone-like exposure on the thermal pain threshold of
young healthy volunteers.
Quality Matters: Systematic Analysis of Endpoints Related to "Cellular Life" in Vitro Data of
Radiofrequency Electromagnetic Field Exposure.
The effect of electromagnetic fields emitted by mobile phones on human sleep.
Mobile phone 'talk-mode' signal delays EEG-determined sleep onset.
The response of human bacteria to static magnetic field and radiofrequency electromagnetic
field.
Exposure to radio-frequency electromagnetic fields and behavioural problems in Bavarian
children and adolescents.
Human sleep EEG under the influence of pulsed radio frequency electromagnetic fields. Results
from polysomnographies using submaximal high power flux densities.
[Effects of radio- and microwaves emitted by wireless communication devices on the functions
of the nervous system selected elements].
Effects of radiation emitted by WCDMA mobile phones on electromagnetic hypersensitive
subjects.
Electromagnetic radiation and behavioural response of ticks: an experimental test.
Effects of Sleep Quality on the Association between Problematic Mobile Phone Use and Mental
Health Symptoms in Chinese College Students.
Investigating short-term exposure to electromagnetic fields on reproductive capacity of
invertebrates in the field situation.
Could myelin damage from radiofrequency electromagnetic field exposure help explain the
functional impairment electrohypersensitivity? A review of the evidence.
Association between exposure to radiofrequency electromagnetic fields assessed by dosimetry
and acute symptoms in children and adolescents: a population based cross-sectional study.
Cochlear implants in the etiopathogenesis of glioblastoma--an interesting observation or
independent finding?
Terrestrial Trunked Radio (TETRA) exposure and its impact on slow cortical potentials.
Influence of electromagnetic fields emitted by GSM-900 cellular telephones on the circadian
patterns of gonadal, adrenal and pituitary hormones in men.
[Prevalence of insomnia in adults aged 18 to 60 years and exposure to electromagnetic fields in
households of Barranquilla, Colombia].
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"Triple M" Effect: A Proposed Mechanism to Explain Increased Dental Amalgam Microleakage
after Exposure to Radiofrequency Electromagnetic Radiation.
The Effect of a Single 30-Min Long Term Evolution Mobile Phone-Like Exposure on Thermal
Pain Threshold of Young Healthy Volunteers.
Pain, pain intensity and pain disability in high school students are differently associated with
physical activity, screening hours and sleep.
Long-Term Evolution Electromagnetic Fields Exposure Modulates the Resting State EEG on
Alpha and Beta Bands.
Microwaves emitted by cellular telephones affect human slow brain potentials.
--Leaf Cluster 41 (125)
Theme - Adverse effects of radiofrequency fields on cells
Titles
The effects of radiofrequency fields on cell proliferation are non-thermal.
Effects of RF-EMF Exposure from GSM Mobile Phones on Proliferation Rate of Human
Adipose-derived Stem Cells: An In-vitro Study.
Effects of radiofrequency exposure emitted from a GSM mobile phone on proliferation,
differentiation, and apoptosis of neural stem cells.
Are the young more sensitive than adults to the effects of radiofrequency fields? An examination
of relevant data from cellular and animal studies.
Comparative study of cell cycle kinetics and induction of apoptosis or necrosis after exposure of
human Mono Mac 6 cells to radiofrequency radiation.
Apoptosis induced by ultraviolet radiation is enhanced by amplitude modulated radiofrequency
radiation in mutant yeast cells.
Review of possible modulation-dependent biological effects of radiofrequency fields.
An in vitro study of the effects of exposure to a GSM signal in two human cell lines: monocytic
U937 and neuroblastoma SK-N-SH.
Ornithine decarboxylase activity is affected in primary astrocytes but not in secondary cell lines
exposed to 872 MHz RF radiation.
Disturbance of cell proliferation in response to mobile phone frequency radiation.
Effects of chronic exposure to radiofrequency electromagnetic fields on energy balance in
developing rats.
Exposure to 835 MHz radiofrequency electromagnetic field induces autophagy in hippocampus
but not in brain stem of mice.
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Continuous exposure to 900MHz GSM-modulated EMF alters morphological maturation of
neural cells.
Enhancement of X-ray Induced Apoptosis by Mobile Phone-Like Radio-Frequency
Electromagnetic Fields in Mouse Spermatocyte-Derived Cells.
Cell oxidation-reduction imbalance after modulated radiofrequency radiation.
Pulse modulated 900 MHz radiation induces hypothyroidism and apoptosis in thyroid cells: a
light, electron microscopy and immunohistochemical study.
1950MHz Radio Frequency Electromagnetic Radiation Inhibits Testosterone Secretion of Mouse
Leydig Cells.
Non-thermal biomarkers of exposure to radiofrequency/microwave radiation.
In vitro non-thermal oxidative stress response after 1800 MHz radiofrequency radiation.
Effect of radiofrequency electromagnetic field exposure on in vitro models of neurodegenerative
disease.
Influence of a 902.4 MHz GSM signal on the human visual system: investigation of the
discrimination threshold.
Biological indicators in response to radiofrequency/microwave exposure.
The protective effect of autophagy on mouse spermatocyte derived cells exposure to 1800MHz
radiofrequency electromagnetic radiation.
Proliferation and apoptosis in a neuroblastoma cell line exposed to 900 MHz modulated
radiofrequency field.
p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic
field exposure.
Microwave exposure of neuronal cells in vitro: Study of apoptosis.
Apoptosis is induced by radiofrequency fields through the caspase-independent mitochondrial
pathway in cortical neurons.
[Impact of radiofrequency/microwave radiation on cell and cytoskeleton structure].
Reaction of the immune system to low-level RF/MW exposures.
Exposure to Global System for Mobile Communication 900 MHz Cellular Phone
Radiofrequency Alters Growth, Proliferation and Morphology of Michigan Cancer Foundation-7
Cells and Mesenchymal Stem Cells.
Exposure to 900 MHz radiofrequency radiation induces caspase 3 activation in proliferating
human lymphocytes.
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Proteomic analysis of continuous 900-MHz radiofrequency electromagnetic field exposure in
testicular tissue: a rat model of human cell phone exposure.
Anthropogenic Radio-Frequency Electromagnetic Fields Elicit Neuropathic Pain in an
Amputation Model.
Effect of high SARs produced by cell phone like radiofrequency fields on mollusk single neuron.
Investigation of the effects of 2.1 GHz microwave radiation on mitochondrial membrane
potential (DeltaPsim), apoptotic activity and cell viability in human breast fibroblast cells.
Comparison of 864 MHz and 935 MHz microwave radiation effects on cell culture.
Free radical release and HSP70 expression in two human immune-relevant cell lines after
exposure to 1800 MHz radiofrequency radiation.
Effects of GSM-modulated radiofrequency electromagnetic fields on B-cell peripheral
differentiation and antibody production.
Effect of radiofrequency radiation in cultured mammalian cells: A review.
Effect of 835 MHz radiofrequency radiation exposure on calcium binding proteins in the
hippocampus of the mouse brain.
Viability and phagocytosis of neutrophils exposed in vitro to 100-MHz radiofrequency radiation.
Effects of 3G cell phone exposure on the structure and function of the human cytochrome P450
reductase.
Possible effects of radiofrequency electromagnetic fields on in vivo C6 brain tumors in Wistar
rats.
In-vitro exposure of neuronal networks to the GSM-1800 signal.
Mitochondrial hyperpolarization and cytochrome-c release in microwave-exposed MCF-7 cells.
Does MW Radiation Affect Gene Expression, Apoptotic Level, and Cell Cycle Progression of
Human SH-SY5Y Neuroblastoma Cells?
Effect of exposure to the edge signal on oxidative stress in brain cell models.
Impact of 864 MHz or 935 MHz radiofrequency microwave radiation on the basic growth
parameters of V79 cell line.
Effect of a 2.45-GHz radiofrequency electromagnetic field on neutrophil chemotaxis and
phagocytosis in differentiated human HL-60 cells.
Effects of low intensity radiofrequency electromagnetic fields on electrical activity in rat
hippocampal slices.
Effects of mobile phone type signals on calcium levels within human leukaemic T-cells (Jurkat
cells).
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Does exposure to a radiofrequency electromagnetic field modify thermal preference in juvenile
rats?
Measurement of the 100MHz EMF radiation in vivo effects on zebrafish D. rerio embryonic
development: A multidisciplinary study.
Microwave effects on the nervous system.
[Effects of radiofrequency electromagnetic fields on mammalian spermatogenesis].
Effects of simultaneous combined exposure to CDMA and WCDMA electromagnetic field on
immune functions in rats.
Microwaves from Mobile Phones Inhibit 53BP1 Focus Formation in Human Stem Cells More
Strongly Than in Differentiated Cells: Possible Mechanistic Link to Cancer Risk.
Effects of 900-MHz radio frequencies on the chemotaxis of human neutrophils in vitro.
Problems in assessment of risks from exposures to microwaves of mobile communication.
Bioassay for assessing cell stress in the vicinity of radio-frequency irradiating antennas.
Heart rate variability affected by radiofrequency electromagnetic field in adolescent students.
Mobile phone radiation alters proliferation of hepatocarcinoma cells.
A new in vitro exposure device for the mobile frequency of 900 MHz.
A radio-frequency system for in vivo pilot experiments aimed at the studies on biological effects
of electromagnetic fields.
Modeling cell dynamics under mobile phone radiation.
Evaluation of the potential of mobile phone specific electromagnetic fields (UMTS) to produce
micronuclei in human glioblastoma cell lines.
Exposure to radiation from single or combined radio frequencies provokes macrophage
dysfunction in the RAW 264.7 cell line.
Responses of neurons to an amplitude modulated microwave stimulus.
Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male
reproductive system.
An HF exposure system for mice with improved efficiency.
Cell phone radiation effects on cytogenetic abnormalities of oral mucosal cells.
Sleep EEG alterations: effects of different pulse-modulated radio frequency electromagnetic
fields.
Effects of exposure to DAMPS and GSM signals on ornithine decarboxylase (ODC) activity: II.
SH-SY5Y human neuroblastoma cells.
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Design, optimization, realization, and analysis of an in vitro system for the exposure of
embryonic stem cells at 1.71 GHz.
Cell physiological effects of radiofrequency electromagnetic fields.
Acute effect of exposure of mollusk single neuron to 900-MHz mobile phone radiation.
[Dependence of the non-thermal radiofrequency electromagnetic field bioeffects on the
typological features of electroencephalogram in humans].
Age-dependent acute interference with stem and progenitor cell proliferation in the hippocampus
after exposure to 1800 MHz electromagnetic radiation.
Biological effects of radiofrequency radiation: concepts and criteria.
Effects of radiofrequency electromagnetic fields on seed germination and root meristematic cells
of Allium cepa L.
Effects of exposure to DAMPS and GSM signals on ornithine decarboxylase (ODC) activity: I.
L-929 mouse fibroblasts.
An investigation of the effects of TETRA RF fields on intracellular calcium in neurones and
cardiac myocytes.
Apoptotic cell death during Drosophila oogenesis is differentially increased by electromagnetic
radiation depending on modulation, intensity and duration of exposure.
Biological effects of amplitude-modulated radiofrequency radiation.
Cell phone radiations affect early growth of Vigna radiata (mung bean) through biochemical
alterations.
The use of FDTD in establishing in vitro experimentation conditions representative of lifelike
cell phone radiation on the spermatozoa.
Effects of RF fields emitted from smart phones on cardio-respiratory parameters: a preliminary
provocation study.
Exposure to 900 MHz electromagnetic field induces an unbalance between pro-apoptotic and
pro-survival signals in T-lymphoblastoid leukemia CCRF-CEM cells.
Basis for optimization of in vitro exposure apparatus for health hazard evaluations of mobile
communications.
In vitro effect of pulsed 900 MHz GSM radiation on mitochondrial membrane potential and
motility of human spermatozoa.
The effect of pulsed 900-MHz GSM mobile phone radiation on the acrosome reaction, head
morphometry and zona binding of human spermatozoa.
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Prenatal exposure to radiofrequencies: effects of WiFi signals on thymocyte development and
peripheral T cell compartment in an animal model.
Combined effects of flow-induced shear stress and electromagnetic field on neural differentiation
of mesenchymal stem cells.
Long-term electromagnetic exposure of developing neuronal networks: A flexible experimental
setup.
Influence of radiofrequency-electromagnetic waves from 3rd-generation cellular phones on
fertilization and embryo development in mice.
Simulation of electromagnetic fields in the human body using Finite Integration Technique
(FIT).
The implications of non-linear biological oscillations on human electrophysiology for
electrohypersensitivity (EHS) and multiple chemical sensitivity (MCS).
Comparison of biological effects between continuous and intermittent exposure to GSM-900-
MHz mobile phone radiation: Detection of apoptotic cell-death features.
[Effects of mobile phones and radar radiofrequencies on the eye].
Exposure to 1950-MHz TD-SCDMA electromagnetic fields affects the apoptosis of astrocytes
via caspase-3-dependent pathway.
Intrauterine effects in animals exposed to radiofrequency and microwave fields.
Effect of cell phone radiation on neutrophil of mice.
In vitro effects of radiofrequency electromagnetic waves on bovine spermatozoa motility.
[Role of modulation in biological effects of electromagnetic radiation].
Numerical and experimental dosimetry of Petri dish exposure setups.
Effects of 2.45-GHz electromagnetic fields with a wide range of SARs on micronucleus
formation in CHO-K1 cells.
Effect of cell phone usage on semen analysis in men attending infertility clinic: an observational
study.
Modulation of oxidative phosphorylation (OXPHOS) by radiation- induced biophotons.
The possible global hazard of cell phone radiation on thyroid cells and hormones: a systematic
review of evidences.
Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering
factor.
Mobile phone electromagnetic radiation affects Amyloid Precursor Protein and alpha-synuclein
metabolism in SH-SY5Y cells.
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Exposure to cell phone radiations produces biochemical changes in worker honey bees.
Human mesenchymal stem cells are sensitive to abnormal gravity and exhibit classic apoptotic
features.
[Surface markers and functions of human dendritic cells exposed to mobile phone 1800 MHz
electromagnetic fields].
Activation of the TRPV1 Thermoreceptor Induced by Modulated or Unmodulated 1800 MHz
Radiofrequency Field Exposure.
Low power radiofrequency electromagnetic radiation for the treatment of pain due to
osteoarthritis of the knee.
Calcium-binding proteins and GFAP immunoreactivity alterations in murine hippocampus after
1 month of exposure to 835 MHz radiofrequency at SAR values of 1.6 and 4.0 W/kg.
Alteration of glycine receptor immunoreactivity in the auditory brainstem of mice following
three months of exposure to radiofrequency radiation at SAR 4.0 W/kg.
Radiofrequency (RF) effects on blood cells, cardiac, endocrine, and immunological functions.
Influence of electromagnetic waves, with maxima in the green or red range, on the
morphofunctional properties of multipotent stem cells.
Can exposure to a terrestrial trunked radio (TETRA)-like signal cause symptoms? A randomised
double-blind provocation study.
Potential protection of green tea polyphenols against 1800 MHz electromagnetic radiation-
induced injury on rat cortical neurons.
Effects of 2450 MHz electromagnetic fields with a wide range of SARs on methylcholanthrene-
induced transformation in C3H10T1/2 cells.
Assessment of intermittent UMTS electromagnetic field effects on blood circulation in the
human auditory region using a near-infrared system.
Skin changes in "screen dermatitis" versus classical UV- and ionizing irradiation-related
damage--similarities and differences.
Fourth Level Cluster 81 (673)
Theme - Adverse impacts of power-line EMF
--Leaf Cluster 9 (43)
Theme - Adverse effects of ELF magnetic field exposures
Titles
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[Electromagnetic noise blocks the gap-junctional intercellular communication suppression
induced by 50 Hz magnetic field].
Developmental effects of magnetic field (50 Hz) in combination with ionizing radiation and
chemical teratogens.
The effect of extremely low frequency magnetic field on the conjunctiva and goblet cells.
Chronic exposure to an extremely low-frequency magnetic field induces depression-like
behavior and corticosterone secretion without enhancement of the hypothalamic-pituitary-
adrenal axis in mice.
Effect of coexposure to 50 Hz magnetic fields and an aneugen on human lymphocytes,
determined by the cytokinesis block micronucleus assay.
[Superposition of noise magnetic fields inhibits clustering of fibroblast membrane surface
receptors induced by 50 Hz magnetic fields in Chinese hamster lungs].
Extremely low frequency magnetic field induces hyperalgesia in mice modulated by nitric oxide
synthesis.
The cardiovascular response to an acute 1800-microT, 60-Hz magnetic field exposure in humans.
Mouse early embryos obtained by natural breeding or in vitro fertilization display a differential
sensitivity to extremely low-frequency electromagnetic fields.
Interaction of MF 50 Hz, 10 mT with high dose of X-rays: evaluation of embryotoxicity in chick
embryos.
Effects on micronuclei formation of 60-Hz electromagnetic field exposure with ionizing
radiation, hydrogen peroxide, or c-Myc overexpression.
Rodent cell transformation and immediate early gene expression following 60-Hz magnetic field
exposure.
[A study on dose-effect of suppression to gap junctional intercellular communication function by
50-Hz magnetic fields].
Effect of magnetic field exposure on anchorage-independent growth of a promoter-sensitive
mouse epidermal cell line (JB6).
Exposure to 60-Hz magnetic fields and proliferation of human astrocytoma cells in vitro.
Activation of Signaling Cascades by Weak Extremely Low Frequency Electromagnetic Fields.
Effects of ELF magnetic fields on protein expression profile of human breast cancer cell MCF7.
[Noise magnetic fields block co-suppression effect induced by power frequency magnetic field
and phorbol ester].
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The response of the human circulatory system to an acute 200-muT, 60-Hz magnetic field
exposure.
Exposure of Drosophila melanogaster embryonic cell cultures to 60-Hz sinusoidal magnetic
fields: assessment of potential teratogenic effects.
Non-thermal effects of power-line magnetic fields (50 Hz) on gene expression levels of
pluripotent embryonic stem cells-the role of tumour suppressor p53.
[Abnormal shift of connexin 43 gap-junction protein induced by 50 Hz electromagnetic fields in
Chinese hamster lung cells].
[Effects of power frequency magnetic field on gap junction intercellular communication of
astrocytes].
Mutation induction by high-density, 50-Hz magnetic fields in human MeWo cells exposed in the
DNA synthesis phase.
Micronucleus induction in Syrian hamster embryo cells following exposure to 50 Hz magnetic
fields, benzo(a)pyrene, and TPA in vitro.
[Estimation of magnetic radiation effects on leucocytes].
[Effects of electromagnetic noise on the enhancement of stress-activated protein kinase(SAPK)
phosphorylation induced by 50 Hz magnetic fields].
Micronucleus formation in human amnion cells after exposure to 50 Hz MF applied horizontally
and vertically.
Immune function and host defense in rodents exposed to 60-Hz magnetic fields.
Effects of 50-Hz magnetic field exposure on hormone secretion and apoptosis-related gene
expression in human first trimester villous trophoblasts in vitro.
Effects of whole-body 50-Hz magnetic field exposure on mouse Leydig cells.
Superposition of an incoherent magnetic field inhibited EGF receptor clustering and
phosphorylation induced by a 1.8 GHz pulse-modulated radiofrequency radiation.
Effects of 50 Hz sinusoidal magnetic fields on Hsp27, Hsp70, Hsp90 expression in porcine aortic
endothelial cells (PAEC).
Effect of 60 Hz magnetic field exposure on c-fos expression in stimulated PC12 cells.
Immune markers and ornithine decarboxylase activity among electric utility workers.
Neural mass modeling of power-line magnetic fields effects on brain activity.
Modulation of natural killer cell function after exposure to 60 Hz magnetic fields: confirmation
of the effect in mature B6C3F1 mice.
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Alteration of tight and adherens junctions on 50-Hz magnetic field exposure in Madin Darby
canine kidney (MDCK) cells.
Genome-wide transcription analysis of Escherichia coli in response to extremely low-frequency
magnetic fields.
Real-time detection of stimulus response in cultured neurons by high-intensity intermediate-
frequency magnetic field exposure.
Magnetic field desensitizes 5-HT(1B) receptor in brain: pharmacological and functional studies.
Influence of combined AC-DC magnetic fields on free radicals in organized and biological
systems. Development of a model and application of the radical pair mechanism to radicals in
micelles.
A 1.8-GHz radiofrequency radiation induces EGF receptor clustering and phosphorylation in
cultured human amniotic (FL) cells.
--Leaf Cluster 17 (55)
Theme - Adverse impacts of EMF on mammary cancer development
Titles
Acceleration of mammary tumorigenesis by exposure of 7,12-dimethylbenz[a]anthracene-treated
female rats in a 50-Hz, 100-microT magnetic field: replication study.
A histopathological study on alterations in DMBA-induced mammary carcinogenesis in rats with
50 Hz, 100 muT magnetic field exposure.
Effects of magnetic fields on mammary tumor development induced by 7,12-
dimethylbenz(a)anthracene in rats.
Significant differences in the effects of magnetic field exposure on 7,12-
dimethylbenz(a)anthracene-induced mammary carcinogenesis in two substrains of Sprague-
Dawley rats.
Effects of weak alternating magnetic fields on nocturnal melatonin production and mammary
carcinogenesis in rats.
Do cocarcinogenic effects of ELF electromagnetic fields require repeated long-term interaction
with carcinogens? Characteristics of positive studies using the DMBA breast cancer model in
rats.
Effect of 26 week magnetic field exposures in a DMBA initiation-promotion mammary gland
model in Sprague-Dawley rats.
Effect of 13 week magnetic field exposures on DMBA-initiated mammary gland carcinomas in
female Sprague-Dawley rats.
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Effects of GSM-900 microwaves on DMBA-induced mammary gland tumors in female Sprague-
Dawley rats.
[Effects of mobile-phone microwave on dimethylbenz (a) anthracene induced mammary
carcinoma development in rats].
Effects of 900 MHz GSM wireless communication signals on DMBA-induced mammary tumors
in rats.
Developmental toxicity evaluation of ELF magnetic fields in Sprague-Dawley rats.
Developmental toxicity study of 60 Hz (power frequency) magnetic fields in rats.
In vivo exposure of rats to a weak alternating magnetic field increases ornithine decarboxylase
activity in the mammary gland by a similar extent as the carcinogen DMBA.
A study on skin tumour formation in mice with 50 Hz magnetic field exposure.
Rat liver foci study on coexposure with 50 Hz magnetic fields and known carcinogens.
5-Iododeoxyuridine-125I incorporation in vivo after exposure to a 50 Hz magnetic field.
Study on potential effects of "902-MHz GSM-type Wireless Communication Signals" on
DMBA-induced mammary tumours in Sprague-Dawley rats.
Anxiogenic effect of chronic exposure to extremely low frequency magnetic field in adult rats.
Acute and subchronic toxicity of 20 kHz and 60 kHz magnetic fields in rats.
Results of lifespan exposure to continuous and intermittent extremely low frequency
electromagnetic fields (ELFEMF) administered alone to Sprague Dawley rats.
Chronic, low-level (1.0 W/kg) exposure of mice prone to mammary cancer to 2450 MHz
microwaves.
Acute effects of 50 Hz magnetic field exposure on human visual task and cardiovascular
performance.
Cancer promotion in a mouse-skin model by a 60-Hz magnetic field: II. Tumor development and
immune response.
Repeated exposure of C3H/HeJ mice to ultra-wideband electromagnetic pulses: lack of effects on
mammary tumors.
[Effects of chronic exposure of power frequency magnetic field on neurobehavior in rats].
Multigeneration reproductive toxicity assessment of 60-Hz magnetic fields using a continuous
breeding protocol in rats.
Assessing the potential carcinogenic activity of magnetic fields using animal models.
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Evaluation of the potential carcinogenicity of 60 Hz linear sinusoidal continuous-wave magnetic
fields in Fischer F344 rats.
Effect of exposure to extremely low electro-magnetic field during prenatal period on mice
spleen.
Effects of magnetic field exposure on the development of lung fibrosis elicited by industrial
pollutants.
Effect of radiofrequency radiation exposure on mouse skin tumorigenesis initiated by 7,12-
dimethybenz[alpha]anthracene.
Recent experimental data on Extremely Low Frequency (ELF) magnetic field carcinogenic risk:
open questions.
Extremely low-frequency magnetic fields modulate nitric oxide signaling in rat brain.
[Modifying effect of light and electromagnetic field on development of mammary tumors
induced by N-nitrosomethyl urea in female rats].
Effects of subchronic extremely low-frequency electromagnetic field exposure on biochemical
parameters in rats.
Effects of gestational exposure to a video display terminal-like magnetic field (20-kHz) on
CBA/S mice.
Evaluation of the developmental toxicity of 60 Hz magnetic fields and harmonic frequencies in
Sprague-Dawley rats.
Testing electromagnetic fields for potential carcinogenic activity: a critical review of animal
models.
Effects of aluminum and extremely low frequency electromagnetic radiation on oxidative stress
and memory in brain of mice.
Skeletal muscle HSP72 and norepinephrine response to static magnetic field in rat.
Effect of chronic exposure to a GSM-like signal (mobile phone) on survival of female Sprague-
Dawley rats: modulatory effects by month of birth and possibly stage of the solar cycle.
Long-term exposure of Sprague Dawley rats to 20 kHz triangular magnetic fields.
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer
344 rats chronically exposed to 836 MHz modulated microwaves.
In vivo studies of the effect of magnetic field exposure on ontogeny of choline acetyltransferase
in the rat brain.
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer
344 rats exposed to frequency-modulated microwave fields.
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Toxicity bioassay in Sprague-Dawley rats exposed to 20 kHz triangular magnetic field for 90
days.
A cerebral primitive neuroectodermal tumor in a squirrel monkey (Saimiri sciureus).
Indication of cocarcinogenic potential of chronic UMTS-modulated radiofrequency exposure in
an ethylnitrosourea mouse model.
A case of hepatocellular carcinoma rupturing after angiography.
A case of recurring hepatocellular carcinoma with a solitary Virchow's lymph node metastasis.
Benzodiazepine system is involved in hyperalgesia in rats induced by the exposure to extremely
low frequency magnetic fields.
[A case report of primary hepatic carcinoid with lymph node metastasis--treatment of hepatic
arterial infusion to post-reoperative liver and radiation to metastasis of para-aortic lymph nodes].
Effects of mobile phone radiation on UV-induced skin tumourigenesis in ornithine
decarboxylase transgenic and non-transgenic mice.
[A case of renal cell carcinoma in a horseshoe kidney].
--Leaf Cluster 6 (67)
Theme - Adverse health effects of magnetic fields associated with magnetic resonance imaging
Titles
Menometrorrhagia in magnetic resonance imaging operators with copper intrauterine
contraceptive devices (IUDS): a case report.
Safety issues in magnetic resonance imaging.
[Magnetic resonance imaging : Recent studies on biological effects of static magnetic and
highfrequency electromagnetic fields].
A review of the current use of magnetic resonance imaging in pregnancy and safety implications
for the fetus.
Retrospective assessment of exposure to static magnetic fields during production and
development of magnetic resonance imaging systems.
[Safety of magnetic resonance imaging in patients with implanted cardiovascular devices].
Implantable pulse generators (pacemakers) and electrodes: safety in the magnetic resonance
imaging scanner environment.
Health risk assessment of occupational exposure to a magnetic field from magnetic resonance
imaging devices.
Calculation of radiofrequency electromagnetic fields and their effects in MRI of human subjects.
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Biological effects of exposure to magnetic resonance imaging: an overview.
The safety of MRI. Considerations for site planning and clinical use.
Interference with cardiac pacemakers by magnetic resonance imaging: are there irreversible
changes at 0.5 Tesla?
Evaluation of occupational exposure in magnetic resonance sites.
Safety of strong, static magnetic fields.
Guidelines and recommendations for MR imaging safety and patient management. III.
Questionnaire for screening patients before MR procedures. The SMRI Safety Committee.
Safety concerns related to magnetic field exposure.
Occupational exposure of healthcare and research staff to static magnetic stray fields from 1.5-7
Tesla MRI scanners is associated with reporting of transient symptoms.
Magnetic resonance imaging safety: implications for cardiovascular patients.
Exposure classification of MRI workers in epidemiological studies.
MRI magnetic field stimulates rotational sensors of the brain.
[Exposure to static magnetic field and health hazards during the operation of magnetic resonance
scanners].
The effects of 1.5T magnetic resonance imaging on early murine in-vitro embryo development.
Effect of electromagnetic field accompanying the magnetic resonance imaging on human heart
rate variability - a pilot study.
A comprehensive analysis of MRI research risks: in support of full disclosure.
Exposure to time varying magnetic fields associated with magnetic resonance imaging reduces
fentanyl-induced analgesia in mice.
MRI effects on craniofacial size and crown-rump length in C57BL/6J mice in 1.5T fields.
RF-EMF exposure of fetus and mother during magnetic resonance imaging.
Effects of static magnetic fields on cognition, vital signs, and sensory perception: a meta-
analysis.
Pilot study investigating the effect of the static magnetic field from a 9.4-T MRI on the
vestibular system.
Exposure to static and time-varying magnetic fields from working in the static magnetic stray
fields of MRI scanners: a comprehensive survey in the Netherlands.
Safety considerations in MR imaging.
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Human exposure to 4.0-Tesla magnetic fields in a whole-body scanner.
Vestibular stimulation by magnetic fields.
EMF exposure variation among MRI sequences from pediatric examination protocols.
Adaptive suppression of power line interference in ultra-low field magnetic resonance imaging in
an unshielded environment.
Exposure, health complaints and cognitive performance among employees of an MRI scanners
manufacturing department.
[ECG changes caused by the effect of static magnetic fields of nuclear magnetic resonance
tomography using magnets with a field power of 0.5 to 4.0 Telsa].
Development of hypertension after long-term exposure to static magnetic fields among workers
from a magnetic resonance imaging device manufacturing facility.
An improved quasi-static finite-difference scheme for induced field evaluation in MRI based on
the biconjugate gradient method.
A trail of artificial vestibular stimulation: electricity, heat, and magnet.
Prediction of specific absorption rate in mother and fetus associated with MRI examinations
during pregnancy.
Effect of 1.5 tesla nuclear magnetic resonance imaging scanner on implanted permanent
pacemakers.
MRI safety: everyone's job.
MR procedures: biologic effects, safety, and patient care.
Operational safety issues in MRI.
Biologic effects and potential hazards of nuclear magnetic imaging.
Novel mechanistic model and computational approximation for electromagnetic safety
evaluations of electrically short implants.
[Possible mutagenic effects of magnetic fields].
[Effect of a static magnetic field (3.5 T) on the reproductive behavior of mice, on the embryo and
fetal development and on selected hematologic parameters].
[Bacterial mutation in high magnetic fields and radiofrequency radiation].
Neurophysiology: vertigo in MRI machines.
Complex magnetic field exposure system for in vitro experiments at intermediate frequencies.
Magnetic-field-induced vertigo: a theoretical and experimental investigation.
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Effects of magnetic stray fields from a 7 tesla MRI scanner on neurocognition: a double-blind
randomised crossover study.
Effect of a 0.5-T static magnetic field on conduction in guinea pig spinal cord.
Cognitive, cardiac, and physiological safety studies in ultra high field magnetic resonance
imaging.
Magnetic resonance imaging of the chest. Where we stand.
Exposure to static magnetic fields and risk of accidents among a cohort of workers from a
medical imaging device manufacturing facility.
MR safety: past, present, and future from a historical perspective.
Pacemaker reed switch behavior in 0.5, 1.5, and 3.0 Tesla magnetic resonance imaging units: are
reed switches always closed in strong magnetic fields?
Offline impedance measurements for detection and mitigation of dangerous implant interactions:
an RF safety prescreen.
[Do strong static magnetic fields in NMR tomography modify tissue perfusion?].
Aneurysm clips: evaluation of magnetic field interactions and translational attraction by use of
"long-bore" and "short-bore" 3.0-T MR imaging systems.
Modeling of the internal fields distribution in human inner hearing system exposed to 900 and
1800 MHz.
Safety aspects of switched gradient fields.
Effect on germination and early growth characteristics in sunflower (Helianthus annuus) seeds
exposed to static magnetic field.
INFLUENCE OF STATIC ELECTRICITY ON RADON MEASUREMENT USING PASSIVE
DETECTORS.
--Leaf Cluster 32 (139)
Theme - Health risks of power-line electromagnetic fields on humans
Titles
An examination of underlying physical principles. The interaction of power-line electromagnetic
fields with the human body.
The establishment of frequency dependent limits for electric and magnetic fields and evaluation
of indirect effects.
Health risks of electric and magnetic fields caused by high-voltage systems in Finland.
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Electric field induced in the human body by uniform 50 Hz electric or magnetic fields:
bibliography analysis and method for conservatively deriving measurable limits.
LEVELS OF EXTREMELY LOW-FREQUENCY ELECTRIC AND MAGNETIC FIELDS
FROM OVERHEAD POWER LINES IN THE OUTDOOR ENVIRONMENT OF
RAMALLAH CITY-PALESTINE.
Exposure of workers in the electric power industry to electric and magnetic fields.
Comparison of cardiac-induced endogenous fields and power frequency induced exogenous
fields in an anatomical model of the human body.
Influence of 50 Hz electric and magnetic fields on the human heart.
Physiologic and dosimetric considerations for limiting electric fields induced in the body by
movement in a static magnetic field.
The influence of 50 Hz electric and magnetic fields on the extrasystoles of human heart.
Computational estimation of magnetically induced electric fields in a rotating head.
[Evaluation of reports on environmental measurements of electromagnetic fields generated by
high voltage transmission lines and substations].
Intensity of electric and magnetic fields from power lines within the business district of 60
Ontario communities.
Current densities in a pregnant woman model induced by simultaneous ELF electric and
magnetic field exposure.
Basic restrictions in EMF exposure guidelines.
Numerical dosimetry at power-line frequencies using anatomically based models.
Impedance method computation of induced currents in a simple model of a child exposed to
electromagnetic fields of an electric blanket.
[Effects of electromagnetic field emitted by electric blankets on brain catecholamine in fetal
mice].
[Practical aspects of taking measurements of electromagnetic fields in the surrounding of
overhead transmission lines].
Electric and magnetic field exposures for people living near a 735-kilovolt power line.
Nerves in a human body exposed to low-frequency electromagnetic fields.
Current densities and total contact currents for 110 and 220 kV power line tasks.
Evaluation and measurement of magnetic field exposure at a typical high-voltage substation and
its power lines.
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Current densities measured in human models exposed to 60-Hz electric fields.
Assessment of exposure to intermediate frequency electric fields and contact currents from a
plasma ball.
Fetal exposure to low frequency electric and magnetic fields.
Dealing with uncertainty in formulating occupational and public exposure limits.
Limiting electric fields of HVDC overhead power lines.
Electric field prediction for a human body-electric machine system.
Evaluation of long-term exposure to the magnetic field produced from power lines.
Exposure Modelling of Extremely Low-Frequency Magnetic Fields from Overhead Power Lines
and Its Validation by Measurements.
Comparison of cardiac and 60 Hz magnetically induced electric fields measured in anesthetized
rats.
Summary and evaluation of guidelines for occupational exposure to power frequency electric and
magnetic fields.
Effects of high-intensity power-frequency electric fields on implanted modern
multiprogrammable cardiac pacemakers.
Evaluation of current densities and total contact currents in occupational exposure at 400 kV
substations and power lines.
A system for simultaneous exposure of small animals to 60-Hz electric and magnetic fields.
Comparison of electric field exposure measurement methods under power lines.
Quandaries in the application of the ICNIRP low frequency basic restriction on current density.
Human body exposure to power lines: relation of induced quantities to external magnetic fields.
Measurement and Modeling of Personal Exposure to the Electric and Magnetic Fields in the
Vicinity of High Voltage Power Lines.
Effects of electric and magnetic fields from high-power lines on female urinary excretion of 6-
sulfatoxymelatonin.
60-Hertz electric-field exposures in transmission line towers.
Possible health effects of 50/60Hz electric and magnetic fields: review of proposed mechanisms.
Pacemaker interference by magnetic fields at power line frequencies.
Non-Hodgkin's lymphoma among electric utility workers in Ontario: the evaluation of alternate
indices of exposure to 60 Hz electric and magnetic fields.
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Fields and currents in the organs of the human body when exposed to power lines and VLF
transmitters.
Assessment of the magnetic field exposure due to the battery current of digital mobile phones.
Health effects relevant to the setting of EMF exposure limits.
Neuroelectric mechanisms applied to low frequency electric and magnetic field exposure
guidelines--part I: sinusoidal waveforms.
Pacemaker interference and low-frequency electric induction in humans by external fields and
electrodes.
High-voltage overhead power lines in epidemiology: patterns of time variations in current load
and magnetic fields.
Comparison of various safety guidelines for electronic article surveillance devices with pulsed
magnetic fields.
Influence of human model resolution on computed currents induced in organs by 60-Hz
magnetic fields.
Current densities and total contact currents associated with 400 kV power line tasks.
Frequency spectra from current vs. magnetic flux density measurements for mobile phones and
other electrical appliances.
Possible mechanisms by which electric fields from power lines might affect airborne particles
harmful to health.
Uncertainty evaluation in the measurement of power frequency electric and magnetic fields from
AC overhead power lines.
Exposure to power-frequency electromagnetic fields in Denmark.
Induced current measurements in whole body exposure condition to radio frequency electric
fields.
Assessment of foetal exposure to the homogeneous magnetic field harmonic spectrum generated
by electricity transmission and distribution networks.
Survey of ELF magnetic field levels in households near overhead power lines in Serbia.
Dose response study of human exposure to 60 Hz electric and magnetic fields.
The monitoring results of electromagnetic radiation of 110-kV high-voltage lines in one urban
location in Chongqing P.R. China.
Occupational exposure to power frequency fields in some electrical transformation stations in
Romania.
[The ecological-hygienic aspects of the study of industrial-frequency magnetic fields].
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Cardiac pacemakers in electric and magnetic fields of 400-kV power lines.
The interference threshold of cardiac pacemakers in electric 50 Hz fields.
Active medical implants and occupational safety--measurement and numerical calculation of
interference voltage.
Current densities and total contact currents during forest clearing tasks under 400 kV power
lines.
[Biological effects of electromagnetic fields (author's transl)].
Clinical study of interference with cardiac pacemakers by a magnetic field at power line
frequencies.
Effects of a high-voltage direct-current transmission line on beef cattle production.
Acute effects of ELF electromagnetic fields: a field study of linesmen working with 400 kV
power lines.
[Diseases in animals associated with exposure to electric and magnetic fields of 50/60 Hz: report
of a case].
Powerline frequency electric and magnetic fields: a pilot study of risk perception.
[Duration of conscious reactions in persons exposed to an electric field of 50 Hz frequency].
Implantable cardioverter defibrillators in electric and magnetic fields of 400 kV power lines.
Effects of low frequency electric fields on synaptic integration in hippocampal CA1 pyramidal
neurons: implications for power line emissions.
[Intensity of electromagnetic field and electric current on human bodies induced by electric
blanket].
Memory loss risk assessment for the students nearby high-voltage power lines-a case study.
Theoretical limits on the threshold for the response of long cells to weak extremely low
frequency electric fields due to ionic and molecular flux rectification.
An In Situ and In Silico Evaluation of Biophysical Effects of 27 MHz Electromagnetic Whole
Body Humans Exposure Expressed by the Limb Current.
Interference with the pacemakers of two workers at electricity substations.
Sensitivity to electricity in the catfish, Parasilurus asotus.
Electric and magnetic fields generated by ac power lines: an application of advanced modelling
tools in order to predict exposure levels.
[The characteristics of the electromagnetic situation close to overhead electric power
transmission lines in St. Petersburg].
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Human perception of electric fields and ion currents associated with high-voltage DC
transmission lines.
[An experimental study of the sciatic nerve injury by high voltage electricity in rabbits].
Magnetic induction at 60 Hz in the human heart: a comparison between the in situ and isolated
scenarios.
Exposure guidelines for low-frequency electric and magnetic fields: report from the Brussels
workshop.
Power lines and ionizing radiation.
COMPUTATIONAL ASSESSMENT OF PREGNANT WOMAN MODELS EXPOSED TO
UNIFORM ELF-MAGNETIC FIELDS: COMPLIANCE WITH THE EUROPEAN CURRENT
EXPOSURE REGULATIONS FOR THE GENERAL PUBLIC AND OCCUPATIONAL
EXPOSURES AT 50 Hz.
[Exposure of workers to electric and magnetic fields from radiofrequency dielectric heaters to
process polyvinyl chloride material].
Effects of 50 Hz electric currents on vigilance and concentration.
Can disturbances in the atmospheric electric field created by powerline corona ions disrupt
melatonin production in the pineal gland?
Experimental and numeric investigation about electromagnetic interference between implantable
cardiac pacemaker and magnetic fields at power line frequency.
SAR changes in a human head model for plane wave exposure (500 - 2500 MHz) and a
comparison with IEEE 2005 safety limits.
The possible consequences for cognitive functions of external electric fields at power line
frequency on hippocampal CA1 pyramidal neurons.
Interference of 16.7-Hz electromagnetic fields on measured electrocardiogram.
Biological effects of a 765-kV transmission line: exposures and thresholds in honeybee colonies.
Power-frequency magnetic fields from electric blankets.
Electric fields in bone marrow substructures at power-line frequencies.
Analysis of the relationship between electromagnetic radiation characteristics and urban
functions in highly populated urban areas.
Chronic exposure of primates to 60-Hz electric and magnetic fields: III. Neurophysiologic
effects.
Exposure of the human body to professional and domestic induction cooktops compared to the
basic restrictions.
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Electricity and the heart.
[Occupational exposure of physical therapists to electric and magnetic fields and the efficacy of
Faraday cages].
Biological effects of exposure to static electric fields in humans and vertebrates: a systematic
review.
Biological effects of electric and magnetic fields on productivity of dairy cows.
Computer screens and brain cancer.
[Clinical analysis of brain injury in patients injured by high voltage electricity].
Studies on eliminating interference by electromagnetic induction from power lines in ECG
signals.
A Shear-Mode Piezoelectric Heterostructure for Electric Current Sensing in Electric Power
Grids.
Provocation of electric hypersensitivity under everyday conditions.
Chronic exposure of primates to 60-Hz electric and magnetic fields: I. Exposure system and
measurements of general health and performance.
Low-voltage electricity-induced lung injury.
Biophysical cancer transformation pathway.
The influence of electromagnetic interference and ionizing radiation on cardiac pacemakers.
Relationship of electric power quality to milk production of dairy herds - field study with
literature review.
[Pathomorphological constellation in death resulting from high voltage electricity].
The urban decline of the house sparrow (Passer domesticus): a possible link with
electromagnetic radiation.
[Injuries caused by electricity].
Compound injury from high-voltage electricity.
Exposure to static electric fields leads to changes in biogenic amine levels in the brains of
Drosophila.
Effects of electric field reduction in visual display units on skin symptoms.
Do induction loops pose a hazard to health?
Effects of concurrent exposure to 60 Hz electric and magnetic fields on the social behavior of
baboons.
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Assessment of motor pathways by magnetic stimulation in human and veterinary medicine.
Cow sensitivity to electricity during milking.
Characteristics and potential human health hazards of charged aerosols generated by high-
voltage power lines.
Elimination of power line interference from ECG signals using recurrent neural networks.
Neuroelectric mechanisms applied to low frequency electric and magnetic field exposure
guidelines--part II: non sinusoidal waveforms.
Electromagnetic field strength levels surrounding electronic article surveillance (EAS) systems.
Suppression of power-line interference by analog notch filtering in the ECG signal for heart rate
variability analysis: to do or not to do?
Return to arc welding following defibrillator implantation.
Fracture due to shock from domestic electricity supply.
Cascading failures in ac electricity grids.
Renal artery thrombosis due to high voltage electricity.
The potential of electricity transmission corridors in forested areas as bumblebee habitat.
--Leaf Cluster 34 (188)
Theme - Adverse effects of low-frequency electromagnetic fields on humans
Titles
An evaluation of the existing evidence on the carcinogenic potential of extremely low frequency
magnetic fields.
Possible mechanisms by which extremely low frequency magnetic fields affect opioid function.
Effects of 60 Hz magnetic fields on teenagers and adults.
Do extremely low frequency magnetic fields enhance the effects of environmental carcinogens?
A meta-analysis of experimental studies.
Biological interactions and potential health effects of extremely-low-frequency magnetic fields
from power lines and other common sources.
Effects of extremely low-frequency magnetic field on growth and differentiation of human
mesenchymal stem cells.
[Morphological characteristics and various theories on the mechanism of biological effect of
magnetic fields].
Developmental effects of extremely low frequency electric and magnetic fields.
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[Very low frequency electric and magnetic fields and the immune system].
Concern that "EMF" magnetic fields from power lines cause cancer.
Effects of low-frequency magnetic fields on embryonic development and pregnancy.
Perspectives on health effects of electric and magnetic fields.
Assessment of ELF magnetic fields produced by independent power lines.
Low-frequency magnetic fields and cancer. What you should know and what to tell your
patients.
Extremely low frequency magnetic field (50 Hz, 0.5 mT) modifies fitness components and
locomotor activity of Drosophila subobscura.
Extremely low frequency magnetic field effects on metabolite of Aspergillus niger.
Extremely-low frequency magnetic field effects on sulfate reducing bacteria viability.
Extremely low frequency (ELF) magnetic fields and apoptosis: a review.
Variability and consistency of electric and magnetic field occupational exposure measurements.
The genotoxic potential of electric and magnetic fields: an update.
Power frequency electromagnetic fields and health. Where's the evidence?
Interaction of static and extremely low frequency electric and magnetic fields with living
systems: health effects and research needs.
[Biological influences of electromagnetic fields].
[Biological and health effects on electric and magnetic fields at extremely low frequencies].
[Biological effects of nonionizing radiation: low frequency electromagnetic fields].
Extremely low-frequency magnetic fields of transformers and possible biological and health
effects.
EMF and health.
[Evaluation of the effects of electric and magnetic fields in humans].
Induction of kinetochore-positive and kinetochore-negative micronuclei in CHO cells by ELF
magnetic fields and/or X-rays.
Epidemiological studies of work with video display terminals and adverse pregnancy outcomes
(1984-1992).
Possible health hazards from exposure to power-frequency electric and magnetic fields--a
COMAR Technical Information Statement.
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Extremely low frequency (ELF) magnetic fields enhance chemically induced formation of
apurinic/apyrimidinic (AP) sites in A172 cells.
Occupational exposure to intermediate frequency and extremely low frequency magnetic fields
among personnel working near electronic article surveillance systems.
[The role of free radicals in mechanisms of biological function exposed to weak, constant and net
magnetic fields].
Behavioural evidence that magnetic field effects in the land snail, Cepaea nemoralis, might not
depend on magnetite or induced electric currents.
The effect of a 50 Hz magnetic field on cognitive function in humans.
Exposure assessment for electric and magnetic fields.
Assessment of occupational exposure to extremely low frequency magnetic fields in hospital
personnel.
Origins of electromagnetic hypersensitivity to 60 Hz magnetic fields: A provocation study.
Exposure to magnetic fields of railway engine drivers: a case study in Italy.
Acute exposure to 50-Hz magnetic fields increases interleukin-6 in young healthy men.
A review of the literature on potential reproductive and developmental toxicity of electric and
magnetic fields.
[Influence of low magnetic field on lipid peroxidation].
50-Hz magnetic field exposure system for small animals.
Typical exposure of children to EMF: exposimetry and dosimetry.
[Risks of electromagnetic fields for humans].
Low-frequency pulsed electromagnetic field exposure can alter neuroprocessing in humans.
A critical review of the genotoxic potential of electric and magnetic fields.
Occupational exposures of pharmacists and pharmaceutical assistants to 60 Hz magnetic fields.
Evaluation of in vitro effects of 50 and 60 Hz magnetic fields in regional EMF exposure
facilities.
Exposure system to study hypotheses of ELF and RF electromagnetic field interactions of mobile
phones with the central nervous system.
Exposure of welders and other metal workers to ELF magnetic fields.
Safety of the magnetic field generated by a neuronal magnetic stimulator: evaluation of possible
mutagenic effects.
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Exposure of high resolution fetuses in advanced pregnant woman models at different stages of
pregnancy to uniform magnetic fields at the frequency of 50 Hz.
The epidemiology of electric and magnetic field exposures in the power frequency range and
reproductive outcomes.
Food and Drug Administration low-level extremely-low-frequency magnetic field exposure
facility.
Analyses of magnetic-field peak-exposure summary measures.
Increased resorptions in CBA mice exposed to low-frequency magnetic fields: an attempt to
replicate earlier observations.
Cancer promotion in a mouse-skin model by a 60-Hz magnetic field: I. Experimental design and
exposure system.
Influence of weak static and 50 Hz magnetic fields on the redox activity of cytochrome-C
oxidase.
Evaluating alternative exposure indices in epidemiologic studies on extremely low-frequency
magnetic fields.
Amyotrophic lateral sclerosis (ALS) and extremely-low frequency (ELF) magnetic fields: a
study in the SOD-1 transgenic mouse model.
Can low-level 50/60 Hz electric and magnetic fields cause biological effects?
Effects of information and 50 Hz magnetic fields on cognitive performance and reported
symptoms.
Electromagnetic radiation from VDT units: study of the effectiveness of an active shielding
device.
Extremely low-frequency magnetic fields and heart disease.
The wonders of magnetism.
Human exposure to 60-Hz magnetic fields: neurophysiological effects.
Effects of extremely low-frequency magnetic field exposure on cognitive functions: results of a
meta-analysis.
Long-term exposure to extremely low-frequency magnetic fields impairs spatial recognition
memory in mice.
Human electrophysiological and cognitive effects of exposure to ELF magnetic and ELF
modulated RF and microwave fields: a review of recent studies.
Biophysical mechanisms: a component in the weight of evidence for health effects of power-
frequency electric and magnetic fields.
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Cardiac autonomic control mechanisms in power-frequency magnetic fields: a multistudy
analysis.
Magnetic fields of video display terminals and pregnancy outcome.
[Exposure to low electromagnetic fields and the carcinogenesis process].
[Sister chromatid exchange (SCE)and high-frequency cells in workers professionally exposed to
extremely low-frequency magnetic fields (ELF)].
Bio-effects of high magnetic fields: a study using a simple animal model.
Exposure to ELF magnetic and ELF-modulated radiofrequency fields: the time course of
physiological and cognitive effects observed in recent studies (2001-2005).
Micronucleus induction in cells co-exposed in vitro to 50 Hz magnetic field and benzene, 1,4-
benzenediol (hydroquinone) or 1,2,4-benzenetriol.
Evaluation of residential exposure to intermediate frequency magnetic fields.
Effect of 60-Hz magnetic fields on ultraviolet light-induced mutation and mitotic recombination
in Saccharomyces cerevisiae.
The effect of 60-Hz magnetic fields on co-promotion of chemically induced skin tumors on
SENCAR mice: a discussion of three studies.
Stochastic Dosimetry for the Assessment of Children Exposure to Uniform 50 Hz Magnetic
Field with Uncertain Orientation.
Individual subject sensitivity to extremely low frequency magnetic field.
Assessment of magnetic field exposures for a mortality study at a uranium enrichment plant.
Human cognitive performance in a 3 mT power-line frequency magnetic field.
[Problem of studying influence of electric and magnetic fields on human health. Results and
prospects].
Effects of magnetic field exposure on open field behaviour and nociceptive responses in mice.
Biological effects of extremely low-frequency electromagnetic fields: in vivo studies.
Effects in rodents of a 1-month exposure to magnetic fields (200-1200 Gauss).
Symptoms of the musculoskeletal system and exposure to magnetic fields in an aluminium plant.
Children's exposure to magnetic fields produced by U.S. television sets used for viewing
programs and playing video games.
Provocation study of persons with perceived electrical hypersensitivity and controls using
magnetic field exposure and recording of electrophysiological characteristics.
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Implantable cardioverter defibrillator and 50-Hz electric and magnetic fields exposure in the
workplace.
A study of heart rate and heart rate variability in human subjects exposed to occupational levels
of 50 Hz circularly polarised magnetic fields.
Measuring exposed magnetic fields of welders in working time.
Intermittent exposures to nanoTesla range, 7 Hz, amplitude-modulated magnetic fields increase
regeneration rates in planarian.
Cancer from exposure to 50/60 Hz electric and magnetic fields--a major scientific debate.
Chronic or intractable medical problems associated with prolonged exposure to unsuspected
harmful environmental electric, magnetic or electro-magnetic fields radiating in the bedroom or
workplace and their exacerbation by intake of harmful light and heavy metals from common
sources.
Physiological variables and subjective symptoms by 60 Hz magnetic field in EHS and non-EHS
persons.
[Analysis on outer hair cells hazards from occupational exposure to low frequency electric and
magnetic fields and magnetic fields and its related factors].
Possible cocarcinogenic effects of ELF electromagnetic fields may require repeated long-term
interaction with known carcinogenic factors.
Psychological effects of chronic exposure to 50 Hz magnetic fields in humans living near extra-
high-voltage transmission lines.
Effects of short term exposure to 60 Hz electromagnetic fields on interleukin 1 and interleukin 6
production by peritoneal exudate cells.
Apoptosis in haemopoietic progenitor cells exposed to extremely low-frequency magnetic fields.
ELF magnetic fields in a city environment.
Assessing compliance with 60-hertz magnetic-field exposure guidelines.
[Epidemiological study of populations exposed to high levels of 50 Hz magnetic fields].
Temporally incoherent magnetic fields mitigate the response of biological systems to temporally
coherent magnetic fields.
Evaluation of potential health effects of 10 kHz magnetic fields: a short-term mouse toxicology
study.
Magnetic fields and radical reactions: recent developments and their role in nature.
Ambient 60-Hz magnetic flux density in an urban neighborhood.
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Brief exposure to a 50 Hz, 100 microT magnetic field: effects on reaction time, accuracy, and
recognition memory.
The influence of a temporary magnetic field on chicken hatching.
Characterization of Children's Exposure to Extremely Low Frequency Magnetic Fields by
Stochastic Modeling.
Natural killer cell activity decreases in workers occupationally exposed to extremely low
frequency magnetic fields exceeding 1 microT.
A quick and easy method for checking compliance of multi-frequency magnetic fields with
ICNIRP's guidelines.
Measurement of low frequency magnetic fields from digital cellular telephones.
Magnetic fields of video display terminals and spontaneous abortion.
Epidemiologic studies of electric and magnetic fields and cancer: a case study of distortions by
the media.
Non-ionizing electromagnetic radiation: a study of carcinogenic and cancer treatment potential.
Electromagnetic field exposure and cancer: a review of epidemiologic evidence.
[State of peripheral blood of technical personnel exposed to constant magnetic fields].
Magnetic field exposure and arrythmic risk: evaluation in railway drivers.
Prevalence of self-reported hypersensitivity to electric or magnetic fields in a population-based
questionnaire survey.
Involvement of eddy currents in the mutagenicity of ELF magnetic fields.
The effects of weak magnetic fields on radical pairs.
Urban exposure to ELF magnetic field due to high-, medium- and low-voltage electricity supply
networks.
[The effect of low-frequency electromagnetic fields on the development of experimental
mammary tumors].
ECG changes in humans exposed to 50 Hz magnetic fields.
On the role of the interactions of ions with external magnetic fields in physiologic processes and
their importance in chronobiology.
Relative-risk-estimate bias and loss of power in the Mantel test for trend resulting from the use
of magnetic-field point-in-time ("spot") measurements in epidemiological studies based on an
ordinal exposure scale.
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[Mercury and creatinine in urine of employees exposed to magnetic fields. A study of a group
electrolysis-operators in Norzink A/S in Odda].
Some non neoplastic effects of ELF magnetic fields in experimental animals.
Alternate indices of electric and magnetic field exposures among Ontario electrical utility
workers.
[The effect of electromagnetic fields on living organisms: plants, birds and animals].
Calcium homeostasis and low-frequency magnetic and electric field exposure: A systematic
review and meta-analysis of in vitro studies.
Exposure to magnetic field harmonics in the vicinity of indoor distribution substations.
Comparison between personal exposure to 60 Hz magnetic fields and stationary home
measurements for people living near and away from a 735 kV power line.
A 60 Hz electric and magnetic field exposure facility for nonhuman primates: design and
operational data during experiments.
Reduction of laser-induced retinal injury applying the combination of the 3D variable electric
and magnetic fields in "vivo".
[Effect of magnetic fields on embryonic mortality].
Speculations on the influence of electromagnetism on genomic and associated structures.
Methodology of a study on the French population exposure to 50 Hz magnetic fields.
Hypersensitivity of human subjects to environmental electric and magnetic field exposure: a
review of the literature.
MYC mRNA abundance is unchanged in subcultures of HL60 cells exposed to power-line
frequency magnetic fields.
Do naturally occurring magnetic nanoparticles in the human body mediate increased risk of
childhood leukaemia with EMF exposure?
Free radical mechanism for the effects of environmental electromagnetic fields on biological
systems.
Facility for chronic exposure of rats to ELF magnetic fields.
Dynamic characteristics of membrane ions in multifield configurations of low-frequency
electromagnetic radiation.
Flight deck magnetic fields in commercial aircraft.
Cardiovascular alterations in Macaca monkeys exposed to stationary magnetic fields:
experimental observations and theoretical analysis.
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Personal power-frequency magnetic field exposure in women recruited at an infertility clinic:
association with physical activity and temporal variability.
Evaluating exposure cutpoint bias in epidemiologic studies of electric and magnetic fields.
Specific patterns of weak (1 microTesla) transcerebral complex magnetic fields differentially
affect depression, fatigue, and confusion in normal volunteers.
Effects of 50 Hz magnetic field exposure on human heart rate variability with passive tilting.
Comment on "designing EMF experiments: what is required to characterize 'exposure'?".
[Effect of high intensity magnetic field on the processes of early growth in plant seeds and
development of honeybees].
Low-frequency electromagnetic radiation enhances the induction of rat mammary tumors by
nitrosomethyl urea.
Possible disruption of remote viewing by complex weak magnetic fields around the stimulus site
and the possibility of accessing real phase space: a pilot study.
60 Hertz magnetic field exposure assessment for an investigation of leukemia in telephone
lineworkers.
The heliogeophysical aspects of circumpolar health.
The effects of continuous exposure to 20-kHz sawtooth magnetic fields on the litters of CD-1
mice.
[Magnetic field on the deranged accommodation of visual detector terminal operators].
Macro- and trace element concentrations in blood plasma and cerebrospinal fluid of dairy cows
exposed to electric and magnetic fields.
Assessment of occupational exposure patterns by frequency-domain analysis of time series data.
Field enhancement of nonreciprocal electromagnetic wave supported by magnetic surface
plasmon.
Residential magnetic field measurements in France: comparison of indoor and outdoor
measurements.
Sleep EEG alterations: effects of pulsed magnetic fields versus pulse-modulated radio frequency
electromagnetic fields.
Hypothesis on a casual link between EMF and an evolutionary class of cancer and spontaneous
abortion.
Exposure to alternating electromagnetic fields and effects on the visual and visuomotor systems.
Statistical review of the henhouse experiments: the effects of a pulsed magnetic field on chick
embryos.
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A pilot study on the reproductive risks of maternal exposure to magnetic fields from electronic
article surveillance systems.
How do honeybees use their magnetic compass? Can they see the North?
Temporal trends and misclassification in residential 60 Hz magnetic field measurements.
The precautionary principle and electric and magnetic fields.
[Assessment of exposure to extremely low frequency magnetic field emitted from monitors].
Anthropogenic electromagnetic noise disrupts magnetic compass orientation in a migratory bird.
A comparison of rheumatoid arthritis and fibromyalgia patients and healthy controls exposed to a
pulsed (200 microT) magnetic field: effects on normal standing balance.
An Investigation on the Effect of Extremely Low Frequency Pulsed Electromagnetic Fields on
Human Electrocardiograms (ECGs).
Patient reactions to some electromagnetic fields from dental chair and unit: a pilot study.
Occupational 50 Hz magnetic field exposure measurements among female sewing machine
operators in Hungary.
Anatomical localization of human detection of weak electromagnetic radiation: experiments with
dowsers.
Paroxysmal itching in multiple sclerosis during treatment with external magnetic fields.
Natural very-low-frequency sferics and headache.
Nanoscale Design of Nano-Sized Particles in Shape-Memory Polymer Nanocomposites Driven
by Electricity.
Effect of the alternative magnetic stimulation on peripheral circulation for regenerative medicine.
Influence of 50-Hz electromagnetic field on anurian (Xenopus laevis) metamorphosis.
--Leaf Cluster 40 (116)
Theme - Adverse effects of low-frequency magnetic fields on rodents
Titles
Influence of 60-Hertz magnetic fields on leukemia.
Long-term exposure of male and female mice to 50 Hz magnetic field: effects on fertility.
Effects of extremely low-frequency electromagnetic fields (ELF-EMF) exposure on B6C3F1
mice.
Deficits in spatial learning after exposure of mice to a 50 Hz magnetic field.
Eight-week toxicity study of 60 Hz magnetic fields in F344 rats and B6C3F1 mice.
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Dominant lethal studies in male mice after exposure to a 50-Hz electric field.
Long term effects of a 50 Hz electric field on the life-expectancy of mice.
Effect of a 9 mT pulsed magnetic field on C3H/Bi female mice with mammary carcinoma. A
comparison between the 12 Hz and the 460 Hz frequencies.
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in F344/N
rats.
Effects of power frequency alternating magnetic fields on reproduction and pre-natal
development of mice.
Hematopoietic neoplasia in C57BL/6 mice exposed to split-dose ionizing radiation and circularly
polarized 60 Hz magnetic fields.
A gross morphologic, histologic, hematologic, and blood chemistry study of adult and neonatal
mice chronically exposed to high magnetic fields.
Behavioral effects of long-term exposure to magnetic fields in rats.
Behavioral studies with mice exposed to DC and 60-Hz magnetic fields.
Carcinogenicity test of 50 Hz sinusoidal magnetic fields in rats.
Dominant lethal studies in male mice after exposure to a 50 Hz magnetic field.
Toxic effects of 50 Hz electromagnetic field on memory consolidation in male and female mice.
Behavioral sensitivity of rats to extremely-low-frequency magnetic fields.
Rats are not aversive when exposed to 60-Hz magnetic fields at 3.03 mT.
Effects of low-frequency magnetic fields on fetal development in rats.
Effect of pulsed magnetic fields on leukemia-prone AKR mice. No-effect on mortality through
five generations.
Teratogenic effect of broad-band electromagnetic field on neonatal mice (Mus musculus).
Effect of a magnetic field on ascorbate system in mice.
Spatial learning deficit in the rat after exposure to a 60 Hz magnetic field.
Biologic effects of prolonged exposure to ELF electromagnetic fields in rats: II. 50 Hz magnetic
fields.
Neurodevelopmental anomalies of the hippocampus in rats exposed to weak intensity complex
magnetic fields throughout gestation.
Assessment of biological changes of continuous whole body exposure to static magnetic field
and extremely low frequency electromagnetic fields in mice.
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[VDT pulse magnetic field enhances teratogenic effect of ara-c in mice].
Electric field exposure and evidence of stress in mice.
Subchronic in vivo effects of a high static magnetic field (9.4 T) in rats.
Exposure to a theta-burst patterned magnetic field impairs memory acquisition and consolidation
for contextual but not discrete conditioned fear in rats.
Radial maze proficiency of adult Wistar rats given prenatal complex magnetic field treatments.
Lymphoma development of simultaneously combined exposure to two radiofrequency signals in
AKR/J mice.
Teratogenic effects of static magnetic field on mouse fetuses.
Effect of electric field in conditioned aversion response.
Acute exposure to a 50 Hz magnetic field impairs consolidation of spatial memory in rats.
Effects of radiofrequency electromagnetic fields (UMTS) on reproduction and development of
mice: a multi-generation study.
Combined effects of complex magnetic fields and agmatine for contextual fear learning deficits
in rats.
Enhanced mortality of rat pups following inductions of epileptic seizures after perinatal
exposures to 5 nT, 7 Hz magnetic fields.
DEXA analysis on the bones of rats exposed in utero and neonatally to static and 50 Hz electric
fields.
Gender- and age-specific impairment of rat performance in the Morris water maze following
prenatal exposure to an MRI magnetic field.
Repeated exposure attenuates the behavioral response of rats to static high magnetic fields.
Metallothionein content increased in the liver of mice exposed to magnetic fields.
[Alternating magnetic field damages the reproductive function of murine testes].
Initial exposure to 30 kV/m or 60 kV/m 60 Hz electric fields produces temporary cessation of
operant behavior of nonhuman primates.
Extremely low-frequency magnetic fields can impair spermatogenesis recovery after reversible
testicular damage induced by heat.
Teratological evaluation of mouse fetuses exposed to a 20 kHz EMF.
Fetal loss in mice exposed to magnetic fields during early pregnancy.
Effects of pulsed magnetic fields on the developing mouse embryo.
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The effect of the prenatal and post-natal long-term exposure to 50 Hz electric field on growth,
pubertal development and IGF-1 levels in female Wistar rats.
Carcinogenicity study of GSM and DCS wireless communication signals in B6C3F1 mice.
Lymphoma induced in mice chronically exposed to very strong low-frequency electromagnetic
field.
Short-term memory in mice is affected by mobile phone radiation.
Nonhuman primates will not respond to turn off strong 60 Hz electric fields.
[Effects of 1800 MHz GSM-like exposure on the gonadal function and hematological parameters
of male mice].
Detection thresholds for 60 Hz electric fields by nonhuman primates.
Effects of exposure to a 50 Hz electric field on plasma levels of lactate, glucose, free Fatty acids,
triglycerides and creatine phosphokinase activity in hind-limb ischemic rats.
Transient and cumulative memory impairments induced by GSM 1.8 GHz cell phone signal in a
mouse model.
The effect of very low dose pulsed magnetic waves on cochlea.
Lymphoma development in mice chronically exposed to UMTS-modulated radiofrequency
electromagnetic fields.
Effects of combined ferrous sulphate administration and exposure to static magnetic field on
spatial learning and motor abilities in rats.
Autism-relevant social abnormalities in mice exposed perinatally to extremely low frequency
electromagnetic fields.
Urinary 6-sulphatoxymelatonin excretion is increased in rats after 24 hours of exposure to
vertical 50 Hz, 100 microT magnetic field.
Developmental effects of perinatal exposure to extremely weak 7 Hz magnetic fields and nitric
oxide modulation in the Wistar albino rat.
Developmental profiles of growth-associated protein (Gap43), Ngfb, Bndf and Ntf4 mRNA
levels in the rat forebrain after exposure to 60 Hz magnetic fields.
Prenatal exposures to LTP-patterned magnetic fields: quantitative effects on specific limbic
structures and acquisition of contextually conditioned fear.
Effects of exposure to a 60-kV/m, 60-Hz electric field on the social behavior of baboons.
Effects of a 60 Hz magnetic field on central cholinergic systems of the rat.
Electromagnetic waves of 900 MHz in acute pentylenetetrazole model in ontogenesis in mice.
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Reduced litter sizes following 48-h of prenatal exposure to 5 nT to 10 nT,0.5 Hz magnetic fields:
implications for sudden infant deaths.
Effects of Electromagnetic Radiation from Smartphones on Learning Ability and Hippocampal
Progenitor Cell Proliferation in Mice.
Rats avoid exposure to HVdc electric fields: a dose response study.
Biological effects of long-duration, high-field (4 T) MRI on growth and development in the
mouse.
Behavioral in-effectiveness of high frequency electromagnetic field in mice.
Does static electric field from ultra-high voltage direct-current transmission lines affect male
reproductive capacity? Evidence from a laboratory study on male mice.
Carcinogenicity study of 217 Hz pulsed 900 MHz electromagnetic fields in Pim1 transgenic
mice.
Five-tesla static magnetic fields suppress food and water consumption and weight gain in mice.
[The effect of alternating electric field of industrial frequency on testicles of white mice].
Theta-gamma coupling in hippocampus during working memory deficits induced by low
frequency electromagnetic field exposure.
[An ultrastructural analysis of the testes in mice subjected to long-term exposure to a 17-kHz
electrical field].
Evaluation of mouse embryos produced in vitro after electromagnetic waves exposure;
Morphometric study.
Biological accounts emerging from some kinds of electromagnetic waves in the environment.
Effect of electromagnetic waves on sensitivity of fungi of the genus Candida to miconazole.
Effects of exposure to static magnetic field on motor skills and iron levels in plasma and brain of
rats.
Morphometric and structural study of the pineal gland of the Wistar rat subjected to the pulse
action of a 52 Gauss, (50 Hz) magnetic field. Evolutive analysis over 21 days.
Direct suppressive effects of weak magnetic fields (50 Hz and 16 2/3 Hz) on melatonin synthesis
in the pineal gland of Djungarian hamsters (Phodopus sungorus).
Effect of a 20 kHz sawtooth magnetic field exposure on the estrous cycle in mice.
[Pathomorphological reactions of the cerebral cortex nerve elements during treatment with an
alternating magnetic field].
[Effect of an electric field of industrial frequency on selected biochemical parameters in the
guinea pig liver].
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Alterations in the rat electrocardiogram induced by stationary magnetic fields.
Effect of ELF electric field on some on biochemistry characters in the rat serum.
Repeated application of an electric field increases BDNF in the brain, enhances spatial learning,
and induces infarct tolerance.
Pulsed magnetic field from video display terminals enhances teratogenic effects of cytosine
arabinoside in mice.
Fetal radiofrequency radiation exposure from 800-1900 mhz-rated cellular telephones affects
neurodevelopment and behavior in mice.
Liver and spleen morphology, ceruloplasmin activity and iron content in serum of guinea pigs
exposed to the magnetic field.
[Effects of pregnant exposure to electromagnetic field emitted by electric blankets on brain
catecholamine and behavior in offspring mice].
Variable E-cadherin expression in a MNU-induced colon tumor model in rats which exposed
with 50 Hz frequency sinusoidal magnetic field.
Low frequency electromagnetic radiation and hearing.
Pretraining exposure to physiologically patterned electromagnetic stimulation attenuates fear-
conditioned analgesia.
Influence of combined DC and AC magnetic fields on rat behavior.
Radiofrequency fields and teratogenesis.
Chronic exposure of primates to 60-Hz electric and magnetic fields: II. Neurochemical effects.
[Biological effects of pulsing electromagnetic fields (PEMFs) on ICR mice].
Effects of Simulated Mobile Phone Electromagnetic Radiation on Fertilization and Embryo
Development.
Effect of low frequency, low amplitude magnetic fields on the permeability of cationic liposomes
entrapping carbonic anhydrase: I. Evidence for charged lipid involvement.
The influences of extremely low frequency magnetic fields on drug-induced convulsion in
mouse.
Effects of pulsed magnetic field treatment of soybean seeds on calli growth, cell damage, and
biochemical changes under salt stress.
What is the impact of electromagnetic waves on epileptic seizures?
Intensity threshold for 60-Hz magnetically induced behavioral changes in rats.
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Neuritin reverses deficits in murine novel object associative recognition memory caused by
exposure to extremely low-frequency (50 Hz) electromagnetic fields.
[Standardization of electromagnetic fields of 3-30 MHz with reference to the time factor].
[Biological effects of the action of permanent magnetic fields of various intensities].
The influence of low intensity 50 Hz electromagnetic field exposure on blood Na, K and Cl
concentrations in humans.
Effects of exposure of animals to ultra-wideband pulses.
A controlled trial of daily left prefrontal cortex TMS for treating depression.
[The reaction of the systems of hormonal mediator regulation to a weak geomagnetic field
against a background of ionizing radiation exposure].
--Leaf Cluster 2 (27)
Theme - Effects of electromagnetic fields on chicken embryos
Titles
Effects of sinusoidal electromagnetic fields on histopathology and structures of brains of
preincubated white Leghorn chicken embryos.
Teratogenic effects of sinusoidal extremely low frequency electromagnetic fields on morphology
of 24 hr chick embryos.
Effects of MR exposure at 1.5 T on early embryonic development of the chick.
Histopathological and ultrastructural studies on the effects of electromagnetic fields on the liver
of preincubated white Leghorn chicken embryo.
Study of potential health effects of electromagnetic fields of telephony and Wi-Fi, using chicken
embryo development as animal model.
Development of preincubated chicken eggs following exposure to 50 Hz electromagnetic fields
with 1.33-7.32 mT flux densities.
Effect of electric power network frequency magnetic field on embryonic development of Ascaris
suum (Nematoda).
Development of chicken embryos in a pulsed magnetic field.
Influence of continuous electromagnetic fields on the stage, weight and stature of the chick
embryo.
Growth Retardation Of Chick Embryo Exposed To A Low Dose Of Electromagnetic Waves.
Effects of the ELF-MFs on the development of spleens of preincubated chicken embryos.
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Effects of exposing chicken eggs to a cell phone in "call" position over the entire incubation
period.
Effects of 50 Hz electromagnetic fields on the histology, apoptosis, and expression of c-Fos and
beta-catenin on the livers of preincubated white Leghorn chicken embryos.
Chick embryo development can be irreversibly altered by early exposure to weak extremely-low-
frequency magnetic fields.
Effects of static electromagnetic fields on chick embryo pineal gland development.
Survival Assessment of Mouse Preimplantation Embryos After Exposure to Cell Phone
Radiation.
Effect of ambient levels of power-line-frequency electric fields on a developing vertebrate.
Lethal and teratogenic effects of long-term low-intensity radio frequency radiation at 428 MHz
on developing chick embryo.
Biological effects of continuous exposure of embryos and young chickens to electromagnetic
fields emitted by video display units.
Effects of electromagnetic fields on fecundity in the chicken.
[The influence of ultrasound and constant magnetic field on gametes, zygotes, and embryos of
the sea urchin].
Developmental changes in Drosophila melanogaster following exposure to alternating
electromagnetic fields.
Effect of exposure to radio frequency radiation emitted by cell phone on the developing dorsal
root ganglion of chick embryo: a light microscopic study.
First cell cycles of sea urchin Paracentrotus lividus are dramatically impaired by exposure to
extremely low-frequency electromagnetic field.
Assessment of the effects of electromagnetic field modification on egg-laying hens in
commercial flocks as indicated by production measures.
Superimposing spatially coherent electromagnetic noise inhibits field-induced abnormalities in
developing chick embryos.
Sex-linked recessive lethal test of Drosophila melanogaster after exposure to 50-Hz magnetic
fields.
--Leaf Cluster 12 (38)
Theme - Impact of static and low-frequency magnetic fields on melatonin secretion
Titles
Geomagnetic activity and human melatonin metabolite excretion.
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Melatonin suppression by static and extremely low frequency electromagnetic fields: relationship
to the reported increased incidence of cancer.
Human melatonin during continuous magnetic field exposure.
The influence of long-term exposure of mice to randomly varied power frequency magnetic
fields on their nocturnal melatonin secretion patterns.
Geomagnetic disturbances are associated with reduced nocturnal excretion of a melatonin
metabolite in humans.
Melatonin metabolite levels in workers exposed to 60-Hz magnetic fields: work in substations
and with 3-phase conductors.
Magnetic fields and pineal function in humans: evaluation of nocturnal acute exposure to
extremely low frequency magnetic fields on serum melatonin and urinary 6-sulfatoxymelatonin
circadian rhythms.
Nocturnal excretion of a urinary melatonin metabolite among electric utility workers.
Multi-night exposure to 60 Hz magnetic fields: effects on melatonin and its enzymatic
metabolite.
Chronic exposure to 2.9 mT, 40 Hz magnetic field reduces melatonin concentrations in humans.
Is melatonin the hormonal missing link between magnetic field effects and human diseases?
Chronic exposure to ELF magnetic fields during night sleep with electric sheet: effects on
diurnal melatonin rhythms in men.
Reduced excretion of a melatonin metabolite in workers exposed to 60 Hz magnetic fields.
Melatonin and magnetic fields.
Examination of the melatonin hypothesis in women exposed at night to EMF or bright light.
Effects of 60-Hz magnetic field exposure on nocturnal 6-sulfatoxymelatonin, estrogens,
luteinizing hormone, and follicle-stimulating hormone in healthy reproductive-age women:
results of a crossover trial.
Increases in geomagnetic activity are associated with increases in thyroxine levels in a single
patient: implications for melatonin levels.
Rapid-onset/offset, variably scheduled 60 Hz electric and magnetic field exposure reduces
nocturnal serum melatonin concentration in nonhuman primates.
Nocturnal 6-hydroxymelatonin sulfate excretion in female workers exposed to magnetic fields.
Acute exposure to 50 Hz magnetic fields with harmonics and transient components: lack of
effects on nighttime hormonal secretion in men.
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Age-dependent association of exposure to television screen with children's urinary melatonin
excretion?
Effects of electric and magnetic fields on nocturnal melatonin concentrations in dairy cows.
Relationship between amyloid beta protein and melatonin metabolite in a study of electric utility
workers.
Non-linear relation of heart rate variability during exercise recovery with local geomagnetic
activity.
Graded response of heart rate variability, associated with an alteration of geomagnetic activity in
a subarctic area.
Evaluation of the nocturnal levels of urinary biogenic amines in men exposed overnight to 50-Hz
magnetic field.
Nocturnal exposure to intermittent 60 Hz magnetic fields alters human cardiac rhythm.
[Biological effects produced by the influence of low frequency electromagnetic fields on
hormone secretion].
Circasemiannual chronomics: half-yearly biospheric changes in their own right and as a
circannual waveform.
Endocrine functions in young men exposed for one night to a 50-Hz magnetic field. A circadian
study of pituitary, thyroid and adrenocortical hormones.
Effects of exposure to 16.7 Hz magnetic fields on urinary 6-hydroxymelatonin sulfate excretion
of Swiss railway workers.
Chronic exposure to ELF fields may induce depression.
[Dependence of acoustic-motor reaction of healthy individuals from geomagnetic activity].
Is motivation influenced by geomagnetic activity?
Is geomagnetic activity a risk factor for sudden unexplained death in epilepsies?
[Exacerbation of hypertension and disturbances of the geomagnetic field].
Magnetic storm effect on the circulation of rabbits.
Exercise testing in the evaluation of human responses to powerline frequency fields.
Fourth Level Cluster 85 (540)
Theme - Adverse impacts of low-frequency EMF, emphasizing cancer and neurodegenerative
diseases
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--Leaf Cluster 4 (97)
Theme - Exposure to power lines and risk of childhood cancer
Titles
Distance from residence to power line and risk of childhood leukemia: a population-based case-
control study in Denmark.
Living near overhead high voltage transmission power lines as a risk factor for childhood acute
lymphoblastic leukemia: a case-control study.
Residential exposure to electric power transmission lines and risk of lymphoproliferative and
myeloproliferative disorders: a case-control study.
Epidemiological study of power lines and childhood cancer in the UK: further analyses.
Exposure to Electromagnetic Fields of High Voltage Overhead Power Lines and Female
Infertility.
Acute childhood leukemias and exposure to magnetic fields generated by high voltage overhead
power lines - a risk factor in Iran.
Childhood cancer in relation to distance from high voltage power lines in England and Wales: a
case-control study.
Residential mobility of populations near UK power lines and implications for childhood
leukaemia.
Electromagnetic fields and cancer in children residing near Norwegian high-voltage power lines.
Magnetic fields and cancer in children residing near Swedish high-voltage power lines.
Exposure of children to residential magnetic fields in Norway: is proximity to power lines an
adequate predictor of exposure?
Residential exposure to magnetic fields generated by 110-400 kV power lines in Finland.
Childhood cancer and magnetic fields from high-voltage power lines in England and Wales: a
case-control study.
Estimating magnetic fields of homes near transmission lines in the California Power Line Study.
Proximity to overhead power lines and childhood leukaemia: an international pooled analysis.
Childhood leukaemia and distance from power lines in California: a population-based case-
control study.
Childhood leukemia risk in the California Power Line Study: Magnetic fields versus distance
from power lines.
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Residential distance to high-voltage power lines and risk of neurodegenerative diseases: a Danish
population-based case-control study.
Residential proximity to high-voltage power lines and risk of childhood hematological
malignancies.
Magnetic fields and leukemia--risk for adults living close to power lines.
Overhead electricity power lines and childhood leukemia: a registry-based, case-control study.
Preterm birth among women living within 600 meters of high voltage overhead Power Lines: a
case-control study.
Are children living near high-voltage power lines at increased risk of acute lymphoblastic
leukemia?
Health responses to a new high-voltage power line route: design of a quasi-experimental
prospective field study in the Netherlands.
Reanalysis of risks of childhood leukaemia with distance from overhead power lines in the UK.
Adult cancers near high-voltage overhead power lines.
Methods used to estimate residential exposure to 50 Hz magnetic fields from overhead power
lines in an epidemiological study in France.
Magnetic fields of high voltage power lines and risk of cancer in Finnish adults: nationwide
cohort study.
Risks of leukaemia among residents close to high voltage transmission electric lines.
Childhood leukaemia close to high-voltage power lines--the Geocap study, 2002-2007.
Risk of cancer in Finnish children living close to power lines.
Exposure to magnetic fields and childhood acute lymphocytic leukemia in Sao Paulo, Brazil.
"These Power Lines Make Me Ill": A Typology of Residents' Health Responses to a New High-
Voltage Power Line.
Increased risk of childhood acute lymphoblastic leukemia (ALL) by prenatal and postnatal
exposure to high voltage power lines: a case control study in Isfahan, Iran.
[Childhood leukaemia in a residential area with a high-voltage power line: approach according to
the Dutch Community Health Services' guideline 'Cancer Clusters'].
Magnetic fields and childhood cancer: an epidemiological investigation of the effects of high-
voltage underground cables.
Epidemiologic study of residential proximity to transmission lines and childhood cancer in
California: description of design, epidemiologic methods and study population.
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Residence near power lines and the risk of birth defects.
Leukaemia and residence near electricity transmission equipment: a case-control study.
Adult mortality from leukemia, brain cancer, amyotrophic lateral sclerosis and magnetic fields
from power lines: a case-control study in Brazil.
Residential and occupational exposure to 50 Hz magnetic fields and malignant melanoma: a
population based study.
Distance to high-voltage power lines and risk of childhood leukemia--an analysis of confounding
by and interaction with other potential risk factors.
Residential and occupational exposure to 50 Hz magnetic fields and hematological cancers in
Norway.
Childhood cancer and residential proximity to power lines. UK Childhood Cancer Study
Investigators.
[Environmental exposure to electromagnetic fields and the risk of cancer].
Residential magnetic fields, contact voltage and their relationship: the effects of distribution
unbalance and residential proximity to a transmission line.
Magnetic fields, leukemia, and central nervous system tumors in Swedish adults residing near
high-voltage power lines.
Residential distance from high-voltage overhead power lines and risk of Alzheimer's dementia
and Parkinson's disease: a population-based case-control study in a metropolitan area of
Northern Italy.
Maternal exposure to magnetic fields from high-voltage power lines and the risk of birth defects.
Magnetic fields exposure from high-voltage power lines and risk of amyotrophic lateral sclerosis
in two Italian populations.
Residence near power lines and mortality from neurodegenerative diseases: longitudinal study of
the Swiss population.
Symptom reporting after the introduction of a new high-voltage power line: a prospective field
study.
Risk of hematological malignancies associated with magnetic fields exposure from power lines:
a case-control study in two municipalities of northern Italy.
Nocebo responses to high-voltage power lines: Evidence from a prospective field study.
Role of Electromagnetic Field Exposure in Childhood Acute Lymphoblastic Leukemia and No
Impact of Urinary Alpha- Amylase--a Case Control Study in Tehran, Iran.
Residence near high voltage facilities and risk of cancer in children.
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[Residence close to high-tension electric power lines and its association with leukemia in
children].
Relation between suicide and the electromagnetic field of overhead power lines.
Methods used to calculate exposures in two epidemiological studies of power lines in the UK.
Risk of selected birth defects by maternal residence close to power lines during pregnancy.
The effects of electric power lines on the breeding ecology of greater sage-grouse.
Birth defects and high voltage power lines: an exploratory study based on registry data.
[Electromagnetic fields from high-voltage installations and cancer in childhood].
Understanding Local Policy Elites' Perceptions on the Benefits and Risks Associated with High-
Voltage Power Line Installations in the State of Arkansas.
Maternal residential proximity to sources of extremely low frequency electromagnetic fields and
adverse birth outcomes in a UK cohort.
Experimental validation of a statistical model for evaluating the past or future magnetic field
exposures of a population living near power lines.
Residential exposure to overhead high-voltage lines and the risk of testicular cancer: results of a
population-based case-control study in Hamburg (Germany).
Childhood cancer and exposure to corona ions from power lines: an epidemiological test.
[Epidemiological studies on neurotic disturbances, anxiety and depression disorders in a
population living near an overhead high voltage transmission line (400 kV)].
Magnetic fields of transmission lines and depression.
Power lines and the geomagnetic field.
The relationship between residential proximity to extremely low frequency power transmission
lines and adverse birth outcomes.
Effect of Power Line Interference on Microphone Calibration Measurements Made at or Near
Harmonics of the Power Line Frequency.
Maternal proximity to extremely low frequency electromagnetic fields and risk of birth defects.
Morbidity experience in populations residentially exposed to 50 hz magnetic fields: methodology
and preliminary findings of a cohort study.
Case-control study on maternal residential proximity to high voltage power lines and congenital
anomalies in France.
Case-only study of interactions between DNA repair genes (hMLH1, APEX1, MGMT, XRCC1
and XPD) and low-frequency electromagnetic fields in childhood acute leukemia.
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Environmental justice: a contrary finding for the case of high-voltage electric power transmission
lines.
Comparison of Two Methods for Judging Distances Near Overhead Power Lines.
Relative contribution of residential and occupational magnetic field exposure over twenty-four
hours among people living close to and far from a power line.
Depressive symptomatology in women and residential proximity to high-voltage transmission
lines.
Childhood cancer occurrence in relation to power line configurations: a study of potential
selection bias in case-control studies.
Power lines, roads, and avian nest survival: effects on predator identity and predation intensity.
Symptom prevalence and worry about high voltage transmission lines.
Re-examining the association between residential exposure to magnetic fields from power lines
and childhood asthma in the Danish National Birth Cohort.
Comparison of three different ways of measuring distances between residences and high voltage
power lines.
Association between high voltage overhead transmission lines and mental health: a cross-
sectional study.
Residential proximity to electromagnetic field sources and birth weight: Minimizing residual
confounding using multiple imputation and propensity score matching.
[Health effects of electromagnetic fields].
Association between exposure to electromagnetic fields from high voltage transmission lines and
neurobehavioral function in children.
Theory of oncogene activation by chemicals and antioncogene inactivation by radiations -
possible carcinogenic effect of power-lines.
Radiofrequency field exposure and cancer: what do the laboratory studies suggest?
Cancer cluster among young Indian adults living near power transmission lines in Bom Jesus do
Tocantins, Para, brazil.
The Origin and Role of Trust in Local Policy Elites' Perceptions of High-Voltage Power Line
Installations in the State of Arkansas.
A note on the charging of aerosols by overhead line corona.
[Heliogeophysical correlates of early biodemographic variables in the south of western Siberia].
Experimental evidence of a potentially increased thrombo-embolic disease risk by domestic
electromagnetic field exposure.
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--Leaf Cluster 15 (131)
Theme - Residential magnetic fields and childhood leukemia
Titles
A pooled analysis of magnetic fields, wire codes, and childhood leukemia. Childhood Leukemia-
EMF Study Group.
Residential magnetic fields predicted from wiring configurations: II. Relationships To childhood
leukemia.
Childhood leukemia and personal monitoring of residential exposures to electric and magnetic
fields in Ontario, Canada.
Residential exposure to magnetic fields and acute lymphoblastic leukemia in children.
A case-control study of childhood leukemia in southern Ontario, Canada, and exposure to
magnetic fields in residences.
Do studies of wire code and childhood leukemia point towards or away from magnetic fields as
the causal agent?
Case-control study of childhood cancer and exposure to 60-Hz magnetic fields.
Power-frequency electric and magnetic fields and risk of childhood leukemia in Canada.
Exposure to residential electric and magnetic fields and risk of childhood leukemia.
Magnetic field exposure assessment in a case-control study of childhood leukemia.
Assessment of selection bias in the Canadian case-control study of residential magnetic field
exposure and childhood leukemia.
Childhood leukemia and electromagnetic fields: results of a population-based case-control study
in Germany.
[Infantile leukemia and exposure to 50/60 Hz magnetic fields: review of epidemiologic evidence
in 2000].
Factors that explain the power line configuration wiring code-childhood leukemia association:
what would they look like?
Electric and magnetic fields at power frequencies.
Residential magnetic field exposure and childhood brain cancer: a meta-analysis.
Childhood cancer in relation to a modified residential wire code.
Occupational and residential magnetic field exposure and leukemia and central nervous system
tumors.
A pooled analysis of magnetic fields and childhood leukaemia.
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Electrical power lines and childhood leukemia: a study from Greece.
Childhood leukemia, electric and magnetic fields, and temporal trends.
Residential mobility and childhood leukemia.
Residential wire codes: reproducibility and relation with measured magnetic fields.
Childhood leukemia: electric and magnetic fields as possible risk factors.
Childhood leukemia and magnetic fields in Japan: a case-control study of childhood leukemia
and residential power-frequency magnetic fields in Japan.
Hypothesis: the risk of childhood leukemia is related to combinations of power-frequency and
static magnetic fields.
Selection bias from differential residential mobility as an explanation for associations of wire
codes with childhood cancer.
Do confounding or selection factors of residential wiring codes and magnetic fields distort
findings of electromagnetic fields studies?
Residential magnetic fields and childhood leukemia: a meta-analysis.
Residential magnetic fields as a risk factor for childhood acute leukaemia: results from a German
population-based case-control study.
The residential case-specular method to study wire codes, magnetic fields, and disease.
Wire codes, magnetic fields, and childhood cancer.
Residential EMF exposure and childhood leukemia: meta-analysis and population attributable
risk.
The potential impact of bias in studies of residential exposure to magnetic fields and childhood
leukemia.
Magnetic fields and childhood cancer--a pooled analysis of two Scandinavian studies.
Do magnetic fields cause increased risk of childhood leukemia via melatonin disruption?
[Electromagnetic residential fields and childhood cancers: state of epidemiological research].
[Synthesis of the epidemiological evidence concerning childhood leukemia in relation to
exposure to 50 Hz. electric and magnetic fields].
Childhood leukemia and magnetic fields in infant incubators.
Electromagnetic fields and cancer risks.
[Risk of childhood leukemia and environmental exposure to ELF electromagnetic fields].
Magnetic fields and acute leukemia in children with Down syndrome.
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Residential exposure to electromagnetic fields and childhood leukaemia: a meta-analysis.
Combined risk estimates for two German population-based case-control studies on residential
magnetic fields and childhood acute leukemia.
Magnetic fields and acute lymphoblastic leukemia in children: a systematic review of case-
control studies.
Adult and childhood leukemia near a high-power radio station in Rome, Italy.
Residential proximity to electricity transmission and distribution equipment and risk of
childhood leukemia, childhood lymphoma, and childhood nervous system tumors: systematic
review, evaluation, and meta-analysis.
Variation in cancer risk estimates for exposure to powerline frequency electromagnetic fields: a
meta-analysis comparing EMF measurement methods.
Maternal occupational exposure to extremely low frequency magnetic fields during pregnancy
and childhood leukemia.
Residential magnetic fields predicted from wiring configurations: I. Exposure model.
Estimating exposure in studies of residential magnetic fields and cancer: importance of short-
term variability, time interval between diagnosis and measurement, and distance to power line.
Childhood leukemia in relation to radio frequency electromagnetic fields in the vicinity of TV
and radio broadcast transmitters.
Pooled analysis of recent studies on magnetic fields and childhood leukaemia.
Occupational electric and magnetic field exposure and leukemia. A meta-analysis.
Description of a new computer wire coding method and its application to evaluate potential
control selection bias in the Savitz et al. childhood cancer study.
Aetiology of childhood leukemia.
Maternal occupational exposure to electromagnetic fields before, during, and after pregnancy in
relation to risks of childhood cancers: findings from the Oxford Survey of Childhood Cancers,
1953-1981 deaths.
Exposure to power-frequency magnetic fields and the risk of childhood cancer. UK Childhood
Cancer Study Investigators.
Exposure to magnetic fields and survival after diagnosis of childhood leukemia: a German cohort
study.
A case-control pilot study of traffic exposures and early childhood leukemia using a geographic
information system.
Influence of power frequency electric and magnetic fields on human health.
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Rate of occurrence of transient magnetic field events in U.S. residences.
Epidemiologic studies of electric and magnetic fields and cancer: strategies for extending
knowledge.
Suggestion of concomitant changes of electric power consumption and childhood leukemia in
Greece.
Association between childhood acute lymphoblastic leukemia and use of electrical appliances
during pregnancy and childhood.
Nighttime exposure to electromagnetic fields and childhood leukemia: an extended pooled
analysis.
The possible role of contact current in cancer risk associated with residential magnetic fields.
Leukemia in electric utility workers: the evaluation of alternative indices of exposure to 60 Hz
electric and magnetic fields.
Exposure to radio-frequency electromagnetic fields from broadcast transmitters and risk of
childhood cancer: a census-based cohort study.
Leukemia and lymphoma incidence in rodents exposed to low-frequency magnetic fields.
Do power frequency magnetic fields cause leukemia in children?
Viral contacts confound studies of childhood leukemia and high-voltage transmission lines.
Residential exposure to magnetic fields and risk of canine lymphoma.
[Occupational and residential exposure to electric and magnetic field and its relationship on
acute myeloid leukemia in adults - A Meta-analysis].
Acute nonlymphocytic leukemia and residential exposure to power frequency magnetic fields.
Modification of the 1979 "Denver wire code" for different wire or plumbing types.
Risk of childhood leukemia in areas passed by high power lines.
Risk factors for leukemia in Thailand.
Determinants of power-frequency magnetic fields in residences located away from overhead
power lines.
Risk of leukemia in children living near high-voltage transmission lines.
Los Angeles study of residential magnetic fields and childhood brain tumors.
Residential electric consumption and childhood cancer in Canada (1971-1986)
Selection bias and its implications for case-control studies: a case study of magnetic field
exposure and childhood leukaemia.
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Extremely low-frequency magnetic fields and childhood acute lymphoblastic leukemia: an
exploratory analysis of alternative exposure metrics.
Childhood brain tumors and residential electromagnetic fields (EMF).
Power-frequency magnetic fields and childhood brain tumors: a case-control study in Japan.
Electromagnetic field exposures and childhood leukaemia in New Zealand.
Childhood cancer in relation to indicators of magnetic fields from ground current sources.
[A review of epidemiological studies on the relationship of residential electromagnetic exposure
to cancer].
Investigation of the sources of residential power frequency magnetic field exposure in the UK
Childhood Cancer Study.
Electric and magnetic fields and health outcomes--an overview.
Estimation of population attributable fractions from fitted incidence ratios and exposure survey
data, with an application to electromagnetic fields and childhood leukemia.
The determinants of Canadian children's personal exposures to magnetic fields.
Correlation of year-to-year magnetic field exposure metrics among children in a leukemia
survival study.
Contact voltage measured in residences: implications to the association between magnetic fields
and childhood leukemia.
Exposure to power frequency electric fields and the risk of childhood cancer in the UK.
Investigation of increased incidence in childhood leukemia near radio towers in Hawaii:
preliminary observations.
Adult glioma in relation to residential power frequency electromagnetic field exposures in the
San Francisco Bay area.
A precautionary public health protection strategy for the possible risk of childhood leukaemia
from exposure to power frequency magnetic fields.
[Leukemia mortality and incidence of infantile leukemia near the Vatican Radio Station of
Rome].
A pooled analysis of extremely low-frequency magnetic fields and childhood brain tumors.
Health effects of magnetic fields generated from power lines: new clues for an old puzzle.
Association of childhood cancer with residential traffic density.
Designs and analyses for exploring the relationship of magnetic fields to childhood leukaemia: a
pilot project for the Danish National Birth Cohort.
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A Bayesian approach to hazard identification. The case of electromagnetic fields and cancer.
[Risk of neoplastic diseases in conditions of exposure to power magnetic fields--epidemiologic
investigations].
Potential motion related bias in the worn dosimeter measurements of two childhood leukemia
studies.
Early pregnancy loss and exposure to 50-Hz magnetic fields.
Extra low frequency electric and magnetic fields in the bedplace of children diagnosed with
leukaemia: a case-control study.
Environmental factors and childhood acute leukemias and lymphomas.
Are the stray 60-Hz electromagnetic fields associated with the distribution and use of electric
power a significant cause of cancer?
An alternate hypothesis for the association between electrical wiring configurations and cancer.
Magnetic field exposure and long-term survival among children with leukaemia.
Decreased survival for childhood leukemia in proximity to television towers.
Exposure to electromagnetic fields and risk of leukemia.
An evaluation of exposure metrics in an epidemiologic study on radio and television broadcast
transmitters and the risk of childhood leukemia.
[Meta-analysis and its application in epidemiology].
Does our electricity distribution system pose a serious risk to public health?
Magnetic fields and leukaemia risks in UK electricity supply workers.
Childhood incidence of acute lymphoblastic leukaemia and exposure to broadcast radiation in
Sydney--a second look.
50-Hz electromagnetic environment and the incidence of childhood tumors in Stockholm
County.
Assessment of non-response bias in a survey of residential magnetic field exposure in Taiwan.
The relative merits of contemporary measurements and historical calculated fields in the Swedish
childhood cancer study.
A population-based case-control study of radiofrequency exposure in relation to childhood
neoplasm.
A unified approach to the analysis of case-distribution (case-only) studies.
A richer conceptualization of "exposure" for epidemiological studies of the "EMF mixture".
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High incidence of acute leukemia in the proximity of some industrial facilities in El Bierzo,
northwestern Spain.
Exposure measurement errors, risk estimate and statistical power in case-control studies using
dichotomous analysis of a continuous exposure variable.
Deaths from electricity.
RF personal exposimetry on employees of elementary schools, kindergartens and day nurseries
as a proxy for child exposures.
Attributable fractions: bias from broad definition of exposure.
--Leaf Cluster 13 (113)
Theme - Electromagnetic fields and cancer, especially breast cancer
Titles
Breast cancer and electromagnetic fields--a review.
Follow-up of radio and telegraph operators with exposure to electromagnetic fields and risk of
breast cancer.
Electric power, pineal function, and the risk of breast cancer.
Electric blanket use and breast cancer in the Nurses' Health Study.
Electric blanket or mattress cover use and breast cancer incidence in women 50-79 years of age.
Electric blanket use and breast cancer risk among younger women.
Electric blanket use and breast cancer on Long Island.
Risk of premenopausal breast cancer and use of electric blankets.
Occupational exposure to electromagnetic field and breast cancer risk in a large, population-
based, case-control study in the United States.
The relationship between electromagnetic field and light exposures to melatonin and breast
cancer risk: a review of the relevant literature.
Residential and occupational exposures to 50-Hz magnetic fields and breast cancer in women: a
population-based study.
Use of electric blankets and risk of postmenopausal breast cancer.
Electromagnetic fields and male breast cancer.
Environmental factors and breast cancer.
Electromagnetic fields and female breast cancer.
Environmental risk factors and female breast cancer.
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Occupational and residential magnetic field exposure and breast cancer in females.
Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca2+ signaling
molecular pathways in breast cancer.
Occupational exposures to extremely low frequency magnetic fields and postmenopausal breast
cancer.
Population-based case-control study of occupational exposure to electromagnetic fields and
breast cancer.
Exposure to electromagnetic fields from use of electric blankets and other in-home electrical
appliances and breast cancer risk.
Residential magnetic field exposure and breast cancer risk: a nested case-control study from a
multiethnic cohort in Los Angeles County, California.
Evaluation of potential confounders in planning a study of occupational magnetic field exposure
and female breast cancer.
Risk for leukaemia and brain and breast cancer among Danish utility workers: a second follow-
up.
Breast cancer and electric power.
Residential exposure to 60-Hertz magnetic fields and adult cancers in Taiwan.
Occupational exposure to magnetic fields in relation to male breast cancer and testicular cancer:
a Swedish case-control study.
The melatonin hypothesis: electric power and breast cancer.
Incidence of breast cancer in a Norwegian cohort of women with potential workplace exposure
to 50 Hz magnetic fields.
Magnetic fields and breast cancer in Swedish adults residing near high-voltage power lines.
Electromagnetic fields and breast cancer on Long Island: a case-control study.
Occupational magnetic fields and female breast cancer: a case-control study using Swedish
population registers and new exposure data.
A meta-analysis of epidemiologic studies of electric and magnetic fields and breast cancer in
women and men.
Residential magnetic fields and the risk of breast cancer.
A cluster of male breast cancer in office workers.
Induction of tamoxifen resistance in breast cancer cells by ELF electromagnetic fields.
Electromagnetic field exposure and male breast cancer risk: a meta-analysis of 18 studies.
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Relationship between exposure to extremely low-frequency electromagnetic fields and breast
cancer risk: a meta-analysis.
Shift work, light at night, and breast cancer on Long Island, New York.
Extremely low-frequency electromagnetic fields exposure and female breast cancer risk: a meta-
analysis based on 24,338 cases and 60,628 controls.
Use of electric bedding devices and risk of breast cancer in African-American women.
Epidemiological appraisal of studies of residential exposure to power frequency magnetic fields
and adult cancers.
Magnetic fields and mammary cancer in rodents: a critical review and evaluation of published
literature.
Breast cancer, occupation, and exposure to electromagnetic fields among Swedish men.
[Risk of cancer among Danish electricity workers. A cohort study].
Meta-analysis of extremely low frequency electromagnetic fields and cancer risk: a pooled
analysis of epidemiologic studies.
Occupational magnetic field exposure and site-specific cancer incidence: a Swedish cohort study.
Risk of cancer among Danish utility workers--a nationwide cohort study.
Occupational exposures associated with male breast cancer.
Incidence of cancer in persons with occupational exposure to electromagnetic fields in Denmark.
Cancer incidence in California flight attendants (United States).
Overview of epidemiologic research on electric and magnetic fields and cancer.
Exposure to extremely low frequency magnetic fields among working women and homemakers.
Endometrial cancer incidence in relation to electric blanket use.
[Carcinogenic risk of extremely-low-frequency electromagnetic fields: state of the art].
Increased incidence of cancer in a cohort of office workers exposed to strong magnetic fields.
Socioeconomic status, social mobility and cancer occurrence during working life: a case-control
study among French electricity and gas workers.
Extremely low frequency electromagnetic fields (EMF) and brain cancer in adults and children:
review and comment.
Incidence of cancer in the vicinity of Korean AM radio transmitters.
Cancer incidence and magnetic field exposure in industries using resistance welding in Sweden.
Use of electric blankets and risk of testicular cancer.
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Use of electric blankets and association with prevalence of endometrial cancer.
Personal radio use and cancer risks among 48,518 British police officers and staff from the
Airwave Health Monitoring Study.
[Use of cellular telephones and risk of cancer. A Danish cohort study].
Cancer incidence near radio and television transmitters in Great Britain. I. Sutton Coldfield
transmitter.
Cancer incidence among Norwegian airline pilots.
Radio-frequency radiation exposure from AM radio transmitters and childhood leukemia and
brain cancer.
Biologically based epidemiological studies of electric power and cancer.
Cancer incidence vs. FM radio transmitter density.
A new electromagnetic exposure metric: high frequency voltage transients associated with
increased cancer incidence in teachers in a California school.
Primary brain cancer in adults and the use of common household appliances: a case-control
study.
Extremely low frequency electromagnetic fields and cancer: the epidemiologic evidence.
Cancer incidence near radio and television transmitters in Great Britain. II. All high power
transmitters.
Epidemiological studies of radio frequency exposures and human cancer.
Cancer mortality and residence near electricity transmission equipment: a retrospective cohort
study.
Effects of 50- or 60-hertz, 100 microT magnetic field exposure in the DMBA mammary cancer
model in Sprague-Dawley rats: possible explanations for different results from two laboratories.
Brain tumor risk in children in relation to use of electric blankets and water bed heaters. Results
from the United States West Coast Childhood Brain Tumor Study.
Electromagnetic fields: a cancer promoter?
Prostate cancer in relation to the use of electric blanket or heated water bed.
Cancer in radar technicians exposed to radiofrequency/microwave radiation: sentinel episodes.
Brain cancer risk and electromagnetic fields (EMFs): assessing the geomagnetic component.
Incidence of Seminoma Cancer in Staffs that Worked in Electromagnetic Waves Station; Three
Cases Report.
Incidence of cancer in Norwegian workers potentially exposed to electromagnetic fields.
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Human cancer from environmental pollutants: the epidemiological evidence.
Electric blanket use during pregnancy in relation to the risk of congenital urinary tract anomalies
among women with a history of subfertility.
Magnetic field exposure related to cancer subtypes.
Increasing incidence of thyroid cancer in the Nordic countries with main focus on Swedish data.
[Electromagnetic fields: is there any probability of the risk of cancer?].
Electric Blanket Use and Risk of Thyroid Cancer in the Women's Health Initiative Observational
Cohort.
Epidemiology and aetiological factors of male breast cancer: a ten years retrospective study in
eastern Turkey.
Radio frequency radiation-related cancer: assessing causation in the occupational/military
setting.
Spontaneous abortion and exposure to electric blankets and heated water beds.
[Environment and cancer risk].
[Geomagnetic field variation in early ontogenesis as a risk factor for oncopathology].
Cancer in the electric power industry.
The use of electric bed heaters and the risk of clinically recognized spontaneous abortion.
The role of household electromagnetic fields in the development of mammary tumors in women:
clinical case-record observations.
[Evaluation of genotoxic and/or co-genotoxic effects in cells exposed in vitro to extremely-low
frequency electromagnetic fields].
Trends in incidence of primary brain cancer in New Zealand, 1995 to 2010.
Myelogenous leukemia and electric blanket use.
Panel exploring pro and con arguments as to whether EMFs cause childhood brain cancer.
[Recent data from the literature on the biological and pathologic effects of electromagnetic
radiation, radio waves and stray currents].
Chronic toxicity/oncogenicity evaluation of 60 Hz (power frequency) magnetic fields in B6C3F1
mice.
Biological effects of power-frequency fields as they relate to carcinogenesis.
[Age diseases depending on geomagnetic field activity inside the womb period].
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[Enhancement of efficacy of neoadjuvant polychemotherapy in combined treatment of lung
cancer].
Cancer versus FM radio polarization types.
Genetic damage in humans exposed to extremely low-frequency electromagnetic fields.
[Male breast tumors in railway engine drivers: investigation of 5 cases].
Exposure to electromagnetic fields during pregnancy with emphasis on electrically heated beds:
association with birthweight and intrauterine growth retardation.
Melanoma incidence and frequency modulation (FM) broadcasting.
Malignant melanoma of the skin - not a sunshine story!
Multimodal treatment of hepatocellular carcinoma.
--Leaf Cluster 18 (62)
Theme - Mortality studies of electrical utility workers, focusing on electromagnetic field
exposures
Titles
Magnetic field exposure in relation to leukemia and brain cancer mortality among electric utility
workers.
A mortality study of electrical utility workers in Quebec.
Cohort and nested case-control studies of hematopoietic cancers and brain cancer among electric
utility workers.
[Cancer mortality among electricity utility workers in a the state of Sao Paulo, Brazil].
Radiofrequency exposure and mortality from cancer of the brain and lymphatic/hematopoietic
systems.
Magnetic field exposure and neurodegenerative disease mortality among electric utility workers.
Exposure to electromagnetic fields and suicide among electric utility workers: a nested case-
control study.
[Preliminary study of cause-specific mortality of a population exposed to 50 Hz magnetic fields,
in a district of Rome municipality].
Exposure to electromagnetic fields and suicide among electric utility workers: a nested case-
control study.
Mortality from brain cancer and leukaemia among electrical workers.
Mortality in workers exposed to electromagnetic fields.
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Comparative analyses of the studies of magnetic fields and cancer in electric utility workers:
studies from France, Canada, and the United States.
Leukemia following occupational exposure to 60-Hz electric and magnetic fields among Ontario
electric utility workers.
Mortality from amyotrophic lateral sclerosis, other chronic disorders, and electric shocks among
utility workers.
Electromagnetic fields and health effects--epidemiologic studies of cancer, diseases of the central
nervous system and arrhythmia-related heart disease.
Mortality of workers exposed to ionizing radiation at the French National Electricity Company.
Association between exposure to pulsed electromagnetic fields and cancer in electric utility
workers in Quebec, Canada, and France.
[Mortality of personnel operating electric power objects with 500 kV voltage].
Electromagnetic fields, polychlorinated biphenyls, and prostate cancer mortality in electric utility
workers.
Mortality of plastic-ware workers exposed to radiofrequencies.
Mortality among workers in the geothermal power plants at Larderello, Italy.
A population-based cohort study of occupational exposure to magnetic fields and cardiovascular
disease mortality.
Exposure to 50-Hz electric field and incidence of leukemia, brain tumors, and other cancers
among French electric utility workers.
Cancer in Korean war navy technicians: mortality survey after 40 years.
[Occupational exposure to electromagnetic fields and its health effects in electric energy
workers].
Leukemia, brain tumors, and exposure to extremely low frequency electromagnetic fields in
Swiss railway employees.
Electric and magnetic field exposure and brain cancer: a review.
[Remote effects of occupational and non-occupational exposure to electromagnetic fields of
power-line frequency. Epidemiological studies].
Occupational exposures and brain cancer mortality: a preliminary study of east Texas residents.
[Mortality of people residing near electric power supply line with voltage of 500 kV].
Cancer incidence and mortality and proximity to TV towers.
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Cardiovascular mortality and exposure to extremely low frequency magnetic fields: a cohort
study of Swiss railway workers.
Mortality of persons resident in the vicinity of electricity transmission facilities.
A case cohort study of suicide in relation to exposure to electric and magnetic fields among
electrical utility workers.
Mortality from neurodegenerative disease and exposure to extremely low-frequency magnetic
fields: 31 years of observations on Swiss railway employees.
Refinements in magnetic field exposure assignment for a case-cohort study of electrical utility
workers.
Leukaemia, brain tumours and exposure to extremely low frequency magnetic fields: cohort
study of Swiss railway employees.
Magnetic field exposure and cardiovascular disease mortality among electric utility workers.
[Mortality indices for hemoblastoses in Rivno Province before and after the accident at the
Chernobyl Atomic Electric Power Station].
Incidence of cancer among workers in Norwegian hydroelectric power companies.
Fatal occupational injuries among electric power company workers.
Exposure to electromagnetic fields and the risk of leukemia.
Biological effects on human health due to radiofrequency/microwave exposure: a synopsis of
cohort studies.
Increased mortality in amateur radio operators due to lymphatic and hematopoietic malignancies.
Risk of severe cardiac arrhythmia in male utility workers: a nationwide danish cohort study.
Occupational magnetic field exposure, cardiovascular disease mortality, and potential
confounding by smoking.
Invited commentary: electromagnetic fields and cancer in railway workers.
Multiple sclerosis among utility workers.
Annals of conflicting results: looking back on electromagnetic field research.
Ecological study on residences in the vicinity of AM radio broadcasting towers and cancer death:
preliminary observations in Korea.
Feasibility of a cohort study on health risks caused by occupational exposure to radiofrequency
electromagnetic fields.
[An epidemiological study of cancer morbidity and mortality among the population living in
areas close to thermal and atomic electric power stations].
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Practical limitations of epidemiologic methods.
Causes of death among Belgian professional military radar operators: a 37-year retrospective
cohort study.
Effects upon health of occupational exposure to microwave radiation (radar).
Leukemia in telephone linemen.
Cancer incidence among welders: possible effects of exposure to extremely low frequency
electromagnetic radiation (ELF) and to welding fumes.
Uncertainty in the relation between exposure to magnetic fields and brain cancer due to
assessment and assignment of exposure and analytical methods in dose-response modeling.
Accidental deaths caused by electricity in Sweden, 1975-2000.
Cancer morbidity in subjects occupationally exposed to high frequency (radiofrequency and
microwave) electromagnetic radiation.
Pregnancy outcomes after paternal radiofrequency field exposure aboard fast patrol boats.
Home and leisure injuries among the French electricity and gas company active employees:
circumstances and short-term consequences.
--Leaf Cluster 27 (137)
Theme - Occupational exposure to electromagnetic fields, emphasizing neurodegenerative
disease and cancer
Titles
Occupational exposures and the risk of amyotrophic lateral sclerosis.
Dementia and occupational exposure to magnetic fields.
Occupational exposure to magnetic fields in case-referent studies of neurodegenerative diseases.
Amyotrophic lateral sclerosis and occupational exposure to electromagnetic fields.
Occupational Exposures and Neurodegenerative Diseases-A Systematic Literature Review and
Meta-Analyses.
Occupational magnetic field exposure and neurodegenerative disease.
Association between extremely low-frequency electromagnetic fields occupations and
amyotrophic lateral sclerosis: a meta-analysis.
Paternal occupational exposure to electro-magnetic fields as a risk factor for cancer in children
and young adults: a case-control study from the North of England.
Occupational exposure and amyotrophic lateral sclerosis in a prospective cohort.
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Neurodegenerative diseases in welders and other workers exposed to high levels of magnetic
fields.
Parental occupational exposure to magnetic fields and childhood cancer (Sweden).
Association between occupational exposure to power frequency electromagnetic fields and
amyotrophic lateral sclerosis: a review.
Magnetic field exposure and neurodegenerative diseases--recent epidemiological studies.
Occupational and residential exposure to electromagnetic fields and risk of brain tumors in
adults: a case-control study in Gironde, France.
Electrical occupations and neurodegenerative disease: analysis of U.S. mortality data.
Occupational exposure to magnetic fields and brain tumours in central Sweden.
Occupational exposure to extremely low frequency electric and magnetic fields and Alzheimer
disease: a meta-analysis.
Amyotrophic Lateral Sclerosis and Occupational Exposures: A Systematic Literature Review
and Meta-Analyses.
Case-Control Study on Occupational Exposure to Extremely Low-Frequency Electromagnetic
Fields and the Association with Meningioma.
Occupational exposure to extremely low frequency magnetic fields and risk of Alzheimer
disease: A systematic review and meta-analysis.
Occupational exposure to electromagnetic fields and Alzheimer disease.
Risk of childhood acute lymphoblastic leukaemia following parental occupational exposure to
extremely low frequency electromagnetic fields.
Brain cancer and occupational exposure to magnetic fields among men: results from a Canadian
population-based case-control study.
Occupational exposure to high-frequency electromagnetic fields and brain tumor risk in the
INTEROCC study: An individualized assessment approach.
Occupational exposure to power frequency magnetic fields and risk of non-Hodgkin lymphoma.
Parental occupational exposure to extremely low frequency magnetic fields and childhood
cancer: a German case-control study.
[News in occupational cancers].
Exposure to magnetic fields among electrical workers in relation to leukemia risk in Los Angeles
County.
Occupational exposure to magnetic fields and the risk of brain tumors.
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Occupational electric and magnetic field exposure and brain cancer: a meta-analysis.
Risk factors for Alzheimer disease: a population-based case-control study in Istanbul, Turkey.
Acute leukemia in electrical workers: a New Zealand case-control study.
Brain tumor risk in offspring of men occupationally exposed to electric and magnetic fields.
Work related etiology of amyotrophic lateral sclerosis (ALS): a meta-analysis.
Occupational exposure to low frequency magnetic fields and the risk of low grade and high
grade glioma.
Occupational magnetic field exposure among women in Stockholm County, Sweden.
Occupational risk factors for cancer of the central nervous system: a case-control study on death
certificates from 24 U.S. states.
Are occupational, hobby, or lifestyle exposures associated with Philadelphia chromosome
positive chronic myeloid leukaemia?
Berkson error adjustment and other exposure surrogates in occupational case-control studies,
with application to the Canadian INTEROCC study.
Paternal occupational exposure to radiofrequency electromagnetic fields and risk of adverse
pregnancy outcome.
Electromagnetic field exposures and childhood cancers in New Zealand.
Occupational exposure to electromagnetic fields and acute leukaemia: analysis of a case-control
study.
Maternal occupational exposure to extremely low frequency magnetic fields and the risk of brain
cancer in the offspring.
Elevated risk of Alzheimer's disease among workers with likely electromagnetic field exposure.
[Epidemiological risk assessment of pathology development in occupational exposure to
radiofrequency electromagnetic fields].
Review of the epidemiologic literature on EMF and Health.
Occupational risk factors in Alzheimer's disease: a review assessing the quality of published
epidemiological studies.
Exposure to extremely low frequency electromagnetic fields and the risk of malignant diseases--
an evaluation of epidemiological and experimental findings.
Interactions between occupational exposure to extremely low frequency magnetic fields and
chemicals for brain tumour risk in the INTEROCC study.
The effect of male occupational exposure in infertile couples in Norway.
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[Amyotrophic lateral sclerosis and exposure to metals and other occupational/environmental
hazardous materials: state of the art].
Occupational exposure to radio frequency/microwave radiation and the risk of brain tumors:
Interphone Study Group, Germany.
Relationships between occupational history and serum concentrations of organochlorine
compounds in exocrine pancreatic cancer.
Risk agents related to work and amyotrophic lateral sclerosis: An occupational medicine focus.
[A case-control study on the risk factors of Alzheimer's disease in military elderly men].
Occupational exposures obtained by questionnaire in clinical practice and their association with
semen quality.
Leukemia and occupational exposure to electromagnetic fields: review of epidemiologic surveys.
Occupational exposure to ionizing and non-ionizing radiation and risk of non-Hodgkin
lymphoma.
Case-control study on occupational exposure to extremely low-frequency electromagnetic fields
and glioma risk.
Risk of birth defects by parental occupational exposure to 50 Hz electromagnetic fields: a
population based study.
Environmental risk factors for non-Hodgkin's lymphoma: a population-based case-control study
in Languedoc-Roussillon, France.
Exposure to electromagnetic fields and risk of central nervous system disease in utility workers.
[Exposure to electromagnetic fields and risk of central nervous system diseases among
employees at Danish electric companies].
Neurodegenerative diseases, suicide and depressive symptoms in relation to EMF.
Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer's
disease.
Occupational risk factors for lung cancer in the French electricity and gas industry: a case-
control survey nested in a cohort of active employees.
Parental occupational exposures to electromagnetic fields and radiation and the incidence of
neuroblastoma in offspring.
Occupational exposure to ionizing radiation and electromagnetic fields in relation to the risk of
thyroid cancer in Sweden.
[Parental occupational exposures and autism spectrum disorder in children].
Acute leukaemia in workers exposed to electromagnetic fields.
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Parental heat exposure and risk of childhood brain tumor: a Children's Oncology Group study.
Occupational magnetic field exposure and the risk of acoustic neuroma.
Leukemia risk and occupational electric field exposure in Los Angeles County, California.
Neurodegenerative disease and magnetic field exposure in UK electricity supply workers.
Occupational exposure to low frequency magnetic fields and dementia: a case-control study.
Occupation and malignant lymphoma: a population based case control study in Germany.
A nested case-control study of residential and personal magnetic field measures and
miscarriages.
Need for a European approach to the effects of extremely low-frequency electromagnetic fields
on cancer. ELF-EMF European Feasibility Study Group.
Incidence of leukaemia and brain tumours in some "electrical occupations".
A population-based prospective cohort study of personal exposure to magnetic fields during
pregnancy and the risk of miscarriage.
Risk of cognitive impairment in relation to elevated exposure to electromagnetic fields.
Occupational factors of anxiety and depressive disorders in the French National Electricity and
Gas Company. The Anxiety-Depression Group.
Occupational electromagnetic field exposures associated with sleep quality: a cross-sectional
study.
Testicular cancer and electromagnetic fields (EMF) in the workplace: results of a population-
based case-control study in Germany.
Occupational exposure to electromagnetic fields and the occurrence of brain tumors. An analysis
of possible associations.
Occupational magnetic field exposure and myocardial infarction incidence.
Magnetic fields and brain tumour risks in UK electricity supply workers.
[The potential hazard for the development of leukemia from exposure to electromagnetic
radiation (a review of the literature)].
Neuroblastoma and paternal occupation. A case-control analysis.
Self-reported electrical appliance use and risk of adult brain tumors.
Non-specific physical symptoms and electromagnetic field exposure in the general population:
can we get more specific? A systematic review.
Occupational risk factors for acute leukaemia: a case-control study.
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Occupational hazards for the male reproductive system.
Amyotrophic lateral sclerosis and environmental factors.
Environmental risk factors for brain tumors.
Occupational exposure to electromagnetic fields and sex-differential risk of uveal melanoma.
Maternal cumulative exposure to extremely low frequency electromagnetic fields and pregnancy
outcomes in the Elfe cohort.
[Non dietetic environmental risk factors in prostate cancer].
[Environmental risk factors and epidemiologic study].
[Paternal exposure to occupational electromagnetic radiation and sex ratio of the offspring: a
meta-analysis].
[Occupational risk and its prophylaxis for female workers engaged in radio-electronic instrument
industry].
Interactive effect of chemical substances and occupational electromagnetic field exposure on the
risk of gliomas and meningiomas in Swedish men.
[Delayed biological effect of electromagnetic fields action].
Prevalence of musculoskeletal disorders and related occupational causative factors among
electricity linemen: A narrative review.
Paternal work in the power industry: effects on children at delivery.
Miscarriages among female physical therapists who report using radio- and microwave-
frequency electromagnetic radiation.
Radiation exposure, socioeconomic status, and brain tumor risk in the US Air Force: a nested
case-control study.
Risk factors, health risks, and risk management for aircraft personnel and frequent flyers.
Video display terminal use during pregnancy and reproductive outcome--a meta-analysis.
[Difficulties of expert testimony in microwave disease].
Radiofrequency electromagnetic fields; male infertility and sex ratio of offspring.
Exposure to magnetic fields and the risk of poor sperm quality.
Myeloid leukemias and myelodysplastic syndromes: chemical exposure, histologic subtype and
cytogenetics in a case-control study.
[Evaluation of occupational risk caused by exposure to electromagnetic rays].
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An apparently incongruous exposure-response relationship resulting from the use of job
description to assess magnetic field exposure.
Carcinogenicity test in B6C3F1 mice after parental and prenatal exposure to 50 Hz magnetic
fields.
Congenital malformations and exposure to high-frequency electromagnetic radiation among
Danish physiotherapists.
[The IARC carcinogenicity evaluation of radio-frequency electromagnetic field: with special
reference to epidemiology of mobile phone use and brain tumor risk].
Limitations of interview-based risk assessment of RF exposure from appliances.
Case-control study on uveal melanoma (RIFA): rational and design.
Gender-specific reproductive outcome and exposure to high-frequency electromagnetic radiation
among physiotherapists.
Search for teratogenic risks with the aid of malformation registries.
[Effect of early pregnancy electromagnetic field exposure on embryo growth ceasing].
Development and evaluation of a tool for retrospective exposure assessment of selected
endocrine disrupting chemicals and EMF in the car manufacturing industry.
Environmental risk factors in the history of male patients of an infertility clinic.
Environmental exposure assessment in European birth cohorts: results from the ENRIECO
project.
Maternal exposure to magnetic fields during pregnancy in relation to the risk of asthma in
offspring.
Life styles, anxiety, expertise: the perception of risk from electromagnetic fields.
Epidemiologic evidence relevant to radar (microwave) effects.
Exposure to electromagnetic fields during pregnancy.
A literature review of medical side effects from radio-frequency energy in the human
environment: involving cancer, tumors, and problems of the central nervous system.
Does exposure to computers affect the routine parameters of semen quality?
Gender ratio of offspring and exposure to shortwave radiation among female physiotherapists.
Clinical teratology.
Electricity and bones.
[A historic case of Wegener's granulomatosis: the physicist who discovered the electromagnetic
waves: Heinrich Hertz].
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A possible association between fetal/neonatal exposure to radiofrequency electromagnetic
radiation and the increased incidence of autism spectrum disorders (ASD).
Fourth Level Cluster 83 (668)
Theme - Adverse effects of mobile phone use, especially brain tumors, and brain and neural
function
--Leaf Cluster 30 (321)
Theme - Adverse health symptoms from mobile phone use
Titles
The risk of subjective symptoms in mobile phone users in Poland--an epidemiological study.
Problematic Use of Mobile Phones in Australia...Is It Getting Worse?
Use of mobile phones and cancer risk.
Health hazards of mobile phones: an Indian perspective.
Nomophobia: A Cross-sectional Study to Assess Mobile Phone Usage Among Dental Students.
Evidence-based policy? The use of mobile phones in hospital.
A survey study of the association between mobile phone use and daytime sleepiness in California
high school students.
Electroencephalographic, personality, and executive function measures associated with frequent
mobile phone use.
[Radiation from mobile phone and the health].
Is human saliva an indicator of the adverse health effects of using mobile phones?
Use of mobile phones by medical staff at Queen Elizabeth Hospital, Barbados: evidence for both
benefit and harm.
Mobile phone induced sensorineural hearing loss.
[Mobile phones radiate--risk to the health?].
An international prospective cohort study of mobile phone users and health (COSMOS): Factors
affecting validity of self-reported mobile phone use.
Mobile phone use and location of glioma: a case-case analysis.
Exposure to mobile phone electromagnetic fields and subjective symptoms: a double-blind study.
Adverse effects of excessive mobile phone use.
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Mobile phone radiation causes brain tumors and should be classified as a probable human
carcinogen (2A) (review).
Are mobile phones harmful?
[Subjective symptoms related to mobile phone use--a pilot study].
Mobile phone radiation and the risk of cancer; a review.
Review on health effects related to mobile phones. Part II: results and conclusions.
Effects of thirty minutes mobile phone use on the human sensory cortex.
Significance of micronuclei in buccal smears of mobile phone users: A comparative study.
[Psychophysiological indicators for children using mobile phones. Communication 1. Current
state of the problem].
Audiologic disturbances in long-term mobile phone users.
Does chronic exposure to mobile phones affect cognition?
Mobile phones: influence on auditory and vestibular systems.
Cellular phones: are they detrimental?
Analysis of mobile phone use among young patients with brain tumors in Japan.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep
disturbance in Saudi population.
Association between vestibular schwannomas and mobile phone use.
Acute effects of 3G mobile phone radiations on frontal haemodynamics during a cognitive task
in teenagers and possible protective value of Om chanting.
Ethical considerations of mobile phone use by patients in KwaZulu-Natal: Obstacles for
mHealth?
The use of cell phone and insight into its potential human health impacts.
Mobile phones, in combination with a computer locator system, improve the response times of
emergency medical services in central London.
Mobile phone use, school electromagnetic field levels and related symptoms: a cross-sectional
survey among 2150 high school students in Izmir.
Mobile phone related-hazards and subjective hearing and vision symptoms in the Saudi
population.
Thermal effects of mobile phones on human auricle region.
Mobile phones and health: a literature overview.
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Radiation from mobile phone systems: Is it perceived as a threat to people's health?
Child and Adolescent Use of Mobile Phones: An Unparalleled Complex Developmental
Phenomenon.
Micronucleus frequency in buccal mucosa cells of mobile phone users.
Exposure of magnetic bacteria to simulated mobile phone-type RF radiation has no impact on
mortality.
The assessment of electromagnetic field radiation exposure for mobile phone users.
Mobile phones: Reservoirs for the transmission of nosocomial pathogens.
Headache, tinnitus and hearing loss in the international Cohort Study of Mobile Phone Use and
Health (COSMOS) in Sweden and Finland.
Analysis of ear side of mobile phone use in the general population of Japan.
Questionnaire-based evaluation of mobile phone interference with medical-electrical equipment
in Swedish hospitals.
Mobile Phone-Use Habits Among Adolescents: Predictors of Intensive Use.
[Effect of stress and intesity of mobile phone using on the health and subjective symptoms in
GSM workers].
Epidemiological risk assessment of mobile phones and cancer: where can we improve?
Impact of one's own mobile phone in stand-by mode on personal radiofrequency electromagnetic
field exposure.
Mobile phones, radiofrequency fields, and health effects in children--epidemiological studies.
Self-reported mobile phone use and semen parameters among men from a fertility clinic.
Recall of mobile phone usage and laterality in young people: The multinational Mobi-Expo
study.
Psychological factors associated with self-reported sensitivity to mobile phones.
Real versus Simulated Mobile Phone Exposures in Experimental Studies.
Time trends (1998-2007) in brain cancer incidence rates in relation to mobile phone use in
England.
Neurological changes induced by a mobile phone.
Survey of mobile phone use and their chronic effects on the hearing of a student population.
Mobile phone use and stress, sleep disturbances, and symptoms of depression among young
adults--a prospective cohort study.
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[SAR values of mobile phones. Safety evaluation and risk perception].
Assessment of extremely low frequency magnetic field exposure from GSM mobile phones.
EEG Changes Due to Experimentally Induced 3G Mobile Phone Radiation.
Effects of thirty-minute mobile phone exposure on saccades.
Cell phone radiation exposure on brain and associated biological systems.
Effects of chronic exposure of electromagnetic fields from mobile phones on hearing in rats.
Do mobile 'phones have a detrimental impact on auditory function?
[Hearing level and intensive use of mobile phones].
Preliminary report: symptoms associated with mobile phone use.
Validation of exposure assessment and assessment of recruitment methods for a prospective
cohort study of mobile phone users (COSMOS) in Finland: a pilot study.
Studying the effects of mobile phone use on the auditory system and the central nervous system:
a review of the literature and future directions.
Mobile-phone pulse triggers evoked potentials.
Association between General Health and Mobile Phone Dependency among Medical University
Students: A Cross-sectional Study in Iran.
Mobile phones and children: is precaution warranted?
[Determining health policy for sensible mobile phone use--current world status].
Comparison of cytotoxic and genotoxic effects of plutonium-239 alpha particles and mobile
phone GSM 900 radiation in the Allium cepa test.
Mobile phones: time to rethink and limit usage.
Bedtime mobile phone use and sleep in adults.
Mobile phones and seizures: drug-resistant epilepsy is less common in mobile-phone-using
patients.
Estimation of head tissue-specific exposure from mobile phones based on measurements in the
homogeneous SAM head.
Mobile phones, heat shock proteins and cancer.
Can evidence change belief? Reported mobile phone sensitivity following individual feedback of
an inability to discriminate active from sham signals.
Distribution of RF energy emitted by mobile phones in anatomical structures of the brain.
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Association between mobile phone use and depressed mood in Japanese adolescents: a cross-
sectional study.
Effects of thirty-minute mobile phone use on visuo-motor reaction time.
The controversy about a possible relationship between mobile phone use and cancer.
Association between Excessive Use of Mobile Phone and Insomnia and Depression among
Japanese Adolescents.
Electromagnetic interference of GSM mobile phones with the implantable deep brain stimulator,
ITREL-III.
Association between overuse of mobile phones on quality of sleep and general health among
occupational health and safety students.
Effect of mobile phones on micronucleus frequency in human exfoliated oral mucosal cells.
A study on the effect of prolonged mobile phone use on pure tone audiometry thresholds of
medical students of Sikkim.
Factors that influence the radiofrequency power output of GSM mobile phones.
Analysis of mobile phone design features affecting radiofrequency power absorbed in a human
head phantom.
Does the Brain Detect 3G Mobile Phone Radiation Peaks? An Explorative In-Depth Analysis of
an Experimental Study.
Effects of mobile phone use on brain tissue from the rat and a possible protective role of vitamin
C - a preliminary study.
Effects of a 902 MHz mobile phone on cerebral blood flow in humans: a PET study.
Analysis of the influence of handset phone position on RF exposure of brain tissue.
Are thyroid dysfunctions related to stress or microwave exposure (900 MHz)?
Exposure to mobile phone electromagnetic field radiation, ringtone and vibration affects anxiety-
like behaviour and oxidative stress biomarkers in albino wistar rats.
Clear policies on mobile phones vital.
Personal exposure to mobile phone frequencies and well-being in adults: a cross-sectional study
based on dosimetry.
Self-report of physical symptoms associated with using mobile phones and other electrical
devices.
Mobile phones as mediators of health behavior change in cardiovascular disease in developing
countries.
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Experimental and numerical assessment of low-frequency current distributions from UMTS and
GSM mobile phones.
Are men talking their reproductive health away?
The effect of mobile phone to audiologic system.
The effects of 884 MHz GSM wireless communication signals on headache and other symptoms:
an experimental provocation study.
Associations between problematic mobile phone use and psychological parameters in young
adults.
Effects on auditory function of chronic exposure to electromagnetic fields from mobile phones.
Mobile phones are good for you, p0.36! Observations on Keetley, Wood, Spong and Stough
(2006).
Cordless telephone use: implications for mobile phone research.
Mobile phone exposure and spatial memory.
Prevalence of subjective poor health symptoms associated with exposure to electromagnetic
fields among university students.
Mobile phone headache: a double blind, sham-controlled provocation study.
Human short-term exposure to electromagnetic fields emitted by mobile phones decreases
computer-assisted visual reaction time.
Evaluation of the effects of mobile phones on the neural tube development of chick embryos.
Mobile telephone use is associated with changes in cognitive function in young adolescents.
Mobile phone use, blood lead levels, and attention deficit hyperactivity symptoms in children: a
longitudinal study.
Is mobile phone radiation genotoxic? An analysis of micronucleus frequency in exfoliated buccal
cells.
Mobile Phone, Computer, and Internet Use Among Older Homeless Adults: Results from the
HOPE HOME Cohort Study.
Mobile phones carry the personal microbiome of their owners.
Mobile phones and sex work in South India: the emerging role of mobile phones in condom use
by female sex workers in two Indian states.
Spatial memory performance of Wistar rats exposed to mobile phone.
The effect of the duration of exposure to the electromagnetic field emitted by mobile phones on
human attention.
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Interference of GSM mobile phones with communication between Cardiac Rhythm Management
devices and programmers: A combined in vivo and in vitro study.
Guidance for exposure design of human studies addressing health risk evaluations of mobile
phones.
Exposure to non-ionizing electromagnetic fields emitted from mobile phones induced DNA
damage in human ear canal hair follicle cells.
Effects of mobile phone radiofrequency on the structure and function of the normal human
hemoglobin.
Impact of head morphology on local brain specific absorption rate from exposure to mobile
phone radiation.
Can the Accuracy of Home Blood Glucose Monitors be affected by the Received Signal Strength
of 900 MHz GSM Mobile Phones?
Are some people sensitive to mobile phone signals? Within participants double blind randomised
provocation study.
Women's mobile phone use in birth suite: A West Australian perspective.
Effect of mobile telephones on sperm quality: a systematic review and meta-analysis.
Social behavioral testing and brain magnetic resonance imaging in chicks exposed to mobile
phone radiation during development.
[Effects of electromagnetic fields emitted by cellular phone on auditory and vestibular labyrinth].
Mobile phone hygiene: potential risks posed by use in the clinics of an Indian dental school.
Impact of Adolescents' Screen Time and Nocturnal Mobile Phone-Related Awakenings on Sleep
and General Health Symptoms: A Prospective Cohort Study.
The association between use of mobile phones after lights out and sleep disturbances among
Japanese adolescents: a nationwide cross-sectional survey.
The influence of direct mobile phone radiation on sperm quality.
The effect of mobile phone on the number of Purkinje cells: a stereological study.
Some ocular symptoms experienced by users of mobile phones.
Radio frequency exposure in mobile phone users: implications for exposure assessment in
epidemiological studies.
Mobile phone use facilitates memory in male, but not female, subjects.
Use of mobile phones and changes in cognitive function in adolescents.
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Assessment of the radio-frequency electromagnetic fields induced in the human body from
mobile phones used with hands-free kits.
An epidemiological review of mobile telephones and cancer.
Interaction of mobile phones with superficial passive metallic implants.
The effect of electromagnetic field emitted by a mobile phone on the inhibitory control of
saccades.
Effects of GSM 900 MHz on middle cerebral artery blood flow assessed by transcranial Doppler
sonography.
How to encourage children to use mobile phones safely.
Effects of electromagnetic fields from mobile phones on depression and anxiety after titanium
mesh cranioplasty among patients with traumatic brain injury.
Individual differences in the effects of mobile phone exposure on human sleep: rethinking the
problem.
[Correlation of health literacy and mobile phone use dependence with psychopathological
symptoms in middle school students].
Acute effects of using a mobile phone on CNS functions.
Effect of electromagnetic fields emitted by cellular phones on the latency of evoked
electrodermal activity.
Evaluation of the effect of using mobile phones on male fertility.
Effect of prenatal exposure to mobile phone on pyramidal cell numbers in the mouse
hippocampus: a stereological study.
Mobile phone use on a young person's unit.
Mobile phones: are children at higher risk?
Effects of mobile phone radiation on reproduction and development in Drosophila melanogaster.
Quantitative changes in testicular structure and function in rat exposed to mobile phone
radiation.
The effects of the duration of mobile phone use on heart rate variability parameters in healthy
subjects.
Specific absorption rate variation in a brain phantom due to exposure by a 3G mobile phone:
problems in dosimetry.
[Acute ear trauma caused by failure of mobile phone/cellular phone].
Assessment of auditory evoked potential in long-term mobile phone users.
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Is exposure to personal music players a confounder in adolescent mobile phone use and hearing
health studies?
Interference to medical equipment from mobile phones.
Identifying seasonal mobility profiles from anonymized and aggregated mobile phone data.
Application in food security.
Effects of mobile phone electromagnetic fields: critical evaluation of behavioral and
neurophysiological studies.
Estimation of RF energy absorbed in the brain from mobile phones in the Interphone Study.
[Electromagnetic fields in the vicinity of DECT cordless telephones and mobile phones].
Thermal effects of mobile phones on facial nerves and surrounding soft tissue.
Intraoperative observation of changes in cochlear nerve action potentials during exposure to
electromagnetic fields generated by mobile phones.
An old issue and a new look: electromagnetic hypersensitivity caused by radiations emitted by
GSM mobile phones.
Can mobile phone emissions affect auditory functions of cochlea or brain stem?
Influence on the mechanisms of generation of distortion product otoacoustic emissions of mobile
phone exposure.
Does acute exposure to the electromagnetic field emitted by a mobile phone influence visual
evoked potentials? A pilot study.
The estimation of 3D SAR distributions in the human head from mobile phone compliance
testing data for epidemiological studies.
The acute auditory effects of exposure for 60 minutes to mobile`s electromagnetic field.
Long-term digital mobile phone use and cognitive decline in the elderly.
Mobile Phone: A Possible Vector of Bacterial Transmission in Hospital Setting.
Electrophysiological Assessment of the Impact of Mobile Phone Radiation on Cognition in
Persons With Epilepsy.
Mobile phone affects cerebral blood flow in humans.
Association between mobile phone use and semen quality: a systemic review and meta-analysis.
Effects of Mobile Phones on Children's and Adolescents' Health: A Commentary.
[Activity of vestibular organ in people using mobile phones professionally].
Analysis of three-dimensional SAR distributions emitted by mobile phones in an
epidemiological perspective.
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Perception of the electromagnetic field emitted by a mobile phone.
[ Effects of electromagnetic fields generated by mobile phones on the nervous system].
Effects of high frequency electromagnetic field (EMF) emitted by mobile phones on the human
motor cortex.
[Cellular phones and cancer: current status].
Local vasodilator response to mobile phones.
Electromagnetic hypersensitivity (EHS) and subjective health complaints associated with
electromagnetic fields of mobile phone communication--a literature review published between
2000 and 2004.
Mobile phone types and SAR characteristics of the human brain.
Diverse radiofrequency sensitivity and radiofrequency effects of mobile or cordless phone near
fields exposure in Drosophila melanogaster.
Biophysical evaluation of radiofrequency electromagnetic field effects on male reproductive
pattern.
The semen quality of the mobile phone users.
Tinnitus and mobile phone use.
Association of excessive mobile phone use during pregnancy with birth weight: an adjunct study
in Kumamoto of Japan Environment and Children's Study.
Is problematic mobile phone use explained by chronotype and personality?
Effects of mobile phone emissions on human brain activity and sleep variables.
Effect of Bluetooth headset and mobile phone electromagnetic fields on the human auditory
nerve.
Cranial and postcranial skeletal variations induced in mouse embryos by mobile phone radiation.
Effects of exposure to a mobile phone on testicular function and structure in adult rabbit.
"MXing it up": how African adolescents may affect social change through mobile phone use.
Mobile-phone-based home exercise training program decreases systemic inflammation in COPD:
a pilot study.
Effects of short-term radiation emitted by WCDMA mobile phones on teenagers and adults.
Diseases of modern living: neurological changes associated with mobile phones and
radiofrequency radiation in humans.
GSM mobile phone radiation suppresses brain glucose metabolism.
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The electromagnetic interference of mobile phones on the function of a gamma-camera.
Effects of mobile phone exposure on biochemical parameters of cord blood: A preliminary study.
[An analysis of the pathogenetic significance of irradiations from mobile phones].
Self-reported symptoms associated with exposure to electromagnetic fields: a questionnaire
study.
The mobile phone decreases fructose but not citrate in rabbit semen: a longitudinal study.
Mobile phone use and subjective symptoms. Comparison of symptoms experienced by users of
analogue and digital mobile phones.
Acute effects of the electromagnetic waves emitted by mobile phones on attention in emergency
physicians.
Multiple assessment methods of prenatal exposure to radio frequency radiation from
telecommunication in the Mothers and Children's Environmental Health (MOCEH) study.
Mobile phone use and possible cancer risk: Current perspectives in India.
Symptomatic complex partial status epilepticus manifesting as utilization behavior of a mobile
phone.
Genotoxic and carcinogenic effects of non-ionizing electromagnetic fields.
"Mate! I'm running 10 min late": An investigation into the self-regulation of mobile phone tasks
while driving.
Dose related shifts in the developmental progress of chick embryos exposed to mobile phone
induced electromagnetic fields.
Growing concern over the safety of using mobile phones and male fertility.
Is there any exposure from a mobile phone in stand-by mode?
[Biological effects of mobile phone electromagnetic field on chick embryo (risk assessment
using the mortality rate)].
MEMO--a mobile phone depression prevention intervention for adolescents: development
process and postprogram findings on acceptability from a randomized controlled trial.
Relationship between Mobile Phone Addiction and the Incidence of Poor and Short Sleep among
Korean Adolescents: a Longitudinal Study of the Korean Children & Youth Panel Survey.
Neurodevelopment for the first three years following prenatal mobile phone use, radio frequency
radiation and lead exposure.
Electromagnetic safety of children using wireless phones: a literature review.
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Histological and histochemical study of the protective role of rosemary extract against harmful
effect of cell phone electromagnetic radiation on the parotid glands.
Mobile phone use for contacting emergency services in life-threatening circumstances.
Effect of Mobile Phone-Induced Electromagnetic Field on Brain Hemodynamics and Human
Stem Cell Functioning: Possible Mechanistic Link to Cancer Risk and Early Diagnostic Value of
Electronphotonic Imaging.
Fetal and neonatal responses following maternal exposure to mobile phones.
Is the effect of mobile phone radiofrequency waves on human skin perfusion non-thermal?
Systematic review and meta-analysis of psychomotor effects of mobile phone electromagnetic
fields.
[Cell phone communication: hygienic characteristics, biological action, standardization (a
review)].
Age-dependent tissue-specific exposure of cell phone users.
Comments on "Association of excessive mobile phone use during pregnancy with birth weight:
an adjunct study in Kumamoto of Japan Environment and Children's Study".
Neuropsychological sequelae of digital mobile phone exposure in humans.
Effects of radiofrequency electromagnetic radiation (RF-EMF) on honey bee queen development
and mating success.
Genotoxicity evaluation of electromagnetic fields generated by 835-MHz mobile phone
frequency band.
A survey study on some neurological symptoms and sensations experienced by long term users
of mobile phones.
Does evening exposure to mobile phone radiation affect subsequent melatonin production?
Nocebo as headache trigger: evidence from a sham-controlled provocation study with RF fields.
Mobile phones and elderly people: a noisy communication.
Recall of past use of mobile phone handsets.
Mobile phone use and willingness to pay for SMS for diabetes in Bangladesh.
Electromagnetic absorption in the head of adults and children due to mobile phone operation
close to the head.
Preliminary evaluation of nanoscale biogenic magnetite-based ferromagnetic transduction
mechanisms for mobile phone bioeffects.
[Mobile phones, web chat, and sex among Norwegian adolescents].
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Comparison of FDTD-calculated specific absorption rate in adults and children when using a
mobile phone at 900 and 1800 MHz.
Effects of the Effect of Ultra High Frequency Mobile Phone Radiation on Human Health.
Dosimetric comparison of the specific anthropomorphic mannequin (SAM) to 14 anatomical
head models using a novel definition for the mobile phone positioning.
Can electromagnetic fields emitted by mobile phones stimulate the vestibular organ?
Analysis on the effect of the distances and inclination angles between human head and mobile
phone on SAR.
The use of a 'phantom scalp' to assess the possible direct pickup of mobile phone handset
emissions by electroencephalogram electrode leads.
[Change settings for visual analyzer of child users of mobile communication: longitudinal study].
Determinants of mobile phone output power in a multinational study: implications for exposure
assessment.
Effects of electromagnetic radiation of mobile phones on the central nervous system.
Noncommunicable Disease Risk Factors and Mobile Phones: A Proposed Research Agenda.
Effect of mobile phone usage time on total antioxidant capacity of saliva and salivary
immunoglobulin a.
Mobile cell-phones (M-phones) in telemicroscopy: increasing connectivity of isolated
laboratories.
A new problem in inflammatory bladder diseases: use of mobile phones!
Effects of mobile phone exposure on metabolomics in the male and female reproductive systems.
The pattern of the electromagnetic field emitted by mobile phones in motor vehicle driving
simulators.
Derangement of chick embryo retinal differentiation caused by radiofrequency electromagnetic
fields.
Mobile-phone dispatch of laypersons for CPR in out-of-hospital cardiac arrest.
Numerical assessment of induced ELF currents in the human head due to the battery current of a
digital mobile phone.
Moving the Agenda on Noncommunicable Diseases: Policy Implications of Mobile Phone
Surveys in Low and Middle-Income Countries.
Effect of mobile phone use on salivary concentrations of protein, amylase, lipase,
immunoglobulin A, lysozyme, lactoferrin, peroxidase and C-reactive protein of the parotid
gland.
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Wi-Fi technology--an uncontrolled global experiment on the health of mankind.
Phantom vibration and phantom ringing among mobile phone users: A systematic review of
literature.
Structural and kinetic effects of mobile phone microwaves on acetylcholinesterase activity.
Tinnitus and cell phones: the role of electromagnetic radiofrequency radiation.
[Psychophysiological indicators for children using mobile phones. Communication 2. Results of
four-year monitoring].
Who reaps the benefits, who bears the risks? Comparative optimism, comparative utility, and
regulatory preferences for mobile phone technology.
Electromagnetic Fields of Mobile Phone Jammer Exposure on Blood Factors in Rats.
Effect of handheld mobile phone use on parotid gland salivary flow rate and volume.
[Mobile phone use as a risk factor for affection of the central nerve system--secondary
publication].
ELF exposure from mobile and cordless phones for the epidemiological MOBI-Kids study.
The Effect of Electromagnetic Radiation due to Mobile Phone Use on Thyroid Function in
Medical Students Studying in a Medical College in South India.
Long-term mobile phone use and the risk of vestibular schwannoma: a Danish nationwide cohort
study.
Cellular phones for reducing battlefield stress: rationale and a preliminary research.
Assessment of SAR and thermal changes near a cochlear implant system for mobile phone type
exposures.
Evaluation of the mobile phone electromagnetic radiation on serum iron parameters in rats.
Asymmetries in hip mineralization in mobile cellular phone users.
Mobile Phone Use Behaviors and Postures on Public Transportation Systems.
Radiofrequency Electromagnetic Radiation and Memory Performance: Sources of Uncertainty in
Epidemiological Cohort Studies.
The effects of multivitamin supplementation on mood and general well-being in healthy young
adults. A laboratory and at-home mobile phone assessment.
[Monitor of ECG signal and heart rate using a mobile phone with Bluetooth communication
protocol].
Safe use of mobile phones in hospitals.
Exposure to mobile phone radiation opens new horizons in Alzheimer's disease treatment.
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[Mobile telephones: a 'new risk'].
Predicting the biological effects of mobile phone radiation absorbed energy linked to the MRI-
obtained structure.
Metal-framed spectacles and implants and specific absorption rate among adults and children
using mobile phones at 900/1800/2100 MHz.
Mobile telephones: a comparison of radiated power between 3G VoIP calls and 3G VoCS calls.
A framework for spatial interaction analysis based on large-scale mobile phone data.
Self-reported depression and anxiety symptoms and usage of computers and mobile phones
among working-age Finns.
Motivating men who have sex with men to get tested for HIV through the internet and mobile
phones: a qualitative study.
The influence of handheld mobile phones on human parotid gland secretion.
Acute effects of 30 minutes of exposure to a smartphone call on in vitro platelet function.
[Effect of high-frequency EMF on public health and its neuro-chemical investigations].
Development of a problematic mobile phone use scale for Turkish adolescents.
Radiofrequency fields, transthyretin, and Alzheimer's disease.
Mobile phone mast effects on common frog (Rana temporaria) tadpoles: the city turned into a
laboratory.
Analysis of RF exposure in the head tissues of children and adults.
SARs for pocket-mounted mobile telephones at 835 and 1900 MHz.
Intravital Computer Morphometry on Protozoa: A Method for Monitoring of the
Morphofunctional Disorders in Cells Exposed in the Cell Phone Communication
Electromagnetic Field.
Estimation of the SAR in the human head and body due to radiofrequency radiation exposure
from handheld mobile phones with hands-free accessories.
Ants can be used as bio-indicators to reveal biological effects of electromagnetic waves from
some wireless apparatus.
Regulating hearing aid compatibility of cell phones: results from a national survey.
Laughter counteracts enhancement of plasma neurotrophin levels and allergic skin wheal
responses by mobile phone-mediated stress.
Recently published papers: take your predictions with a drop of saline... and breathe deeply
before turning on your phone.
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Interactions of problematic mobile phone use and psychopathological symptoms with
unintentional injuries: a school-based sample of Chinese adolescents.
Critical comments on DNA breakage by mobile-phone electromagnetic fields [Diem et al.,
Mutat. Res. 583 (2005) 178-183].
Mobile phone-delivered reminders and incentives to improve childhood immunisation coverage
and timeliness in Kenya (M-SIMU): a cluster randomised controlled trial.
Enhancement of allergic skin wheal responses in patients with atopic eczema/dermatitis
syndrome by playing video games or by a frequently ringing mobile phone.
Pilot study of mobile phone technology in allergic rhinitis in European countries: the MASK-
rhinitis study.
A closed-loop process to recover Li and Co compounds and to resynthesize LiCoO2 from spent
mobile phone batteries.
--Leaf Cluster 1 (36)
Theme - Effects of mobile phones on brain and neural function
Titles
Mobile phone use for 5 minutes can cause significant memory impairment in humans.
Association between mobile phone use and inattention in 7102 Chinese adolescents: a
population-based cross-sectional study.
Clinical features of headache associated with mobile phone use: a cross-sectional study in
university students.
Predictors of mobile telephone use and exposure analysis in Australian adolescents.
Acute Effect of Electromagnetic Waves Emitted from Mobile Phone on Visual Evoked Potential
in Adult Male : A Preliminary Study.
Analysis of the mobile phone effect on the heart rate variability by using the largest Lyapunov
exponent.
Mobile Phone Use and The Risk of Headache: A Systematic Review and Meta-analysis of Cross-
sectional Studies.
Acute mobile phone effects on pre-attentive operation.
Effect Of Electromagnetic Waves Emitted From Mobile Phone On Brain Stem Auditory Evoked
Potential In Adult Males.
Acute effects of radiofrequency electromagnetic field emitted by mobile phone on brain
function.
Psychophysiological tests and provocation of subjects with mobile phone related symptoms.
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The cardiac effects of a mobile phone positioned closest to the heart.
Electromagnetic field of mobile phones affects visual event related potential in patients with
narcolepsy.
Acute mobile phone operation affects neural function in humans.
Use of mobile and cordless phones and cognition in Australian primary school children: a
prospective cohort study.
Effect of mobile phone radiation on heart rate variability.
[Effects of radiation emitted from mobile phones on short- term heart rate variability
parameters].
Mobile phone use and health symptoms in children.
The sensitivity of human event-related potentials and reaction time to mobile phone emitted
electromagnetic fields.
Factors associated with mental health among high school students in Iran: Does mobile phone
overuse associate with poor mental health?
Mobile phone effects on children's event-related oscillatory EEG during an auditory memory
task.
Examining the effects of electromagnetic fields emitted by GSM mobile phones on human event-
related potentials and performance during an auditory task.
Estimating transmitted power density from mobile phone: an epidemiological pilot study with a
software modified phone.
"Nomophobia": impact of cell phone use interfering with symptoms and emotions of individuals
with panic disorder compared with a control group.
Mobile phone use and exposures in children.
The effect of mobile phone electromagnetic fields on the alpha rhythm of human
electroencephalogram.
Use of mobile and cordless phones and change in cognitive function: a prospective cohort
analysis of Australian primary school children.
Neurophysiological effects of mobile phone electromagnetic fields on humans: a comprehensive
review.
[Effect of mobile phone electromagnetic emission on characteristics of cerebral blood circulation
and neurohumoral regulations in humans].
Effects of 2G and 3G mobile phones on human alpha rhythms: Resting EEG in adolescents,
young adults, and the elderly.
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Acute mobile phones exposure affects frontal cortex hemodynamics as evidenced by functional
near-infrared spectroscopy.
Effects of exposure to a mobile phone on sexual behavior in adult male rabbit: an observational
study.
Effects of concurrent caffeine and mobile phone exposure on local target probability processing
in the human brain.
Some ocular symptoms and sensations experienced by long term users of mobile phones.
Nasal colonization and bacterial contamination of mobile phones carried by medical staff in the
operating room.
Headache and sferics.
--Leaf Cluster 25 (68)
Theme - Effects of cell phone radiation on cognitive function and hearing
Titles
Effects of GSM cellular phones on human hearing: the European project "GUARD".
Effects of weak mobile phone - electromagnetic fields (GSM, UMTS) on event related potentials
and cognitive functions.
Mobile phone emission modulates event-related desynchronization of alpha rhythms and
cognitive-motor performance in healthy humans.
Effects of pulsed and continuous wave 902 MHz mobile phone exposure on brain oscillatory
activity during cognitive processing.
Effects of electromagnetic field emitted by cellular phones on the EEG during a memory task.
Effects of weak mobile phone - electromagnetic fields (GSM, UMTS) on well-being and resting
EEG.
Assessment of potential effects of the electromagnetic fields of mobile phones on hearing.
Effects of electromagnetic field emitted by cellular phones on the EEG during an auditory
memory task: a double blind replication study.
Human brain wave activity during exposure to radiofrequency field emissions from mobile
phones.
Effects of electromagnetic fields emitted by cellular phones on the electroencephalogram during
a visual working memory task.
Effects of radiofrequency radiation emitted by cellular telephones on the cognitive functions of
humans.
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Cognitive effects of radiation emitted by cellular phones: the influence of exposure side and
time.
Mobile phone emission modulates interhemispheric functional coupling of EEG alpha rhythms.
Effects of mobile phone exposure on time frequency fine structure of transiently evoked
otoacoustic emissions.
[Effects of electromagnetic field from cellular phones on selected central nervous system
functions: a literature review].
Effects of UMTS cellular phones on human hearing: results of the European project EMFnEAR.
Is the brain influenced by a phone call? An EEG study of resting wakefulness.
Effect of acute exposure to radiofrequency electromagnetic fields emitted by a mobile phone
(GSM 900 MHz) on electrodermal responsiveness in healthy human.
Human brain activity during exposure to radiofrequency fields emitted by cellular phones.
Effects of exposure to electromagnetic fields emitted by GSM 900 and WCDMA mobile phones
on cognitive function in young male subjects.
Preattentive auditory information processing under exposure to the 902 MHz GSM mobile phone
electromagnetic field: a mismatch negativity (MMN) study.
Pulsed and continuous wave mobile phone exposure over left versus right hemisphere: effects on
human cognitive function.
Mobile phone emission increases inter-hemispheric functional coupling of
electroencephalographic alpha rhythms in epileptic patients.
Electromagnetic fields produced by GSM cellular phones and heart rate variability.
Effect of a 902 MHz electromagnetic field emitted by mobile phones on human cognitive
function: A replication study.
The effects of mobile-phone electromagnetic fields on brain electrical activity: a critical analysis
of the literature.
Hypersensitivity symptoms associated with exposure to cellular telephones: no causal link.
Nonlinear heart rate variability measures under electromagnetic fields produced by GSM cellular
phones.
Mobile phone emission modulates inter-hemispheric functional coupling of EEG alpha rhythms
in elderly compared to young subjects.
A study of the effects of cellular telephone microwave radiation on the auditory system in
healthy men.
Cognitive effects of cellular phones: a possible role of non-radiofrequency radiation factors.
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Comparison of the effects of continuous and pulsed mobile phone like RF exposure on the
human EEG.
Mobile phones exposure induces changes of contingent negative variation in humans.
Investigation of potential effects of cellular phones on human auditory function by means of
distortion product otoacoustic emissions.
Effects of microwaves emitted by cellular phones on human slow brain potentials.
Effects of radiofrequency electromagnetic fields on the human nervous system.
Variations in electroencephalography with mobile phone usage in medical students.
Effects of 2G and 3G mobile phones on performance and electrophysiology in adolescents,
young adults and older adults.
The excretion of 6-hydroxymelatonin sulfate in healthy young men exposed to electromagnetic
fields emitted by cellular phone -- an experimental study.
Gender related differences on the EEG during a simulated mobile phone signal.
Cellular Phone Irradiation of the Head Affects Heart Rate Variability Depending on
Inspiration/Expiration Ratio.
Effects of RF exposure of teenagers and adults by CDMA cellular phones.
Effects of 900 MHz electromagnetic fields exposure on cochlear cells' functionality in rats:
evaluation of distortion product otoacoustic emissions.
Effects of the acute exposure to the electromagnetic field of mobile phones on human auditory
brainstem responses.
Do mobile phones pose a potential risk to autonomic modulation of the heart?
Effects of intensive and moderate cellular phone use on hearing function.
A meta-analysis for neurobehavioural effects due to electromagnetic field exposure emitted by
GSM mobile phones.
Mobile phone emissions modulate brain excitability in patients with focal epilepsy.
Mobile phone emissions and human brain excitability.
Effects of pulsed electromagnetic fields on cognitive processes - a pilot study on pulsed field
interference with cognitive regeneration.
Scalp localization of human auditory cortical activity modified by GSM electromagnetic fields.
Effect of 902 MHz mobile phone transmission on cognitive function in children.
Physiological effects of RF exposure on hypersensitive people by a cell phone.
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Effects of mobile phone signals over BOLD response while performing a cognitive task.
Effect of electromagnetic field emitted by cellular phones on fetal heart rate patterns.
Effects of W-CDMA 1950 MHz EMF emitted by mobile phones on regional cerebral blood flow
in humans.
Does acute exposure to mobile phones affect human attention?
Effects of GSM signals during exposure to event related potentials (ERPs).
The effect of GSM and TETRA mobile handset signals on blood pressure, catechol levels and
heart rate variability.
Thermal effects of mobile phone RF fields on children: a provocation study.
Controversies on electromagnetic field exposure and the nervous systems of children.
The influence of the call with a mobile phone on heart rate variability parameters in healthy
volunteers.
[A study on the biological effects of exposure mobile-phone frequency EMF].
Effects of Bluetooth device electromagnetic field on hearing: pilot study.
Evaluation in humans of the effects of radiocellular telephones on the circadian patterns of
melatonin secretion, a chronobiological rhythm marker.
Comparison of earphone radiation recorded from hearing impaired subjects and a resistor
network simulator.
[The influence of hypogeomagnetic field on bioelectric activity of the brain in epilepsy].
Non-ionizing radiofrequency electromagnetic waves traversing the head can be used to detect
cerebrovascular autoregulation responses.
--Leaf Cluster 14 (93)
Theme - Myriad adverse health effects from cellphones
Titles
Cell phone use and acoustic neuroma: the need for standardized questionnaires and access to
industry data.
Cell-phone use and self-reported hypertension: national health interview survey 2008.
Cell phones: modern man's nemesis?
Impact of cell phone use on men's semen parameters.
A preliminary examination of cell phone use and helping behavior.
Cell phone use and behavioural problems in young children.
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An analysis of the impact of cell phone use on depressive symptoms among Japanese elders.
Cell phones and brain tumors: a review including the long-term epidemiologic data.
Prenatal and postnatal exposure to cell phone use and behavioral problems in children.
Maternal cell phone use during pregnancy and child behavioral problems in five birth cohorts.
Maternal cell phone use in early pregnancy and child's language, communication and motor
skills at 3 and 5 years: the Norwegian mother and child cohort study (MoBa).
Cell phones and tumor: still in no man's land.
Cell phones and male infertility: a review of recent innovations in technology and consequences.
Prenatal exposure to cell phone use and neurodevelopment at 14 months.
The effects of cell phone use on peripheral vision.
Factors associated with cell phone use in adolescents in the community of Madrid (Spain).
The Impact of Using Cell Phones After Light-Out on Sleep Quality, Headache, Tiredness, and
Distractibility Among Students of a University in North of Iran.
Prospective study of pregnancy outcomes after parental cell phone exposure: the Norwegian
Mother and Child Cohort Study.
Prenatal and Postnatal Cell Phone Exposures and Headaches in Children.
Cell-Phone Addiction: A Review.
Ambulatory cell phone injuries in the United States: an emerging national concern.
[Cell Phones and Risk of brain and acoustic nerve tumours: the French INTERPHONE case-
control study].
Cell phone usage and erectile function.
Real-world cell phone radiofrequency electromagnetic field exposures.
Cell phone exposures and hearing loss in children in the Danish National Birth Cohort.
Cell Phone Information Seeking Explains Blood Pressure in African American Women.
Habits of cell phone usage and sperm quality - does it warrant attention?
Maternal cell phone use during pregnancy and child cognition at age 5years in 3 birth cohorts.
Cell phones and male infertility: dissecting the relationship.
Augmentative and alternative communication and cell phone use: one off-the-shelf solution and
some policy considerations.
Cell phones and cancer: what is the evidence for a connection?
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Cancer risks related to low-level RF/MW exposures, including cell phones.
Effect of cell-phone radiofrequency on angiogenesis and cell invasion in human head and neck
cancer cells.
Is health literacy related to health behaviors and cell phone usage patterns among the text4baby
target population?
Cell phone use and risk of thyroid cancer: a population-based case-control study in Connecticut.
Cell phones and children: follow the precautionary road.
Association between number of cell phone contracts and brain tumor incidence in nineteen U.S.
States.
Maternal cell phone and cordless phone use during pregnancy and behaviour problems in 5-year-
old children.
The effect of cell phone use on postural balance and mobility in older compared to young adults.
Cell phones change the way we walk.
Effects of cell phone use on semen parameters: Results from the MARHCS cohort study in
Chongqing, China.
Multidrug-Resistant Bacteria Associated with Cell Phones of Healthcare Professionals in
Selected Hospitals in Saudi Arabia.
Effect of cell phone exposure on physiologic and hematologic parameters of male medical
students of Bijapur (Karnataka) with reference to serum lipid profile.
General health of students of medical sciences and its relation to sleep quality, cell phone
overuse, social networks and internet addiction.
The role of anxiety in the perception of technological hazards - a cross-sectional study on cell
phones and masts.
Effect of Cell Phone Radiations on Orofacial Structures: A Systematic Review.
The association of sleep and late-night cell phone use among adolescents.
Cell Phone Use and Child and Adolescent Reading Proficiency.
Reach for your cell phone at your own risk: The cognitive costs of media choice for breaks.
Effects of cell phone radiofrequency signal exposure on brain glucose metabolism.
A forecasting method to reduce estimation bias in self-reported cell phone data.
The incidence rate and mortality of malignant brain tumors after 10 years of intensive cell phone
use in Taiwan.
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Abnormal responses of electronic pocket dosimeters caused by high frequency electromagnetic
fields emitted from digital cellular telephones.
[Cell phones: health risks and prevention].
Does cell phone use increase the chances of parotid gland tumor development? A systematic
review and meta-analysis.
Prevalence of problematic cell phone use in an adult population in Spain as assessed by the
Mobile Phone Problem Use Scale (MPPUS).
Use of mobile phone during pregnancy and the risk of spontaneous abortion.
Cell phones: the psychosocial risks.
Prenatal cell phone use and developmental milestone delays among infants.
Associations of Maternal Cell-Phone Use During Pregnancy With Pregnancy Duration and Fetal
Growth in 4 Birth Cohorts.
Effect of cell phone magnetic fields on adjustable cerebrospinal fluid shunt valves.
Combined effects of varicocele and cell phones on semen and hormonal parameters.
Chatting in the face of the eyewitness: The impact of extraneous cell-phone conversation on
memory for a perpetrator.
Risks to Health and Well-Being From Radio-Frequency Radiation Emitted by Cell Phones and
Other Wireless Devices.
Effect of Mobile Phone Radiofrequency Electromagnetic Fields on.
Absorption of wireless radiation in the child versus adult brain and eye from cell phone
conversation or virtual reality.
Is there a relationship between cell phone use and semen quality?
Cell phone-generated radio frequency electromagnetic field effects on the locomotor behaviors
of the fishes Poecilia reticulata and Danio rerio.
Not So Smart: Cell Phone Use Hurts Our Patients and Profession.
Cell phone etiquette in the clinical arena: A professionalism imperative for healthcare.
Mobile Phones: Potential Sources of Nickel and Cobalt Exposure for Metal Allergic Patients.
[Risk perception of the general public of cell phone towers and cancer: trend and associated
factors, 2005-2010].
Electromagnetic field and brain development.
Impacts of silver-coated antimicrobial screen covers on the cell-phone microbiome of resident
physicians.
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The effects of cell phone conversations on the attention and memory of bystanders.
Effects of cell-phone and text-message distractions on true and false recognition.
Vestibular schwannoma and cell-phones. Results, limits and perspectives of clinical studies.
The psychometric properties of cellular phone dependency questionnaire in students of Isfahan:
A pilot study.
Multidrug-resistant bacteria isolated from cell phones in five intensive care units: Exploratory
dispersion analysis.
[The health problems which can brougth by 3G cell phones to our country].
Exposure limits: the underestimation of absorbed cell phone radiation, especially in children.
Do people understand IARC's 2B categorization of RF fields from cell phones?
Allergic Contact Dermatitis to a Cell Phone.
Impact of pinna compression on the RF absorption in the heads of adult and juvenile cell phone
users.
Do cell phones, iPods/MP3 players, siblings and friends matter? Predictors of child body mass in
a U.S. Southern Border City Middle School.
The role of cellular phone usage by parents in the increase in ASD occurrence: A hypothetical
framework.
Psychophysiological patterns during cell phone text messaging: a preliminary study.
From sweeteners to cell phones-Cancer myths and beliefs among journalism undergraduates.
Can Fish and Cell Phones Teach Us about Our Health?
Cell Phone Counseling Improves Retention of Mothers With HIV Infection in Care and Infant
HIV Testing in Kisumu, Kenya: A Randomized Controlled Study.
Association between problematic cellular phone use and suicide: the moderating effect of family
function and depression.
Symptoms of problematic cellular phone use, functional impairment and its association with
depression among adolescents in Southern Taiwan.
Adolescent in-school cellphone habits: a census of rules, survey of their effectiveness, and
fertility implications.
--Leaf Cluster 7 (44)
Theme - Risks from cell phone use, especially brain tumors
Titles
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Validation of self-reported cellular phone use.
Cellular phone use and brain tumor: a meta-analysis.
[Symptoms reported by mobile cellular telephone users].
Risk of pituitary tumors in cellular phone users: a case-control study.
Cellular and cordless telephone use and the association with brain tumors in different age groups.
Cellular phones, cordless phones, and the risks of glioma and meningioma (Interphone Study
Group, Germany).
Use of cellular telephones and the risk for brain tumours: A case-control study.
Further aspects on cellular and cordless telephones and brain tumours.
Cellular phone use and risk of benign and malignant parotid gland tumors--a nationwide case-
control study.
Cellular-telephone use and brain tumors.
[In vitro and in vivo study of electromagnetic compatibility of cellular phones and pacemakers].
Cellular and cordless telephones and the risk for brain tumours.
Cellular phones and their hazards: the current evidence.
Use of cellular telephones and brain tumour risk in urban and rural areas.
Case-control study on the use of cellular and cordless phones and the risk for malignant brain
tumours.
Characteristics of excessive cellular phone use in Korean adolescents.
Use of cellular or cordless telephones and the risk for non-Hodgkin's lymphoma.
Cellular telephone use and risk of intratemporal facial nerve tumor.
[Study of the influence of cellular phones and personal computers on schoolchildren's health:
hygienic aspects].
Cellular telephone use and time trends for brain, head and neck tumours.
[Experimental data on radiofrequency].
Assessment of radiofrequency exposure from cellular telephone daily use in an epidemiological
study: German Validation study of the international case-control study of cancers of the brain--
INTERPHONE-Study.
Use of cellular and cordless telephones and risk of testicular cancer.
[Cellular phones and public health].
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Estimation of relative exposure levels for cellular phone users using a neural network.
Cellular phone and cellular phone accessory dermatitis due to nickel allergy: report of five cases.
[Health risks of mobile phones].
Brain cancer incidence trends in relation to cellular telephone use in the United States.
Cellular phones and risk of brain tumors.
Correlation between cellular phone use and epithelial parotid gland malignancies.
[On the evaluation of the influence of cellular phones on their users].
Mobile Phone Use and the Risk of Parotid Gland Tumors: A Retrospective Case-Control Study.
Behavioral support to parents through a cellular-phone website that provides the degree of
urgency for medical attention of a child.
Risk perception and public concerns of electromagnetic waves from cellular phones in Korea.
Frequent cellular phone use modifies hypothalamic-pituitary-adrenal axis response to a cellular
phone call after mental stress in healthy children and adolescents: A pilot study.
The relationship between adolescents' well-being and their wireless phone use: a cross-sectional
study.
New Zealand adolescents' cellphone and cordless phone user-habits: are they at increased risk of
brain tumours already? A cross-sectional study.
Prevalence of headache among handheld cellular telephone users in Singapore: a community
study.
[The electromagnetic fields of cellular phones and the health of children and of teenagers (the
situation requiring to take an urgent measure)].
Patterns of cellular phone use among young people in 12 countries: Implications for RF
exposure.
Use of wireless telephones and serum S100B levels: a descriptive cross-sectional study among
healthy Swedish adults aged 18-65 years.
Risks for central nervous system diseases among mobile phone subscribers: a Danish
retrospective cohort study.
The effect of feedback on attitudes toward cellular phone use while driving: a comparison
between novice and experienced drivers.
Radio frequency electromagnetic fields: cancer, mutagenesis, and genotoxicity.
--Leaf Cluster 8 (106)
Theme - Risk of brain tumors/acoustic neuromas from mobile phone use
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Titles
Mobile phone use and risk of glioma in 5 North European countries.
Mobile phone use and brain tumours in the CERENAT case-control study.
Use of mobile phones in Norway and risk of intracranial tumours.
Long-term mobile phone use and brain tumor risk.
Long-term use of cellular phones and brain tumours: increased risk associated with use for > or
=10 years.
Mobile phone use and risk of glioma in adults: case-control study.
A case-case study of mobile phone use and acoustic neuroma risk in Japan.
Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five
Interphone countries.
Mobile phone use and risk of acoustic neuroma: results of the Interphone case-control study in
five North European countries.
Mobile phones, cordless phones and the risk for brain tumours.
Mobile phone use and the risk of acoustic neuroma.
Case-control study of the association between malignant brain tumours diagnosed between 2007
and 2009 and mobile and cordless phone use.
Mobile phone use and glioma risk: A systematic review and meta-analysis.
Mobile phone use and risk of brain neoplasms and other cancers: prospective study.
Pooled analysis of case-control studies on acoustic neuroma diagnosed 1997-2003 and 2007-
2009 and use of mobile and cordless phones.
Long-term mobile phone use and acoustic neuroma risk.
Mobile phone use and risk of brain tumours: a systematic review of association between study
quality, source of funding, and research outcomes.
Mobile phone use and incidence of brain tumour histological types, grading or anatomical
location: a population-based ecological study.
Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and
cordless phones including living and deceased subjects.
Mobile phone use and acoustic neuroma risk in Japan.
Mobile phone use, exposure to radiofrequency electromagnetic field, and brain tumour: a case-
control study.
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Meta-analysis of long-term mobile phone use and the association with brain tumours.
The anatomical distribution of cerebral gliomas in mobile phone users.
Meningioma patients diagnosed 2007-2009 and the association with use of mobile and cordless
phones: a case-control study.
Epidemiologic evidence on mobile phones and tumor risk: a review.
Acoustic neuroma risk in relation to mobile telephone use: results of the INTERPHONE
international case-control study.
The Intracranial Distribution of Gliomas in Relation to Exposure From Mobile Phones: Analyses
From the INTERPHONE Study.
Childhood brain tumour risk and its association with wireless phones: a commentary.
Mobile phone use and risk for intracranial tumors.
Meningioma and mobile phone use--a collaborative case-control study in five North European
countries.
Mobile phone use and glioma risk: comparison of epidemiological study results with incidence
trends in the United States.
The controversy about a possible relationship between mobile phone use and cancer.
Mobile phones and brain tumours: a review of epidemiological research.
Meta-analysis of association between mobile phone use and glioma risk.
Mobile phones and head tumours. The discrepancies in cause-effect relationships in the
epidemiological studies - how do they arise?
Mobile phone use and brain tumors in children and adolescents: a multicenter case-control study.
Mobile phone use and risk of intracranial tumors: a consistency analysis.
Pituitary tumor risk in relation to mobile phone use: A case-control study.
[Long-term use of mobile phone and its association with glioma: a systematic review and meta-
analysis].
Mobile phones, brain tumors, and the interphone study: where are we now?
[Motivation and significance of IARC classification for mobile phone].
Mobile telephones and cancer--a review of epidemiological evidence.
The INTERPHONE study: design, epidemiological methods, and description of the study
population.
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Evaluation of Mobile Phone and Cordless Phone Use and Glioma Risk Using the Bradford Hill
Viewpoints from 1965 on Association or Causation.
Pooled analysis of Swedish case-control studies during 1997-2003 and 2007-2009 on
meningioma risk associated with the use of mobile and cordless phones.
Meta-analysis of mobile phone use and intracranial tumors.
[Association between radiation from mobile phones and tumour risk in adults].
Probabilistic Multiple-Bias Modeling Applied to the Canadian Data From the Interphone Study
of Mobile Phone Use and Risk of Glioma, Meningioma, Acoustic Neuroma, and Parotid Gland
Tumors.
Childhood brain tumours and use of mobile phones: comparison of a case-control study with
incidence data.
Medical exposure to ionising radiation and the risk of brain tumours: Interphone study group,
Germany.
Recall bias in the assessment of exposure to mobile phones.
Lost in laterality: interpreting ''preferred side of the head during mobile phone use and risk of
brain tumour'' associations.
Wireless Phone Use and Risk of Adult Glioma: Evidence from a Meta-Analysis.
Using the Hill viewpoints from 1965 for evaluating strengths of evidence of the risk for brain
tumors associated with use of mobile and cordless phones.
Mobile phone use and risk for intracranial tumors and salivary gland tumors - A meta-analysis.
Use of mobile phones and risk of brain tumours: update of Danish cohort study.
Mobile phone use and risk of tumors: a meta-analysis.
[Mobile phones and head tumours: it is time to read and highlight data in a proper way].
Cellular telephones and risk for brain tumors: a population-based, incident case-control study.
Changes in brain glioma incidence and laterality correlates with use of mobile phones--a
nationwide population based study in Israel.
Survival of glioma patients in relation to mobile phone use in Denmark, Finland and Sweden.
Mobile phone use and the risk for malignant brain tumors: a case-control study on deceased
cases and controls.
A case-control study of risk of leukaemia in relation to mobile phone use.
Validation of self-reported start year of mobile phone use in a Swedish case-control study on
radiofrequency fields and acoustic neuroma risk.
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Environmental risk factors for sporadic acoustic neuroma (Interphone Study Group, Germany).
Use of mobile and cordless phones and survival of patients with glioma.
Impact of random and systematic recall errors and selection bias in case--control studies on
mobile phone use and brain tumors in adolescents (CEFALO study).
Electromagnetic fields and brain tumours: a commentary.
[Radio and microwave frequency radiation and health--an analysis of the literature].
Long-term and frequent cellular phone use and risk of acoustic neuroma.
Validation of short term recall of mobile phone use for the Interphone study.
Systematic review of wireless phone use and brain cancer and other head tumors.
Mobile phone use and incidence of glioma in the Nordic countries 1979-2008: consistency
check.
Selection bias due to differential participation in a case-control study of mobile phone use and
brain tumors.
Decreased survival of glioma patients with astrocytoma grade IV (glioblastoma multiforme)
associated with long-term use of mobile and cordless phones.
Quantifying the impact of selection bias caused by nonparticipation in a case-control study of
mobile phone use.
Analyses of temporal and spatial patterns of glioblastoma multiforme and other brain cancer
subtypes in relation to mobile phones using synthetic counterfactuals.
Estimating associations of mobile phone use and brain tumours taking into account laterality: a
comparison and theoretical evaluation of applied methods.
Mobile phone use and risk of parotid gland tumor.
Epidemiology of brain tumors.
Review of four publications on the Danish cohort study on mobile phone subscribers and risk of
brain tumors.
Evaluation of carcinogenic effects of electromagnetic fields (EMF).
Use of wireless phones and the risk of salivary gland tumours: a case-control study.
Epidemiology and etiology of gliomas.
Epidemiology of Intracranial Gliomas.
The effects of recall errors and of selection bias in epidemiologic studies of mobile phone use
and cancer risk.
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Time trend in incidence of malignant neoplasms of the central nervous system in relation to
mobile phone use among young people in Japan.
A three-dimensional point process model for the spatial distribution of disease occurrence in
relation to an exposure source.
[Risk of major lymphoma subtypes and use of mobile phones].
Simulation of the incidence of malignant brain tumors in birth cohorts that started using mobile
phones when they first became popular in Japan.
Risks of carcinogenesis from electromagnetic radiation of mobile telephony devices.
Current state of our knowledge on brain tumor epidemiology.
Mobile phones, cordless phones and rates of brain tumors in different age groups in the Swedish
National Inpatient Register and the Swedish Cancer Register during 1998-2015.
Has the incidence of brain cancer risen in Australia since the introduction of mobile phones 29
years ago?
Inferring the 1985-2014 impact of mobile phone use on selected brain cancer subtypes using
Bayesian structural time series and synthetic controls.
Location of gliomas in relation to mobile telephone use: a case-case and case-specular analysis.
Mobile phone use and risk of uveal melanoma: results of the risk factors for uveal melanoma
case-control study.
[The probability of developing brain tumours among users of cellular telephones (scientific
information to the decision of the International Agency for Research on Cancer (IARC)
announced on May 31, 2011)].
[Risk of neoplastic diseases in conditions of exposure to radio- and microwave fields--
epidemiologic investigations].
Effects of alternative styles of risk information on EMF risk perception.
Medical students' risk perceptions on decreased attention, physical and social risks in using
mobile phones and the factors related with their risk perceptions.
The possible role of radiofrequency radiation in the development of uveal melanoma.
Mobile phones and multiple sclerosis--a nationwide cohort study in Denmark.
Mobile phone use and the risk of skin cancer: a nationwide cohort study in Denmark.
Use of wireless phones and serum beta-trace protein in randomly recruited persons aged 18-65
years: a cross-sectional study.
Exposure to wireless phone emissions and serum beta-trace protein.
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Fourth Level Cluster 89 (869)
Theme - Human health risks from electromagnetic radiation, including adverse effects on
implanted electronic devices, and possible protections
--Leaf Cluster 0 (63)
Theme - Electromagnetic interference with cardiac pacemakers
Titles
The effects of mobile phones on pacemaker function.
[The effect of cell phones on pacemaker function].
Electromagnetic interference with implantable cardiac pacemakers by video capsule.
Influence of digital and analogue cellular telephones on implanted pacemakers.
[Pacemaker dysfunction during use of a mobile telephone].
Life after pacemaker implantation: management of common problems and environmental
interactions.
[Cardiac pacemakers designed for magnetic resonance environment].
Interference with cardiac pacemakers by cellular telephones.
Pacemakers and magnetic resonance imaging: Current status and survey in Switzerland.
Influence of D-net (European GSM-Standard) cellular phones on pacemaker function in 50
patients with permanent pacemakers.
[Pacemaker dysfunction in the clinical practice].
Interference in pacemakers.
Interactions between pacemakers and security systems.
Electromagnetic interference with pacemakers caused by portable media players.
Electromagnetic compatibility of electronic implants--review of the literature.
Do European GSM mobile cellular phones pose a potential risk to pacemaker patients?
Electromagnetic interference in pacemakers in single-engine fixed-wing aircraft: a European
perspective.
Pacemaker inhibition and asystole in a pacemaker dependent patient.
[Cardiac pacemaker dysfunction secondary to outside interference: a review].
Pacemakers: some of the risks and complications you are not warned about.
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Is there a risk for interaction between mobile phones and single lead VDD pacemakers?
SAR evaluations of mobile phone close to a pacemaker implanted in human body.
[Is there any risk interaction between electromagnetic field generated by mobile phones and
artificial pacemakers].
Electromagnetic interference with cardiac pacemakers and implantable cardioverter-defibrillators
from low-frequency electromagnetic fields in vivo.
Induction ovens and electromagnetic interference: what is the risk for patients with implanted
pacemakers?
Magnetic resonance imaging for patients with permanent pacemakers: initial clinical experience.
Magnetic interference of cardiac pacemakers from a surgical magnetic drape.
Electromagnetic compatibility study of the in-vitro interaction of wireless phones with cardiac
pacemakers.
Do media players cause interference with pacemakers?
Electromagnetic interference of pacemakers by mobile phones.
Interference by cellular phones with permanent implanted pacemakers: an update.
Electrocardiographic "pacemaker pseudo-spikes" and radio frequency interference.
Pacemaker interference.
Reliability of electromagnetic filters of cardiac pacemakers tested by cellular telephone ringing.
Pacemaker interference by 60-Hz contact currents.
The effect of 50 Hz external electrical interference on implanted cardiac pacemakers.
Concerns about sources of electromagnetic interference in patients with pacemakers.
Selective interference with pacemaker activity by electrical dental devices.
Hospital pager systems may cause interference with pacemaker telemetry.
[Environment and permanent cardiac pacing].
Interference with cardiac pacing.
Electromagnetic interference of analog cellular telephones with pacemakers.
The effect of power frequency high intensity electric fields on implanted cardiac pacemakers.
The effect of radar on cardiac pacemakers.
Pacing in high field cardiac magnetic resonance imaging:.
Do induction cooktops interfere with cardiac pacemakers?
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[Interference between cardiac pacemaker and electromagnetic anti-theft devices in stores].
[Effect of external electrical interference on pacemakers].
Effects of an increased air gap on the in vitro interaction of wireless phones with cardiac
pacemakers.
Radiofrequency Scanning for Retained Surgical Items Can Cause Electromagnetic Interference
and Pacing Inhibition if an Asynchronous Pacing Mode Is Not Applied.
Interference between mobile phones and pacemakers: a look inside.
[Electromagnetic interference of electrical dental equipment with cardiac pacemakers].
Electromagnetic interference of an external temporary pacemaker during maxillofacial and neck
surgery.
Effect of electronic apex locators on cardiac pacemaker function.
Mode of operation induced by rapid external chest wall stimulation in patients with normally
functioning QRS-inhibited (VVI) pacemakers.
Disturbances in the function of cardiac pacemaker caused by short wave and microwave
diathermies and pulsed high frequency current.
[Cardiac Pacemakers, implantable defibrillators and IRM].
The safety of digital mobile cellular telephones with minute ventilation rate adaptive
pacemakers.
Electromagnetic interference of implantable unipolar cardiac pacemakers by an induction oven.
[Health Council Report 'Radiofrequency electromagnetic fields (300 Hz-300 GHz). The Health
Council of the Netherlands].
Characteristics of telemetry interference with pacemakers caused by digital media players.
Influence of mobile magnetic resonance imaging on implanted pacemakers.
[Compatibility of active implants in the professional environment].
--Leaf Cluster 16 (103)
Theme - Electromagnetic interference on implanted cardiac devices
Titles
Incidence of electromagnetic interference in implantable cardioverter defibrillators.
Effects of electromagnetic interference on implanted cardiac devices and their management.
Electromagnetic interference in cardiac rhythm management devices.
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Surgical management of the patient with an implanted cardiac device: implications of
electromagnetic interference.
Electromagnetic interference and implanted cardiac devices: the nonmedical environment (part
I).
[The influence of non-ionizing electromagnetic fields on implantable cardiac medical devices].
Electromagnetic interference and implanted cardiac devices: the medical environment (part II).
Potential interference of small neodymium magnets with cardiac pacemakers and implantable
cardioverter-defibrillators.
Implanted devices and electromagnetic interference: case presentations and review.
Are patients with cardiac implants protected against electromagnetic interference in daily life and
occupational environment?
Safety of the colonoscope magnetic imaging device (ScopeGuide) in patients with implantable
cardiac devices.
Intermittent, erratic behaviour of an implantable cardioverter defibrillator secondary to a hidden
magnetic source of interference.
Shock whilst gardening--implantable defibrillators & lawn mowers.
An update on mobile phones interference with medical devices.
Characterization of electromagnetic interference of medical devices in the hospital due to cell
phones.
Mobile phone interference with medical equipment and its clinical relevance: a systematic
review.
Electromagnetic interference in implantable cardioverter defibrillators: present but rare.
Electromagnetic interference with implantable cardioverter-defibrillators at power frequency: an
in vivo study.
Cellular phone interference with external cardiopulmonary monitoring devices.
Do airport metal detectors interfere with implantable pacemakers or cardioverter-defibrillators?
Electromagnetic interference of dental equipment with implantable cardioverter defibrillators.
Treatment of patients with cardiac pacemakers and implantable cardioverter-defibrillators during
radiotherapy.
AANA Journal Course: update for nurse anesthetists. Arrhythmia management devices and
electromagnetic interference.
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In-vivo testing of digital cellular telephones in patients with implantable cardioverter-
defibrillators.
[Magnets, pacemaker and defibrillator: fatal attraction?].
Induction ovens and electromagnetic interference: what is the risk for patients with implantable
cardioverter defibrillators?
Electromagnetic Interference (EMI) and arrhythmic events in ICD patients undergoing
gastrointestinal procedures.
Radiofrequency interference with medical devices. A technical information statement.
How do mobile phones affect electromedical devices?
Cell phones and electromagnetic interference revisited.
Patient safety and electromagnetic protection: a review.
[Return to work of a pacemaker bearing worker: the relationship between health problems and
electromagnetic interferences].
Report of the American Medical Association (AMA) Council on Scientific Affairs and AMA
recommendations to medical professional staff on the use of wireless radio-frequency equipment
in hospitals.
Implantable cardioverter defibrillators and cellular telephones: is there any interference?
Wireless technologies and patient safety in hospitals.
[Magnetic resonance imaging in patients with pacemakers and implantable cardioverter-
defibrillators: a systematic review].
[Medical implantable devices and electromagnetic compatibility].
Electromagnetic interference in critical care.
In vitro tests reveal sample radiofrequency identification readers inducing clinically significant
electromagnetic interference to implantable pacemakers and implantable cardioverter-
defibrillators.
[Do mobile telephones have adverse effects on the functions of implantable cardioverter
defibrillators?].
A follow-up study of electromagnetic interference of cellular phones on electronic medical
equipment in the emergency department.
Electromagnetic interference can cause hospital devices to malfunction, McGill group warns.
Electromagnetic interference from radio frequency identification inducing potentially hazardous
incidents in critical care medical equipment.
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Electromagnetic interference of endodontic equipments with cardiovascular implantable
electronic device.
Is magnetic resonance safe in implanted cardiac devices patients?
Safety Considerations in Magnetic Resonance Imaging of Patients With Implanted Medical
Devices.
Cardiac devices and electromagnetic interference revisited: new radiofrequency technologies and
implications for dermatologic surgery.
State of the science: pacemaker and defibrillator interference from wireless communication
devices.
Measurements of electromagnetic fields radiated from communication equipment and of
environmental electromagnetic noise: impact on the use of communication equipment within the
hospital.
Dosimetry of electromagnetic field exposure of an active armlet and its electromagnetic
interference to the cardiac pacemakers using adult, child and infant models.
Implanted medical devices in workers exposed to radio-frequency radiation.
[Radiotherapy in patients with a pacemaker or an implantable cardioverter defibrillator].
Electromagnetic interference of communication devices on ECG machines.
Interference by new-generation mobile phones on critical care medical equipment.
[Use of mobile phones in hospitals do not jeopardise the safety of the patients].
Electromagnetic interference between external defibrillator and cardiac resynchronization
therapy-pacemaker (CRT-P) devices.
Interference of electrical dental equipment with implantable cardioverter-defibrillators.
Electromagnetic interference of cardiac rhythmic monitoring devices to radio frequency
identification: analytical analysis and mitigation methodology.
A practical procedure to prevent electromagnetic interference with electronic medical equipment.
Clinically significant magnetic interference of implanted cardiac devices by portable
headphones.
Electromagnetic interference from GSM and TETRA phones with life-support medical devices.
Electromagnetic interference to infusion pumps. Update2008 from GSM mobile phones.
Electronic article surveillance systems and interactions with implantable cardiac devices: risk of
adverse interactions in public and commercial spaces.
Electromagnetic immunity of infusion pumps to GSM mobile phones: a systematic review.
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Avoidance behaviors in patients with implantable cardioverter defibrillators.
Electromagnetic interference of implantable cardiac devices from a shoulder massage machine.
Deaths associated with implantable cardioverter defibrillator failure and deactivation reported in
the United States Food and Drug Administration Manufacturer and User Facility Device
Experience Database.
Cochlear implants: in vitro investigation of electromagnetic interference at MR imaging--
compatibility and safety aspects.
Electromagnetic interference with electronic medical equipment induced by automatic
conveyance systems.
Possible electromagnetic interference with electronic medical equipment by radio waves coming
from outside the hospital.
Interactions between electronic article surveillance systems and implantable cardioverter-
defibrillators.
Risk of cellular phone interference with an implantable loop recorder.
Interference of electrocardiographic recordings by a mobile telephone.
Electromagnetic interference with infusion pumps from GSM mobile phones.
An implanted spherical head model exposed to electromagnetic fields at a mobile
communication frequency.
Biomedical concerns in wireless communications.
In vitro study of the electromagnetic interaction between wireless phones and an implantable
neural stimulator.
Safety aspects of radiofrequency power deposition in magnetic resonance.
Electromagnetic interference of bone-anchored hearing aids by cellular phones revisited.
Fatal collision? Are wireless headsets a risk in treating patients?
Ventricular fibrillation induced by radiofrequency energy delivery for premature ventricular
contractions arising from the right ventricular outflow tract: is
implantablecardioverterdefibrillator indicated?
Interaction of radio frequency electromagnetic fields and passive metallic implants--a brief
review.
Use of mobile phones in ICU--why not ban?
Clinical testing of cellular phone ringing interference with automated external defibrillators.
Electromagnetic immunity of implantable pacemakers exposed to wi-fi devices.
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Effect of digital cellular phones on tachyarrhythmia analysis of automated external defibrillators.
Interference with the operation of medical devices resulting from the use of radio frequency
identification technology.
The impact of dental devices on neurostimulators.
Detection of refrigerator-associated 60 Hz alternating current as ventricular fibrillation by an
implantable defibrillator.
Solutions to electromagnetic interference problems between cochlear implants and GSM phones.
[Electromagnetic fields of mobile telephone systems--thresholds, effects and risks for cochlear
implant patients and healthy people].
[Interference testing in certification of medical equipment].
Assessment of the exposure to WLAN frequencies of a head model with a cochlear implant.
Mobile phones to improve the practice of neurology.
Is electromagnetic interference still a risk?
Cellular phone interference with the operation of mechanical ventilators.
[Electromagnetic fields in hospitals: wireless-LAN as a risk factor?].
[Influence of electromagnetic waves on portable electronic instruments in medicine].
Electromagnetic energy radiated from mobile phone alters electrocardiographic records of
patients with ischemic heart disease.
Nullification of electromagnetic radiation: 50 Hz artifact during electroencephalogram recording.
Development of a silicon retinal implant: cortical evoked potentials following focal stimulation
of the rabbit retina with light and electricity.
[Influence of the radiofrequency current on the left ventricular systolic function].
Smart phone: a popular device supports amylase activity assay in fisheries research.
--Leaf Cluster 5 (120)
Theme - Health risks from mobile phone base stations
Titles
Epidemiological evidence for a health risk from mobile phone base stations.
Mobile phone base stations and adverse health effects: phase 1 of a population-based, cross-
sectional study in Germany.
Perception of mobile phone and base station risks.
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Effect of mobile phone station on micronucleus frequency and chromosomal aberrations in
human blood cells.
Public exposure to radio waves near GSM microcell and picocell base stations.
Mobile phone base stations and well-being--A meta-analysis.
Mobile phone base stations and adverse health effects: phase 2 of a cross-sectional study with
measured radio frequency electromagnetic fields.
Assessment of exposure to mobile telecommunication electromagnetic fields.
Assessment of radiofrequency/microwave radiation emitted by the antennas of rooftop-mounted
mobile phone base stations.
Electromagnetic field pattern in the environment of GSM base stations.
[Electormagnetic field of the mobile phone base station: case study].
Determination of exposure due to mobile phone base stations in an epidemiological study.
Variographic analysis of public exposure to electromagnetic radiation due to cellular base
stations.
[Subjective symptoms reported by people living in the vicinity of cellular phone base stations:
review].
Neurobehavioral effects among inhabitants around mobile phone base stations.
[Assessment of electromagnetic fields intensity emitted by cellular phone base stations in
surrounding flats--a preliminary study].
Effects of short-term W-CDMA mobile phone base station exposure on women with or without
mobile phone related symptoms.
Statistical analysis of electromagnetic radiation measurements in the vicinity of indoor microcell
GSM/UMTS base stations in Serbia.
Estimates of Environmental Exposure to Radiofrequency Electromagnetic Fields and Risk of
Lymphoma Subtypes.
[Level of microwave radiation from mobile phone base stations built in residential districts].
Do mobile phone base stations affect sleep of residents? Results from an experimental double-
blind sham-controlled field study.
Effect of electromagnetic radiations from mobile phone base stations on general health and
salivary function.
Use of portable exposure meters for comparing mobile phone base station radiation in different
types of areas in the cities of Basel and Amsterdam.
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[Investigation on the health of people living near mobile telephone relay stations: I/Incidence
according to distance and sex].
Statistical analysis of electromagnetic radiation measurements in the vicinity of GSM/UMTS
base station antenna masts.
Impact of radiofrequency radiation on DNA damage and antioxidants in peripheral blood
lymphocytes of humans residing in the vicinity of mobile phone base stations.
Analysis of the effect of mobile phone base station antenna loading on localized SAR and its
consequences for measurements.
Public safety assessment of electromagnetic radiation exposure from mobile base stations.
Survey of RF exposure levels from mobile telephone base stations in Australia.
Subjective complaints of people living near mobile phone base stations in Poland.
Time averaged transmitter power and exposure to electromagnetic fields from mobile phone base
stations.
[Symptoms experienced by people in vicinity of base stations: II/ Incidences of age, duration of
exposure, location of subjects in relation to the antennas and other electromagnetic factors].
[Danger of cellular telephones and their relay stations].
Mobile phone base stations and early childhood cancers: case-control study.
Exposure to non-ionizing electromagnetic radiation from mobile telephony and the association
with psychiatric symptoms.
Feasibility of future epidemiological studies on possible health effects of mobile phone base
stations.
Electromagnetic fields from mobile phone base station - variability analysis.
Assessment of RF radiation levels in the vicinity of 60 GSM mobile phone base stations in Iran.
Biological responses of mobile phone frequency exposure.
Radio frequency electromagnetic field compliance assessment of multi-band and MIMO
equipped radio base stations.
A possible effect of electromagnetic radiation from mobile phone base stations on the number of
breeding house sparrows (Passer domesticus).
Statistical analysis of electromagnetic radiation measurements in the vicinity of GSM/UMTS
base station installed on buildings in Serbia.
A cross-sectional case control study on genetic damage in individuals residing in the vicinity of a
mobile phone base station.
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Does short-term exposure to mobile phone base station signals increase symptoms in individuals
who report sensitivity to electromagnetic fields? A double-blind randomized provocation study.
Modeled and Perceived Exposure to Radiofrequency Electromagnetic Fields From Mobile-
Phone Base Stations and the Development of Symptoms Over Time in a General Population
Cohort.
Determination of safety distance limits for a human near a cellular base station antenna, adopting
the IEEE standard or ICNIRP guidelines.
Subjective symptoms, sleeping problems, and cognitive performance in subjects living near
mobile phone base stations.
Occupational exposure to base stations-compliance with EU directive 2004/40/EC.
Measurement and analysis of radiofrequency radiations from some mobile phone base stations in
Ghana.
UMTS base station-like exposure, well-being, and cognitive performance.
Outdoor and indoor sources of residential radiofrequency electromagnetic fields, personal cell
phone and cordless phone use, and cognitive function in 5-6 years old children.
[Increased occurrence of nuclear cataract in the calf after erection of a mobile phone base
station].
Impact of a small cell on the RF-EMF exposure in a train.
A large-scale measurement, analysis and modelling of electromagnetic radiation levels in the
vicinity of GSM/UMTS base stations in an urban area.
Determinants of exposure to electromagnetic fields from mobile phones.
Improving the efficiency of measurement procedures for assessing human exposure in the
vicinity of mobile phone (GSM/DCS/UMTS) base stations.
Population exposure to electromagnetic fields generated by radio base stations: evaluation of the
urban background by using provisional model and instrumental measurements.
On the safety assessment of human exposure in the proximity of cellular communications base-
station antennas at 900, 1800 and 2170 MHz.
What input data are needed to accurately model electromagnetic fields from mobile phone base
stations?
Methods of evaluating human exposure to electromagnetic fields radiated from operating base
stations in Korea.
Non-specific physical symptoms in relation to actual and perceived proximity to mobile phone
base stations and powerlines.
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[Mobile communication: radiobiology problems and evaluation of danger].
Temporal and spatial variability of personal exposure to radio frequency electromagnetic fields.
The precautionary principle in the context of mobile phone and base station radiofrequency
exposures.
Adolescents' risk perceptions on mobile phones and their base stations, their trust to authorities
and incivility in using mobile phones: a cross-sectional survey on 2240 high school students in
Izmir, Turkey.
Systematic review on the health effects of exposure to radiofrequency electromagnetic fields
from mobile phone base stations.
Radiofrequency electromagnetic fields emitted from base stations of DECT cordless phones and
the risk of glioma and meningioma (Interphone Study Group, Germany).
Mobile telecommunications and health: report of an investigation into an alleged cancer cluster
in Sandwell, West Midlands.
Study of variations of radiofrequency power density from mobile phone base stations with
distance.
Health risks from the use of mobile phones.
Mobile phones, mobile phone base stations and cancer: a review.
Animal carcinogenicity studies on radiofrequency fields related to mobile phones and base
stations.
Association of Exposure to Radio-Frequency Electromagnetic Field Radiation (RF-EMFR)
Generated by Mobile Phone Base Stations with Glycated Hemoglobin (HbA1c) and Risk of
Type 2 Diabetes Mellitus.
Assessment of the temporal trend of the exposure of people to electromagnetic fields produced
by base stations for mobile telephones.
Risk and benefit perceptions of mobile phone and base station technology in Bangladesh.
Clinically defined non-specific symptoms in the vicinity of mobile phone base stations: A
retrospective before-after study.
Specific absorption rate and electric field measurements in the near field of six mobile phone
base station antennas.
Output power levels from mobile phones in different geographical areas; implications for
exposure assessment.
Influence of mobile phone traffic on base station exposure of the general public.
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Residential exposure to RF-EMF from mobile phone base stations: Model predictions versus
personal and home measurements.
Physics and biology of mobile telephony.
Longitudinal associations between risk appraisal of base stations for mobile phones, radio or
television and non-specific symptoms.
Exposure assessment of mobile phone base station radiation in an outdoor environment using
sequential surrogate modeling.
Exposure of farm workers to electromagnetic radiation from cellular network radio base stations
situated on rural agricultural land.
Mobile phones. precautionary options.
Aggregated data from two double-blind base station provocation studies comparing individuals
with idiopathic environmental intolerance with attribution to electromagnetic fields and controls.
GSM base stations: short-term effects on well-being.
Sensitivity to electricity--temporal changes in Austria.
How does long term exposure to base stations and mobile phones affect human hormone
profiles?
Effects of exposure to GSM mobile phone base station signals on salivary cortisol, alpha-
amylase, and immunoglobulin A.
Determinants and stability over time of perception of health risks related to mobile phone base
stations.
[Cellular radio systems. Problems faced in assessing exposure to electromagnetic fields].
Effect of radiofrequency radiation on reproductive health.
Exposure assessment in front of a multi-band base station antenna.
Protect children from EMF.
Symptoms of ill health ascribed to electromagnetic field exposure--a questionnaire survey.
Spatial electromagnetic field intensity modelling of global system for mobile communication
base stations in the Istanbul Technical University Ayazaga campus area.
[Protection against electromagnetic fields emitted by mobile phone facilities in Poland and the
European Union countries].
Prevalence of nuclear cataract in Swiss veal calves and its possible association with mobile
telephone antenna base stations.
[GSM fields and health: an updated literature review].
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Knowledge and perceptions of the health effects of environmental hazards in the general
population in Italy.
Dynamics of the public concern and risk communication program implementation.
Microwaves in the cold war: the Moscow embassy study and its interpretation. Review of a
retrospective cohort study.
Health effects of living near mobile phone base transceiver station (BTS) antennae: a report from
Isfahan, Iran.
Replication of heart rate variability provocation study with 2.4-GHz cordless phone confirms
original findings.
[Reports on the impact of objects emitting electromagnetic fields on the environment: issues
concerning their better understanding by non-specialists in telecommunication].
Cognitive and physiological responses in humans exposed to a TETRA base station signal in
relation to perceived electromagnetic hypersensitivity.
Mortality by neoplasia and cellular telephone base stations in the Belo Horizonte municipality,
Minas Gerais state, Brazil.
Are wireless phones safe? A review of the issue.
A novel method to assess human population exposure induced by a wireless cellular network.
[Metrology of pulse modulated electromagnetic fields with diode-type meters].
Radiofrequency radiation injures trees around mobile phone base stations.
Comparison of temporal realistic telecommunication base station exposure with worst-case
estimation in two countries.
[Cellular telephones and their relay stations: a health risk?].
[Evaluation of the levels of radiofrequency electromagnetic fields in the territory of the city of
Bari in outside and inside environments].
A geographical model of radio-frequency power density around mobile phone masts.
[Ecological aspects of electromagnetic radiation emitted by mobile stations of communication
means].
Assessment of nuclear abnormalities in exfoliated cells from the oral epithelium of mobile phone
users.
Occupational exposure to radiofrequency fields in antenna towers.
Joint minimization of uplink and downlink whole-body exposure dose in indoor wireless
networks.
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--Leaf Cluster 19 (84)
Theme - Electromagnetic hypersensitivity
Titles
Does electromagnetic hypersensitivity originate from nocebo responses? Indications from a
qualitative study.
Symptoms, personality traits, and stress in people with mobile phone-related symptoms and
electromagnetic hypersensitivity.
Electromagnetic field induced biological effects in humans.
Development and evaluation of the electromagnetic hypersensitivity questionnaire.
Hypothesis on how to measure electromagnetic hypersensitivity.
[Subjective non-specific symptoms related with electromagnetic fields: description of 2 cases].
Characteristics of perceived electromagnetic hypersensitivity in the general population.
Electromagnetic hypersensitivity--an increasing challenge to the medical profession.
Idiopathic environmental intolerance attributed to electromagnetic fields (formerly
'electromagnetic hypersensitivity'): An updated systematic review of provocation studies.
Cognitive and neurobiological alterations in electromagnetic hypersensitive patients: results of a
case-control study.
Becoming electro-hypersensitive: A replication study.
Hypersensitivity to RF fields emitted from CDMA cellular phones: a provocation study.
Electromagnetic hypersensitivity: fact or fiction?
IEI-EMF provocation case studies: A novel approach to testing sensitive individuals.
A systematic review of treatments for electromagnetic hypersensitivity.
[Hypersensitivity syndrome].
Electromagnetic hypersensitivity: a systematic review of provocation studies.
Symptom attribution and risk perception in individuals with idiopathic environmental intolerance
to electromagnetic fields and in the general population.
Polluted places or polluted minds? An experimental sham-exposure study on background
psychological factors of symptom formation in 'Idiophatic Environmental Intolerance attributed
to electromagnetic fields'.
Is There a Connection Between Electrosensitivity and Electrosensibility? A Replication Study.
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Idiopathic environmental intolerance attributed to electromagnetic fields (IEI-EMF): a
systematic review of identifying criteria.
Electromagnetic hypersensitivity (EHS) in occupational and primary health care: A nation-wide
survey among general practitioners, occupational physicians and hygienists in the Netherlands.
"Hypersensitivity to Electricity" in the Office; Symptoms and Improvement.
Do people with idiopathic environmental intolerance attributed to electromagnetic fields display
physiological effects when exposed to electromagnetic fields? A systematic review of
provocation studies.
Hypersensitivity to electricity: working definition and additional characterization of the
syndrome.
Are media warnings about the adverse health effects of modern life self-fulfilling? An
experimental study on idiopathic environmental intolerance attributed to electromagnetic fields
(IEI-EMF).
Medical and social prognosis for patients with perceived hypersensitivity to electricity and skin
symptoms related to the use of visual display terminals.
Blood laboratory findings in patients suffering from self-perceived electromagnetic
hypersensitivity (EHS).
Representative survey on idiopathic environmental intolerance attributed to electromagnetic
fields in Taiwan and comparison with the international literature.
Can explicit suggestions about the harmfulness of EMF exposure exacerbate a nocebo response
in healthy controls?
Idiopathic environmental intolerance attributed to electromagnetic fields: a content analysis of
British newspaper reports.
A cognitive-behavioral treatment of patients suffering from "electric hypersensitivity".
Subjective effects and reactions in a double-blind provocation study.
Development and evaluation of an electromagnetic hypersensitivity questionnaire for Japanese
people.
Increasing levels of saliva alpha amylase in electrohypersensitive (EHS) patients.
Are media reports able to cause somatic symptoms attributed to WiFi radiation? An experimental
test of the negative expectation hypothesis.
Electrical hypersensitivity in humans--fact or fiction?
Electromagnetic hypersensitivity: evidence for a novel neurological syndrome.
Effect of short exposure to radiofrequency electromagnetic fields on saliva biomarkers: a study
on the electrohypersensitive individuals.
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[Electromagnetic fields hypersensitivity].
Heavy metal exposure in patients suffering from electromagnetic hypersensitivity.
[Controversies around electromagnetic fields and electromagnetic hypersensitivity. The
construction of "low noise" public problems].
Coping and self-image in patients with visual display terminal-related skin symptoms and
perceived hypersensitivity to electricity.
Neurophysiological effects of flickering light in patients with perceived electrical
hypersensitivity.
Effects of personalised exposure on self-rated electromagnetic hypersensitivity and sensibility -
A double-blind randomised controlled trial.
Psychologic aspects of patients with symptoms presumed to be caused by electricity or visual
display units.
Odontologic survey of referred patients with symptoms allegedly caused by electricity or visual
display units.
Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple
chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder.
[Idiopathic environmental intolerance: 2 disabling entities to recognize].
Neurophysiological study of patients with perceived 'electrical hypersensitivity'.
Description of persons with symptoms presumed to be caused by electricity or visual display
units--oral aspects.
Provocation with stress and electricity of patients with "sensitivity to electricity".
Functional brain MRI in patients complaining of electrohypersensitivity after long term exposure
to electromagnetic fields.
Association of tinnitus and electromagnetic hypersensitivity: hints for a shared pathophysiology?
The microwave syndrome or electro-hypersensitivity: historical background.
[Pseudostenocardia due to exposure to "electrosmog"].
Altered cortical excitability in subjectively electrosensitive patients: results of a pilot study.
An assessment of the autonomic nervous system in the electrohypersensitive population: a heart
rate variability and skin conductance study.
Provocation of the electromagnetic distress syndrome.
Skin problems from visual display units. Provocation of skin symptoms under experimental
conditions.
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Cognitive behavioural therapy for patients with electric sensitivity - a multidisciplinary approach
in a controlled study.
Self-reporting of symptom development from exposure to radiofrequency fields of wireless
smart meters in victoria, australia: a case series.
Improvement of gastroesophageal reflux symptoms after radiofrequency energy: a randomized,
sham-controlled trial.
Does "electromagnetic pollution" cause illness? An inquiry among Austrian general
practitioners.
"Struggle to obtain redress": Women's experiences of living with symptoms attributed to dental
restorative materials and/or electromagnetic fields.
Environmental illness: fatigue and cholinesterase activity in patients reporting hypersensitivity to
electricity.
The views of primary care physicians on health risks from electromagnetic fields.
Review of extensive workups of 34 patients overexposed to radiofrequency radiation.
Providing cell phone numbers and e-mail addresses to patients: The patient's perspective, a cross
sectional study.
[Effects of millimetric electromagnetic waves on regional blood flow and effectiveness of
multimodal therapy of patients with pulmonary tuberculosis].
Environmental illness: evaluation of salivary flow, symptoms, diseases, medications, and
psychological factors.
30-MINUTES-TUMT. Use of the visual analogue scale to investigate patients' pain perception,
different cocktail options and tolerability during 30 minutes' treatment.
Non-ionizing radiation exposure causing ill-health and alopecia areata.
Low-frequency pulsed electromagnetic field therapy in fibromyalgia: a randomized, double-
blind, sham-controlled clinical study.
Electrohypersensitivity: a functional impairment due to an inaccessible environment.
Accidental exposure to electromagnetic fields from the radar of a naval ship: a descriptive study.
[Mechanism of biotropic effects of regional electromagnetic fields in patients with left
ventricular ischemic dysfunction].
A comparision of percutaneous radiofrequency trigeminal neurolysis and microvascular
decompression of the trigeminal nerve for the treatment of tic douloureux.
Medical aspects of radiofrequency radiation overexposure.
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Prospective, randomized, single-blind, sham treatment-controlled study of the safety and efficacy
of an electromagnetic field device for the treatment of chronic low back pain: a pilot study.
Atrial fibrillation therapies: lest we forget surgery.
Non-resection approaches for colorectal liver metastases.
[Indices of thrombocyte conductance and permeability in microwave fields in ischemic and
hemorrhagic stroke patients].
Health care utilisation and attitudes towards health care in subjects reporting environmental
annoyance from electricity and chemicals.
A primer of magnetic stimulation as a tool for neuropsychology.
--Leaf Cluster 43 (202)
Theme - Health risks from low-frequency electromagnetic fields
Titles
Health risks of electromagnetic fields. Part I: Evaluation and assessment of electric and magnetic
fields.
The Bernal Lecture 2004 Are low-frequency electromagnetic fields a health hazard?
Electric and magnetic fields (EMF): what do we know about the health effects?
EUROPAEM EMF Guideline 2016 for the prevention, diagnosis and treatment of EMF-related
health problems and illnesses.
[Non-thermal bioeffects of static and extremely low frequency electromagnetic fields].
Effects of extremely low frequency electromagnetic fields on health.
Exposure assessment for power frequency electric and magnetic fields (EMF) and its application
to epidemiologic studies.
The question of health effects from exposure to electromagnetic fields.
[Influence of low frequency electromagnetic fields on the nervous system].
Biological responses to electromagnetic fields.
Teratogen update: electromagnetic fields.
Intrauterine effects of electromagnetic fields--(low frequency, mid-frequency RF, and
microwave): review of epidemiologic studies.
The effects of electromagnetic fields from power lines on avian reproductive biology and
physiology: a review.
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The effects of extremely low-frequency magnetic fields on melatonin and cortisol, two marker
rhythms of the circadian system.
The sensitivity of children to electromagnetic fields.
Electromagnetic fields and cancer: the cost of doing nothing.
Biological effects from electromagnetic field exposure and public exposure standards.
[Low frequency electromagnetic fields in the working environment--exposure and health effects.
Elevated risk of cancer, reproductive hazards or other unwanted health effects?].
Designing EMF experiments: what is required to characterize "exposure"?
Electromagnetic fields and public health.
[Current state of knowledge on health and electromagnetic fields].
Health risks associated with residential exposure to extremely low frequency electromagnetic
radiation.
Electromagnetic fields and health outcomes.
[Biological mechanisms and health effects of emf in view of requirements of reports on the
impact of various installations on the environment].
[Exposure to low-frequency electromagnetic fields and pregnancy outcome: a review of the
literature with particular attention to exposure to video terminals].
Fielding a current idea: exploring the public health impact of electromagnetic radiation.
A literature review: the cardiovascular effects of exposure to extremely low frequency
electromagnetic fields.
Exposure to low-frequency electromagnetic fields--a health hazard?
Human disease resulting from exposure to electromagnetic fields.
Electromagnetic radiation.
Future needs of occupational epidemiology of extremely low frequency electric and magnetic
fields: review and recommendations.
Comparative health risk assessment of electromagnetic fields.
[Effects of electromagnetic fields on health].
WHO health risk assessment process for static fields.
A review of cancer induction by extremely low frequency electromagnetic fields. Is there a
plausible mechanism?
Reproductive and teratologic effects of electromagnetic fields.
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Developing policy in the face of scientific uncertainty: interpreting 0.3 microT or 0.4 microT
cutpoints from EMF epidemiologic studies.
[Electromagnetic fields--effects on health].
Biologic effects and health consequences of low and high (radio) frequency electromagnetic
fields.
[Electromagnetic pollution (electrosmog)--potential hazards of our electromagnetic future].
Risk governance for mobile phones, power lines, and other EMF technologies.
[Bioeffects of electromagnetic fields--safety limits of each frequency band, especially less than
radio one].
Setting prudent public health policy for electromagnetic field exposures.
Effects of extremely low frequency electromagnetic field on the health of workers in automotive
industry.
Electromagnetic fields: low dose exposure, current update.
Effects of extremely low frequency electromagnetic fields on distortion product otoacoustic
emissions in rabbits.
Exposure to extremely-low-frequency electromagnetic fields and radiofrequency radiation:
cardiovascular effects in humans.
Effects of electromagnetic field exposure on the heart: a systematic review.
Current Understanding of the Health Effects of Electromagnetic Fields.
Personal digital assistant (PDA) cell phone units produce elevated extremely-low frequency
electromagnetic field emissions.
Biological effects of low frequency electromagnetic fields.
Exposure to extremely low frequency electromagnetic fields during pregnancy and the risk of
spontaneous abortion: a case-control study.
[Neurotic disturbances, depression and anxiety disorders in the population living in the vicinity
of overhead high-voltage transmission line 400 kV. Epidemiological pilot study].
The effect of extremely low frequency electromagnetic fields on pregnancy and fetal growth, and
development.
The Effects of Electromagnetic Field on the Endocrine System in Children and Adolescents.
EMF and current cancer concepts.
Attitudes about electric and magnetic fields: do scientists and other risk experts perceive risk
similarly?
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[Effects of extremely low frequency electromagnetic radiation on cardiovascular system of
workers].
Perception of health risks of electromagnetic fields by MRI radiographers and airport security
officers compared to the general Dutch working population: a cross sectional analysis.
[Electromagnetic poles and reproduction].
[Biophysical mechanisms of electromagnetic fields interaction and health effects].
Resveratrol may reverse the effects of long-term occupational exposure to electromagnetic fields
on workers of a power plant.
ELF noise fields: a review.
[The health risks of exposure to electromagnetic fields in work environments].
Scientific panel on electromagnetic field health risks: consensus points, recommendations, and
rationales.
Fundamental issues on electromagnetic fields (EMF).
Study of extremely low frequency electromagnetic fields in infant incubators.
Intensity-time dependence dosing criterion in the EMF exposure guidelines in Russia.
[Electromagnetic fields: their biological effects and regulation].
Can EMF exposure during development leave an imprint later in life?
Combined effects of electromagnetic fields on immune and nervous responses.
Effects of dietary green tea polyphenol supplementation on the health of workers exposed to
high-voltage power lines.
Effects of noise and electromagnetic fields on reproductive outcomes.
Health and safety implications of exposure to electromagnetic fields in the frequency range 300
Hz to 10 MHz.
The role of electromagnetic fields in neurological disorders.
Biophysical estimation of the environmental importance of electromagnetic fields.
[Biological effects of electromagnetic fields].
Effects of electromagnetic fields exposure on plasma hormonal and inflammatory pathway
biomarkers in male workers of a power plant.
The epidemiology of exposure to electromagnetic fields: an overview of the recent literature.
Microwave electromagnetic field regulates gene expression in T-lymphoblastoid leukemia
CCRF-CEM cell line exposed to 900 MHz.
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Effects of 60 Hz electromagnetic field exposure on APP695 transcription levels in differentiating
human neuroblastoma cells.
Ambiguous evidence and institutional interpretation: an alternative view of electric and magnetic
fields.
[Combined biological effect of electromagnetic fields and chemical substances (toxic)].
EMFs: cutting through the controversy.
The effect of chronic exposure to extremely low-frequency electromagnetic fields on sleep
quality, stress, depression and anxiety.
[Norms and standards for radiofrequency electromagnetic fields in Latin America: guidelines for
exposure limits and measurement protocols].
Health risk assessment of electromagnetic fields: a conflict between the precautionary principle
and environmental medicine methodology.
[Constant low-frequency electrical and electromagnetic fields (biological action and hygienic
evaluation)].
[Electrical field exposure and human health. Risk assessment and problems relative to
bureaucratic procedures and to the role of instituitional organizations in control and prevention].
Possible health effects of EMF.
Electromagnetic fields enhance chemically-induced hyperploidy in mammalian oocytes.
Electromagnetic field exposure assessment in Europe radiofrequency fields (10 MHz-6 GHz).
Exposure of the critically ill patient to extremely low-frequency electromagnetic fields in the
intensive care environment.
Biological effects of electromagnetic fields on vertebrates. A review.
Electromagnetic effects on people.
Time-dependent hematological changes in workers exposed to electromagnetic fields.
Characterisation of exposure to non-ionising electromagnetic fields in the Spanish INMA birth
cohort: study protocol.
Electromagnetic fields in neonatal incubators: the reasons for an alert.
[Electromagnetic fields and people's health].
Electromagnetic fields: mechanism, cell signaling, other bioprocesses, toxicity, radicals,
antioxidants and beneficial effects.
Project NEMESIS: perception of a 50 Hz electric and magnetic field at low intensities
(laboratory experiment).
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Non-ionising electromagnetic environments on manned spacecraft.
Health hazards and electromagnetic fields.
The design, construction and calibration of a carefully controlled source for exposure of
mammalian cells to extremely low-frequency electromagnetic fields.
[HEALTH STATUS OF ELECTROTECHNICAL PERSONNEL EXPOSED TO THE
COMBINED IMPACT OF ELECTROMAGNETIC FIELDS OF 50 HZ AND CHEMICALS].
EMF recommendations specific for children?
[Electromagnetic fields emitted in radio- and microwave- frequency range: equipment and
methods for the environment protection and survey measurements].
Health-Economics Analyses Applied to ELF Electric and Magnetic Fields.
Alterations in human EEG activity caused by extremely low frequency electromagnetic fields.
Adverse human reproductive outcomes and electromagnetic fields: a brief summary of the
epidemiologic literature.
Nonionizing electromagnetic fields and cancer: a review.
Recommended minimal requirements and development guidelines for exposure setups of bio-
experiments addressing the health risk concern of wireless communications.
Genetic damage in mammalian somatic cells exposed to extremely low frequency electro-
magnetic fields: a meta-analysis of data from 87 publications (1990-2007).
Health effects of low-level electromagnetic fields: phantom or not-so-phantom risk?
"Dirty electricity": what, where, and should we care?
Basic problems of diversely reported biological effects of radio frequency fields.
Investigation of the spinal cord as a natural receptor antenna for incident electromagnetic waves
and possible impact on the central nervous system.
Assessment of electromagnetic field levels from surrounding high-tension overhead power lines
for proposed land use.
Effects of electromagnetic fields on photophasic circulating melatonin levels in American
kestrels.
How dangerous are mobile phones, transmission masts, and electricity pylons?
Understanding the effects of electromagnetic field emissions from Marine Renewable Energy
Devices (MREDs) on the commercially important edible crab, Cancer pagurus (L.).
Actual and perceived exposure to electromagnetic fields and non-specific physical symptoms: an
epidemiological study based on self-reported data and electronic medical records.
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Is newborn melatonin production influenced by magnetic fields produced by incubators?
Does exposure to environmental radiofrequency electromagnetic fields cause cognitive and
behavioral effects in 10-year-old boys?
Cardiovascular diseases and the work environment. A critical review of the epidemiologic
literature on nonchemical factors.
Public health hazards from electricity-producing plants.
[Saccharomyces cerevisiae as a model organism for studying the carcinogenicity of non-ionizing
electromagnetic fields and radiation].
How to approach complex mixtures: lessons from the epidemiology of electromagnetic fields.
[The role of chemical and physical factors in cancer development].
[Possible outer hair cells hazards from occupational exposure to very low frequency electric and
magnetic fields: a pilot study].
Effects of electromagnetic fields on the reproductive success of American kestrels.
A 50-Hz electromagnetic field impairs sleep.
A structured literature review for risk assessment: EMF and human health risk.
Is MRI imaging in pediatric age totally safe? A critical reprisal.
Health effects of microwave exposures: a review of the recent (1995-1998) literature.
Epidemiological studies of human exposures to radiofrequency radiation. A critical review.
Human adverse reproductive outcomes and electromagnetic field exposures: review of
epidemiologic studies.
The infant incubator in the neonatal intensive care unit: unresolved issues and future
developments.
Biologic effects of low-level electromagnetic fields: current issues and controversies.
[Non-thermal electromagnetic fields and estimation of the convulsive syndrome probable
development].
[The precautionary principle: scientific evidence and decision processes].
Study of self-reported hypersensitivity to electromagnetic fields in California.
Occupational EMF exposure from radar at X and Ku frequency band and plasma catecholamine
levels.
Clustering of excess health concerns for electromagnetic fields among health personnel: A
quantitative and qualitative approach.
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Biological effects of environmental electromagnetic fields: molecular mechanisms.
[Biological effects of exposure to electromagnetic fields: introduction].
Effects of low-level radio-frequency (3kHz to 300GHz) energy on human cardiovascular,
reproductive, immune, and other systems: a review of the recent literature.
Human performance and physiology: a statistical power analysis of ELF electromagnetic field
research.
Psychological studies in nonionizing electromagnetic energy research.
Potential emotional and cognitive disorders associated with exposure to EMFs. A review.
Electric power plant emissions and public health.
Electromagnetic fields produced by incubators influence heart rate variability in newborns.
Study of human neurovegetative and hematologic effects of environmental low-frequency (50-
Hz) electromagnetic fields produced by transformers.
[The influence of occupational environment and professional factors on the risk of
cardiovascular disease].
Synergistic health effects between chemical pollutants and electromagnetic fields.
Effect of short-term 50 Hz electromagnetic field exposure on the behavior of rats.
Estimating air pollution and health loss embodied in electricity transfers: An inter-provincial
analysis in China.
Alternative functional relationships between ELF field exposure and possible health effects:
report on an expert workshop.
[Impact of electromagnetic fields on a computer user].
Mechanisms of electromagnetic interaction with cellular systems.
Opinion on potential health effects of exposure to electromagnetic fields.
Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes
and multiple sclerosis.
The "Moscow signal" epidemiological study, 40 years on.
Effects of EMF emissions from undersea electric cables on coral reef fish.
Exposure to electric power generator noise among small scale business operators in selected
communities in Ibadan, Nigeria.
Northern cardiometeopathies.
EMF-cancer link: the ferritin hypothesis.
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Effect of occupational EMF exposure from radar at two different frequency bands on plasma
melatonin and serotonin levels.
Dirty electricity, chronic stress, neurotransmitters and disease.
[The perceptibility of a microwave field under experimental conditions].
Women growing older with environmental sensitivities: A grounded theory model of meeting
one's needs.
A perspective on environmental health in the USSR: research and practice.
[Clinical variants of the disease caused by exposure to radio-frequency electromagnetic fields].
Work environment and cardiovascular diseases. A short review of the literature.
Noise, impulse noise, and other physical factors: combined effects on hearing.
[Characteristics of electromagnetic situation in Far North regions].
Fifty Hertz electromagnetic field exposure stimulates secretion of beta-amyloid peptide in
cultured human neuroglioma.
[Ethical values in the regulation of the exposure to electromagnetic fields].
[Ecological significance of electromagnetic fields: the 20th century--century of electricity, the
21st--century of magnetism].
[Video display terminals: their electromagnetic safety].
Male proportion in offspring of parents exposed to strong static and extremely low-frequency
electromagnetic fields in Norway.
Video display terminals: risk of electromagnetic radiation.
[The evaluation of the exposure of seamstresses to electromagnetic fields, emitted by sewing
machines].
Scientometric study of the effects of exposure to non-ionizing electromagnetic fields on fertility:
A contribution to understanding the reasons of partial failure.
[Influences of solar and geomagnetic activity on health status of people with various nosological
forms of diseases].
Earthing: health implications of reconnecting the human body to the Earth's surface electrons.
Prevalence of annoyance attributed to electrical equipment and smells in a Swedish population,
and relationship with subjective health and daily functioning.
Fetal loss associated with two seasonal sources of electromagnetic field exposure.
Use of kappa statistic in determining validity of quality filtering for meta-analysis: a case study
of the health effects of electromagnetic radiation.
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[Health risks from the use of NMR tomography and in vivo NMR spectroscopy].
Geomagnetics and society interact in weekly and broader multiseptans underlying health and
environmental integrity.
[Contribution of physical factors to the complex anthropogenic load in an industrial town].
Evidence that dirty electricity is causing the worldwide epidemics of obesity and diabetes.
Possible effects of electric blankets and heated waterbeds on fetal development.
Environmental variables and the risk of disease.
[The use of geographic information technologies in the sanitary control of an environmental
electromagnetic field].
[Personal computer: physical factors, effect on the user].
A low cost, re-usable electricity-free infant warmer: evaluation of safety, effectiveness and
feasibiliy.
Iatrogenic environmental hazards in the neonatal intensive care unit.
Space weather and human deaths distribution: 25 years' observation (Lithuania, 1989-2013).
Acute myocardial infarction (AMI) (n-11026) on days of zero geomagnetic activity (GMA) and
the following week: differences at months of maximal and minimal solar activity (SA) in solar
cycles 23 and 24.
Current strategies in the management of atrial fibrillation.
--Leaf Cluster 33 (91)
Theme - Health risks to workers in different occupations
Titles
[Levels of occupational exposure to extremely low frequency magnetic fields among workers in
different jobs].
[Occupational exposure to 50 Hz magnetic fields in workers employed in various jobs].
[Exposure to electromagnetic fields with frequencies of 50 Hz and changes in the circulatory
system in workers at electrical power stations].
Absenteeism and mortality of workers exposed to electromagnetic fields in the French Electricity
Company.
[Evaluation of selected parameters of circulatory system function in various occupational groups
exposed to high frequency electromagnetic fields. II. Electrocardiographic changes].
[Fitness of workers with particular sensitivity to non-ionizing radiation].
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Health of workers exposed to electric fields.
[Health protection of workers occupationally exposed to effects of electromagnetic fields in
Poland and in the European Union member states].
[Occupational exposure to electromagnetic fields of extremely low frequency (with particular
regard to power plants) and the health status of workers, based on a literature review].
A biomonitoring study of genotoxic risk to workers of transformers and distribution line stations.
[Health effects of occupational exposure to electromagnetic fields in view of studies performed
in Poland and abroad].
[Evaluation of the genotoxicity of the extremely low frequency-magnetic fields (ELF-MF) in
workers exposed for professional reasons].
[Evaluation of selected parameters of circulatory system function in various occupational groups
of workers exposed to high frequency electromagnetic fields].
[Health status of railway workers using magnetic powder flaw detectors].
[Health effects of occupational exposure to static magnetic fields used in magnetic resonance
imaging: a review].
Health problems among workers of iron welding machines: an effect of electromagnetic fields.
[Health and work ability of workers of the electricity sector in Sao Paulo].
[Hygienic assessment of working conditions and functional resistance in electric power station
workers].
Should the threshold limit value for power frequency (60 Hz) magnetic fields be changed?
Perceptions among scientists and other risk experts.
Prevalence of depression among electrical workers.
[Health status of the workers exposed to strong, constant magnetic fields].
[Observations of changes in neurobehavioral functions in workers exposed to high-frequency
radiation].
Occupational exposure to electromagnetic fields of uninterruptible power supply industry
workers.
Neurovegetative disturbances in workers exposed to 50 Hz electromagnetic fields.
[Possible consequence on measures for the protection of electromagnetic fields exposed
workers].
Extremely low frequency-magnetic fields (ELF-EMF) occupational exposure and natural killer
activity in peripheral blood lymphocytes.
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Evaluation of chromosomal alteration in electrical workers occupationally exposed to low
frequency of electro magnetic field (EMFs) in Coimbatore population, India.
Injuries among electric power industry workers, 1995-2013.
Health status of personnel occupationally exposed to radiowaves.
[Effect of exposure to extremely low-frequency electromagnetic fields on liver function of
workers].
[Evaluation of selected functional circulation parameters of workers from various occupational
groups exposed to electromagnetic fields of high frequency. III. 24-h monitoring of arterial blood
pressure (ABP)].
Depression in high voltage power line workers.
[A methodological approach to studying the values of 50-Hz electromagnetic fields that
influence the workers of power enterprises].
Guidance note: risk management of workers with medical electronic devices and metallic
implants in electromagnetic fields.
ECG changes in factory workers exposed to 27.2 MHz radiofrequency radiation.
Low-back pain among electric power supply workers and their attitude toward its prevention and
the treatment.
Exposure to high-frequency transient electromagnetic fields.
[Exposure to VHF and UHF electromagnetic fields among workers employed in radio and TV
broadcast centers. I. Assessment of exposure].
Heart rate variability (HRV) analysis in radio and TV broadcasting stations workers.
[Functional status of workers engaged in connecting high-voltage electric power lines].
[Offshore substation workers' exposure to harmful factors - Actions minimizing risk of hazards].
[Medical and biologic research of electromagnetic fields in radiofrequencies range. Results and
prospects].
[Health surveillance guidelines after the European directive on electromagnetic fields].
Monitoring of people and workers exposure to the electric, magnetic and electromagnetic fields
in an Italian National Cancer Institute.
[Risk of electromagnetic fields in electric power stations and substations of a petrochemical
plant].
An analysis of fatal and non-fatal injuries and injury severity factors among electric power
industry workers.
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[Hygienic optimization of the use of chemical protective means on railway transport].
[High-frequency electromagnetic field exposure on reproductive and endocrine functions of
female workers].
Assessment of levels of occupational exposure to workers in radiofrequency fields of two
television stations in Accra, Ghana.
[Evaluation of vital activity of workers with obliterating diseases of lower extremities servicing
electric transmission lines].
[Occupational health evaluation of electromagnetic fields in electric trains and subway
technologic areas].
[Reports on electromagnetic field strength measurements issued for occupational health and
safety needs in the opinion of radio communication station users].
Health problems among operators of plastic welding machines and exposure to radiofrequency
electromagnetic fields.
[Various psychological parameters in subjects occupationally exposed to radiofrequencies].
Ocular medical surveillance on microwave and laser workers.
Evaluation of non ionizing radiation around the dielectric heaters and sealers: a case report.
The psychosocial work environment and skin symptoms among visual display terminal workers:
a case referent study.
The strategy of targetted health surveillance. II. Genetically determined susceptibility to
chemical substances and other issues related to health surveillance.
[Screen dermatitis and visual display units].
[Occupational risks in grocery stores].
Health Effects of Electromagnetic Fields on Reproductive-Age Female Operators of Plastic
Welding Machines in Fuzhou, China.
Reproductive hazards among workers at high voltage substations.
[Evaluation of various psychologic parameters in a group of workers occupationally exposed to
radiofrequency].
Occupational influences on male fertility and sexuality. I.
[Radiation safety at atomic electric power stations].
[Effect of wide-band modulated electromagnetic fields on the workers of high-frequency
telephone exchanges].
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[Effect of ultra high frequency electromagnetic waves and lead on the workers' health;
phytotherapy of the disorders].
Biosomatic effects of the electromagnetic fields on view of the physiotherapy personnel health.
[On prevention of electromagnetic rays effects in workers exposed to extreme climate
conditions].
Microwave sickness: a reappraisal.
Building an index of activity of inhabitants from their activity on the residential electrical power
line.
Radiofrequency electromagnetic leakage fields from plastic welding machines. Measurements
and reducing measures.
Rate of change of frequency under line contingencies in high voltage electric power networks
with uncertainties.
Risk-management and risk-analysis-based decision tools for attacks on electric power.
Exposure from occupational versus other sources.
Occupational exposure of herbicide applicators to herbicides used along electric power
transmission line right-of-way.
[Clinical monitoring in areas of exposure to radiofrequency electromagnetic fields].
Electromagnetic noise superimposed on the electric power supply to electronic medical
equipment.
Cardiovascular risk in operators under radiofrequency electromagnetic radiation.
Occupational exposure to physical agents: the new Italian database for risk assessment and
control.
Erratic electricity supply (Dumsor) and anxiety disorders among university students in Ghana: a
cross sectional study.
[A survey on diabetes mellitus in the staff of electric power system in Baotou city].
Correction: The effects of electric power lines on the breeding ecology of greater sage-grouse.
[Risk of electromagnetic fields in control board and switchboard rooms at petrochemical plants].
Biomonitoring of 20 trace elements in blood and urine of occupationally exposed workers by
sector field inductively coupled plasma mass spectrometry.
Effects of atmospheric electricity on some substrates of disordered social behavior.
Electricity prices in Italy: Data registered during photovoltaic activity interval.
[Dermatitis in VDT operators: a review of the literature].
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Black sky: Exposing electricity as the Achilles' heel of resilience.
[Danger of electricity in the bathtub].
The role of microwave radiometry in carotid artery disease. Diagnostic and clinical prospective.
--Leaf Cluster 36 (84)
Theme - Precautionary measures to reduce potential EMF health risks
Titles
Workgroup report: base stations and wireless networks-radiofrequency (RF) exposures and
health consequences.
Recent advances in research on radiofrequency fields and health: 2004-2007.
Recent advances in research on radiofrequency fields and health: 2001-2003.
International and national expert group evaluations: biological/health effects of radiofrequency
fields.
Low-level exposure to radiofrequency electromagnetic fields: health effects and research needs.
Public responses to precautionary information from the Department of Health (UK) about
possible health risks from mobile phones.
Health risks of electromagnetic fields. Part II: Evaluation and assessment of radio frequency
radiation.
The precautionary principle and risk perception: experimental studies in the EMF area.
[Autoimmune processes after long-term low-level exposure to electromagnetic fields (the results
of an experiment). Part 1. Mobile communications and changes in electromagnetic conditions for
the population. Needs for additional substantiation of the existing hygienic standards].
[In the consumers' interest: precautionary principles for protection against electromagnetic
fields].
Exposure Knowledge and Perception of Wireless Communication Technologies.
Epidemiology of health effects of radiofrequency exposure.
World Health Organization, radiofrequency radiation and health - a hard nut to crack (Review).
Public perception of risk concerning celltowers and mobile phones.
Risks perception of electromagnetic fields in Taiwan: the influence of psychopathology and the
degree of sensitivity to electromagnetic fields.
The prevalence of symptoms attributed to electromagnetic field exposure: a cross-sectional
representative survey in Switzerland.
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The development of human exposure standards for radio-frequency fields.
Recent advances in research on radiofrequency fields and health.
Searching for the perfect wave: the effect of radiofrequency electromagnetic fields on cells.
[Mutagenic, carcinogenic and teratogenic effects induced by radiofrequency electromagnetic
field of mobile phone].
Cell phones and health concerns: impact of knowledge and voluntary precautionary
recommendations.
An international prospective cohort study of mobile phone users and health (Cosmos): design
considerations and enrolment.
Risk of brain tumors from wireless phone use.
Does precautionary information about electromagnetic fields trigger nocebo responses? An
experimental risk communication study.
Vehicle-mounted high-power microwave systems and health risk communication in a deployed
environment.
Mobile phone health risk policy in Germany: the role of the federal government and the Federal
Office for Radiation Protection.
Electromagnetic fields (EMF): do they play a role in children's environmental health (CEH)?
Improving Precautionary Communication in the EMF Field? Effects of Making Messages
Consistent and Explaining the Effectiveness of Precautions.
Discourse and policy making on consumer protection in the areas of mobile telecommunication
and tanning.
Source of funding and results of studies of health effects of mobile phone use: systematic review
of experimental studies.
Radiofrequency exposure from wireless LANs utilizing Wi-Fi technology.
Near-field radiofrequency electromagnetic exposure assessment.
Wi-Fi and health: review of current status of research.
[Mobile communication and health of population: estimation of danger, social and ethical
problems].
Improved classification of evidence for EMF health risks.
German wide cross sectional survey on health impacts of electromagnetic fields in the view of
general practitioners.
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Thermal and non-thermal health effects of low intensity non-ionizing radiation: An international
perspective.
Cell phone radiation: Evidence from ELF and RF studies supporting more inclusive risk
identification and assessment.
Assessment of cellular telephone and other radio frequency exposure for epidemiologic research.
Potential health risks due to telecommunications radiofrequency radiation exposures in Lagos
State Nigeria.
[Electromagnetic fields: damage to health due to the nocebo effect].
Radiofrequency exposure in the French general population: band, time, location and activity
variability.
Public health and the radio frequency radiation emitted by cellphone technology, smart meters
and WiFi.
[Fundamentally new electromagnetic pollution and the lack of adequate regulatory framework--
on the risk assessment (analysis of modern domestic and foreign data)].
[Application criteria of the precautionary principle].
Health response of two communities to military antennae in Cyprus.
Physicians appeals on the dangers of mobile communication--what is the evidence? Assessment
of public health data.
[Ionizing and non-ionizing radiation (comparative risk estimations)].
Radiofrequency exposure in young and old: different sensitivities in light of age-relevant natural
differences.
Drosophila oogenesis as a bio-marker responding to EMF sources.
Radiofrequency electromagnetic radiation exposure inside the metro tube infrastructure in
Warszawa.
Electromagnetic Fields, Pulsed Radiofrequency Radiation, and Epigenetics: How Wireless
Technologies May Affect Childhood Development.
Radiofrequency (RF) sickness in the Lilienfeld Study: an effect of modulated microwaves?
Neurological effects of radiofrequency radiation.
[French general practitioners and electromagnetic fields].
The (co-)production of public uncertainty: UK scientific advice on mobile phone health risks.
Procedure for assessment of general public exposure from WLAN in offices and in wireless
sensor network testbed.
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Exposure caused by wireless technologies used for short-range indoor communication in homes
and offices.
Scientific basis for the Soviet and Russian radiofrequency standards for the general public.
[Effects of electromagnetic radiation from cellular telephone handsets on symptoms of
neurasthenia].
Genetic, carcinogenic and teratogenic effects of radiofrequency fields.
Assessment of guidelines for limiting exposures to emf using methods of probabilistic risk
analysis.
General practitioners using complementary and alternative medicine differ from general
practitioners using conventional medicine in their view of the risks of electromagnetic fields: a
postal survey from Germany.
Risk perception, somatization, and self report of complaints related to electromagnetic fields--a
randomized survey study.
Exposure to radio frequency electromagnetic fields from wireless computer networks: duty
factors of Wi-Fi devices operating in schools.
[Effects of electromagnetic radiation from handsets of cellular telephone on neurobehavioral
function].
Measurement and mapping of the electromagnetic radiation in the urban environment.
A radio-frequency monitor for protection against overexposure from RF heaters.
Radiofrequency electromagnetic fields (300 Hz-300 GHz) summary of an advisory report.
Health Council of The Netherlands: Radiofrequency Radiation Committee.
Prevalence and psychiatric comorbidity of self-reported electromagnetic field sensitivity in
Taiwan: a population-based study.
WHO research agenda for radiofrequency fields.
Occupational safety: effects of workplace radiofrequencies on hearing function.
[Problems of harmonization of sanitary regulations of the electromagnetic fields of mobile radio
communication equipment].
[New methodic approach to hygienic evaluation of electromagnetic energy absorption in near-
field zone of irradiation source].
Long-term exposure to mobile communication radiation: an analysis of time-variability of
electric field level in GSM900 downlink channels.
IEEE Committee on Man and Radiation--COMAR technical information statement
radiofrequency safety and utility Smart Meters.
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[Hygienic regulation of electromagnetic radiation of 300-3000 MHz frequency range].
[Formation of electromagnetic load under urban conditions].
[The effect of a high-frequency electromagnetic field (2.45 GHz) on perceptual processes,
psychological performance and well-being].
Occupational exposure to ambient electromagnetic fields of technical operational personnel
working for a mobile telephone operator.
Involuntary human hand movements due to FM radio waves in a moving van.
[Best practices in prevention public health].
Effects of exposure to very high frequency radiofrequency radiation on six antenna engineers in
two separate incidents.
Increased mercury release from dental amalgam restorations after exposure to electromagnetic
fields as a potential hazard for hypersensitive people and pregnant women.
--Leaf Cluster 42 (122)
Theme
–
Regulatory protections against electromagnetic fields
Titles
[Proposal for magnetic/electromagnetic fields protection norms on national level].
Exposure of humans to electromagnetic fields. Standards and regulations.
[Limitations of occupational exposure to electromagnetic fields adopted by Polish law from the
perspectives of international documents with particular reference to fields of low and medium
frequencies].
[Patient exposure to electromagnetic fields in magnetic resonance scanners: a review].
International workshop on non-ionizing radiation protection in medicine.
[National and international standards for limiting exposure to electromagnetic fields].
An historical overview of the activities in the field of exposure and risk assessment of non-
ionizing radiation in Bulgaria.
[The problem of hygienic standardization of commercial electric and magnetic fields in Russia
and other countries].
[Polish guidelines of 2001 for maximum admissible intensities in high frequency EMF versus
European Union recommendations].
[Hazards of radio frequency magnetic field and their prevention and control].
[Measurement and study report as a part of the control system for human safety and health
protection against electromagnetic fields and electromagnetic radiation (0 Hz-300 GHz)].
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[Protection against electromagnetic fields 0-300 GHz in Poland. New regulations and
perspectives if their harmonization wit the European Union requirements].
[Biological effects and health risks of electromagnetic fields at levels classified by INCRIP ans
admissible among occupationally exposed workers: a study of the Nofer Institute of
Occupational Medicine, Lodz].
EU Directive, ICNIRP guidelines and Polish legislation on electromagnetic fields.
[Measurements of electromagnetic fields and evaluation of occupational exposure: PN-T-
06580:2002 requirements and principles adopted in the European Union].
[Hygienic assessment of sources of electromagnetic fields using revised and new standards of
maximum admissible intensities].
Assessment of physiotherapists' occupational exposure to radiofrequency electromagnetic fields
from shortwave and microwave diathermy devices: a literature review.
Occupational Electromagnetic Fields exposure in Magnetic Resonance Imaging systems -
Preliminary results for the RF harmonic content.
[ASSESSMENT OF OCCUPATIONAL EXPOSURE TO RADIO FREQUENCY
ELECTROMAGNETIC FIELDS].
[Recent concept of protection of workers and general population against electromagnetic fields
in the European countries].
[Improvement in the hygienic standards for radio-frequency electromagnetic fields in member
countries of the COMECON].
Application of EMF emission measurement techniques to wireless communications systems for
compliance with directive 2004/40/EC.
[Occupational exposure to electromagnetic fields in physiotherapy departments].
Non-ionising radiation human exposure assessment near telecommunication devices in Croatia.
Evaluation of the safety of users of active implantable medical devices (AIMD) in the working
environment in terms of exposure to electromagnetic fields - Practical approach to the
requirements of European Directive 2013/35/EU.
Effective Analysis of Human Exposure Conditions with Body-worn Dosimeters in the 2.4 GHz
Band.
Occupational exposure to electromagnetic fields. The situation in Greece.
European regulations of the radio spectrum, ISM use and safety.
Impact of electromagnetic field exposure limits in Europe: is the future of interventional MRI
safe?
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[Modern concepts and methodology of means, methods of protection, and safety measures for
servicemen affected by nonionizing radiation].
Biological effects of electromagnetic fields and recently updated safety guidelines for strong
static magnetic fields.
[Hygienic regulation of electromagnetic fields for the preservation of workers' health].
Occupational exposure to electromagnetic fields in physiotherapy departments.
[Exposure of nurses to electromagnetic fields].
An evaluation of safety guidelines to restrict exposure to stray radiofrequency radiation from
short-wave diathermy units.
[European Directive 2004/40/EC on workers' exposure to electromagnetic fields from MRI].
[HYGIENIC ASSESSMENT OF WORKING CONDITIONS OF EMPLOYEES OF
BROADCASTING CENTER].
[Contemporary state of hygienic regulation of electromagnetic fields and prospective
harmonizing with foreign standards].
[Basic science to evaluate efficiency of means protecting from electromagnetic fields].
An evaluation of radio frequency exposure from therapeutic diathermy equipment.
[Electrosmog as a health risk factor: sources of artificial electromagnetic fields, evaluation of
health risk, prevention methods].
Incorporation of epidemiological findings into radiation protection standards.
Inaccurate official assessment of radiofrequency safety by the Advisory Group on Non-ionising
Radiation.
[Numerical modeling of emf distribution around transmitters in view of the latest environmental
protection regulations].
[Electrosmog, cellular phones, sunbeds etc. -- adverse health effects from radiation? Health
aspects of non-ionizing radiation].
Health risks of exposure to non-ionizing radiation--myths or science-based evidence.
[Safety of use assessment in a radio-frequency medical device].
Electromagnetic field occupational exposure: non-thermal vs. thermal effects.
Exposure assessment of electromagnetic fields near electrosurgical units.
[Polish regulations on maximum admissible intensities for electric and magnetic frequencies of
60 Hz and the European Union recommendations for electrical power engineering].
Mechanisms of biological effects of radiofrequency electromagnetic fields: an overview.
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Monitoring Electromagnetic Radiation Emissions in Buildings and Developing Strategies for
Improved Indoor Environmental Quality.
Exposure to electromagnetic fields from laptop use of "laptop" computers.
[Hygienic evaluation of contemporary light sources].
Electromagnetic fields in offices.
[Criterial parameter of hygienic regulation for exposure to rarely repeated ultrashort
electromagnetic impulses].
[Criterion for the hygienic standardization of exposure to infrequent ultra-short electromagnetic
pulses].
[Environment protection against electromagnetic fields. Legal point of view].
The potential carcinogenic hazards of electromagnetic radiation: a review.
Microwave emissions from police radar.
Measurement of the environmental broadband electromagnetic waves in a mid-size European
city.
[The hygienic protective area of the Kaliakra Medium-Wave Radio Station].
[Optimization of methods for measurement and assessment of occupational exposure to
electromagnetic fields in physiotherapy (SW diathermy)].
The effects of ionizing radiation, microwaves, and ultrasound on the developing embryo: clinical
interpretations and applications of the data.
[Problems with implementation of Polish standards on admissible electromagnetic field levels by
the State Sanitary Inspectorate and of the measuring teams].
On the issues related to compliance of LF pulsed exposures with safety standards and guidelines.
[Dosimetry in setting practical hygienic standards for radio-wave irradiation].
[Levels of the electromagnetic field in the vicinity of therapeutic devices using radiofrequency
and microwaves].
[Novelties in hygienic evaluation of electromagnetic conditions on computerized workplaces].
Outdoor characterization of radio frequency electromagnetic fields in a Spanish birth cohort.
The effect of embryonic and fetal exposure to x-ray, microwaves, and ultrasound: counseling the
pregnant and nonpregnant patient about these risks.
Significant RF-EMF and thermal levels observed in a computational model of a person with a
tibial plate for grounded 40 MHz exposure.
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Analysis of exposure to electromagnetic fields in a healthcare environment: simulation and
experimental study.
[Health state and performance of operators in electric discharge facilities--sources of
electromagnetic impulses].
Trends in nonionizing electomagnetic radiation bioeffects research and related occupational
health aspects.
[Organization of monitoring of electromagnetic radiation in the urban environment].
[Effective methods of protection from technogenic electromagnetic irradiation and information-
wave diagnostic means].
[Assessment of the safety of toys with special reference to electromagnetic safety in view of
binding regulations: a pilot study].
Electrical stimulation vs thermal effects in a complex electromagnetic environment.
Exposure of radio officers to radio frequency radiation on Danish merchant ships.
The effects of embryonic and fetal exposure to x-ray, microwaves, and ultrasound.
Occupational exposure to non-ionizing radiation and an association with heart disease: an
exploratory study.
Radiofrequency/microwave protection guides.
Summary of measured radiofrequency electric and magnetic fields (10 kHz to 30 GHz) in the
general and work environment.
[Emission of electromagnetic radiation from selected computer monitors].
[Hygienic standardization of electromagnetic radiation from two-channel meteorological radar
stations].
[Hygienic evaluation of work conditions for shielded compartments staff].
[Evaluation of maximum permissible intensity of electromagnetic fields].
The Possibility of Decreasing 50-Hz Electric Field Exposure near 400-kV Power Lines with Arc
Flash Personal Protective Equipment.
Damage criteria for determining microwave exposure.
Variability in electromagnetic field levels over time, and Monte-Carlo simulation of exposure
parameters.
A survey of the potential impact of the European Union Physical Agents Directive (EU PAD) on
electromagnetic fields (EMF) on MRI research practice in the United Kingdom.
Safety protocols for interventional MRI.
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The spatial statistics formalism applied to mapping electromagnetic radiation in urban areas.
Continuous electromagnetic radiation monitoring in the environment: analysis of the results in
Greece.
Occupational health effects of nonionizing radiation.
Can exposure to electromagnetic radiation in diathermy operators be estimated from interview
data? A pilot study.
[Protection of personnel exposed to very high frequency electromagnetic fields (author's transl)].
[A hygienic assessment of the work of students on Macintosh computers].
Dangerous-electricity annunciator and detector.
Assessment of human body influence on exposure measurements of electric field in indoor
enclosures.
Perspectives on setting limits for RF contact currents: a commentary.
[In vitro and in vivo studies of the "VITA" device].
An investigation into the effectiveness of ELF protective clothing when exposed to RF fields
between 65 MHz and 3 GHz.
In situ LTE exposure of the general public: Characterization and extrapolation.
Science and standards. RF-hazards and standards: an historical perspective.
[The current problems of electromagnetic safety in computer classes].
Ultrashort electromagnetic signals: biophysical questions, safety issues, and medical
opportunities.
[Possible consequences of urban pollution caused by radio frequency].
[The health problems of computer operators].
Exposure to radio-frequency radiation from an aircraft radar unit.
[Occupational assessment of computer placement in school areas].
A novel apparatus for non-contact measurement of heart rate variability: a system to prevent
secondary exposure of medical personnel to toxic materials under biochemical hazard conditions,
in monitoring sepsis or in predicting multiple organ dysfunction syndrome.
Biological effects and mechanisms of shortwave radiation: a review.
[Experience of the development special medical technical laboratory for studies of effects caused
by potent electromagnetic radiation in biologic objects].
The electromagnetic spectrum: current and future applications in oncology.
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A cross-sectional study of the temporal evolution of electricity consumption of six commercial
buildings.
[Strategies in approaches to requirements in the control of electromagnetic irradiation levels].
20:60:20--differences in energy behaviour and conservation between and within households with
electricity monitors.
Parametric and non-parametric convergence analysis of electricity intensity in developed and
developing countries.
[Shielding of the geomagnetic field in apartment houses].
Monochromatic electromagnetic wavelets and the huygens principle.
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Appendix 5
–
Potential Impact of Wireless Radiation Exposure on the Opioid Crisis and
Coronavirus Pandemic
A5-A. Potential Impact on Opioid Crisis
The previous findings of wireless radiation adverse effects reported in Chapter 2 of this
monograph are based on
hard evidence
and have been
validated
in numerous studies. The
present section on the link of wireless radiation to the opioid crisis is based on
hard evidence
as
well, but the link of wireless radiation to the opioid crisis is
not as far along in the validation
process.
It should be viewed as a hypothesis at this point, and serve as a basis for discussion and
further research.
The opioid crisis (drug dependence and overdosing) has become of increasing concern
since the 1990s (coincidentally, when mobile networking technology was being introduced on a
larger scale). This appendix addresses potential relationships between wireless radiation and
increasing dependence on drugs.
“Over the past two decades, the United States has experienced a growing crisis of
substance abuse and addiction that is illustrated most starkly by the rise in deaths from drug
overdoses. Since 2000, the annual number of drug overdose deaths has quadrupled from 17,500
to 70,000 in 2017…..Most of these deaths involved opioids, including heroin, prescription
painkillers, and
synthetic opioids such as fentanyl.” [Planalp, Hest, Lahr, 2019].
According to the US Department of Health and Human Services [HHS, 2019], 47,600
people died from overdosing on opioids in 2018, 10.3 million people misused prescription
opioids in 2018, and 2 million people had an opioid misuse disorder in 2018. While there can be
myriad contributing factors to such a widespread disorder, wireless radiation exposure (which
increased dramatically over the same period that drug overdose deaths increased dramatically)
may be a significant contributing factor. The reasons follow.
An analogy to climate change would be helpful in framing the perspective. The
contribution of fossil fuel combustion to anthropogenic (man-made) climate change is
conceptually
similar to the contribution of wireless radiation to opioid overuse. The climate
change analogy will be presented initially, since it crystallizes the nature of the causative effect.
It will then be followed by the analogous details of the wireless radiation link.
The main contributing factor to anthropogenic climate change is the combustion of fossil
fuels. The combustion process produces two major products relevant to climate change: carbon
dioxide (CO2) and fossil sulphates/nitrates [Dutton, 2019].
CO2 from fossil fuel combustion percolates to the upper atmosphere and remains there
for decades. It is transparent to the high frequency solar radiation and is partially absorbent of
the lower frequency radiation returning from the Earth, thereby trapping some of the incoming
solar energy in the atmosphere (and especially the ocean).
Decades are required for the Earth’s
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global mean surface temperature to come into equilibrium with the levels of CO2 in the
atmosphere.
The fossil sulphates and nitrates rise in the atmosphere, form small particles called
aerosols, remain there for very short periods of time (days or weeks), then precipitate to Earth.
They increase the effective albedo of the atmosphere (the albedo is a measure of the
reflectiveness of the Earth’s atmosphere to the incoming solar
radiation), and this partial
mirroring effect reduces the level of
solar flux reaching the Earth’s surface.
Thus, from the perspective of climate change, there is 1) an apparent
positive short-
term
effect from the aerosol shielding of the solar radiation, and 2) a
negative long-term
effect
from the energy trapping of the CO2.
The positive short-term effect is masking the harmful
effects of the negative long-term effect!
What is the analogy of the climate change phenomena described above to the impact of
wireless radiation on the opioid crisis? Consider the endogenous opioid system. This innate
pain-relieving
system “consists of widely scattered neurons that produce three opioids: beta-
endorphin, the met- and leu-enkephalins, and the dynorphins. These opioids act as
neurotransmitters and neuromodulators at three major classes of receptors, termed mu, delta, and
kappa, and produce analgesia” and other effects [Holden
et al, 2005].
It has been shown many times that one impact of wireless radiation (at myriad
frequencies) is release of endogenous opioids [e.g., Radzievsky et al, 2008; Lai et al, 1983]. This
release of endogenous opioids can enable analgesic effects by itself [Wu et al, 2012], or can
enhance the analgesic effects of exogenous analgesics [Emilie et al, 2012; Thomas et al, 1979].
This has been demonstrated at pulsed millimeter-wave frequencies [Miryutova et al, 2001;
Radzievsky et al, 2008; Hura et al, 2011], WiFi frequencies [Maillefer and Quock, 1992 ],
mobile phone frequencies [Bodera et al, 2019], radiofrequencies [Foley-Nolan, 1992], and
extremely low frequencies [Ozdemir et al, 2017; Demirkazik et al, 2019]. Additionally, as has
been demonstrated by the results of the current monograph, wireless radiation at all the above
frequencies has resulted in serious mid-term and especially long-term adverse health effects.
Therefore, analogous to the climate change example, wireless radiation exposure,
especially at cell phone, WiFi, and millimeter-wave pulsed and modulated frequencies, generates
1) analgesic and pleasurable short-term effects and 2) serious adverse mid- and long-term
effects.
There would be some exceptions for the short-term, such as electrohypersensitivity
(EHS) sufferers, who are immediately affected adversely by wireless radiation exposure.
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For most people, the enhanced analgesic short-term effects of the wireless radiation
would in effect mask the long-term damage from this radiation, analogous to the short-term
positive effects from the aerosols masking the long-term negative effects from the CO2 in
the climate change example.
Consider the following cases. In the first case, a person with ordinary pains and aches
starts using a cell phone or WiFi system. There will be an almost immediate feeling of less pain
and pleasurable sensations, similar to that experienced after a modest period of exercise (another
stimulant of endogenous opioids) [Boecker et al, 2008]. This feeling can last for a short to
intermediate length of time, after which another bout of stimulation is required to release further
endogenous opioids. The cell phone/WiFi user will get conditioned to associating the immediate
positive feelings with the wireless radiation-emitting devices. As time proceeds, the latent
longer-term adverse effects of the wireless radiation will result in various levels of increasing
discomfort and unpleasant symptoms, if not outright diseases. The immediate analgesic effects
from the wireless devices will become even more important, but may be insufficient to overcome
the increased levels of discomfort due to prolonged wireless radiation exposure. The individual
will then be forced to use 1) exogenous opioids and narcotics and 2) wireless radiation devices to
help attenuate the increasing feelings of discomfort, leading to possible addiction.
In the second case, a person with serious pain-producing disease or injury starts using a
cell phone or WiFi system. This person has already been prescribed pain-killers of various
types. Research has shown that wireless radiation of selected frequency characteristics in the
parameter ranges discussed above not only exhibits an enhanced analgesic effect in its own right,
but can enhance further the analgesic effects of exogenous analgesics [Emilie et al, 2012;
Thomas et al, 1979]. Again, this person will become conditioned to the short-term analgesic and
analgesic-enhancing effects of the wireless radiation devices. And, again, the increasing levels
of discomfort eventually produced by prolonged wireless radiation exposure (augmented in
many cases by adverse long-term effects of prolonged analgesics (
https://www.painedu.org/pain-
medications-long-term/
) will increase the need for 1) further wireless radiation exposure and 2)
additional exogenous analgesics. This positive feedback mechanism will lead to
two forms of
addiction:
exogenous pain-killers and wireless radiation.
Finally, consider the following. Alcohol has been shown to have analgesic effects
[Thompson et al, 2017]. In Lai’s experiments involving microwave irradiation and consumption
of a mixture containing ethanol, microwave irradiation enhanced consumption of ethanol by
about 25% [Lai et al, 1984]. As Lai pointed out, microwave irradiation may stress the rats, and
consumption of ethanol may serve to reduce stress. So, the microwave irradiation triggers the
release of endogenous opioids, producing a calming/analgesic effect, and at the same time
increases stress or other adverse symptoms, driving the rodents to seek analgesia from an
external source.
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The above examples focus on positive short-term analgesic effects from wireless
radiation followed by negative long-term addictive effects. There is no reason to believe this
short-term long-term dichotomy is limited to analgesic effects. Wireless radiation
short-term
performance enhancements
of many types accompanied by
long-term detrimental effects
cannot be ruled out (witness such effects for anabolic steroids on the performance of athletes in
myriad sports [Vorona and Niesshlag, 2018], where short-term athletic performance is enhanced,
with long-term adverse health consequences).
While the non-wireless radiation determinants of the opioid crisis should not be
downplayed, a credible component of the opioid crisis may be the downward spiral of the self-re-
enforcing positive feedback mechanisms generated by the wireless radiation. While there are
obviously cultural influences, peer-presssure influences, over-prescribing of medications, etc, the
pain and discomfort induced by the wireless radiation exposure may directly impact increased
use of wireless radiation devices.
There is some overlap between the opioid crisis and the increased suicide crisis in the
USA relative to wireless radiation exposure [Cheatle, 2011, 2016; Racine et al, 2017]. There are
the same reasons existing for an increase in discomfort due to wireless radiation exposure, and
the increase in suicide-related opioid abuse from wireless radiation, but the suicide crisis will not
be addressed further in the current monograph.
A5-B. Potential Impact on Coronavirus Pandemic
The previous findings of wireless radiation adverse effects reported in Chapter 2 of this
monograph are based on
hard evidence
and have been
validated
in numerous studies. The
present section linking wireless radiation to exacerbation of the coronavirus pandemic is based
on
hard evidence
as well, but the link of wireless radiation to exacerbation of the coronavirus
pandemic is
not as far along in the validation process.
It should be viewed as a hypothesis at
this point, and serve as a basis for discussion and further research.
The fundamental hypothesis in this section is that wireless radiation weakens the immune
system, and a weakened immune system increases the chances that exposure to the
coronavirus (or any virus) will translate into symptoms/disease.
Almost a decade ago, I published a paper on potential treatments for SARS [Kostoff,
2011], the China-based pandemic of 2002-2003 that was associated with another coronavirus.
As in the present China-based coronavirus pandemic, the SARS zoonotic virus/disease was
thought to originate with infected bats. These bats then infected other species, which were then
sold in open-air markets, and eventually infected their buyers.
Approximately 8,000 people globally presented with SARS symptoms, and
approximately 10% of those who presented died. However, those who succumbed were not a
random ten percent. Most had many co-morbidities, and it appeared their immune systems could
not handle yet another insult.
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The SARS pandemic was not ended with drugs or vaccines. None of these measures
worked. Instead, quarantine and good hygiene contributed most to ending the pandemic.
After the pandemic ended, a number of physicians (especially in Asia) reviewed the
records of all patients they had examined for various health issues (or standard annual physical
examinations) during the pandemic, and concentrated especially on the blood test results. There
were many cases where the coronavirus antibodies had shown up in the blood tests,
but the
patient had exhibited none of the SARS symptoms.
In other words, the patient's adaptive immune system was sufficiently strong to operate
properly and neutralize the coronavirus to which the patient had been exposed!
To me, that was the key finding, and contributed to the approach I have taken for
developing protocols to reverse chronic diseases [e.g., Kostoff, Porter, and Buchtel, 2018].
There are on the order of 300,000 viruses, many/most of which have zoonotic potential.
To develop vaccines for all of these viruses (before an epidemic or pandemic strikes) is
unreasonable (based on present technology) because of the sheer numbers involved. To develop
vaccines for any specific virus
during
an epidemic or pandemic (which was the mainstream
approach taken for the coronavirus during the SARS pandemic of 2002-2003) is completely
unrealistic, because of the lead times required for vaccine development, efficacy testing,
credible
mid-and long-term safety testing, and implementation.
Those who succumbed during the SARS pandemic had 1) myriad co-morbidities and 2)
weakened immune systems unable to neutralize the SARS coronavirus. Having a strong immune
system that allowed a smooth transition from innate immune system operation to adaptive
immune system operation
was the one intrinsic defense that worked!
The SARS experience
showed that the best and most realistic approach for defense against any potential viral attack is
reversing immune-degrading lifestyles well before any pandemic or epidemic outbreaks. In that
case, the immune system would be sufficiently strong to be able to handle viral exposure on its
own without the emergence of serious symptoms, as was the case with those exposed to the
SARS coronavirus (with coronavirus antibodies in their serum) who exhibited no (or minimal)
symptoms.
This gets to the link between wireless radiation exposure and the latest coronavirus
pandemic. Wireless radiation adversely affects the immune system (see boxed references at end
of this section). To the degree that non-ionizing radiation exposure (superimposed on the myriad
toxic stimuli to which many people are exposed by choice or imposition) degrades the operation
of the innate and adaptive immune systems, it would increase the likelihood that the immune
system could not counteract the exposure to the coronavirus (or any other virus) as nature
intended. Thus,
wireless radiation would contribute to the exacerbation of adverse effects from
coronavirus exposure.
The bottom line is that exposures to essentially ALL the exogenous
immune-damaging toxic stimuli (including, but not limited to, wireless radiation) need to be
removed before resistance to viruses of any type can be improved substantially.
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ADVERSE IMPACT OF WIRELESS RADIATION ON IMMUNE SYSTEM-
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Korenstein-Ilan A, Barbul A, Hasin P, Eliran A, Gover A, Korenstein R. Terahertz radiation
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Lasalvia M, Scrima R, Perna G, Piccoli C, Capitanio N, Biagi PF, et al. Correction: Exposure
to 1.8 GHz electromagnetic fields affects morphology, DNA-related Raman spectra and
mitochondrial functions in human lympho-monocytes. PloS one. 2018;13(6):e0198892.
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Li Y-z, Chen S-h, Zhao K-f, Gui Y, Fang S-x, Xu Y, et al. Effects of electromagnetic
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Lopez-Furelos A, Salas-Sanchez AA, Ares-Pena FJ, Leiro-Vidal JM, Lopez-Martin E.
Exposure to radiation from single or combined radio frequencies provokes macrophage
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Lushnikov KV, Gapeev AB, Sadovnikov VB, Cheremis NK. Effect of extremely high
frequency electromagnetic radiation of low intensity on parameters of humoral immunity in
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Maes A, Collier M, Slaets D, Verschaeve L. 954 MHz microwaves enhance the mutagenic
properties of mitomycin C. Environmental and molecular mutagenesis. 1996;28(1):26-30.
Mazor R, Korenstein-Ilan A, Barbul A, Eshet Y, Shahadi A, Jerby E, et al. Increased levels of
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Pershin SB, Frenkel ID, Kuz'min SN, Ponomarev IT, Galenchik AI. Immunosuppressive
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wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese
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Zhang D-y, Xu Z-p, Chiang H, Lu D-q, Zeng Q-l. Effects of GSM 1800 MHz radiofrequency
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Zhang M-B, He J-L, Jin L-F, Lu D-Q. Study of low-intensity 2450-MHz microwave exposure
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Appendix 6
–
Funding Source Bias on Research Outcomes
Upton Sinclair, noted muckracker and one-time candidate for Governor of California,
once stated:
“It is difficult to get a man to understand something, when his salary depends upon
his not understanding it!” (
https://www.brainyquote.com/quotes/upton_sinclair_138285
). In a
nutshell, this crystallizes the central problem of integrity and credibility of the biomedical
literature, especially for topics of commercial, military, and political sensitivity.
There have been many studies addressing how researcher and institutional conflicts-of-
interest relate to their published findings. The following article titles reflect only the tip of the
iceberg of biased outcomes related to funding sources. Since research manipulations to achieve
a predetermined agenda tend not to be advertised (e.g., see section 3.2.2 of Kostoff [2016]), what
eventually sees the light of day is truly the very small tip of a very large iceberg. In these
sensitive topical areas,
bias may in fact be closer to the norm than to the exception!
Titles of Sample Records
(to obtain Abstracts, insert titles into Pubmed, or similar search engines, if available)
A matter of influence: graduate medical education and commercial sponsorship. The New
England journal of medicine. 1988;318(1):52-4.
AAMC Task Force issues first Financial Conflict of Interest Guidelines, and GAO urges HHS to
reexamine financial conflict of interest guidance and regulations for NIH-funded research.
Association of American Medical Colleges. U.S. General Accounting Office. Department of
Health and Human Services. Journal of investigative medicine : the official publication of the
American Federation for Clinical Research. 2002;50(2):82-3.
AAMC Task Force releases recommendations on institutional conflicts of interest. Journal of
investigative medicine: the official publication of the American Federation for Clinical Research.
2002;50(6):389-90.
Aaron DG, Siegel MB. Sponsorship of National Health Organizations by Two Major Soda
Companies. American journal of preventive medicine. 2017;52(1):20-30.
Abaid LN, Grimes DA, Schulz KF. Reducing publication bias of prospective clinical trials
through trial registration. Contraception. 2007;76(5):339-41.
Abaid LN, Grimes DA, Schulz KF. Reducing publication bias through trial registration.
Obstetrics and gynecology. 2007;109(6):1434-7.
Abbas EE. Industry-sponsored research in developing countries. Contemporary clinical trials.
2007;28(6):677-83.
Abbas M, Pires D, Peters A, Morel CM, Hurst S, Holmes A, et al. Conflicts of interest in
infection prevention and control research: no smoke without fire. A narrative review. Intensive
Care Medicine. 2018;44(10):1679-90.
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Abdel-Sattar M, Krauth D, Anglemyer A, Bero L. The Relationship between Risk of Bias
Criteria, Research Outcomes, and Study Sponsorship in a Cohort of Preclinical
Thiazolidinedione Animal Studies: A Meta-Analysis. Evidence-based preclinical medicine.
2014;1(1):11-20.
Abdoul H, Perrey C, Tubach F, Amiel P, Durand-Zaleski I, Alberti C. Non-financial conflicts of
interest in academic grant evaluation: a qualitative study of multiple stakeholders in France. PloS
one. 2012;7(4):e35247.
Abou-Setta AM, Rabbani R, Lix LM, Turgeon AF, Houston BL, Fergusson DA, et al. Can
authorship bias be detected in meta-analysis? Canadian Journal of Anesthesia-Journal Canadien
D Anesthesie. 2019;66(3):287-92.
Abraham A, Ahn R, Woodbridge A, Madden E, Keyhani S, Korenstein D. What Constitutes an
Independent Statistical Analysis? Journal of General Internal Medicine. 2018;33(6):786-8.
Abraham J. On the prohibition of conflicts of interest in pharmaceutical regulation:
precautionary limits and permissive challenges. A commentary on Sismondo (66:9, 2008, 1909-
14) and O'Donovan and Lexchin. Social science & medicine (1982). 2010;70(5):648-51.
Abrams P. Editorial comment: Re: Brubaker L. Conflict of interest: what is the role of our
professional societies? Neurourol Urodyn 2012;31:1217-1218. Neurourology and urodynamics.
2012;31(8):1219-20.
Abrams P. Letter to the editor: conflicts of interest. Neurourology and urodynamics.
2008;27(4):359; discussion
Abramson J, Redberg R. Conflicts of Interest. The New England journal of medicine.
2015;373(8):778.
Abramson J, Starfield B. The effect of conflict of interest on biomedical research and clinical
practice guidelines: can we trust the evidence in evidence-based medicine? The Journal of the
American Board of Family Practice. 2005;18(5):414-8.
Abratt RP. Who will guard the guards? Medical leadership and conflict of interest in South
African healthcare. South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde.
2016;106(2):129.
Acar F, Seurinck R, Eickhoff SB, Moerkerke B. Assessing robustness against potential
publication bias in Activation Likelihood Estimation (ALE) meta-analyses for fMRI. PloS one.
2018;13(11):e0208177.
Achkar E, Richter JE, Talley NJ. American Journal of Gastroenterology conflict of interest
policy. The American journal of gastroenterology. 2008;103(2):260-1.
Achkar E, Richter JE, Talley NJ. Conflict of interest policy of the American Journal of
Gastroenterology: new and improved. The American journal of gastroenterology.
2008;103(2):259.
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Achkar E. Conflict of interest policy for medical journals: just a first step. The American journal
of gastroenterology. 2007;102(6):1145.
Ackerman AB. Reviewer conflicts of interest should be disclosed. Journal of the American
Academy of Dermatology. 2005;52(3 Pt 1):538; author reply ; discussion -9.
Acquavella J. Conflict of interest: a hazard for epidemiology. Annals of Epidemiology.
2019;34:8-11.
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Pediatric dentistry. 2006;28(4):309.
Adamczyk A. Extracurricular activities and teens' alcohol use: The role of religious and secular
sponsorship. Social science research. 2012;41(2):412-24.
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Gynecology. Journal of pediatric and adolescent gynecology. 2019;32(1):1-2.
Adashi EY. Conflict of Interest in Medicine: Plausible Deniability? The American journal of
bioethics : AJOB. 2017;17(6):30-1.
Addeo A, Weiss GJ, Gyawali B. Association of Industry and Academic Sponsorship With
Negative Phase 3 Oncology Trials and Reported Outcomes on Participant Survival: A Pooled
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Adibi S, Abidi S, Bebermeyer RD. Conflicts of interest in research: is clinical decision-making
compromised? An opinion paper. Texas dental journal. 2010;127(8):735-41.
Adler G. Does financing researchers and research at university clinics entail a conflict of
interests and dependence? Zeitschrift fur Gastroenterologie. 1999;Suppl 2:28-32.
Agema WRP, Jukema JW, Zwinderman AH, van der Wall EE. A meta-analysis of the
angiotensin-converting enzyme gene polymorphism and restenosis after percutaneous
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2002;144(5):760-8.
Agich GJ, Forster H. Conflicts of interest and management in managed care. Cambridge
quarterly of healthcare ethics : CQ : the international journal of healthcare ethics committees.
2000;9(2):189-204.
Agoritsas T, Neumann I, Mendoza C, Guyatt GH. Guideline conflict of interest management and
methodology heavily impacts on the strength of recommendations: comparison between two
iterations of the American College of Chest Physicians Antithrombotic Guidelines. Journal of
clinical epidemiology. 2017;81:141-3.
Agra Tunas C, Rujido Freire S, Rodriguez Nunez A. How do residents and medical students
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Agrawal D, Haque W. Transparent Disclosure of Conflicts of Interest. Jama. 2019;321(17):1728.
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Agrawal S. Pharmaceutical industry and sponsorship of delegates for national conferences.
Indian pediatrics. 2002;39(5):445-8.
Aguilar A. Editors of biomedical journals and the disclosure of their own conflicts of interest.
Archivos argentinos de pediatria. 2018;116(1):3-4.
Aguilar KM, Hou Q, Miller RM. Impact of Employer-Sponsored Onsite Pharmacy and
Condition Management Programs on Medication Adherence. Journal of managed care &
specialty pharmacy. 2015;21(8):670-7.
Aguilar-Salinas CA, Pascual-Ramos V, Sierra-Madero JG, Loria-Acereto A, Zambrano-
Gonzalez E, Kaufer-Horwitz M, et al. III. THE ROLE OF THE RESEARCH ETHICS
COMMITTEES IN THE REGULATION OF PHARMA-SPONSORED STUDIES. Revista de
investigacion clinica; organo del Hospital de Enfermedades de la Nutricion. 2019;71(5):297-305.
Ahlawat A, Narayanaswami P. Financial relationships between neurologists and industry The
2015 Open Payments database. Neurology. 2018;90(23):1063-70.
Ahlawat A, Narayanaswami P. Financial relationships between neurologists and industry The
2015 Open Payments database. Neurology. 2019;92(21):1006-13.
Ahmadi Nasab Emran S. An intellectual virtue "vaccination" for physician-pharmaceutical
industry interactions. Academic medicine : journal of the Association of American Medical
Colleges. 2015;90(1):30-2.
Ahmed AA, Holliday EB, Fakhreddine M, Yoo SK, Deville C, Jagsi R. Trends in Disclosures of
Industry Sponsorship. International Journal of Radiation Oncology Biology Physics.
2016;95(4):1093-101.
Ahmed AA, Holliday EB, Fakhreddine M, Yoo SK, Deville C, Jagsi R. Trends in Disclosures of
Industry Sponsorship. International journal of radiation oncology, biology, physics.
2016;95(4):1093-101.
Ahmed AA, Yoo SK, Mehta S, Holliday EB, Deville C, Vapiwala N, et al. Meaningful and
Accurate Disclosure of Conflict of Interest at the ASTRO National Meeting: A Need for
Reassessment of Current Policies. Journal of oncology practice. 2018:JOP1800121.
Ahmed AA, Yoo SK, Mehta S, Holliday EB, Deville C, Vapiwala N, et al. Meaningful and
Accurate Disclosure of Conflict of Interest at the ASTRO National Meeting: A Need for
Reassessment of Current Policies. Journal of Oncology Practice. 2018;14(11):687-+.
Ahmed I, Sutton AJ, Riley RD. Assessment of publication bias, selection bias, and unavailable
data in meta-analyses using individual participant data: a database survey. BMJ (Clinical
research ed). 2012;344:d7762.
Ahmer S, Arya P, Anderson D, Faruqui R. Conflict of interest in psychiatry. Psychiatric Bulletin.
2005;29(8):302-4.
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Ahn R, Woodbridge A, Abraham A, Saba S, Korenstein D, Madden E, et al. Financial ties of
principal investigators and randomized controlled trial outcomes: cross sectional study. BMJ
(Clinical research ed). 2017;356:i6770.
Ahn R, Woodbridge A, Abraham A, Saba S, Korenstein D, Madden E, et al. Financial ties of
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Aimah E. Tobacco sponsorship is not inevitable. Promotion & education. 2005;Suppl 4:34.
Aitken DG. WHO handling of conflicts of interest. International journal of occupational and
environmental health. 2003;9(1):91; author reply 2.
Akabayashi A, Slingsby BT, Takimoto Y. Conflict of interest: a Japanese perspective.
Cambridge quarterly of healthcare ethics : CQ : the international journal of healthcare ethics
committees. 2005;14(3):277-80.
Akl EA, El-Hachem P, Abou-Haidar H, Neumann I, Schunemann HJ, Guyatt GH. Considering
intellectual, in addition to financial, conflicts of interest proved important in a clinical practice
guideline: a descriptive study. Journal of clinical epidemiology. 2014;67(11):1222-8.
Akl EA, Karl R, Guyatt GH. Methodologists and context experts disagreed regarding managing
conflicts of interest of clinical practice guidelines panels. Journal of clinical epidemiology.
2012;65(7):734-9.
Akpinar I, Ohinmaa A, Thording L, Tran DT, Fedorak RN, Richer L, et al. The Costs of
Industry-Sponsored Medical Device Clinical Trials in Alberta. PharmacoEconomics - open.
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Alasbali T, Smith M, Geffen N, Trope GE, Flanagan JG, Jin YP, et al. Discrepancy between
Results and Abstract Conclusions in Industry- vs Nonindustry-funded Studies Comparing
Topical Prostaglandins. American Journal of Ophthalmology. 2009;147(1):33-8.
Al-Badriyeh D, Alameri M, Al-Okka R. Cost-effectiveness research in cancer therapy: a
systematic review of literature trends, methods and the influence of funding. Bmj Open.
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Albersheim SG, Golan A. The Physician's Relationship with the Pharmaceutical Industry: Caveat
Emptor ... Buyer Beware! Israel Medical Association Journal. 2011;13(7):389-93.
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emptor...buyer beware! The Israel Medical Association journal : IMAJ. 2011;13(7):389-93.
Albert HB. Answer to the Letter to the Editor of Benjamin John Floyd Dean et al. entitled "No
conflict of interest?" concerning "Antibiotic treatment in patients with chronic low back pain and
vertebral bone edema (Modic type 1 changes): a double-blind randomized controlled trial of
efficacy" by Albert HB et al., Eur Spine J (2013) 22:697-707. European spine journal : official
publication of the European Spine Society, the European Spinal Deformity Society, and the
European Section of the Cervical Spine Research Society. 2013;22(8):1701.
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Albert SM, Kim S. Are we doing enough to manage financial conflicts of interest? Neurology.
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Aldairy Y, Nguyen PL, Jatoi A. Bone pain from granulocyte colony stimulating factor: does
clinical trial sponsorship by a pharmaceutical company influence its reporting? European journal
of cancer care. 2011;20(1):72-6.
Aleksandrova OA, Komolova OA. The conflict of interests and organizational structures in
conditions of health care commercialization. Problemy sotsial'noi gigieny, zdravookhraneniia i
istorii meditsiny. 2019;27(4):384-8.
Alexander GC. Seeding Trials and the Subordination of Science. Archives of Internal Medicine.
2011;171(12):1107-8.
Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of Interest
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Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of interest
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Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of interest
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Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of interest
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Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of interest
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Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of Interest
Policies and Disclosure Requirements Among European Society of Cardiology National
Cardiovascular Journals. Hellenic Journal of Cardiology. 2012;53(3):179-88.
Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of Interest
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Alfonso F, Timmis A, Pinto FJ, Ambrosio G, Ector H, Kulakowski P, et al. Conflict of interest
policies and disclosure requirements among European Society of Cardiology National
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Appendix 7
–
Adverse Effects of Wireless Radiation Related to Implants and Appendages
A7-A. Overview
Adverse impacts of wireless radiation on myriad medical implants and appendages
don’t
get much discussion in the literature, especially passive medical implants (A7-B2), non-medical
implant analogues (A7-B3), and metallic appendages (defined below), and especially with regard
to radiofrequency radiation. The FCC has raised concerns about the interactions of RF radiation
with passive implants. Paragraph 230 of [FCC, 2013] states: “Electrically
conductive objects in
or on the body may interact with sources of RF energy in ways that are not easily predicted.
Examples of conductive objects in the body include implanted metallic objects. Examples of
conductive objects on the body include eyeglasses, jewelry, metallic accessories, etc.”
A number of articles in the database addressed non-organic implants, which are foreign
bodies inserted into humans and animals for medical purposes. Non-organic implants addressed
in the present database are typically not rejected by the immune system like organic foreign
substances (although some adjuvants such as metal could induce autoimmune responses [Loyo et
al, 2013]). Non-rejection does not imply safety, especially from exposure to wireless radiation.
There were two major types of implants covered by the database articles showing adverse
effects: active implants that produced electrical signals mainly for controlling heart irregularities
(e.g., pacemakers, defibrillators) and hearing deficiencies (e.g., cochlear implants), and passive
metallic implants for structural support (e.g., dental implants, bone pins, plates, etc). The active
implants also have a passive component, since their structural components are imbedded in, and
interactive with, the incoming RF. Additionally, there are articles addressing adverse effects
from wireless radiation in the vicinity of
metallic
appendages (e.g., eyeglasses, jewelry, etc).
The external EMF from microwaves (and other sources) could 1) impact the electrical
operation of the active implants adversely, 2) increase the Specific Absorption Rate (SAR)
values of tissue in the vicinity of the passive implants substantially, and 3) increase the flow rate
and acidity of saliva. While the EMF effects on the cochlear implants could adversely affect
auditory capability, EMF effects on the heart-related implants could potentially be life-
threatening. The increased SAR values around the passive metal implants could result in
increased tissue temperatures, and could adversely impact integration and longevity of the
passive metallic implants. In the mouth, the combination of 1) increased tissue temperatures in
proximity to the implant, and 2) increased saliva flow rate and acidity, could lead to 3) increased
leaching of heavy metals from metallic orthodontic structures. This also raises the question:
what other adverse health effects from the exposure of both the active and passive implants to
increasing levels of wireless radiation have not been identified or addressed or reported?
While
Table A7-1
shows that substantial research has been done on exogenous electrical
interference with cardiac pacemakers and defibrillators, the impacts of automotive-based
electrical sources on these active implants have not been promulgated widely.
Appendix 8
addresses the larger issue of automotive-based wireless radiation at myriad frequencies,
including adverse impacts on these active implants.
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A7-B. Specific Impacts from Passive Implants
A7-B1. Overview
This sub-section of Appendix 7 examines two types of passive implants: passive metallic
medical implants (dental implants, orthodontic structures, nails, plates, etc) and passive
micro/nano implant analogues. The former types of implants are well-known, and the latter are
much less well-known, especially in their interactions with radiofrequency radiation. The latter
include exogenous nanoparticles that could also enhance absorption of RF radiation. Section
A7-B2 focuses on the passive metallic medical implants, and section A7-B3 focuses on passive
micro/nano implant analogues.
A7-B2. Impacts from Passive Metallic Medical Implants
The potential interference from external electromagnetic fields on implanted devices that
emit electromagnetic signals is somewhat obvious, and has been the subject of extensive study.
Some relevant documentation will be presented later. Less studied is the impact from external
electromagnetic fields on passive metallic medical implants and appendages. What are the
technical issues surrounding these EMF-implant interactions?
A good summary of these interactions is contained in Virtanen et al [2006]. The
following excerpts are most relevant, and critical issues are highlighted.
“When
a conductive object like an implant lies close to the source of the EM field, it
affects the shape of the radiated field and thus the SAR distribution. Within a perfectly
conducting object, the E field disappears; and outside the implant E field,
lines bend
perpendicular to the surface of the implant.
If the surface area is small, a
dense EM flux may
arise near the implant.
In lossy tissues, this leads to
higher power absorption near the implant
compared to the same tissue volume with no implant present. Correspondingly, tissue volumes
with lower power absorption also occur as the implant redistributes the SAR pattern. This
phenomenon may especially occur with implants that are thin…..or have sharp edges or
tips…..Furthermore, the
conductive implant may couple with a radiating source,
for example,
an antenna. The coupling can be either conductive, magnetic, or both…..As a consequence, a
current oscillating on an antenna induces a current on the implant,
too. Furthermore, the
induced surface current produces a secondary EM field, which contributes to the power
absorption, that is, SAR, in tissues around the implant…..Hence the implant acts as a weak
radiating antenna…..or a re-radiator…..in
tissues. At high frequencies, the induced current
flows in a thin surface layer of the implant, that is, at the implant–tissue interface, which may
even slightly warm up due to ohmic losses…..However, this warming is marginal compared to
warming of surrounding tissues.
The size of an implant is essential when evaluating its effect on the SAR
distribution…..If the implant is very small compared to the wavelength, it does not have a strong
effect on the SAR distribution…..Generally intermediate size implants, with dimensions close to
the wave length, and
especially those with resonance dimensions,
may cause strong EM fields
around themselves, and thus
enhanced SAR may occur around such an implant.
Large implants
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again may cause a
major change in the SAR distribution,
since they may
scatter or reflect the
field…..
In addition to other size-related effects, the size affects the magnitude of induced
currents…..A special case of this is the
implant with a resonance dimension…..The
length,
which apparently causes the highest SAR enhancement is about lT/3, where lT is the wavelength
in the media…..or lT/2…..An implant with such a dimension may even
cause enhancement of
SAR1g or SAR10g by a factor of 2–3…..
The shape of an implant is an important factor…..Pin-
or rod-shaped implants
may act as antennas and re-radiate the external field…..Rings
and
other loop structures may act as induction loops and thus
carry high induced currents…..A
gap
in the loop or rod would
induce high SAR in the gap…..Sharp
corners and tips in the implant
may cause
concentration of the EM flux around them.
One essential factor in the interaction is the orientation of an implant with respect to the
external source, that is, polarization of the field in the far field…..Especially for pin- or rod-like
structures, the orientation parallel to the electric field or antenna is the worst case…..In this
orientation, the
implant may act like an antenna
as described earlier. For arbitrary-shaped
implants, the mutual inductance of an antenna and an implant depends on their orientation with
respect to each other and other geometrical factors. The higher the mutual inductance, the
stronger is the interaction…..
Since dielectric properties of tissues vary, the
tissues that surround an implant have a
great impact on the SAR distribution…..If
tissues have high conductivity and relative
permittivity, they are very lossy and
SAR around the implant can be high…..
However, in bone, the
SAR enhancement due to an implant is assumingly higher
because of lower base level.
In general, the larger the relative difference between the dielectric
properties, especially conductivity, of the two media, the
greater is the bending of the EM field
when it enters the more lossy media.
Hence
larger averaged SAR values can be expected in
small volumes on the boundary.
Furthermore, the dielectric properties affect the wavelength of
EM field. In certain (plane wave) cases, the distance between the implant and the skin surface
may match the wavelength in tissue so that constructive interference occurs in the surface
layers…..This may
cause elevated SAR in the surface…..Similar
phenomena may also occur in
other layered structures…..
As a consequence of the described effects, the maximum SAR may occur at a different
location with and without the implant in the EM field…..Usually the SAR will be at maximum
either on the surface of the body, that is, in the skin, or in the tissue with the highest water
content. However, due to the interaction of implant and RF field, the
location of the highest
SAR may be shifted to the proximity of the implant.
This is an important fact for RF exposure
evaluation.”
Key takeaways from this summary are that resonance between the incoming EMF waves
and the implants can contribute to increased SAR levels, and these increased SAR levels can
occur in the bone or soft tissue adjacent to the implant(s).
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Implants, both active and passive, are cornerstones of modern medical treatment, and are
big business. Many of the implant-related articles read for this monograph attempted to
downplay the significance of the EMF effects on passive implants. While some acknowledged
that substantial increases in SAR are possible, especially near the implant(s), some/many
concluded that while SAR was indeed increased, the values averaged over the appropriate
volume (as allowed by the FCC) were small, and well under the FCC exposure limits.
This is misleading. Stating that exposure levels well below those allowed by the FCC
(which bear no relation to safety) are somehow ‘safe’ is disingenuous! There can be very high
SAR levels in volumes smaller than those allowed by the FCC, and this could have a dual
impact. The bonding between the implant and surrounding media could be impacted adversely,
and the myriad other adverse effects associated with SAR levels of that magnitude could be
operable.
Many of the articles identified the presence of ‘hot spots”, where the SARs were very
high, but the effect was numerically attenuated by averaging over a somewhat larger area.
Additionally, most of these measurements/computations were for single stressors only
(the incoming EMF radiation). Adding the real-life combinations of other toxic stimuli would
tend to exacerbate the effect, perhaps substantially. Finally, the measurements and computations
tended to end with a demonstration of the increase in SAR level.
That’s equivalent to
performing a chest x-ray on someone who smoked his first cigarette, and then writing a paper
that smoking had little effect on the lungs and other structures! What are the long-term effects of
the incoming wireless radiation on the passive implants and their supportive tissue/bone, both in
terms of structural integrity and increased incidence of non-communicable disease impacts? The
question about long-term effects and combined toxic stimuli applies to the operation of the active
implants as well.
A recent paper addressing adverse effects of RF impacts on osseointegration (dental
implant integration with underlying bone) illustrates the issues raised above [Kavyashree et al,
2019].
“Forty-eight
implants were placed in tibia and femur bone of rabbits, and after 90 days
the rabbits were sacrificed and bone surrounding the implant was retrieved…..Significantly less
bone-to-implant contact and bone area surrounding implant threads were found in the test groups
compared to the control group. There was a significant difference in regular bone
formation…..among the three groups…..Implants exposed to cell phone radiation showed more
inflammatory reaction when compared to the nonexposed implants, thus indicating that
cellular
phone overuse could affect the maturation of bone and thus delay osseointegration.”
If other toxic stimuli were co-exposed along with EMF radiation, and if longer-term data
were taken, more severe impacts could be expected. Similar effects could be expected for other
types of implants!
Table A7-1
contains an implant taxonomy. The format is category heading followed by a
few selected references. The active implant categories cover cardiac, cochlear, and other
devices, and the passive implant categories cover imbedded implants and appendages.
A sub-category of passive implants called Metal Release was created. This category
reflects adverse effects of wireless radiation that are almost unknown to the general public. The
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focus is on increased corrosive abilities of saliva due to wireless radiation exposure, and the
subsequent release/leaching of metal from myriad orthodonic structures in the mouth. Many of
these metals are heavy metals, such as nickel and chromium, which can be extremely dangerous
when released into the body. Most of the references in
Table A7-1
in this Metal Release
category deal with nickel release from orthodonic appliances.
In these circumstances, the mobile phone radiation stimulates the parotid glands, causing
them to produce more saliva. Not only is the flow of saliva increased, but its properties are
altered, including reduction of pH. Additionally, as the larger passive implant category has
shown, there will be some preferential heating at the saliva-orthodonic appliance interface. The
net effect will be to increase corrosion of the metal appliance, resulting in release of nickel.
Given that children are major customers for many of these dental appliances as well as
increasingly major users of cell phones, WiFi, etc, these children will be adversely impacted by
the wireless radiation through myriad pathways!
Table A7-1
–
Implant Taxonomy
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ACTIVE IMPLANT - CARDIAC
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Electromagnetic interference in implantable cardioverter defibrillators: present but rare.
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Yoshida S, Fujiwara K, Kohira S, Hirose M. Electromagnetic interference of
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Yu SS, Tope WD, Grekin RC. Cardiac devices and electromagnetic interference
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[et al]. 2005;31(8 Pt 1):932-40.
ACTIVE IMPLANT - COCHLEAR
McIntosh RL, Iskra S, McKenzie RJ, Chambers J, Metzenthen B, Anderson V.
Assessment of SAR and thermal changes near a cochlear implant system for mobile phone
type exposures. Bioelectromagnetics. 2008;29(1):71-80.
Parazzini M, Sibella F, Paglialonga A, Ravazzani P. Assessment of the Exposure to
WLAN Frequencies of a Head Model with a Cochlear Implant. Bioelectromagnetics.
2010;31(7):546-55.
Sibella F, Parazzini M, Paglialonga A, Ravazzani P. Assessment of SAR in the tissues
near a cochlear implant exposed to radiofrequency electromagnetic fields. Physics in
Medicine and Biology. 2009;54(8):N135-N41.
Zradzinski P, Karpowicz J, Gryz K, Leszko W. Evaluation of the safety of users of
active implantable medical devices (AIMD) in the working environment in terms of exposure
to electromagnetic fields - Practical approach to the requirements of European Directive
2013/35/EU. International journal of occupational medicine and environmental health.
2018;31(6):795-808.
Zradzinski P, Karpowicz J, Gryz K. Electromagnetic Energy Absorption in a Head
Approaching a Radiofrequency Identification (RFID) Reader Operating at 13.56 MHz in
Users of Hearing Implants Versus Non-Users. Sensors. 2019;19(17).
ACTIVE IMPLANT - OTHER
Baker KB, Phillips MD. Deep Brain Stimulation Safety: MRI and Other
Electromagnetic Interactions. In: Tarsy MD, Vitek JL, Starr PA, Okun MS, editors. Deep
Brain Stimulation in Neurological and Psychiatric Disorders. Current Clinical
Neurology2008. p. 453-72.
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Baker KB, Tkach JA, Phillips MD, Rezai AR. Variability in RF-induced heating of
a deep brain stimulation implant across MR systems. Journal of Magnetic Resonance
Imaging. 2006;24(6):1236-42.
Blomstedt P, Jabre M, Bejjani BP, Koskinen LOD. Electromagnetic environmental
influences on implanted deep brain stimulators. Neuromodulation. 2006;9(4):262-9.
Dustin K. Evaluation of Electromagnetic Incompatibility Concerns for Deep Brain
Stimulators. Journal of Neuroscience Nursing. 2008;40(5):299-+.
Golestanirad L, Kazemivalipour E, Keil B, Downs S, Kirsch J, Elahi B, et al.
Reconfigurable MRI coil technology can substantially reduce RF heating of deep brain
stimulation implants: First in-vitro study of RF heating reduction in bilateral DBS leads at
1.5 T. Plos One. 2019;14(8).
Guerin B, Serano P, Iacono MI, Herrington TM, Widge AS, Dougherty DD, et al.
Realistic modeling of deep brain stimulation implants for electromagnetic MRI safety
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Kainz W, Alesch F, Chan DD. Electromagnetic interference of GSM mobile phones
with the implantable deep brain stimulator, ITREL-III. Biomedical Engineering Online.
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Kiourti A, Nikita KS. Numerical assessment of the performance of a scalp-
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Bioelectromagnetics. 2013;34(3):167-79.
McElcheran CE, Golestanirad L, Iacono MI, Wei PS, Yang B, Anderson KJT, et al.
Numerical Simulations of Realistic Lead Trajectories and an Experimental Verification
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Xu J, Li LM, Hao HW, Ieee. Primary experimental study on safety of Deep Brain
Stimulation in RF electromagnetic field. 2009 Annual International Conference of the Ieee
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PASSIVE IMPLANT
Bernardi P, Pisa S, Cavagnaro M, Piuzzi E, Lin JC. Dosimetry and Temperature
Aspects of Mobile-Phone Exposures. Advances in Electromagnetic Fields in Living Systems,
Vol 5: Health Effects of Cell Phone Radiation. 2009;5:221-76.
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Crouzier D, Selek L, Martz BA, Dabouis V, Arnaud R, Debouzy JC. Risk assessment
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the human body: methods and applications. Physics in Medicine and Biology.
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Kyriakou A, Christ A, Neufeld E, Kuster N. Local tissue temperature increase of a
generic implant compared to the basic restrictions defined in safety guidelines.
Bioelectromagnetics. 2012;33(5):366-74.
Mat MH, Abd Malek MF, Whittow WG, Bibb R. Ear prosthesis evaluation: specific
absorption rate levels in the head due to different angles and frequencies of electromagnetic
exposure. Journal of Electromagnetic Waves and Applications. 2015;29(4):514-24.
Mat MH, Jusoh M, Rahim H, Yusoff MI. A Brief Review of the EMF Interaction:
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Matikka H, Keshvari J, Lappalainen R. Temperature changes associated with
radiofrequency exposure near authentic metallic implants in the head phantom-a near field
simulation study with 900, 1800 and 2450 MHz dipole. Physics in Medicine and Biology.
2010;55(19):5867-81.
Mattei E, Calcagnini G, Censi F, Triventi M, Bartolini P, Ieee. Radiofrequency
Dosimetry in Subjects Implanted with Metallic Straight Wires: A Numerical Study. 2008
30th Annual International Conference of the IEEE Engineering in Medicine and Biology
Society, Vols 1-8. IEEE Engineering in Medicine and Biology Society Conference
Proceedings2008. p. 4387-90.
McIntosh RL, Anderson V, McKenzie RJ. A numerical evaluation of SAR distribution
and temperature changes around a metallic plate in the head of a RF exposed worker.
Bioelectromagnetics. 2005;26(5):377-88.
McIntosh RL, Iskra S, Anderson V. Significant RF-EMF and Thermal Levels
Observed in a Computational Model of a Person With a Tibial Plate for Grounded 40 MHz
Exposure. Bioelectromagnetics. 2014;35(4):284-95.
Miaskowski A, Gas P, Krawczyk A, Ieee. SAR Calculations for Titanium Bar-Implant
Subjected to Microwave Radiation2016.
Miaskowski A, Krawczyk A, Ishihara Y. A numerical evaluation of eddy currents
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Computation and Mathematics in Electrical and Electronic Engineering. 2012;31(5):1441-7.
Miaskowski A, Olchowik G, Krawczyk A, Lada-Tondyra E, Bartosinski A. A
Numerical Evaluation of Electric Field and SAR Distribution Around a Titanium Implant in
the Trunk of a Child. Przeglad Elektrotechniczny. 2012;88(12B):77-9.
Kavyashree M, Harish PV, Mishra SK, Chowdhary R. Cell Phone Radiation Effect on
Bone-to-Implant Osseointegration: A Preliminary Histologic Evaluation in Rabbits.
International Journal of Oral & Maxillofacial Implants. 2019;34(3):643-50.
Moutaouekkil MA, Taybi C, Ziyyat A, Picard D, Ieee. The effect of metal braces on
antenna parameters and the SAR distribution of the head exposed to popular cellular
frequencie. 2017 Mediterranean Microwave Symposium. Mediterranean Microwave
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Nguyen DT, Barham W, Zheng LJ, Dinegar S, Tzou WS, Sauer WH. Effect of
radiofrequency energy delivery in proximity to metallic medical device components. Heart
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Olteanu M, Rafiroiu D, Ieee. Temperature Increase due to Specific Absorption Rate
Enhancement around Metallic Stent Implants. 2011 E-Health and Bioengineering
Conference. E-Health and Bioengineering Conference2011.
Ono T, Hikage T, Nojima T, Nagaoka T, Watanabe S, Ieee. Local SAR in Anatomical
Phantom Implanted with Metallic Osteosynthesis Plates in Mandibular Exposed to 2 GHz RF
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Fields. 2014 Ieee International Workshop on Electromagnetics (Ieee Iwem): Applications and
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Othman N, Samsuri NA, Ellias NA. Evaluation of Specific Absorption Rate due to
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Othman N, Samsuri NA, Rahim MKA, Elias NA, BinSulaiman H, Awang Z, et al.
Analysis on the Specific Absorption Rate due to the Metallic Objects Exposed to Radiation
Source2013. 400-4 p.
Rafiroiu D, Ciupa RV, Iancu A, Lazar A, Tiseanu I, Craciunescu T, et al. Numerical
Analysis of the Electric Field and Temperature Changes around Carotid Stents. 2011 7th
International Symposium on Advanced Topics in Electrical Engineering. International
Symposium on Advanced Topics in Electrical Engineering2011.
Safari M, Abdolali A. Dental Implants and Mobile-Phone Use. Ieee Antennas and
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Saghiri MA, Orangi J, Asatourian A, Mehriar P, Sheibani N. Effect of mobile phone
use on metal ion release from fixed orthodontic appliances. American journal of orthodontics
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Orthodontists, its constituent societies, and the American Board of Orthodontics.
2015;147(6):719-24.
Sanchez-Hernandez DA. The Effect of Metallic Objects on SAR Distributions.
SanchezHernandez DA, editor2009. 175-205 p.
Santini L, Forleo GB, Santini M. Implantable devices in the electromagnetic
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Smondrk M, Benova M, Psenakova Z, Ieee. Evaluation of metallic implant influence
on SAR distribution in a multilayered tissue model2017.
Valic B, Gajsek P, Miklavcic D. Conducting Implant in Low Frequency
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IFMBE Proceedings. 162007. p. 218-+.
Valic B, Gajsek P, Miklavcic D. Current Density in a Model of a Human Body With a
Conductive Implant Exposed to ELF Electric and Magnetic Fields. Bioelectromagnetics.
2009;30(7):591-9.
Vidal N, Lopez-Villegas JM, Sieiro J. Subcutaneous implanted antennas: interaction
with biological tissues. Compel-the International Journal for Computation and Mathematics in
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Vidal N, Lopez-Villegas JM. Changes in Electromagnetic Field Absorption in the
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Virtanen H, Keshvari J, Lappalainen R. Interaction of radio frequency electromagnetic
fields and passive metallic implants - A brief review. Bioelectromagnetics. 2006;27(6):431-9.
Virtanen H, Keshvari J, Lappalainen R. The effect of authentic metallic implants on
the SAR distribution of the head exposed to 900, 1800 and 2450 MHz dipole near field.
Physics in Medicine and Biology. 2007;52(5):1221-36.
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Wang G, Xu YM, Zhang LN, Ye DM, Feng XX, Fu TF, et al. Enhancement of
Apoptosis by Titanium Alloy Internal Fixations during Microwave Treatments for Fractures:
An Animal Study. Plos One. 2015;10(7).
Whittow WG, Edwards RM. A study of changes to specific absorption rates in the
human eye close to perfectly conducting spectacles within the radio frequency range 1.5 to 3.0
GHz. Ieee Transactions on Antennas and Propagation. 2004;52(12):3207-12.
Ye DM, Xu YM, Wang G, Feng XX, Fu TF, Zhang H, et al. Thermal Effects of 2450
MHz Microwave Exposure Near a Titanium Alloy Plate Implanted in Rabbit Limbs.
Bioelectromagnetics. 2015;36(4):309-18.
Ye DM, Xu YM, Zhang H, Fu TF, Jiang L, Bai YH. Effects of Low-Dose Microwave
on Healing of Fractures with Titanium Alloy Internal Fixation: An Experimental Study in a
Rabbit Model. Plos One. 2013;8(9).
Yelkenci T, Paker S. The effects of frequency, polarization, direction and metallic
objects on the SAR values in a human head model for plane wave exposure (500-2500 MHZ).
Frequenz. 2006;60(11-12):215-9.
Yelkenci T. Effects of metallic objects on specific absorption rate in the human head
for 915 and 1900 MHz mobile phones. Frequenz. 2006;60(3-4):46-9.
Yu D, Zhang RY, Liu Q. Influence of dentures on SAR in the visible Chinese human
head voxel phantom exposed to a mobile phone at 900 and 1800 MHz. Bioelectromagnetics.
2012;33(6):508-17.
Zou YZ, Wang G, Xu YM, Bai YH. Comparative study of the proliferative ability of
skeletal muscle satellite cells under microwave irradiation in fractures with titanium alloy
internal fixation in rabbits. Experimental and Therapeutic Medicine. 2018;16(6):4357-66.
PASSIVE IMPLANT
–
METAL RELEASE
Hamzany Y, Feinmesser R, Shpitzer T, Mizrachi A, Hilly O, Hod R, et al. Is Human
Saliva an Indicator of the Adverse Health Effects of Using Mobile Phones? Antioxidants &
Redox Signaling. 2013;18(6):622-7.
Mortazavi G, Haghani M, Rastegarian N, Zarei S, Mortazavi SMJ. Increased Release
of Mercury from Dental Amalgam Fillings due to Maternal Exposure to Electromagnetic
Fields as a Possible Mechanism for the High Rates of Autism in the Offspring: Introducing a
Hypothesis. Journal of biomedical physics & engineering. 2016;6(1):41-6.
Mortazavi SMJ, Paknahad M, Khaleghi I, Eghlidospour M. Effect of radiofrequency
electromagnetic fields (RF-EMFS) from mobile phones on nickel release from orthodontic
brackets: An in vitro study. International Orthodontics. 2018;16(3):562-70.
Nanjannawar LG, Girme TS, Agrawal JM, Agrawal MS, Fulari SG, Shetti SS, et al.
Effect of Mobile Phone Usage on Nickel Ions Release and pH of Saliva in Patients
Undergoing Fixed Orthodontic Treatment. Journal of Clinical and Diagnostic Research.
2017;11(9):ZC84-ZC7.
Saghiri MA, Orangi J, Asatourian A, Mehriar P, Sheibani N. Effect of mobile phone
use on metal ion release from fixed orthodontic appliances. American Journal of Orthodontics
and Dentofacial Orthopedics. 2015;147(6):719-24.
Shivashankara AR, Joy J, Sunitha V, Rai MP, Rao S, Nambranathayil S, et al. Effect
of Cell Phone Use on Salivary Total Protein, Enzymes and Oxidative Stress Markers in
Young Adults: A Pilot Study. Journal of Clinical and Diagnostic Research. 2015;9(2):BC19-
BC22.
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APPENDAGE
Anuar MZ, Samsuri NA, Rahim MKA, Elias NA, Othman N. On the Effect of
Metallic Earring on Antenna Performance and SAR at 2.4 & 5.8 GHz. Jurnal Teknologi.
2012;58.
Cihangir A, Luxey C, Jacquemod G, Pilard R, Gianesello F, Whittow WG, et al.
Investigation of the Effect of Metallic Frames on 4G Eyewear Antennas2014. 60-3 p.
Cihangir A, Whittow W, Panagamuwa C, Jacquemod G, Gianesello F, Luxey C. 4G
antennas for wireless eyewear devices and related SAR. Comptes Rendus Physique.
2015;16(9):836-50.
Cihangir A, Whittow WG, Panagamuwa CJ, Ferrero F, Jacquemod G, Gianesello F, et
al. Feasibility Study of 4G Cellular Antennas for Eyewear Communicating Devices. Ieee
Antennas and Wireless Propagation Letters. 2013;12:1704-7.
Edwards RM, Whittow WG. Applications of a genetic algorithm for identification of
maxima in specific absorption rates in the human eye close to perfectly conducting spectacles.
Iee Proceedings-Science Measurement and Technology. 2005;152(3):89-96.
Fayos-Fernandez J, Arranz-Faz C, Martinez-Gonzalez AM, Sanchez-Hernandez D.
Effect of pierced metallic objects on SAR distributions at 900 MHz. Bioelectromagnetics.
2006;27(5):337-53.
Lan JQ, Du GH. Evaluation of Temperature Elevation in Human Ocular Tissues due
to Wireless Eyewear Devices. Applied Computational Electromagnetics Society Journal.
2019;34(1):17-24.
Lan JQ, Hong T, Liang X, Du GH. Evaluation of Microwave Microdosimetry for
Human Eyes with Glasses Exposed to Wireless Eyewear Devices at Phone Call State.
Progress in Electromagnetics Research M. 2018;63:71-81.
Lan JQ, Huang KM. Evaluation of SAR in a human head with glasses exposed to
radiation of a mobile phone. Journal of Electromagnetic Waves and Applications.
2013;27(15):1919-30.
Lan JQ, Liang X, Hong T, Du GH. On the effects of glasses on the SAR in human
head resulting from wireless eyewear devices at phone call state. Progress in Biophysics &
Molecular Biology. 2018;136:29-36.
Othman N, Samsuri NA, Rahim MKA, Elias NA, Ieee. Specific Absorption Rate in
the Human Leg and Testicle Due to Metallic Coin and Zip. 2015 Ieee International Rf and
Microwave Conference. IEEE International RF and Microwave Conference2015. p. 123-7.
Othman N, Samsuri NA, Rahim MKA. ESTIMATION OF SPECIFIC ABSORPTION
RATE IN THE HUMAN LEG AND TESTICLE DUE TO A METALLIC RING. Jurnal
Teknologi. 2015;77(10):85-90.
Whittow W, Panagamuwa CJ, Edwards R, Vardaxoglou JC, Ieee. Specific absorption
rates in the human head due to circular metallic earrings at 1800mhz2007.
Whittow WG, Panagamuwa CJ, Edwards RM, Vardaxoglou JC. On the effects of
straight metallic jewellery on the specific absorption rates resulting from face-illuminating
radio communication devices at popular cellular frequencies. Physics in medicine and
biology. 2008;53(5):1167-82.
Whittow WG, Panagamuwa CJ, Edwards RM, Vardaxoglou JC. The Energy Absorbed
in the Human Head Due to Ring-Type Jewelry and Face-Illuminating Mobile Phones Using a
Dipole and a Realistic Source. Ieee Transactions on Antennas and Propagation.
2008;56(12):3812-7.
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A7-B3. Impacts from Passive Macro/Nano Implant Analogues
The FCC regulations for RF exposure limits are based on an
average exposure
over a
six-minute period for occupational applications, and thirty-minute period for the general public.
For near-field exposures, the guidelines can be summarized as follows:
“Whole-Body
SAR is
averaged over the entire body; Partial-body SAR is averaged over any 1 g of tissue in the shape
of a cube; SAR for hands, wrists, feet and ankles is averaged over any 10 g of tissue in the shape
of a cube.
SAR limits are not applicable above 6.0 GHz; MPE limits for field strength and power
density should be applied. Categorical exclusion of routine MPE evaluation for mobile
transmitters does not apply to portable devices operating above 6.0 GHz”
(
https://transition.fcc.gov/oet/ea/presentations/files/oct05/RF_Exposure_Concepts_Support_KC.pdf
).
Averaging processes attenuate the extremes. In particular, within the thirty-minute
averaging window used for general population exposure averaging (above), there could be many
examples of RF power fluxes exceeding the FCC guidelines, perhaps substantially. Given that
the FCC Guidelines are based on thermal limits not being exceeded, this means that (within the
thirty-minute averaging window) temperatures (and related thermal stresses) could reach peak
values capable of inflicting serious damage. Neufeld and Kuster [2018] examined RF heating of
skin in the >10 GHz region, and concluded: “Transient
exposure with high PAR [peak-to-
average ratio] can lead to large temperature oscillations, with peak temperature increases in the
skin reaching tens of degrees, thus exceeding tissue damage thresholds after short exposure
durations.”
The computations were made “at
an intensity resulting in a temperature increase of 1
K at
continuous exposure”.
Would implant analogues, such as imbedded nanoparticles in the heated tissue, change
the characteristics of tissue heating from the pulsed RF described above? Section 2E contains
the statement “At
the millimeter carrier wavelengths characteristic of high performance 5G, one
can expect resonance phenomena with small-scale human structures [Betzalel, 2018], as well as
resonances with insects/insect components [Thielens et al, 2018, 2020].” Can this enhanced
heating of tissue due to high-frequency pulsed RF be extended to nanoparticle-imbedded tissue?
These implant analogues could include e.g. tattoos using nanoparticle materials,
nanoparticles from cosmetics and air pollution, possibly nanoparticles from forced-air
occupational situations, etc. These analogues could be metallic or non-metallic. Whether they
would be heated by RF, and how that would vary by particle characteristics, RF characteristics,
and surrounding tissue properties, is an open question. Collins et al [2014] conclude, for gold
nanoparticles: “The
chief conclusion is that in some cases gold nanoparticles immersed in RF
fields heat, and in other cases they do not.”
There is a substantial literature on RF heating of nanoparticles within tissue, motivated by
applications to hyperthermia treatment of diseased tissue, especially cancer [e.g., Huang et al,
2008; Gupta et al, 2010; Hanson et al, 2011; Cardinal et al, 2008; Xu et al, 2008; Tamarov et al,
2016; Ocampo-Garcia et al, 2015; San et al, 2013; Pantano et al, 2017; Nordebo et al, 2017;
Nguyen et al, 2016; Mironava et al, 2017; Mackeyev et al, 2017; Liu et al, 2015; Letfullin et al,
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2015; Kim et al, 2013; Corr et al, 2012; Collins et al, 2014; Chaurasia et al, 2016; Amini et al,
2018; Glazer et al, 2010; Dennis and Ivkov, 2013; Sassaroli et al, 2012; Moran et al, 2009;
Gannon et al, 2008]. The references/bibliography at the end of this section contain more
examples of RF (and other pulsed) heating of nanoparticles, including some non-tissue-related
heating.
There is not uniform consensus on heating mechanisms. While myriad specific
approaches are used for RF heating of nanoparticle-imbedded tissue for cancer therapy, Glazer
and Curley [2011] provide a reasonable summary of the technical issues involved. They state:
“RF
field therapy is a non-invasive method to expose cancers to nonionizing radiation that is
relatively nontoxic in and of itself….. nanoparticle-mediated RF field hyperthermia induces
heating on the scale of approximately 100 μm. Fortunately, noninvasive
RF fields easily
penetrate human tissues and pass through the entire body with minimal perturbations until the RF
fields interact with metal….. The size of the field can be scaled from small, animal-sized
devices….. up to very large volumes that could theoretically treat small (local tumor) or large
regions of the human body. Samples (cells, animals or, theoretically, patients) are placed in an
RF field created by a parallel plate capacitor
…..
This establishes a directional electromagnetic
field that passes through tissues and organs without significant absorbance. Metal, however,
absorbs RF energy and quickly releases heat to the surrounding region. Nanoparticles in general,
and metal nanoparticles specifically, are utilized because of this general principle, as well as their
unique qualities that absorb even more energy (and release even more heat), due to their very
small size and quantum characteristics.
Recent advancements in nanotechnology have resulted in multiple types of nanoparticles
that can be targeted with antibodies, peptides/proteins and sugar residues to cancer cells…..
Thermal therapy is induced with either focused laser irradiation, manipulation of magnetic fields
or RF field exposure….. While these nanoparticles may be more selective than specific, animal
studies have demonstrated promising results without major toxicity….. nanoparticles induce
intracellular hyper-thermia. Unique physicochemical properties of metallic and non-metallic
nanoparticles result in different heating rates for various types of non-ionizing radiation
exposure….. We have found that solid gold nanoparticles less than 50 nm in diameter are safely
taken up by macrophages in the liver and spleen without major toxicity….. large nanoparticles
with a large aspect ratio (i.e., rods or tubes) have been associated with fibrosis and cellular
injury….. Nanoparticle heating in RF fields is a very complex phenomenon. The end result is
that RF fields induce nanoparticle heating rates of 1–3°C/s in various solutions and at various
power levels…..Most RF field devices are based on shortwave RF fields (13.56 MHz) as
licensing agencies permit this frequency for ‘medical use’…..
The power of these devices is
typically from 100–800 W. The energy transfer efficiency from the field generator to actual field
strength varies amongst the devices; determining the exact field strength is problematic….. The
RF electrical field strength in general, however, is approximately 5–15 kV/m…..
In a nanoparticle concentration and field strength-dependent manner, nanoparticles in aqueous
solutions can reach boiling temperatures in 2–3 min. Interestingly, deionized water negligibly
heats in RF fields, while antibody solutions (e.g., with ions or proteins) typically heat around
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five- to ten-times less than nanoparticle solutions….. In the RF field, SWNTs heat in the range of
2–6°C/s, slighter faster than gold…..
There remains some controversy regarding the mechanism in which nanoparticles heat in an RF
field. Our group has demonstrated that gold nanoparticles heat primarily via Joule heating…..
This work has demonstrated that gold nanoparticles behave
as ‘mini-resistors’, where free
electrons on the surface have limitations to their movement. In this way, friction is created at the
individual nanoparticle level, which release heat into the surrounding aqueous solution.
Furthermore, based on these findings, one would predict less heating for larger nanoparticles as
well as much less for aggregates where there are far fewer limitations placed on the movement of
electrons.”
Extrapolation from the cancer (and similar) therapy use of nanoparticles for hyperthermia
destruction of diseased tissue to heating of nanoparticles imbedded in near-surface tissue by
communications-level RF powers is not straight-forward. The therapeutic situation involves
high-power RF targeting nanoparticles with desired pre-selected properties at specific locations
to achieve high temperatures, whereas the communications situation involves low-power RF
interacting with nanoparticles of unknown properties at unknown locations constrained to low
temperature increases. Additionally, the RF therapy situation has typically involved RF
frequencies in the MHz range, whereas the RF communications scenario (especially for 5G)
would involve frequencies in the GHz range (high-band 5G would be in the 10s of GHz).
It is unclear how the effects on tissue surrounding these micro/nanoscale implant
analogues would relate to those of the macro-implants of the previous section. More detailed
computations are required to identify specific temperature excursions and related thermal
stresses for specific nanoscale implant anologues.
As mentioned previously, there may also be electromagnetic and thermal resonances with
insects and other small living creatures and substances. For insects, there could be resonances
based on overall body dimensions [e.g., Thielens, 2018, 2020], and/or resonances based on
specific appendage dimensions. Insects are a critical part of the ecological chain, and severe
functional damage may occur even if only critical organs or appendages are damaged. If
antennae are heated, or experience even moderate cyclic thermal stresses, that may be sufficient
to disable the insect, and eliminate their functional contribution to the ecological chain.
Additionally, for insects, heating at different spatial macroscales may be sufficient to
cause damage, as well as microscale heating. More detailed insect heating computations at the
microscale, and at the macroscale (covering the spectrum of full body resonance to critical
appendage resonance) are required before declarations of safety become credible.
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Appendix 8
–
Adverse Effects of Automotive-Based Wireless Radiation
A8-A. Overview
The modern automobile is a powerful source of wireless radiation at myriad frequencies,
and is subject to external wireless radiation at myriad frequencies as well. The trend has not
been to reduce these sources, but rather to add equipment both to the vehicle and to the external
environment that will increase the wireless radiation flux associated with the vehicle
substantially. The numbers and types of sources are not well-known, even among those experts
and laymen concerned about adverse effects from wireless radiation. This appendix will address
only a few of those sources.
Some/much of the appendix is based on recent personal experience. Over a year ago, I
began looking for a new car. My previous vehicle had almost none of the wireless add-ons that
are promoted extensively by the automotive industry, and I had hoped to replace it with a similar
wireless-free vehicle.
I spent perhaps six months part-time test-driving vehicles, taking some EMF
measurements in selected vehicles, and researching myriad vehicles on the Web. This appendix
uses some of my findings as a starting point to identify the full scope of the radiation flux exiting
and entering the vehicle.
A8-B. Specific Automotive Wireless Radiation Sources
During this automotive evaluation process, I received a very informative response from
Dr. Theodore Metsis. It is summarized at the following link
(
http://www.radiationdangers.com/automotive-radiation/automotive-radiation/
). Of particular
interest is the diagram at the beginning of the article, showing radars and wireless sensors in
modern cars. I would recommend the reader study that diagram in detail, to better appreciate
how ubiquitous are these sources of wireless radiation. Not all the wireless radiation enters the
cabin, since some/much is outward-directed, but some/much of it will enter the cabins of other
cars on the road.
However, that diagram tells only part of the story. Assume there is a car pool commuting
to work from the suburbs of a major city. It is not uncommon
(in today’s world)
for a one-way
trip to take from one-two hours, or more. Even in a regular car, or mid-size SUV, there might be
four or so passengers. They may be using cell phones, WiFi, or both, thereby adding to the
radiation from the automotive-based sensors/transmitters. For example, in an experiment
comparing cell phone-Bluetooth
use inside and outside a car, Dhami [2015] concluded “The
increase in radiation power density with the use of Bluetooth was observed to be 313% higher as
compared to phone alone when measured outside the car…..The power density was observed to
have increased by 393% when cell-phone and Bluetooth were used inside the car with windows
rolled up as compared to using no phone/Bluetooth.”
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There will be cell towers lining the sides of a major highway, thereby increasing the
radiation to the occupants substantially. Depending on conditions, there may be substantial air
pollution to which the occupants are exposed. Additionally, the prolonged sitting is very
dangerous, and is a contributing factor to many serious diseases [Kostoff, 2015]. If the vehicle is
new, there may be substantial out-gassing of toxic chemicals from the interior materials
(
https://www.ecocenter.org/newsletter/2012-02/dangers-lurk-behind-new-car-smell
). Combined
exposure to the wireless radiation, air pollution and other toxic substances, coupled with
prolonged sitting and continual
impacts from the car’s motions, produces a synergistic effect that
exacerbates adverse impacts from any of the constituent components substantially.
A8-B1. Automotive ELF
About a decade ago, the Israeli Ministry of Environmental Protection undertook an
evaluation of the safety of hybrid vehicles with respect to emissions of non-ionizing radiation.
The following excerpt summarizes their findings, and the context
(
https://www.thetruthaboutcars.com/2010/03/israel-preps-worlds-first-hybrid-car-radiation-scale/
):
“Not
exactly flower power, the radiation in question is cast by the electromagnetic field
made by alternating current (AC) flowing from the batteries in the back to the engine up front.
The medical implications of this non ionizing radiation, similar to radiation from cellphone
antennas, are not yet clear.
The Australian Radiation Protection and Nuclear Safety Agency (ARPANSA)
recommends a limit of 1,000 mG (milligauss) for a 24-hour exposure period. While other
guidelines pose similar limits, the International Agency for Research on Cancer (IARC) deemed
extended exposure to electromagnetic fields stronger than 2 mG to be a “possible cause” for
cancer.
Israel’s Ministry of Health recommends a maximum of 4 mG.
The ministry’s foray into this topic is a culmination of a public outcry resulting from
publications in the media regarding possible dangers from radiation in hybrid cars. Last year,
Israeli automotive website Walla! Cars conducted a series of tests on the previous generation
Toyota Prius, Honda Insight and Honda Civic Hybrid, and recorded radiation figures of
up to
100 mG during acceleration.
Measurements also peaked when the batteries were either full (and
in use) or empty (and being charged from the engine), while
normal driving at constant speeds
yielded 14 to 30 mG
on the Prius, depending on the area of the cabin.”
Over the past couple of decades (bracketing the Israeli study), a number of researchers
have conducted studies measuring EMF emissions in conventional gasoline/diesel-powered cars,
hybrids, and electric vehicles. Some of these studies are listed in the first part of
Table A8-1.
The results are all over the map.
One reason is that “there
are alternating magnetic fields
produced by its engine, control systems, air conditioning, sound, video, communications, etc. In
vehicles with tyres, one has to add the magnetic field produced by the magnetized metal of the
wheels” [Paniagua et al, 2017]. Additionally, the results vary by location, vehicle speed, and
braking/acceleration.
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The findings of [Paniagua et al, 2017] are instructive, and provide a good summary of
magnetic fields found in fossil-fuel
powered cars. “Other
works, however, detect magnetic fields
inside cars with values that are comparable to ours. Thus, for example, Milham et al…..found a
range of 0.2 to 2.0μT,
Stankowski et al…..0.1
to 9.5μT,
and Halgamuge et al…..0.3
to 3.5μT.
These studies used instrumentation that measures magnetic fields with frequencies
above 5 Hz.
As in our study, Stankowski et al…..found magnetic fields that were higher in the rear
seats than in the front seats, and higher at floor level than at the seat and head levels. The reason
for the differences between the two sets of studies lies in the frequency ranges used. The rotating
wheels produce spectral peaks that coincide with the rotation frequency, typically 6–12
Hz…..and are
not detectable when using instrumentation whose lowest frequency threshold is
30–40 Hz.
This instrumentation detects the magnetic fields generated by the motor and the
electrical systems of the vehicle, but not those generated by the effect of wheel rotation. One can
therefore conclude that the magnetic fields from the rotating wheels represent a very important
part of the total magnetic field inside the vehicles.”
The maximum exposures reported in the
study by [Panigua et al, 2017] were about twenty milligauss (1
μT=10
milligauss).
In a 2014 article on hybrids [Karabetsos et al, 2014], Figure 8 (cruising at 80-120
kilometers/hour) shows exposures in the right-rear seat reaching over 20% of 1998 ICNIRP
limits for the general public. The article does not provide actual magnetic field numbers for
these exposures, nor does it provide the frequencies at which these magnetic fields were
measured. The 1998 ICNIRP limits are a function of frequency.
The article states: “it
was observed that the major components of the magnetic flux
density appeared at frequencies lower than 100 Hz.”
In this frequency spectrum, the ICNIRP
limits range from 400,000 milligauss at 1 Hz to 500 milligauss at 100 Hz. So, the actual
measurement of ~20% of ICNIRP limit could range from 80,000 milligauss to 100 milligauss,
depending on the frequency(s) at which the measurements were made. For reference, the
ICNIRP limits for power frequency (60 Hz) are 830 milligauss (for the general public), far above
the levels shown as dangerous in the Israeli reference above, and other references in the
biomedical literature.
In Vasilev et al, [2015], magnetic field measurements were made in myriad electric
vehicles and hybrids. The two major sources of magnetic fields were traction currents and
wheels. The findings for each were as follows: “Therefore,
if the traction current has variations
up to ±300 A, the magnetic field could also have
variations of up to ±300 μT.” The upper limit
translates to
3,000 milligauss!
“The
permanent magnetization of steel belted tires is a well
known source of in-vehicle magnetic fields…..Our measurements show that this phenomenon is
responsible for a
magnetic field inside the car of up to 2 μT at the wheel frequency
fw (which
ranges from 0 to 20 Hz for speeds ranging from 0 to 130 km/h).”
This upper limit translates to
twenty milligauss, and is similar to the upper limit above reported by Panigua et al, [2017].
References to other studies are shown in the first section of
Table A8-1.
The hybrids and
EVs are associated with larger magnetic fields (especially at acceleration and braking), due
mainly to large electrical power transfers for all operations. My own measurements in hybrids
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showed magnetic fields around the driver could range up to 15-30 milligauss, depending on the
vehicle. However, the meter I used had a lower limit of 40 Hz, so I could not measure the
powerful magnetic fields shown by the above studies to occur at the extremely low frequencies.
However, in my view, chronic exposure even to the 15-30 milligauss I measured is something to
be avoided at all costs, much less the larger fields at the lower frequencies!
In many of the references shown in
Table A8-1
(and beyond),
the authors don’t present
actual magnetic field numbers, but rather magnetic fields
normalized to ICNIRP
recommended
exposure limits. They usually conclude that, because the ratios are less than one, therefore, the
vehicles are safe. This is fallacious and disingenuous, since the ICNIRP recommended limits
have nothing to do with safety (based on exposures shown to cause harm in the biomedical
literature) and everything to do with providing cover for the wireless radiation promoters.
Additionally, many of the guidelines tend to be based on single stressor experiments.
Vehicle cabins expose their occupants to many types of toxic stimuli (described initially in this
appendix), and the synergies will reduce the levels of EMF exposure at which damage occurs,
sometimes dramatically.
Table A8-1
–
Appendix 8 References
Category/References
Automotive Extremely Low Frequency (ELF) Exposures
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A8-B2. Automotive Radar
Radar has become ubiquitous on modern automotive vehicles. Many of the new ‘safety’
systems use radar in their operation, and in-cabin radars have been proposed to further enhance
‘safety’. How safe are these radar add-ons,
and what are their potential radiation levels?
The FCC used to have a requirement that when cars were stopped, such as in a traffic jam
or at a traffic light, any onboard radars would have to reduce power to minimize longer-term
exposure to humans. In 2009, Toyota applied to relax these rules, for reasons described in the
linked document below. Naturally, the FCC complied with the request, as per the following
2012 directive addressing vehicle radar systems:
https://www.federalregister.gov/documents/2012/08/13/2012-19732/operation-of-radar-systems-
in-the-76-77-ghz-band.
The FCC promulgated the following emission limits:
"In lieu of separate emission limits for in-motion and not-in-motion, the Commission
proposed to increase the average power density limit to 88 µW/cm2 at 3 meters (average EIRP of
50 dBm) and to decrease the peak power density limit to 279 µW/cm2 at 3 meters (peak EIRP of
55 dBm) for vehicular radar systems regardless of the direction of illumination."
Converting units, the average power density limit would be 88*10^4 microwatts/square
meter, or 880,000 microwatts/square meter,
at three meters.
So, in slow moving traffic on a
superhighway, if there was six meters separation between the bumper of the car behind and the
driver of the car ahead (a conservative estimate in bumper-to-bumper traffic), there could be as
much as
220,000 microwatts/square meter radiating the front vehicle,
if the radars were
operating at the allowable limit. Some bands would be absorbed by the glass at these
frequencies, and other bands would penetrate the glass. There could also be side radar coming
from cars other than the rear car.
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However, pedestrians or highway workers would not have whatever protections from
wireless radiation are afforded by vehicle structures. For example, a person walking on a
crosswalk in front of stopped traffic could even be closer to the bumper than three meters, and
could be exposed directly full body to a
million microwatts/square meter,
or more, if the radars
were operating at the allowable limit! Children walking close to a vehicle would be even more
vulnerable, since they are closer to the horizontal plane of bumper antennas. And, these numbers
carry the assumption of being radiated from one car only. If there are multiple cars, with some
emissions spreading to the side, then the cumulative exposures could be well above the FCC
exposure limits at selected points. Walking on streets in high traffic areas may become a
dangerous pastime, and few people realize it!
Are there sources of radar potentially entering the vehicle cabin other than those from the
‘safety’ sensors? The answer is yes (at least in the future
and maybe in the present), as shown in
the following article: https://www.eetimes.com/document.asp?doc_id=1333330.
The author of the above article states:
"For example, the digital processing capability inside the mmWave sensor can filter out
noise, said Wasson, allowing TI’s radar chips to detect very
small movements, even the
breathing that indicates the presence of a person or animal inside a vehicle.
Wasson noted that “child occupancy detection” is likely to become a feature in the Euro
NCAP roadmap. This, he believes, will open the door for TI’s radars
in body, chassis, and in-
cabin applications. As tier ones and OEMs look for the right sensing technology to enable such
detection possibilities, Wasson noted that radars are much better-positioned.
Radar, for example can “see” through a blanket to determine
whether a child is
underneath. TI’s radar chips can even distinguish between a person and a static object like a
duffel bag, explained Wasson, because their on-chip digital signal processing can detect a
heartbeat."
The aim seems to be to deliberately flood the cabin with radar RFR, for various detection
purposes. The article makes no mention about potential power levels.
Another potential in-cabin source would be radar aimed at the driver continuously, to
insure alertness and awareness. For example, consider the following statement:
"Sudipto Bose, director of marketing for automotive radar at Texas Instruments, points
out that in-cabin radar offers a number of benefits. It can alert parents if they've left children in a
car, and it can be used for gesture controls, which let drivers control navigation, phone and stereo
with hand motions. This proximity radar could also identify if a driver's attention is not focused
out the windshield.....If automakers take Texas Instruments up on its new radar sensors, a
production vehicle with radar-based gesture control would still be two to five years away
(https://www.cnet.com/roadshow/news/volkswagen-invests-100-million-to-develop-solid-state-
battery-tech/)."
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There appears to be a developing market focused on occupancy sensing using radar. For
example, “So
radar is no longer the preserve of complex and costly, high-end markets, it's ready
for 100% reliable infant presence detection in cars. Whether our children’s movements are
major, minor or finer, they’ll be detected and the driver can be automatically reminded: ‘Don’t
forget, you have someone very precious in the back seat of your car.’
(
https://www.xethru.com/blog/posts/hot-car-deaths-radar-tech-can-help-save-lives
)”.
As another example:
“Startup
Caaresys imagines its radar-based system monitoring the
respiration and heart rates of everyone in the car, with a particular focus on sensing a child that
might be hidden from view in the back and potentially left behind in the car
(
https://www.cnet.com/roadshow/news/in-car-monitoring-surveillance-technology-privacy/
).”
Novelic (
https://www.novelic.com/applications-and-system-solutions/
) offers radar-based
sensors for car interiors, including: Seat Occupancy Sensor; Vital Signs Detection Sensor;
Passenger Detection Sensor;
“Baby left in a car” Sensor;
Driver and Passengers Fatigue Sensor;
Driver and Passengers Emotion Sensor. Other non-car applications include: Baby crib
monitoring; Assistive Living for Elderly People; Visual Impairments Sensor; Emotion Sensor.
Azcom (
http://www.services.azcomtech.com/index.php/services/mmwave-
sensors/automobile-in-cabin-monitoring/
) promotes continuous in-cabin monitoring as follows:
“In
case of autonomous vehicles, it will also be critical to continuously monitor vehicle occupancy
without creating privacy concerns. Radar sensors, combined with special ad hoc algorithms, are
well-suited for such applications.”
There are even nascent efforts to make some of these systems mandatory. For example,
“U.S.
lawmakers and European safety regulators are considering rules that could mandate "child
presence detection" systems aimed at avoiding hot-car deaths of unattended children. That has
suppliers scrambling to develop new systems for automakers, according to interviews with
several high-tech suppliers at a recent industry conference here….."The moment you have
regulation, things are going to move fast," Melamed told Automotive News. "The timelines are
very, very close."”
(
https://www.autonews.com/regulation-safety/safety-idea-gets-mandate
)
Also, it's not clear how the FCC exposure limits (which are already six orders of
magnitude higher than exposures shown in the biomedical literature to cause damage) would
apply to limit in-cabin radiation levels. Would they apply to each source, or to the total
radiation? The former seems more likely, since it is unclear how they would enforce the latter.
If that is the case, cabin occupants could be exposed theoretically to radiation levels in excess of
the FCC present limits.
In sum, the occupants of a hybrid vehicle with a full load of passengers will be subject to:
*ELF-EMF from the tires and other sources unique to hybrids
*RFR from the
passengers’
cell phones
*RFR from Bluetooth
*RFR from the WiFi 'hot spot' and the devices communicating with the hot spot
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*RFR from the myriad cell towers that dot the sides of most highways
*RFR from the radar sensors of other cars
*RFR from on-board radar sensors to detect motions and driver alertness within the cabin
Almost all these radiation sources will also be operable in a gasoline-powered car, and
there will be some radiation reflections within the cabin because of the surrounding metal.
Our studies on combinations of toxic stimuli including non-ionizing radiation [Kostoff et
al, 2018; Kostoff and Lau, 2013, 2017] showed that adverse health effects are exacerbated when
non-ionizing radiations of different characteristics are combined. What would be the effects of
the above complex combination that goes well beyond EMF constituents?
The middle part of
Table A8-1
contains references to other studies showing deliberate
radar impingement on vehicle occupants.
A8-B3. Automotive Wireless Networks
The past decade has seen an increasing number of wireless networks that are fully or
partially intra-vehicular. The final segment of
Table A8-1
presents only a small part of the
studies that have been done to expand these intra-vehicular wireless networks. The remainder of
this appendix addresses two of these many intra-vehicular networks, and it is based on my
personal experience with these two networks.
A8-B3a. Keyless Access Network
As mentioned at the beginning of this appendix, about six months ago I bought a new car.
One of the features in the particular model trim is the ability to open the doors and allow engine
ignition with a key fob in proximity. This capability is not unique to the model I bought. Far
from it! My search process showed that the push-button start capability is rapidly becoming
ubiquitous in new cars. The strenuous process of turning a key in a lock is thereby bypassed.
According to the Owner's Manual, my new car has a 130+ KHz continuously operating
wireless network that allows 1) the doors to be opened and closed, and 2) the ignition to be
started by push-button, when the key fob is within proximity of the car. The Owner's Manual
also states that the radio waves from the network could potentially interfere with an implanted
pacemaker or defibrillator, and accompanies this statement with a Warning icon.
Luckily, according to the Owner's Manual, this wireless system/function can be disabled.
The disabling is allowed not because of any manufacturer-stated concern for the adverse effects
of wireless radiation on normal humans. It is allowed because it could potentially interfere with
the operation of pacemakers and other similar devices.
The Owner's Manual provides two approaches to disabling the keyless access capability,
thereby converting the key fob to effectively a key with some remote-control functions (like the
TV remote-control). Disabling this capability is not a simple process, as I discovered. I was not
able to do it myself, even though two alternative methods were provided in the Owner's Manual.
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The dealer from whom I bought the vehicle said the disabling was not possible, and the second
dealer I visited required two technicians to experiment before they could finally disable it.
Here's the critical point of this narrative. The technicians (and other service personnel) of
the second dealer told me
no one had ever requested this disabling before!
From the first
dealer's feedback, I'm sure they had never received such a request either.
This means that the customers with implanted electrical devices who purchase these
vehicles are (for the most part) not disabling the 130+ KHz wireless network. My guess is they
don't even know about this network. None of the salespeople I had at any of the dealerships who
offered test drives in cars with keyless access function (and in my case there were probably half
a dozen different brands I drove that had this capability) asked whether I had an implantable
electrical device (I don't) nor mentioned the presence of the 130+ KHz network, or any other
frequency applicable to their model/brand. I doubt whether any of them knew!
Here's the bottom line. If people with implantable devices are not motivated to eliminate
these wireless networks, where there exists a rather obvious potential danger to health, how will
healthy (or relatively healthy) people become motivated to avoid wireless systems/radiation?
Whatever dangers the 130+ KHz network (or different frequency networks of other
brands performing the same function) would pose in isolation, I suspect the adverse effects
would be amplified substantially in combination with the other toxic stimuli sources I mentioned
in previous sections. While one could make arguments about some applications of wireless
radiation being useful/justified in extreme emergencies, installing a potentially harmful wireless
network to eliminate inserting a key into a lock is technology gone mad!
A8-B3b. Tire Pressure Monitoring System
Another intra-vehicular source of wireless radiation entering the automobile cabin is the
tire pressure monitoring system (TPMS). TPMS has been mandated in the USA by the TREAD
Act, and has been installed on all cars for the past decade. (https://en.wikipedia.org/wiki/Tire-
pressure_monitoring_system). It is mandated and used in many other countries as well.
There are myriad types of these sensors. Most Direct TPMS deploy tire pressure sensors
on each wheel of a vehicle. As tire pressure data is collected for each tire, it is sent to one or
more TPMS receivers, using RF (radio frequency) technology. The majority of Direct TPMS
installations transmit their data via UHF (Ultra High Frequency) radio. TPMS data is typically
transmitted in one of two frequency ranges, which depends on the geographical location of the
TPMS: about 433MHz in Europe, and at 315MHz in most other parts of the world.
https://tpms247.com/blogs/tpms-faq/73376901-tpms-frequencies-315-mhz-433mhz.
I didn’t find any articles addressing adverse health effects from the TPMS. That doesn’t
mean they don’t exist. There may be myriad reasons why I didn’t find adverse health effects.
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A8-B4. Other
The latter part of Table A8-1 alludes to many other types of networks being studied, as
well as optimizing some already implemented. Most of these are not mentioned in my new car
Owner’s Manual, since I assume they don’t affect pacemakers and defibrillators (at least
according to whomever has responsibility for monitoring such systems). The only way to fully
understand the levels of wireless radiation to which vehicle occupants are being subjected is
through detailed measurements of the wireless radiation environment.
This would include full spectrum monitoring (from 1 Hz for ELF to >100 GHz for
millimeter-wave communications and detection). Testing would be done under at least four
conditions:
•
•
•
•
no passengers and in an EMF quiet zone, with all on-board electronics operating;
with passengers using myriad wireless devices, in EMF quiet zone, and with all on-board
electronics operating;
no passengers and in a typical urban business high EMF antenna concentration zone, and
with all on-board electronics operating;
with passengers using myriad wireless devices, in high EMF high antenna concentration
zone, and with all on-board electronics operating.
Those results should begin to provide some idea of the complex and potentially dangerous
wireless radiation environment that many commuters face.
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ABOUT THE AUTHOR
Ronald Neil Kostoff received a Ph. D. in Aerospace and Mechanical Sciences from Princeton
University in 1967. He has worked for Bell Laboratories, Department of Energy, Office of
Naval Research, and MITRE Corp. He invented the Wake Shield for producing high vacuum
in low orbit, and used in manned space missions for research and development. He has
published over 200 peer-reviewed articles, served as Guest Editor of four journal Special Issues
since 1994, obtained two text mining system patents, and presently is a Research Affiliate at
Georgia Institute of Technology.
He has published on numerous medical topics in the peer-reviewed literature, including:
•
potential treatments for
o
Multiple Sclerosis,
o
Parkinson's Disease,
o
Raynaud's Phenomenon,
o
Cataracts,
o
SARS,
o
Vitreous Restoration,
o
Peripheral Neuropathy/Peripheral Arterial Disease
o
Alzheimer's Disease, and
o
Chronic Kidney Disease;
•
potential causes of Chronic Kidney Disease;
•
potential causes of Alzheimer's Disease;
•
potential causes of Peripheral Neuropathy/Peripheral Arterial Disease
•
potential impacts of Electromagnetic Fields on health; and
•
synergistic effects of toxic stimuli combinations.
His recent publications in toxicology have shown that regulatory exposure limits to toxic
stimuli are, on average, orders of magnitude too high compared to exposures shown to cause
damage in the biomedical literature, and are not protecting the public from harmful substances.
He is listed in:
•
Who's Who in America, 60th Edition (2006),
•
Who's Who in Science and Engineering, 9th Edition (2006), and
•
2000 Outstanding Intellectuals of the 21st Century, 4th Edition, (2006).
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REPUBBLICA
ITALIANA
Sent. N.
Cron. N.
R. Gen. N.
361/08
IN NOME DEL POPOLO ITALIANO
La Corte d’Appello di Brescia, Sezione Lavoro,
composta dai
Sigg.:
Dott.
Dott.
Dott.
Angelo
Antonella
Anna Luisa
TROPEANO Presidente
NUOVO
TERZI
Consigliere rel.
Consigliere
ha pronunciato la seguente
SENTENZA
nella causa civile promossa in grado d’appello con ricorso depositato
in Cancelleria il giorno 08/07/2008 iscritta al n. 361/08 R.G. Sezione
Lavoro
10/12/2009
da
XXX,
rappresentato e difeso dall’Avv.to Danilo MINA di Brescia,
domiciliatario giusta delega a margine del ricorso in appello
RICORRENTE APPELLANTE
OGGETTO:
contro
Prestazione: indennità
e posta in discussione all’udienza collegiale del
I.N.A.I.L.,
in persona del Direttore Regionale pro tempore,
rendita vitalizia INAIL
rappresentato e difeso dall’Avv.to Sabina LUPO ed elettivamente
o equivalente – altre
domiciliato presso l’Avvocatura Distrettuale I.N.A.I.L di Brescia
ipotesi
giusto mandato generale alle liti
RESISTENTE APPELLATO
In punto: appello a sentenza n. 471/08 del 15/05/2008 del Tribunale
di Brescia.
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CONCLUSIONI
Del ricorrente appellante:
come da ricorso in appello
Del resistente appellato:
come da memoria di costituzione e risposta
Svolgimento del processo
Con ricorso al Tribunale di Brescia, giudice del lavoro,
depositato il 6.7.2007 Innocente XXX conveniva l’INAIL per sentirlo
condannare a corrispondergli le prestazioni di legge in riferimento ad
una grave e complessa patologia cerebrale che aveva origine
professionale. Esponeva, in fatto, di aver svolto attività di dirigente
d’azienda dal 1981, e, da ultimo, presso la S.p.a. Sangiacomo dal
2.9.1991 al 26.9.2003; che in tale mansione aveva utilizzato il
telefono cellulare e il cordless per una media di 5 - 6 ore al giorno e
per un periodo di 12 anni; che, essendo destrimane, teneva
l’apparecchio all’orecchio sinistro in quanto con la mano destra
rispondeva al telefono fisso collocato sulla scrivania o prendeva note
e appunti; che detta attività gli aveva provocato una grave patologia
per la quale il 17.11.03 aveva chiesto all’INAIL le corrispondenti
prestazioni di legge, che l’Istituto aveva rifiutato la richiesta, negando
il nesso causale fra l’attività lavorativa e le affezioni denunciate.
Pertanto insisteva nella domanda, deducendo prova per testi sulle
modalità lavorative ed allegando un’approfondita relazione medico-
legale del neurochirurgo dott.Giuseppe Grasso.
L’INAIL si opponeva al ricorso, sempre sotto il profilo della
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carenza del nesso causale, e deduceva controprova orale, producendo
varia documentazione.
Esperita l’istruttoria testimoniale, che accertava in fatto l’uso
intenso di cellulare e cordless, ed assunta consulenza tecnica
d’ufficio, il primo giudice respingeva la domanda per carenza del
nesso causale, aderendo alle considerazioni svolte dal CTU,
aspramente criticate dal ricorrente.
Appellava il XXX, depositando ulteriore e ponderoso
elaborato del consulente di parte, riportandosi alle considerazioni
critiche ivi svolte e chiedendo che, previo rinnovo della consulenza,
l’INAIL fosse condannato alle prestazioni di legge.
Si
costituiva
l’INAIL
per
la
conferma,
ricordando
l’inesistenza di studi scientifici attendibili in ordine alla nocività delle
onde elettromagnetiche.
Questa Corte rinnovava la consulenza e, a fronte delle
osservazioni svolte dall’INAIL, concedeva termine all’appellante per
depositare le sue controdeduzioni: all’esito, all’udienza odierna, le
parti discutevano e la Corte decideva con sentenza del cui dispositivo
veniva data immediata lettura.
Motivi della decisione
La CTU disposta in questo grado di giudizio, molto
documentata ed accuratamente motivata, individua il nesso, quanto
meno concausale, tra l’utilizzo dei telefoni e la patologia.
Innanzitutto, occorre osservare che l’allegato utilizzo di
cellulare e radiotelefono per molte ore lavorative (5-6 ore / die) e
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l’uso principalmente dell’orecchio sinistro, che consentiva il libero
impiego della mano destra per note scritte, hanno trovato piena
conferma testimoniale e non sono più oggetto di contestazione da
parte dell’INAIL.
Da questo dato, che quantifica il livello di esposizione,
doveva dunque partire il consulente per la sua indagine sul nesso
causale.
Dall’anamnesi clinica risulta che nel giugno 2002 è comparsa
ipoanestesia (perdita parziale della sensibilità) dell’emiviso di
sinistra: eseguita la Risonanza Magnetica Nucleare veniva formulata
diagnosi di “neurinoma del Ganglio di Gasser” che è un tumore
benigno che colpisce i nervi cranici, in particolare il nervo acustico,
mentre più rara è la localizzazione al V nervo cranico (Trigemino),
come nel caso in specie. Secondo la spiegazione fornita dal
consulente, deriva dalle cellule (cellule di Schwann) della guaina di
rivestimento da cui anche la denominazione di Schwannoma. La
localizzazione anatomica di questo tumore dà ragione della severità
delle manifestazioni cliniche correlate.
Subiva quindi un intervento neurochirurgico l’8 novembre
2002 (Ospedale S. Anna di Lucerna) con resezione branca
mandibolare del nervo in quanto non dissociabile, asportazione del
ganglio di Gasser, ma permaneva residuo tumorale dimostrato a RMN
post operatoria.
Gli esiti post intervento possono così essere riassunti: 1)
ulcera corneale sin. (da iposecrezione lacrimale e disturbo
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neurologico). Attuò vari trattamenti per risolverla. E’ in atto un
trattamento cronico con autosiero. Graduale deficit del visus ( 3-4
diottrie); 2)Sindrome algo-distrofica dell’emiviso di sinistra con
dolore cronico severo. Attuati vari e ripetuti trattamenti con farmaci
attivi sul dolore neuropatico con scarso o nullo beneficio. Dall’agosto
1.08.2005 assunzione orale di morfina (Oxicontin 20mg x3 /die) in
associazione con pregabalin (Lyrica 75mg x 3. trattamento del dolore
neuropatico periferico e centrale negli adulti). Valutazione dolore di
5-6 con scala numerica verbale (scala di valutazione del dolore
cronico. Valori da 1-nessun dolore- a 10-il peggiore dolore
immaginabile-. Il dolore si considera controllato per un indice ~4); 3)
Persistenti parestesie sempre all’emiviso; 4) Disturbi della meccanica
masticatoria da mal occlusione secondaria ad atrofia dei muscoli
temporale massetere di sinistra (attua fisiochinesiterapia per
mantenere il trofismo); 5) Incostante diplopia (visione doppia, in
senso orizzontale o verticale, di uno stesso oggetto) 6) Epilessia
parziale
complessa
a
genesi
temporale
da
encefalomalacia
(rammollimento cerebrale legato al trauma chirurgico con perdita di
funzione possibile origine di foci epilettogeni); 7) Deficit cognitivo (
disturbo della fissazione mnesica e ed attenzione); 8) Disturbo
dell’adattamento (Nel Diagnostic and Statistical Manual of mental
disorders [DSM-N] i disturbi dell’adattamento sono definiti come
"sintomi emozionali o comportamentali clinicamente significativi"
che si sviluppano "in risposta a uno o più fattori stressanti psicosociali
identificabili"); 9) sindrome del lobo temporale (sindrome complessa
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da danno del lobo temporale con vari disturbi-olfattivi, gustativi,
dell’equilibrio, visivi, disturbi uditivi e psichiatrici)
Tutte
queste
situazioni
cliniche
sono
ampiamente
documentate negli atti. Ogni patologia è suffragata da consulenze
cliniche specialistiche, anche ripetute, e da opportune indagini
strumentali ed ematochimiche.
Nel 2003 diagnosi di neoformazione surrenalica di destra 5x3
cm con normofunzione. Intervento 30.06.2004 Istituto Europeo di
Oncologia con diagnosi istologica di feocromocitoma (tumore raro
con possibile secrezione di catecolamine [sostanze ormoni e
neurotrasmettitori- prodotte dalla porzione interna del surrene e da
alcuni neuroni] II tumore in presenza di secrezione di catecolamine si
caratterizza per una sindrome clinica peculiare).
Nel caso in specie, non fu dimostrata secrezione di
catecolamine.
E’ seguito da uno psichiatra dal 2003 ed è in terapia con
paroxetina; due ricoveri c/o Servizio Psichiatrico di Diagnosi e Cura
l’ultimo nel marzo 2008.
Attuale terapia comprende Morfina orale, Pregabalin,
Paroxetina (farmaco antidepressivo appartenente alla classe degli
SSRI-inibitori selettivi della ricaptazione della serotonina), Dolore
attuale riferito 5-6 con scala numerica verbale.
Si presente come soggetto magro in mediocri condizioni
generali. Normale sanguinificazione. Sensorio normale orientamento
spazio temporale. Tono dell’umore depresso. Crisi di pianto in corso
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della valutazione clinica. Paresi del VII nervo cranico con ipostenia
del muscolo orbicolare. Anestesia dolorifica abolita sensibilità tattile.
Asimmetria degli emivisi. Dolorabilità alla pressione su articolazione
temporo-mandibolare sin. Lieve tendenza all’intrarotazione mano dx
in estensione.
La prima valutazione del consulente è che gli esiti della
neoplastica son assolutamente severi e del tutto documentati e che la
qualità di vita del sig. XXX è sicuramente gravemente compromessa
da tali esiti.
Quanto alla questione centrale (non essendovi contestazione
sulle conseguenze subite dall’appellante) relativa al nesso causale tra
l’uso dei telefoni e insorgere della patologia, il consulente osserva
innanzitutto che, vel periodo in cui ha lavorato alla San Giacomo SPA
per i primi 3 anni utilizzava telefono cellulare - cordless (deposte 5-6
h al di), dal 1993-4 al cordless fu associato l’uso di telefono cellulare
fino al settembre 2003.
Orbene, i telefoni mobili (cordless) e i telefoni cellulari
funzionano attraverso le onde -elettromagnetiche. Secondo il CTU “In
letteratura gli studi sui tumori cerebrali per quanto riguarda il
neurinoma considerano il tumore con localizzazione al nervo acustico
che è il più frequente. Trattandosi del medesimo istotipo è del tutto
logico assimilare i dati al neurinoma del trigemino”.
Nella CTU, con una tabella molto chiara a cui ci si riporta,
sono riassunti alcuni studi dal 2005 al 2009. “In tre di essi (Hardell
group) e si evidenzia un aumento significativo del rischio relativo di
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neurinoma. (Rischio relativo: misura di associazione fra l’esposizione
ad un particolare fattore di rischio e l’insorgenza di una definita
malattia, calcolata come il rapporto fra i tassi di incidenza negli
esposti [numeratore] e nei non esposti [denominatore]. Esempio: un
rischio relativo di 3 sta a significare che il tasso di incidenza negli
esposti è 3 volte maggiore dei non esposti. Nella tabella il rischio
relativo è derivato dall’odd ratio )
Un recente lavoro, sempre del gruppo di Hardel (Mobile
phones, cordless phones and the risk far brain tumours L. Hardell and
M. Carlberg INTERNATIONAL JOURNAL OF O COLOGY 35: 5-
17, 2009), che si basa sulla revisione degli studi già pubblicati dallo
stesso gruppo, considera altri elementi quali: età dell’esposizione,
ipsilaterlaità e tempo di esposizione. Per quanto riguarda il neurinoma
(dell’acustico) i risultati indicano un Odd ratio per l’uso del cordless
di 1,5 e per il telefono cellulare di 1,7. Considerando l’uso> di 10
anni, gli Odd ratio sono rispettivamente di 1,3 e di 1,9.
L’Odds ratio è il rapporto tra la frequenza con la quale un
evento si verifica in un gruppo di pazienti e la frequenza con la quale
lo stesso evento si verifica in un gruppo pazienti di controllo. Se il
valore dell’odds ratio è superiore a 1 significa che la probabilità che si
verifichi l’evento considerato (per esempio una malattia) in un gruppo
(per esempio tra gli esposti) è superiore rispetto a quella di un altro
gruppo (per esempio tra i non esposti). Significato opposto ha un
valore inferiore a 1 (riduzione del rischio legato all’esposizione). Se il
valore è pari a 1 significa che non vi è differenza tra i gruppi. In caso
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di eventi rari l’odds ratio ha un valore molto vicino a quello del
rischio relativo. L’odds ratio è una misura particolarmente utile negli
studi caso-controllo come stima del rischio relativo, che in questo tipo
di studi non può essere misurato direttamente.
Una recente review della The International Commission on
Non-Ionizing Radiation Protection (Exposure to high frequency
electromagnetic fields, biological effects and health consequences
100 kHz-300 GHz. Review of the scientific evidence on dosimetry,
biologicaI
effects,
epidemiological
observations,
and
health
consequences concerning exposure to high frequency electromagnetic
fields 100 kHz to 300 GHz, 2009) evidenzia i limiti degli studi
epidemiologici fin’ora attuati. I principali "bias" riguardano la
modalità di arruolamento, spesso l’assenza di un gruppo di controllo
con ricorso a registri di popolazione, l’impossibilità di standardizzare
l’entità e la durata complessiva di esposizione. Gli autori concludono
che, allo stato attuale, non vi è una convincente evidenza del ruolo
delle radiofrequenze nella genesi dei tumori, ma aggiungono che gli
studi non ne hanno escluso l’associazione (pag 336 "Results of
epidemiological studies to date give no consistent or convincing
evidence of a causal relation between RF exposure and any adverse
health effect. On the other hand, these studies have too many
deficiencies to rule out an association").
A questo punto è utile dedicare spazio ad un’altra review del
tutto autorevole.
Kundi nel 2009 (The Controversy about a Possible
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Relationship between Mobile Phone Use and Cancer Michael Kundi
Environ Health Perspect. 2009 March; 117,3: 316-324) L’autore
conferma i dubbi che gli studi epidemiologici inducono per quanto
riguarda il tempo di esposizione e conclude per rischio individuale
basso, ma presente. L’esposizione può incidere sulla storia naturale
della neoplasia in vari modi: interagendo nella fase iniziale di
induzione, intervenendo sul tempo di sviluppo dei tumori a lenta
crescita, come i neurinomi, accelerandola ed evitando la possibile
naturale involuzione.
L’analisi della letteratura non porta a un giudizio esaustivo,
ma con tutti i limiti insiti nella tipologia degli studi, un rischio
aggiuntivo per i tumori cerebrali, ed in particolare per il neurinoma, è
documentato dopo esposizione per anni (>10) a radiofrequenze
emesse da telefoni portatili e cellulari.
Il dato anamnestico di esposizione supera il limite dei 10
anni.
Il tempo di esposizione è elemento valutativo molto rilevante.
Nello studio di 2006 l’esposizione per più di 10 anni comportava un
rischio relativo calcolato di 2,9 sicuramente significativo (pur
considerando i limiti metodologici già illustrati) Si tratta quindi di una
situazione "individuale" che gli esperti riconducono al "modello
probabilistico-induttivo" ed alla "causalità debole" (Angelo Fiori Atti
VI Convegno Nazionale di Medicina Legale Previdenziale 2006), che
ha comunque valenza in sede previdenziale.
Un ruolo quindi, almeno concausale, delle radiofrequenze
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nella genesi della neoplasia che ha patito il sig. XXX è "probabile"
(probabilità qualificata)” (vedi CTU dott. Di Stefano pag. 8 e 9).
L’esito della malattia ha condotto ad una menomazione
stimata nella misura, incontestata, del 80%.
L’Inail ha criticato l’elaborato sostenendo in primo luogo che
la prima asserzione del CTU sarebbe errata: utilizzare gli studi relativi
al neurinoma dell’acustico per analizzare un caso di neurinoma del
trigemino non sarebbe possibile in quanto si tratterebbe di tumore a
diversa localizzazione in quanto relativa a diverso distretto
anatomico.
La
censura
non
merita
accoglimento:
infatti,
come
correttamente spiegato dal consulente, i due neurinomi appartengono
al medesimo distretto corporeo in quanto entrambi i nervi interessati
si trovano nell’angolo ponto-cerebellare, che è una porzione ben
definita e ristretta dello spazio endocranico certamente compresa nel
campo magnetico che si genera dall’utilizzo dei telefoni cellulari e
cordless.
Una seconda censura riguarda gli studi utilizzati dal CTU per
rispondere positivamente al quesito: si tratterebbe infatti di studi su
un basso numero di casi mentre lo studio del 2000 dell’OMS ha
escluso effetti negativi sulla salute. Anche questa censura però non
coglie nel segno.
Lo studio dell’OMS, risalente appunto al 2000 e basato su
dati, ovviamente, ancora più risalenti, non tiene conto dell’uso più
recente, ben più massiccio e diffuso, di tali apparecchi e del fatto che
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- 12 -
si tratta di tumori a lenta insorgenza: pertanto gli studi del 2009,
basati su dati più recenti, sono di per sé più attendibili. Inoltre, come
ha osservato nelle controdeduzioni il ct di parte del XXX, non si tratta
di studi su un basso numero di casi, ma, al contrario, del tutto
esaustivo in quanto tratta di 678 casi, che sono il numero totale che si
verifica in un anno in Italia (trattandosi di tumore non frequente).
Inoltre, a differenza dello studio della IARC, co-finanziato dalla ditte
produttrici di telefoni cellulari, gli studi citati dal dott. Di Stefano
sono indipendenti.
Naturalmente, secondo il costante insegnamento della
Suprema Corte, nel caso di malattia professionale non tabellata, come
anche in quello di malattia ad eziologia multifattoriale, la prova della
causa di lavoro, che grava sul lavoratore, deve essere valutata in
termini di ragionevole certezza, nel senso che, esclusa la rilevanza
della mera possibilità dell’origine professionale, questa può essere
invece ravvisata in presenza di un rilevante grado di probabilità. A
tale riguardo, il giudice deve non solo consentire all’assicurato di
esperire i mezzi di prova ammissibili e ritualmente dedotti, ma deve
altresì valutare le conclusioni probabilistiche del consulente tecnico in
tema di nesso causale, considerando che la natura professionale della
malattia può essere desunta con elevato grado di probabilità dalla
tipologia delle lavorazioni svolte, dalla natura dei macchinari presenti
nell’ambiente di lavoro, dalla durata della prestazione lavorativa e
dall’assenza di altri fattori extralavorativi, alternativi o concorrenti,
che possano costituire causa della malattia.
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Nel caso di specie, il CTU ha spiegato i valori di odd ratio
che lo portano a sostenere la probabilità qualificata del ruolo, quanto
meno,
concausale,
dell’uso
dei
telefoni
nella
causazione
dell’infortunio, ma, per rendere più evidente la reale portata di quanto
affermato, appare utile dar conto dell’esempio che il ct di parte ha
fatto nelle contro-osserazioni depositate il 25.11.2009. Partendo dai
dati indicati dal CTU, il dott. Grasso afferma essere utile confrontare
il dato di rischio individuale ottenuto dal consulente (2,9) con quello
ricavato per il fattore di rischio, universalmente riconosciuto,
dell’esposizione alle radiazioni ionizzanti. Afferma il dott. Grasso:
“Orbene: nei soggetti esposti a 1Gy di RI, come i sopravvissuti alle
esplosioni atomiche giapponesi di Hiroshima e Nagasaki, è stato
accertato un rischio relativo di tipo oncologico di 1,39 per “tutti i
tumori” con un minimo di 1,22 per i tumori di “utero e cervice” ed un
massimo di 4,92 per la “leucemia”, il che significa che il rischio
oncogeno medio delle RI è inferiore a quello che si ha per
l’esposizione alle radio frequenze in riferimento ai neurinomi
endocranici” (vedi relazione dott. Grasso depositata il 25.11.2009
pag.7 e 8).
Appare, quindi, evidentemente integrato il requisito di elevata
probabilità che integra il nesso causale richiesto dalla normativa.
Ne consegue che l’INAIL deve essere condannato a
corrispondere al XXX la rendita per malattia professionale prevista
per l’invalidità all’80%, con arretrati ed interessi di legge.
Le spese seguono la soccombenza e si liquidano per il primo
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- 14 -
grado in
€.1.800,00
(di cui euro 650 per diritti) e per il presente grado
in
€.2.000,00
(di cui euro 700 per diritti) con distrazione in favore del
procuratore antistatario. Le spese di CTU restano definitivamente a
carico dell’INAIL.
P.Q.M.
In riforma della sentenza n. 471/08 del Tribunale di Brescia
condanna l’INAIL a corrispondere all’appellante la rendita per
malattia professionale prevista per l’invalidità all’80%, con arretrati
ed interessi di legge; condanna l’INAIL alla rifusione delle spese di
ambo i gradi liquidate per il I grado in
€.1.800,00
e per il presente
grado in
€.2.000,00.
Brescia 10.12.2009
Il Consigliere est.
Il Presidente
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MOLECULAR AND CLINICAL ONCOLOGY 12: 247-257, 2020
COMMENT
Appeals that matter or not on a moratorium on the deployment
of the fifth generation, 5G, for microwave radiation
LENNART HARDELL
1,3
and
RAINER NYBERG
2,4
1
Department of Oncology, Faculty of Medicine and Health, Örebro University, SE‑701 82 Örebro, Sweden;
2
Faculty of Education and Welfare Studies, Åbo Akademi University, 65100 Vasa, Finland
Received September 21, 2019; Accepted January 3, 2020
DOI: 10.3892/mco.2020.1984
Abstract.
Radiofrequency (RF) radiation in the frequency
range of 30 kHz‑300 GHz is classified as a ‘possible’ human
carcinogen, Group 2B, by the International Agency for
Research on Cancer (IARC) since 2011. The evidence has since
then been strengthened by further research; thus, RF radiation
may now be classified as a human carcinogen, Group 1. In spite
of this, microwave radiations are expanding with increasing
personal and ambient exposure. One contributing factor is
that the majority of countries rely on guidelines formulated
by the International Commission on Non‑Ionizing Radiation
Protection (ICNIRP), a private German non‑governmental
organization. ICNIRP relies on the evaluation only of thermal
(heating) effects from RF radiation, thereby excluding a large
body of published science demonstrating the detrimental effects
caused by non‑thermal radiation. The fifth generation, 5G, for
microwave radiation is about to be implemented worldwide in
spite of no comprehensive investigations of the potential risks
to human health and the environment. In an appeal sent to the
EU in September, 2017 currently >260 scientists and medical
doctors requested for a moratorium on the deployment of 5G
until the health risks associated with this new technology have
been fully investigated by industry‑independent scientists. The
appeal and four rebuttals to the EU over a period of >2 years,
have not achieved any positive response from the EU to date.
Unfortunately, decision makers seem to be uninformed or even
misinformed about the risks. EU officials rely on the opinions
of individuals within the ICNIRP and the Scientific Committee
on Emerging and Newly Identified Health Risks (SCENIHR),
most of whom have ties to the industry. They seem to dominate
evaluating bodies and refute risks. It is important that these
circumstances are described. In this article, the warnings on the
health risks associated with RF presented in the 5G appeal and
the letters to the EU Health Commissioner since September,
2017 and the authors' rebuttals are summarized. The responses
from the EU seem to have thus far prioritized industry profits to
the detriment of human health and the environment.
Introduction
Over the years, numerous international appeals on radiofre-
quency (RF) radiation and health and the environment have
been published (e.g., www.emfscientist.org). These seem to
have had little or no impact on those proposing limits on RF
radiation and on the deployment of this technology. On the
contrary, ambient RF radiation exposure has increased and is
a potential health risk based on the current knowledge of the
biological effects of RF radiation (1‑8). There seems to be an
‘unholy’ alliance between the telecom industry and certain
scientists, organizations (even WHO), and some politicians,
thus reducing the potential for precautionary actions (9,10).
The International Agency for Research on Cancer (IARC)
of WHO in 2011 classified RF radiation in the frequency
range of 30 kHz‑300 GHz as a ‘possible’ human carcinogen,
Group 2B (11,12). Since then, the evidence of the adverse
effects of RF radiation has strengthened based on human
epidemiological (7,8,13) and animal studies (14‑16). These
results add scientific evidence to a previous evaluation (17).
Thus, RF radiation may now be classified as a human carcin-
ogen, Group 1. That is the strongest classification, which is the
same as that for e.g., asbestos and smoking.
The IARC cancer classification seems to have had little
or no impact on protecting the public against risks associ-
ated with RF exposure. A major hampering factor has been
the exposure guidelines by the International Commission
on Non‑Ionizing Radiation Protection (ICNIRP) based only
on the acute and very short‑term thermal (heating) effects
of RF radiation. These guidelines are used by the majority
of countries worldwide. These guidelines were initially
published approximately 20 years ago (18) and were updated
in 2009 (19); however, no changes were made to adapt to the
The Environment and Cancer Research Foundation, Studievägen 35,
SE‑702 17, Örebro, Sweden
E‑mail: [email protected]
3
Correspondence to:
Professor Lennart Hardell,
Present address:
Present address:
4
Fredsgatan 16 A 35, 65100 Vasa, Finland
radiofrequency electromagnetic field, EMF, 5G, EU, WHO,
moratorium, health risks, non‑ionizing radiation guidelines
Key words:
appeals, microwave radiation, radiofrequency radiation,
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248
HARDELL and
NYBERG: APPEALS ON THE DEPLOYMENT OF 5G
rapidly increasing evidence of the harmful effects of RF and
new RF signal characteristics and exposure from new technolo-
gies. ICNIRP, with the support of the WHO (10) and the major
telecom companies, has made considerable efforts to convince
countries worldwide to follow their guidelines. However, with
the deployment of the 5th generation of microwave radiation,
5G, even the obsolete ICNIRP guidelines may be exceeded
and may become an obstacle for the deployment of 5G (20).
Thus, ICNIRP is preparing new guidelines that are briefly
commented on below. However, as already published (9,10),
the ICNIRP guidelines may be contradictory to a vast number
of existing scientific reports demonstrating the harmful effects
of RF radiation (21). Furthermore, there may perhaps also be
conflicts of interests in terms of ties to the industry.
ICNIRP
On July 11, 2018, the ICNIRP released a draft of the guidelines
for limiting exposure to time‑varying electric, magnetic and
electromagnetic fields (100 kHz‑300 GHz). It was open for
public consultations until October 9, 2018. Appendix B was
based on the assessment of the health risks based on a literature
survey (https://www.icnirp.org/en/activities/public‑consulta-
tion/index.html).
Of note, in the background material to the new ICNIRP guidelines,
the IARC classification from 2011 of RF exposure as class 2B,
‘possibly’ carcinogenic to humans (11,12) was not included.
Notably, one of the ICNIRP commission members, Martin
Röösli (https://www.icnirp.org/en/about‑icnirp/commis-
sion/index.html), was also one of the IARC experts evaluating
the scientific RF carcinogenicity in May, 2011 (https://mono-
graphs.iarc.fr/wp‑content/uploads/2018/06/mono102‑F05.
pdf), which classified RF exposure as a class 2B ‘possible’
carcinogen. Thus, he should be aware of the IARC classifica-
tion. Of note, one of the authors of this article (L.H.) was a
member of the IARC expert group.
Below, eight excerpts/quotes from the 2018 ICNIRP
draft guidelines are presented (https://www.icnir p.
org /c m s /uploa d /c on su lt at ion _ uploa d / IC N I R P_ R F_
Guidelines_PCD_2018_07_11.pdf). These assertions in the
ICNIRP evaluation do not seem to represent the valid evalu-
ation of the published literature on the health risks associated
with RF:
i)
Brain physiology and function.
‘In summary, there is no
evidence of effects of radiofrequency EMF [electromagnetic
field] on physiological processes or eye pathology that impair
health in humans. Some evidence of superficial eye damage
has been shown in rabbits at exposures of at least 1.4 kW m-2,
although the relevance of this to humans has not been demon-
strated’.
ii)
Auditory, vestibular, and ocular function.
‘In summary,
no effects on auditory, vestibular, or ocular function relevant
to human health have been substantiated’.
iii)
Neuroendocrine system.
‘In summary, the lowest level at
which an effect of radiofrequency EMF on the neuroendocrine
system has been observed is 4 W kg-1 (in rodents and
primates), but there is no evidence that this translates to
humans or is relevant to human health. No other effects have
been substantiated’.
iv)
Neurodegenerative diseases.
‘In summary, no adverse
effects on neurodegenerative diseases have been substanti-
ated’.
v)
Cardiovascular system, autonomic nervous system and
thermoregulation.
‘In summary, no effects on the cardiovas-
cular system, autonomic nervous system, or thermoregulation
that compromise health have been substantiated for exposures
with whole body average SARs below approximately 1 W kg-1,
and there is some evidence that 4 W kg‑1 is not sufficient to
alter body core temperature in hamsters. However, there
is strong evidence that whole body exposures in rats that
are sufficient to increase body core temperature by several
degrees centigrade can cause serious adverse health effects
in rats’.
vi)
Immune system and hematology.
‘The few human studies
have not indicated any evidence that radiofrequency EMF
affects health in humans via the immune system or haema-
tology’.
vii)
Fertility, reproduction and childhood development.
‘In
summary, no adverse effects of radiofrequency EMF exposure
on fertility, reproduction or development relevant to human
health have been substantiated’.
viii)
Cancer.
‘In summary, no effects of radiofrequency EMF
on cancer have been substantiated’.
Since the ICNIRP 2018 draft guidelines excluded a large
number of science‑based evidence of health hazards from RF
radiation, numerous rebuttals have been sent to the ICNIRP.
However, it remains unknown as to whether these rebuttals
have been taken into account or not.
Thus, the ICNIRP does not acknowledge the health effects
caused by RF radiation. This has been rebutted by several
scientists (21-24).
Details and proofs of scientific misinterpretation were
outlined in a comprehensive response by Dr Martin Pall (21).
He demonstrated that the denials of scientific facts concerning
health risks seem to be the rule in the Health Risk Assessments
of the ICNIRP 2018 Draft Guidelines. ICNIRP confirmed
that Pall's response was received on October 8, 2018 (tinyurl.
se/pall). As outlined above in all eight summarizing state-
ments, the ICNIRP denies that any scientific reports exist
which demonstrate harmful effects below the ICNIRP guide-
lines. However, as Dr Pall demonstrated, a large number of
peer‑reviewed studies have been published over a period of
>20 years contradicting the ICNIRP evaluations. Independent
peer‑reviewed scientific articles (1,7,8) have demonstrated the
harmful effects even far below the current public safety limits
based on ICNIRP 1998 reference levels 10 W/m
2
for 2-300
GHz and 2‑10 W/m
2
for 400 to 2,000 MHz (18).
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MOLECULAR AND CLINICAL ONCOLOGY 12: 247-257, 2020
249
The ICNIRP also seems to have disregarded previously
published animal studies (14‑16) on carcinogenesis. The NTP
results have been discussed in a commentary (25) and clari-
fied to that degree that they should have been considered in
full. These findings supported human epidemiology results on
cancer risks from RF radiation (6,26). The final new ICNIRP
guidelines have yet to be published.
In fact, a hint of the ICNIRP final document may be found
in a presentation by the ICNIRP chairman Eric van Rongen
at a meeting held on April 17, 2019 https://www.anfr.
fr/fileadmin/mediatheque/documents/expace/workshop‑5G/2
0190417‑Workshop‑ANFR‑ICNIRP‑presentation.pdf.
van Rongen stated that there is no evidence that RF EMF
causes diseases, such as cancer and that the US NTP (14-15)
and Ramazzini Institute (16) studies are not convincing for
carcinogenesis. ICNIRP seems still to hold the view, which
is clearly beneficial to the industry, that only thermal effects
exist for RF radiation and not any non‑thermal effects, which
have been proven in research by the majority of scientists in
this field.
ICNIRP recently published a note on the NTP and Ramazzini
Institute animal studies (27). Some of their incorrect state-
ments are commented on below. The ICNIRP claims that
there is no verified mechanism for RF radiation carcinogen-
esis, in spite of well‑designed studies showing the contrary,
e.g., oxidative stress (25,28) and DNA damage (25,29). The
ICNIRP claims that the histopathological evaluation was not
blinded in these studies; however, this is not true, as supported
by the methods described in these studies. Furthermore, the
ICNIRP claims that the body core temperature was increased
in the NTP study (15) and suggested it to be a factor increasing
cancer risk, although heat is not a known carcinogen. The
ICNIRP also claims that only the Hardell group found an
increased risk for acoustic neuroma although the Interphone
study had similar findings (7). ICNIRP does not seem to take
into account the concordance between the tumor types found
in human epidemiological and animal studies. These are just
a few examples.
It is noteworthy that ICNIRP repeats certain debatable state-
ments in spite of being rebutted by Melnick (25) and should
have been known to the 13 ICNIRP Commission members
(https://www.icnirp.org/en/about‑icnirp/commission/index.
html) with their names listed at the end of the article (27).
Perhaps this ICNIRP article lacks scientific authorization. As
previously suggested, they seem to create doubt (30,31). Thus,
one must be cautious when also interpreting other publications
by the 13 Commission members.
The ICNIRP points out an important scientific problem: How
incorrect data can achieve lives of their own and gain respect-
ability and credence with inappropriate repetition. Corrections
and clarifications (25), seem to have difficult time to coun-
teract any possible errors, which is to the disadvantage of both
good science and public health. Of note, President Franklin
D. Roosevelt stated that
‘Repetition does not transform a lie
into a truth’
(https://www.azquotes.com/quote/377323).
Finland, in a new regulation, 1045/2018, dated December 15,
2018, allowed higher average radiation, 200 W, in narrow
areas of 1x1 cm (1 cm
2
) (please see Table 1.5, Note 3 (in
Swedish): (https://www.finlex.fi/data/sdliite/liite/6943.pdf).
This was probably decided in order to accommodate the
steerable, beam‑formed, narrow 5G fields, which will be used
by most 5G equipment. The Director of the Radiation Safety
Agency in Finland claims that this is no problem, as if you
disperse the effect of 200 W (on 1 cm
2
) upon a whole square
meter it will still be within the ICNIRP guideline of 10 W/m
2
(private communication from Petteri Tiippana, 2018, please
see https://www.dropbox.com/s/89cm7bmb410em8w/200W%
3Am2‑STUK.pdf?dl=0).
On top of the other flaws which ICNIRP members are
presenting, they also suggest that only the ‘mean values’ of RF
radiation should be measured. However, the interferences and
the supra‑additive effects between pulses from different RF
radiation sources can lead to ‘hundreds of thousands higher
density’ short‑time pulses than the power density mean values
with the guideline of 10 W/m
2
. This has been well‑documented
in a report from the Finnish Radiation Safety Agency (32).
Panagopoulos (29) has clearly demonstrated that using mean
values for RF radiation may underestimate the risk. Intensity,
frequency, exposure duration, polarization, pulsing and modu-
lation are crucial parameters for the bioactivity. Puranen (32)
states that the instant effect density can be much stronger than
the mean values. However, the guidelines only consider the
mean values.
Appeals to the EU and responses from the EU
The impact of the many international appeals on RF radiation
safety, if any, is unclear. However, they will be historical docu-
ments on warnings that have been thus far ignored by the EU
and the WHO. This is exemplified below.
The deployment of 5G for microwave radiation has given
increasing awareness and concern among individuals
regarding the risks to human health and the environment
resulting in massive protests and even a moratorium in certain
EU countries and US cities (https://tinyurl.se/5gstoppers). 5G
uses a different technology compared with previous genera-
tions, such as 2G, 3G and 4G. In the following, our 5G appeal
to EU is discussed (www.5Gappeal.eu). This has currently
been signed by >260 scientists and medical doctors from a
number of countries. It is still open for endorsement.
a) The 5G Appeal, September 13, 2017 and response.
Below,
the full text, with included links to references, is presented
although it can also be found online (www.5gappeal.eu), and
also at (https://www.environmentandcancer.com/5g‑appeal/).
Scientists and doctors warn of potential severe health effects
of 5G.
‘We the undersigned scientists and doctors recommend
a moratorium on the roll‑out of the fifth generation, 5G, for
telecommunication until potential hazards for human health
and the environment have been fully investigated by scientists
independent from industry. 5G will substantially increase
exposure to radiofrequency electromagnetic fields (RF‑EMF)
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on top of the 2G, 3G, 4G, Wi‑Fi, etc. for telecommunications
already in place. RF-EMF has been proven to be harmful for
humans and the environment’.
5G leads to the marked increase of mandatory exposure
to wireless radiation.
‘5G technology is effective only over
short distance. [The range of 5G radiation is decreased due
to its increased carrier frequency (up to ~100 GHz) compared
to previous mobile telephony generations and other existing
microwave telecommunications radiations such as Wi-Fi
(up to 2.6 GHz), and according to Rayleigh's law which
explains that the intensity of scattered electromagnetic radia-
tion (Jscat) is proportional to f 4 (where f is the frequency
of the radiation) when the dimensions of the scattering
particles - such as the molecules of the air, of the building
materials, etc. - are smaller than the wavelength (which is the
case for all mobile telephony radiations): Jscat
∝
f 4 (33)]. It is
poorly transmitted through solid material. Many new [base]
antennas will be required and full-scale implementation will
result in antennas every 10 to 12 houses in urban areas,
thus
massively increasing mandatory exposure’.
‘[Moreover, apart from the increase in background exposure,
5G is likely to induce significant thermal effects in addition
to the already non‑thermal ones, again due to its significantly
higher frequency (34)]’.
‘With “the ever more extensive use of wireless technolo-
gies,” (35) nobody can avoid to be exposed. Because on top
of the increased number of 5G‑transmitters (even within
housing, shops and in hospitals) according to estimates,
“10 to 20 billion connections” (36) (to refrigerators, washing
machines, surveillance cameras, self-driving cars and buses,
etc.) will be parts of the Internet of Things. All these together
can cause a substantial increase in the total, long term
RF-EMF exposure to all EU citizens’.
Harmful effects of RF-EMF exposure have already been
proven.
‘Over 230 scientists from >40 countries [now
252 scientists from 43 nations] (37) have expressed their
“serious concerns” regarding the ubiquitous and increasing
exposure to EMF generated by electric and wireless devices
already before the additional 5G roll‑out. They refer to the
fact that “numerous recent scientific publications have
shown that EMFs affect living organisms at levels well below
most international and national guidelines”. Effects include
increased cancer risk, cellular stress, increase in harmful free
radicals, genetic damages, structural and functional changes
of the reproductive system, learning and memory deficits,
neurological disorders, and negative impacts on general
well-being in humans. Damage goes well beyond the human
race, as there is growing evidence of harmful effects (38) to
both plants (39) and animals (40)’.
‘After the scientists’ appeal was written in 2015 additional
research has convincingly confirmed serious health risks from
RF‑EMF fields from wireless technology. The world's largest
study (25 million US dollar) National Toxicology Program
(NTP) (41), shows statistically significant increase in the inci-
dence of brain and heart cancer in animals exposed to EMF
[intensities] below the ICNIRP (International Commission on
Non-Ionizing Radiation Protection) guidelines followed by
most countries. These results support results in human epide-
miological studies (17) on RF radiation and brain tumour
risk. A large number of peer‑reviewed scientific reports (2)
demonstrate harm to human health from EMFs’.
‘The International Agency for Research on Cancer (IARC), the
cancer agency of the World Health Organization (WHO), in
2011 concluded that EMFs of frequencies 30 KHz ‑ 300 GHz
are possibly carcinogenic to humans (Group 2B) (12,42).
However, new studies like the NTP study mentioned above and
several epidemiological investigations including the latest
studies on mobile phone use and brain cancer risks confirm
that RF‑EMF radiation is carcinogenic to humans (17)’.
‘The EUROPA EM‑EMF Guideline 2016 (1) states that ”there
is strong evidence that long-term exposure to certain EMFs is
a risk factor for diseases such as certain cancers, Alzheimer's
disease, and male infertility…Common EHS (electromagnetic
hypersensitivity) symptoms include headaches, concentra-
tion difficulties, sleep problems, depression, lack of energy,
fatigue, and flu‑like symptoms”’.
‘An increasing part of the European population is affected
by ill health symptoms that have for many years been linked
to exposure to EMF and wireless radiation in the scientific
literature. The International Scientific Declaration on EHS &
multiple chemical sensitivity (MCS), Brussels (43), declares
that: “In view of our present scientific knowledge, we thereby
stress all national and international bodies and institutions…
to recognize EHS and MCS as true medical conditions which
acting as sentinel diseases may create a major public health
concern in years to come worldwide i.e. in all the countries
implementing unrestricted use of electromagnetic field‑based
wireless technologies and marketed chemical substances…
Inaction is a cost to society
and is not an option anymore…
we unanimously acknowledge this serious hazard to public
health…that major primary prevention measures are adopted
and prioritized, to face this
worldwide pan-epidemic
in
perspective”’.
Precautions.
‘The Precautionary Principle (44) was adopted
by EU 2005 (45): “When human activities may lead to morally
unacceptable harm that is scientifically plausible but uncer-
tain, actions shall be taken to avoid or diminish that harm”’.
‘The Council of Europe Resolution 1815 (46): “Take all
reasonable measures to reduce exposure to electromagnetic
fields, especially to radio frequencies from mobile phones,
and particularly the exposure to children and young people
who seem to be most at risk from head tumours…Assembly
strongly recommends that the ALARA (as low as reasonably
achievable) principle is applied, covering both the so-called
thermal effects and the athermic [non‑thermal] or biological
effects of electromagnetic emissions or radiation” and to
“improve risk-assessment standards and quality”’.
‘The Nuremberg code (47) applies to all experiments on
humans, thus including the roll‑out of 5G with new, higher
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RF-EMF exposure. All such experiments: “should be based
on previous knowledge (e.g., an expectation derived from
animal experiments) that justifies the experiment. No experi-
ment should be conducted, where there is an a priori reason
to believe that death or disabling injury will occur; except,
perhaps, in those experiments where the experimental physi-
cians also serve as subjects,” Nuremberg code pts 3‑5 (47).
Already published scientific studies show that there is “a
priori reason to believe” in real health hazards’.
‘The European Environment Agency (48) is warning for
“Radiation risk from everyday devices” in spite of the radia-
tion being below the WHO/ICNIRP standards (49). EEA also
concludes: “There are many examples of the failure to use the
precautionary principle in the past, which have resulted in
serious and often irreversible damage to health and environ-
ments…harmful exposures can be widespread before there is
both ‘convincing’ evidence of harm from long-term exposures,
and biological understanding [mechanism] (50) of how that
harm is caused”’.
‘Safety
guidelines’ protect the industry, not health.
‘The
current ICNIRP “safety guidelines” are obsolete. All proofs
of harm mentioned above arise although the radiation is
below the ICNIRP “safety guidelines” (49). Therefore new
safety standards are necessary. The reason for the misleading
guidelines is that “conflict of interest of ICNIRP members (10)
due to their relationships with telecommunications or electric
companies undermine the impartiality that should govern the
regulation of Public Exposure Standards for non-ionizing
radiation…To evaluate cancer risks it is necessary to include
scientists with competence in medicine, especially oncology’.
‘The current ICNIRP/WHO guidelines for EMF are based on
the obsolete hypothesis that “The critical effect of RF-EMF
exposure relevant to human health and safety is heating of
exposed tissue” (51). However, scientists have proven that
many different kinds of illnesses and harms are caused
without heating (“non‑thermal effect”) (52) at radiation levels
well below ICNIRP guidelines’.
The authors thus urge the EU to carry out the following.
i) ‘To take all reasonable measures to halt the 5G RF‑EMF
expansion until independent scientists can assure that
5G and the total radiation levels caused by RF‑EMF (5G
together with 2G, 3G, 4G, and WiFi) will not be harmful for
EU-citizens, especially infants, children and pregnant women,
as well as the environment’. ii) ‘To recommend that all EU
countries, especially their radiation safety agencies, follow
Resolution 1815 and inform citizens, including, teachers
and physicians, about health risks from RF-EMF radiation,
how and why to avoid microwave radiation, particularly
in/near e.g., daycare centers, schools, homes, workplaces,
hospitals and elderly care’. iii) ‘To appoint immediately,
without industry influence, an EU task force of independent,
truly impartial EMF‑and‑health scientists with no conflicts
of interest (to re-evaluate the health risks and: a) To decide
about new, safe “maximum total exposure standards” for
all microwave radiation within EU. b) To study the total
and cumulative exposure affecting EU-citizens. c) To create
rules that will be prescribed/enforced within the EU about
how to avoid exposure exceeding new EU “maximum total
exposure standards” concerning all kinds of EMFs in order
to protect citizens, especially infants, children and pregnant
women’. iv) ‘To prevent the wireless/telecom industry through
its lobbying organizations from persuading EU‑officials to
make decisions about further propagation of RF radiation
including 5G in Europe’. v) ‘To favor and implement wired
digital telecommunication instead of wireless’.
First reply from the EU.
A reply from the EU was sent on
October 13, 2017 by the Directorate‑General Health and
Food Safety (Public health, country knowledge, crisis
management) in Luxembourg. It was not replied to by the
Commissioner Andriukaitis, but instead by Mr. John F. Ryan,
Director (for the full text please see: http://www.5gappeal.
eu/wp‑content/uploads/2018/06/reply_ryan.pdf). Some para-
graphs are presented below:
‘It is worth underlining that for the Commission health
protection is always taken into account in all of its proposals.
There is consistent evidence presented by national and inter-
national bodies (International Commission on Non Ionising
Radiation Protection - ICNIRP, Scientific Committee on
Emerging and Newly Identified Health Risks ‑ SCENIHR)
that exposure to electromagnetic fields does not repre-
sent a health risk, if it remains below the limits set by
Council Recommendation 1999/519/EC (https://ec.europa.
eu/health//sites/health/files/electromagnetic_ fields/docs/emf_
rec519_en.pdf)’.
‘The Scientific Committee on Emerging and Newly Identified
Health Risks, which is independent of the Commission, has a
standing mandate to provide this update’.
‘It has already produced five opinions. The last opinion was
adopted in January 2015 on “Potential health effects of exposure
to electromagnetic fields”. (https://ec.europa.eu/health/scien-
tific_committees/emerging/docs/scenihr_o_041.pdf)’.
‘These scientific opinions have not provided any scientific
justification for revising the exposure limits (basic restric-
tions and reference levels) under Council Recommendation
1999/519/EC’.
‘Digital technologies and mobile communication technolo-
gies, including high speed internet, will be the backbone of
Europe's future economy, allowing all citizens to be connected.
At the same time, all citizens deserve appropriate protec-
tion against electromagnetic fields from all types of sources
including from wireless devices’.
‘Most 5G networks are expected to use smaller cells than
previous generations with lower electromagnetic fields expo-
sure levels. This is confirmed by the experience so far gained.
The introduction of 3G and 4G has not increased exposure
from environmental fields and this has been published also
in peer-reviewed journals. In particular, the introduction of
3G has lowered exposure of mobile phone users for calls,
compared to 2G’.
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‘Related to the issue of the alleged conflicts of interests, the
Commission is not aware of any conflicts of interests of members
of international bodies such as ICNIRP or the members of
SCENIHR. Please be informed that the Ombudsman conclu-
sion in case 208/2015/P concerning conflicts of interests in
a Commission expert group on electromagnetic fields is that
there was no maladministration by the European Commission
(https://www.ombudsman.europa.eu/en/cases/decision.
faces/en/78175/html.bookmark)’.
‘Please be assured that the Commission will pursue scrutiny
of the independent scientific evidence available to ensure the
highest health protection of our citizens’.
Comment: There are obvious misconceptions in this reply
such as:
‘The introduction of 3G and 4G has not increased
exposure from environmental fields and this has been
published also in peer-reviewed journals’.
On the contrary,
numerous peer‑reviewed articles have demonstrated that expo-
sure to ambient RF radiation has increased substantially, as
discussed (3‑6).
In addition, the statement that:
‘the Commission is not aware
of any conflicts of interests of members of international bodies
such as ICNIRP or the members of SCENIHR’
does not repre-
sent the scientific evidence of inherent conflicts of interest
both in ICNIRP and SCENIHR (9,10). The very Commission
seems to be ill‑informed or even misinformed, as the EU
seems to take information mainly from these two fraudulent
organizations, but not from independent researchers. The EU
does not seem to rely on sound science and thereby downplays
the RF-related risks (7-12,53,54).
b) First rebuttal to the EU and the response.
On
November 13, 2017, a rebuttal was sent to the EU
Commissioner of Health, Dr Andriukaitis. The whole
letter can be found at: https://www.environmentandcancer.
com/letter‑to‑vytenis‑andriukaitis‑13‑11‑2017/.
‘We suppose that you know that Director John F. Ryan,
October 13, 2017 replied (Ares 2017 5015409 ‑ Reply to the EU
5G‑appeal, and that he said: “There is
consistent evidence
that exposure to electromagnetic fields
does not represent a
health risk… if below the limits
…” His conclusion is based
on the opinions of ICNIRP and SCENIHR’.
‘As early as February 1, 2016, in a Comment on SCENIHR
to Mr.
Ryan it was shown in article and letter by Drs.
[Sage],
Carpenter and Hardell, representing BioInitiative and ECERI,
that: ”The evidence in the SCENIHR Final Opinion on EMF
clearly and convincingly establishes the potential for health
effects of exposure to electromagnetic fields
[EMF]. Based
on the evidence provided in this Opinion, the Committee is
obligated to draw to the attention of the [EU] Commission
that EMF is a new and emerging problem that may pose an
actual or potential threat”’ (55).
‘In spite of all this, Mr Ryan in his reply to us still continues
to claim that EMF ‘does not represent a health risk’ and -
without any other references than ICNIRP and SCENIHR
‑ defends industry's standpoint that EMFs are harmless if
below the ICNIRP “safety guidelines”. In addition he ignores
the IARC evaluations on both ELF-EMF and RF-EMF to be
‘possible’ human carcinogens, Group 2B’.
‘In the 5G‑Appeal we urge EU to appoint a truly independent
expert group of EMF-and-health researchers (contrary to
ICNIRP and SCENIHR) to decide about new safe guidelines
for EMF exposure. It is imperative to
immediately apply
EU:s Precautionary Principle (and ALARA)
enabling rapid
response to stop distribution of 5G products in order to
diminish the harm that has already been proven by scientists.
A
European pan-epidemic
may follow if you don't do so’.
Second reply from EU on 29 November, 2017.
This was sent
from the European Commission, Cabinet of Commissioner
Vytenis Andriukaitis, Head of Cabinet Brussels, written
by Arūnas Vinciunas. The full reply can be found at:
http://www.5gappeal.eu/wp‑content/uploads/2018/06/reply_
vinciunas.pdf).
‘When Mr Ryan answered your email, in which you stated
your disagreement with the Commission's stance on the 5G
appeal, he presented the conclusions of roughly two decades
of research on the potential health effects of EMF, and the
views expressed in the Scientific Opinions produced by the
independent Scientific Committees. [ICNIRP ‑ International
Commission on Non-Ionizing Radiation Protection and
SCENIHR ‑ Scientific Committee on Emerging and Newly
Identified Health Risks]. The Committee's last Opinion on
EMF, published in 2015, is based on hundreds of peer‑reviewed
studies published worldwide and is the fourth Opinion on
EMF published since EMF legislation was adopted in 1999.
The Committee's conclusion in this latest Opinion was based
on exposure studies, epidemiological studies and in vivo and
in vitro studies, and studies on any suggestions of causality
were considered for the weighting’.
‘The Commission services are confident that the advice
provided by the Scientific Committees is unbiased, accurate
and scientifically sound and therefore do not feel it necessary
to appoint an independent expert group of EMF-and-health
researchers to discuss new safe guidelines for EMF exposure’.
‘The recourse to the EU's Precautionary Principle to stop the
distribution of 5G products appears too drastic a measure. We
first need to see how this new technology will be applied and
how the scientific evidence will evolve. Please rest assured
that the Commission will keep abreast of future developments
in view of safeguarding the health of the European citizens at
the highest level possible and in line with its mandate’.
Comment: This reply from EU is far from adequate. It does
not represent a sound evaluation of the RF‑related radiation
risks based on published peer‑reviewed studies. This is again
outlined in our response to the EU.
c) Second rebuttal to the EU and the response.
On January 17,
2018, a letter was sent to Dr. Vytenis Andriukaitis, EU
Commissioner of Health. Sections of this letter are presented
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below and the full text can be found at: https://www.environ-
mentandcancer.com/letter‑to‑vytenis‑andriukaitis‑and‑donald
‑tusk‑17‑01‑18/.
‘Following the letter and the Scientist Appeal calling for a
moratorium on 5G (“The 5G Appeal”), which we sent to your
office, we received a response from Director John F. Ryan
on October 13, 2017 and then, upon our reply, a letter from
Mr. Arūnas Vinciūnas dated 29.11.2017’.
‘Despite the conclusive evidence presented in our letters, both
Director Ryan and Mr. Vinciūnas gave generic responses and
continued to claim that EMF “does not represent a health
risk”. In doing so they only refer to ICNIRP and SCENIHR
opinions without explaining why they disregarded the compel-
ling evidence and references under the 5G‑Appeal headline:
“Harmful effects of RF-EMF exposure are already proven”’.
‘The ICNIRP exposure limits are dependent on an unproven
hypothesis that “only heat from EMF can cause health
hazards”. This hypothesis has clearly been rejected in a large
number of scientific studies’.
‘Both EU officials defend the industry‑supportive standpoint
that EMFs are harmless if below the ICNIRP “guidelines”.
However, many of the scientists on both ICNIRP's and
SCENIHR's committees are connected to the telecom industry
with obvious conflicts of interest’.
‘Mr Vinciūnas stated in his letter: “The recourse to the EU's
Precautionary Principle to stop the distribution of 5G prod-
ucts appears
too drastic a measure.”
Mr Vinciūnas finishes
his letter: “we need to see … how the scientific
evidence will
evolve”’.
‘According to Communication from the Commission on
the precautionary principle: “Whether or not to invoke the
Precautionary Principle is a decision exercised where scien-
tific information is insufficient, inconclusive, or uncertain
and where there are indications that the possible effects on
the environment, or human, animal or plant health may be
potentially dangerous and inconsistent with the chosen level
of protection.” That describes the situation with 5G perfectly.
Existing data shows that 5G frequencies [radiations] are
hazardous. However, additional studies will be necessary to
fully determine the extent of the risk’.
Third reply from the EU.
This letter was replied to on
April 27, 2018 by Mr. Arūnas Vinčiūnas from the Cabinet of
Commissioner Vytenis Andriukaitis. For the full third reply
to our appeals please see: https://www.environmentandcancer.
com/answer‑from‑arunas‑vinciunas‑27‑04‑2018/.
‘Thank you very much for your letter of 15 March 2018 which
was also transmitted by email on 19 March. Commissioner
Andriukaitis has asked me to reply to you on his behalf’.
‘Finally, let me refer to the previous correspondence you have
had with John F. Ryan, Director of Public Health and me
(29 November 2017, 13 October 2017 and 19 February 2018)
where we have comprehensively explained our position with
regard to the arguments you have raised. It is my view that we
have now extensively deliberated on the matter and that we
should refrain from further repetition’.
‘Please rest assured that the Commission will remain
committed to safeguarding the health of the European citizens,
at the highest level possible and in line with his mandate’.
d) Third rebuttal to the EU and the response.
This
rebuttal had the title
“Request for a moratorium on the
5G rollout. Request for guidelines based on independent
research. Request for documents showing that 5G is safe”.
On May 20, 2019 a letter with these requests was sent to
Dr Karmenu Vella, EU Commissioner of Environment and
Dr Vytenis Andriukaitis, EU Commissioner of Health. For
the full text please see: https://www.environmentandcancer.
com/letter‑to‑vytenis‑andriukaitis‑20‑05‑2019/.
‘We make reference to the Precautionary Principle (PP) (56) It
”enables a rapid response to be given in the face of a possible
danger to human health…institutions may take protective
measures without having to wait until the reality… of risks
become apparent … preventive action should be taken” (57).
Research confirms 5G to be a risk to all life on earth’.
‘With this communication we touch upon three points:’
i) ‘Firstly, we request in the 5G Appeal to EU (www.5gappeal.
eu), of which you are a public servant and representative, to
declare an immediate
moratorium
on 5G deployment. The
5G appeal to EU is now confirmed by 230+ truly independent
scientists and physicians from 36 countries. The Space 5G
appeal (58) has more than 83,000 affirmations from 168 coun-
tries. According to PP (56) and EU IP/00/96 (59) “protection
of health takes precedence over economic considerations.”’
ii) ‘Secondly, we ask for groups of truly industry-independent
researchers to establish
new guidelines for exposure.
An
“In‑depth analysis” of the deployment of 5G (60), published
by EU in April 2019, needs to be seriously considered. It
stated that” One aspect, for example, that is not well under-
stood today is the unpredictable propagation patterns that
could result in unacceptable levels of human exposure to
electromagnetic radiation.”(p. 6)’. iii) ‘Thirdly, with this letter
we are formally requesting, in accordance with Art. 42 (61)
on EU Fundamental Rights,
access to all documents
in your
possession, either created by you or at your disposal, related
to the effects of EMF to human health and the environment.
Once in possession of such a list, we will decide which of those
documents, if any, are of interest and show that 5G is safe. The
list of the documents, and the ways to access them, should be
sent to the email addresses below’.
‘We note that, while the EU is eagerly promoting the rollout
of 5G, a new EU report admits (60) “the problem is that
currently it is not possible to accurately simulate or measure
5G emissions in the real world” (p.
12).
“Significant concern
is emerging over the possible impact on health and safety
arising from potentially much higher exposure to radiofre-
quency electromagnetic radiation arising from 5G” (p. 4).
The EU report also stresses dangers: ”Increased exposure
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HARDELL and
NYBERG: APPEALS ON THE DEPLOYMENT OF 5G
may result not only from the use of much higher frequencies in
5G but also from the potential for the aggregation of different
signals, their dynamic nature, and the complex interference
effects that may result, especially in dense urban areas.”
(p. 11)’.
Fourth reply from the EU.
Finally, a response was delivered
by the EU on September 5, 2019, although with reference to the
wrong date of our letter. It was sent by Arunas Vinciunas from
the Cabinet of Commissioner Vytenis Andriukaitis. The full
response can be read at: https://www.environmentandcancer.
com/answer‑from‑arunas‑vinciunas‑05‑09‑2019/.
‘Thank you for your email of 7 July 2019 to Commissioner
Andriukaitis in which you request to halt the 5G expansion
in the EU immediately in order to allow a moratorium for
industry independent research. Commissioner Andriukaitis
has asked me to reply to you on his behalf’.
‘In my latter note to you I already expressed my view that we
had extensively deliberated on the matter and that we should
refrain from further repetition’.
‘As regards your request to halt the launch of the new 5G
technology, I would like to confirm the view already expressed
in my note of 29 November 2017 to you that stopping the
distribution of 5G products appears too drastic a measure. I
repeat that first there is a need to see how this new technology
will be applied and how the scientific evidence will evolve’.
‘Concerning your call for a scientific evaluation and new
guidelines for exposure, the second point you have raised,
let me stress that the Commission will review the situation
once the review of the guidelines issued by the International
Commission on Non-Ionizing Protection (ICNIRP) will be
finalised which is expected in due course’.
‘As regards your third point, documents related to the
effects of electromagnetic fields to human health and
the environment, please be referred to the opinion of the
Commission's Scientific Committee on Emerging and
Newly Identified Health Risks of 20 January 2015 on
potential health effects of exposure to electromagnetic
fields (EMF) (https://ec.europa.eu/health/scientific_commit-
tees/emerging/docs/scenihr_ o_ 041.pdf) that provides an
extensive list of references to scientific literature on this issue’.
Comment on the fourth reply from the EU appeal: There is no
new evidence of the safety in this letter from EU compared with
the earlier replies. Of note, the EU relies on documentation of
risk only on old and biased selection of references in one single
report from SCENIHR (https://ec.europa.eu/health/scien-
tific_committees/emerging/docs/scenihr_o_041.pdf). Thus,
EU officials still seem to base the evaluation of the health
risks on reports from the ICNIRP and SCENIHR that have
been seriously criticized. Of note, the EU relies on a report
from 2015 as to scientific publications on the safety of 5G,
a technology that was not developed during that time. This
suggests that perhaps the EU is reluctant to deal with the safety
issues associated with 5G technology.
e) Fourth rebuttal to the EU.
On October 24, 2019 a fourth
rebuttal was sent to the EU (https://www.environmentand-
cancer.com/letter‑to‑arunas‑vinciunas‑24‑10‑2019). We wrote
that
‘Specifically now, as we wish to assist the Commissioner
in giving due response, it can be further specified from this
side that we need the
list of documents
related to EMFs
created by RF/Radiofrequencies (so: not by ELF) and even
more specifically, to the list of those documents based on which
the Commission is basing its current position that 5G should
not be stopped nor subject to a moratorium (see the statement
of your letter that “first there is a need to see how this new
technology will be applied and how the scien6fic evidence
will evolve”). We leave aside our total disagreement on the
merits of such position at this time: formally, we are entitled
to receive from you such a list of documents based on which
the Commissioner determined that 5G is safe. Based on that
list we will decide which of those documents, are of interest.
Please provide such list by email no later than October 31,
2019. This is urgent’.
Fifth reply from the EU.
In this response, dated December 19,
2019, it was stated that new ICNIRP guidelines are expected.
Thus, the same approach to this issue as previously and no new
commitment (https://www.environmentandcancer.com/answe
r‑from‑martin‑seychell‑19‑12‑2019).
Appeals to the Nordic Prime Ministers
The 5G Appeal was also sent to the Nordic Prime
Ministers (https://www.environmentandcancer.com /
letter‑to‑nordic‑ministers‑27‑6‑2018/); (https://www.environ-
mentandcancer.com/letter‑to‑nordic‑ministers‑5‑3‑2019/). The
only reply, dated March 29, 2019, was sent from the Swedish
government (Ministry of Enterprise and Innovation, Mari
Mild). It was stated that the government relies on Swedish
Radiation Safety Authority (SSM) and their yearly update of
health risks and that no new health risks have been reported.
According to the letter there is no reason for a moratorium on
the deployment of 5G, see (in Swedish) (https://www.miljooch-
cancer.com/svar‑fran‑naringsdepartementet‑29‑3‑2019/). SSM
relies on ICNIRP.
Discussion
Our experience with the EU and the Governments of the
Nordic countries suggests that the majority of decision makers
are scientifically uninformed on health risks from RF radia-
tion (62). In addition, they seem to be uninterested to being
informed by scientists representing the majority of the scien-
tific community, i.e., those scientists who are concerned about
the increasing evidence or even proof of harmful health effects
below the ICNIRP guidelines (www.emfscientist.org). Instead,
they rely on evaluations with inborn errors of conflicts, such
as ICNIRP. In fact, the ICNIRP, with the support of WHO
and major telecommunications companies, has been rather
successful in implementing their views in the EU and world-
wide. Their guidelines seem to be based on the omission of
scientific facts. Thus, their possible ignorance of the health
risks is of concern, as well as their reluctance to adhere to
warnings from large numbers of scientists around the world.
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255
It is striking that 5G is deployed without previous scientific
evaluation of health risks. Not only cancer risks, but also other
health effects such as fertility, cognitive and neurobehavioral
effects, oxidative stress and electromagnetic hypersensitivity
(EHS) have been associated with RF exposure [for a more
detailed discussion on this tope, please see previous publica-
tions (1,7,8,28,35)]. It is thus noteworthy that the ICNIRP
thermal paradigm is still used for the evaluation of the health
risks associated with RF radiation. One issue of major concern
is that there seems to be conflicts of interest among persons
in the evaluating groups. Furthermore the same persons
may often be found in different bodies, thereby in fact citing
themselves representing a cartel (https://www.saferemr.
com/2018/07/icnirps‑exposure‑guidelines‑for‑radio.html).
This has been outlined in peer‑reviewed publications (9,10).
This is also an ethical question. Thus, it would not be
possible to test a new drug on individuals without informa-
tion and signed permission by each individual. Certainly, this
principle should apply to 5G that is furthermore, mandatory.
Exposure to RF radiation from 5G must be regarded as a
medical experiment with potential health risks, some known
and expected based on current knowledge, some unknown
since this is a new untested technology. A letter of information
to those exposed must be sent for informed consent. However,
it must be concluded that such a letter, affirming no risk,
cannot be formulated based on the limited number of studies
on 5G, in fact most of them with no assurance of no risks.
This is also a moral question for all the individuals
involved in the propagation of 5G. It is to be noted that indi-
viduals within e.g., ICNIRP, national governmental bodies and
the EU, partly a cartel, seem to neglect scientific warnings.
They instead seem to follow the no‑risk paradigm. It is thus
questionable as to how it is possible to thereby disregard the
diseases caused by this technology and to not consider the
affected persons.
Taking the history of e.g., tobacco and smoking and the long
period of time it took for cancer classification into account, it
is fully understandable that RF radiation is still in the begin-
ning of that history. However, if no action is currently taken,
the costs to society will most likely be very high in terms of
premature deaths, deteriorated public health and damage to
the ecological system. It is however, important to publish the
history of neglected RF radiation warnings. The EU seems
to perhaps lacking in that respect. It must be concluded that
the polluter has to pay the full cost of harm from this tech-
nology (63). Those in responsible positions in governments
and organizations intended to protect the public and the envi-
ronment from harm (WHO and ICNIRP), but who fail to do so
by ignoring the increasing warnings from scientists worldwide
about the dangers of 5G, should also be held responsible
for the harm to the public that they thereby induce (64). No
doubt damage to the environment by the business sector
may be substantial (https://www.theguardian.com/environ-
ment/2010/feb/18/worlds‑top‑firms‑environmental‑damage).
The EU principle that the Polluter Pays (Article 191, pt 2)
states:
‘Union policy on the environment shall aim at
a high
level of protection taking
into account the diversity of situa-
tions in the various regions of the Union.
It shall be based on the
precautionary principle
and on the principles that
preventive
action should be taken,
that environmental damage should as
a priority be rectified at source and that
the polluter should
pay’.
(https://eur‑lex.europa.eu/LexUriServ/LexUriServ.do?uri
=CELEX:12008E191:EN:HTML).
‘The
fundamental principle of this Directive should
therefore be that an operator whose activity has caused the
environmental damage or the imminent threat of such damage
is to be held financially liable, in order to induce operators
to adopt measures and develop practices to minimise the
risks of environmental damage so that their exposure to
financial liabilities is reduced’ (65) (https://eur‑lex.europa.
eu/legal‑content/EN/TXT/HTML/?uri=CELEX:32004L0035
&from=EN).
The industry tries to convince us that the super
high frequencies of 5G are so weak and its milli-
meter waves will penetrate only the outer surface of
the skin. The opposite was proven in USSR research
already in 1977 (https://www.cia.gov/library/reading-
room/docs/CIA‑RDP88B01125R000300120005‑6.pdf ).
High frequencies (37‑60 GHz), which will be used in 5G,
caused several kinds of detrimental effects in experimental
rats. The high frequencies seem to be worse than the lower
frequencies. The USSR experiments were made more than
40 years ago ‑ when we had no digital pulsed radiation ‑ with
a generator producing sinus curves. Peaks of pulsed radiation
used in 5G with unpredictable intensity changes seem to be an
important parameter for the bioactivity of RF radiation (29).
In conclusion, this article demonstrates that the EU
has given mandate to a 13‑member, non‑governmental
private group, the ICNIRP, to decide upon the RF radiation
guidelines. The ICNIRP, as well as SCENIHR, are well
shown not to use the sound evaluation of science on the
detrimental effects of RF radiation, which is documented
in the research which is discussed above (9,10,21‑24,54,55).
These two small organizations are producing reports which
seem to deny the existence of scientific published reports on
the related risks. It should perhaps be questioned whether it
is in the realm of protecting human health and the environ-
ment by EU and whether the safety of EU citizens and the
environment can be protected by not fully understanding
the health-related risks.
Acknowledgements
Not applicable.
Funding
No funding was received.
Availability of data and materials
The information generated and analyzed during the current
study is available from the corresponding author on reasonable
request.
Authors' contributions
Both authors (LH and RN) participated in the conception,
design and writing of the manuscript, and have read and
approved the final version.
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256
HARDELL and
NYBERG: APPEALS ON THE DEPLOYMENT OF 5G
Ethics approval and consent to participate
Not applicable.
Patient consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
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This work is licensed under a Creative Commons
Attribution-NonCommercial-NoDerivatives 4.0
International (CC BY-NC-ND 4.0) License.
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N. 00500/2019 REG.PROV.COLL.
N. 08373/2018 REG.RIC.
REPUBBLICA ITALIANA
IN NOME DEL POPOLO ITALIANO
Il Tribunale Amministrativo Regionale per il Lazio
(Sezione Terza Quater)
ha pronunciato la presente
SENTENZA
sul ricorso numero di registro generale 8373 del 2018, proposto da
Associazione per la prevenzione e la lotta all'elettrosmog, in persona del legale rappresentante pro tempore,
rappresentata e difesa dagli avvocati Renato Ambrosio, Stefano Bertone, Chiara Ghibaudo, Luigi M. Angeletti, con
domicilio digitale come da PEC da Registri di Giustizia e domicilio eletto presso lo studio dell’avv.to Marco De Fazi
in Roma, via della Giuliana n. 44;
contro
Ministero della Salute; Ministero dello Sviluppo Economico; Ministero dell'Istruzione, dell'Università e della Ricerca;
Ministero dell'Ambiente e della Tutela del Territorio e del Mare, in persona del legale rappresentante pro tempore,
rappresentati e difesi dall'Avvocatura Generale dello Stato, domiciliata ex lege in Roma, via dei Portoghesi n. 12;
nei confronti
Brondi s.p.a., in persona del legale rappresentante pro tempore, rappresentata e difesa dagli avvocati Riccardo
Prandi, Alessandro Massaia, Gianluca Contaldi, con domicilio digitale come da PEC da Registri di Giustizia e
domicilio eletto presso lo studio dell’avv.to Gianluca Contaldi in Roma, via Pier Luigi da Palestrina n. 63;
per l’accertamento e la declaratoria dell’illegittimità
dell’inerzia serbata dalle Autorità intimate in relazione all'atto di diffida del 28 giugno 2017, formulato dalla
ricorrente e diretto a promuovere l’adozione di tutti i provvedimenti finalizzati all'informazione capillare della
popolazione, compresa la fascia dei soggetti più a rischio (bambini, adolescenti) sui rischi a breve e lungo termine
per la salute dovuti all'uso dei telefoni mobili (cellulari e cordless) e sulle indispensabili misure cautelative da adottare
durante il loro utilizzo;
per il conseguente accertamento dell'obbligo di provvedere in capo alle Autorità intimate in relazione al medesimo
atto di diffida, mediante l'adozione di ogni idoneo provvedimento espresso, finalizzato ad assicurare alla popolazione
idonea informazione sui rischi per la salute dei cittadini, a breve e lungo termine, quali descritti nelle più recenti
acquisizioni scientifiche, dovuti all'uso dei telefoni mobili (cellulari e cordless) e sulle indispensabili misure
cautelative da adottare durante il loro utilizzo, con particolare riferimento alla fascia dei soggetti più a rischio
(bambini, adolescenti);
nonché per l’accertamento
dell'obbligo in capo al Ministero della Salute, e/o al Ministero dell'Ambiente, e/o al Ministero dello Sviluppo
Economico (già Ministero dell'Industria) e/o al Ministero dell'Istruzione, dell'Università e della Ricerca, tenendo
conto della multiculturalità presente in Italia, di provvedere all'emanazione senza ritardo del decreto di cui all'art. 12
della legge 22 febbraio 2001, n. 36 "Legge quadro sulla protezione dalle esposizioni a campi elettrici, magnetici ed
elettromagnetici", anche al fine di indicare al pubblico “le informazioni che i fabbricanti di apparecchi e dispositivi,
in particolare di uso domestico, individuale o lavorativo, generanti campi elettrici, magnetici ed elettromagnetici,
sono tenuti a fornire agli utenti, ai lavoratori e alle lavoratrici, mediante apposite etichettature o schede informative”;
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Visti il ricorso e i relativi allegati;
Visti gli atti di costituzione in giudizio del Ministero della Salute, del Ministero dello Sviluppo Economico, del
Ministero dell'Istruzione dell'Università e della Ricerca, del Ministero dell'Ambiente e della Tutela del Territorio e del
Mare e della società Brondi s.p.a.
Visti tutti gli atti della causa;
Relatore nella camera di consiglio del giorno 13 novembre 2018 il dott. Paolo Marotta e uditi per le parti i difensori
come specificato nel verbale;
Con ricorso notificato in data 30 giugno 2018 e depositato il 13 luglio successivo, l’Associazione ricorrente ha
impugnato il silenzio – inadempimento asseritamente formatosi sulla istanza – diffida del 28 – 30 giugno 2017,
diretta all’adozione da parte delle Autorità intimate di tutte le iniziative finalizzate ad informare la popolazione sui
danni a breve e lungo termine connessi all’uso dei telefoni mobili (cordless e cellulari).
La parte ricorrente ha formulato anche istanza cautelare.
A fondamento della propria legittimazione ad agire, la ricorrente richiama il proprio Statuto e segnatamente l’art. 6
dello Statuto, che individua quale scopo dell’associazione quello di tutelare la salute degli esseri viventi e
dell’ambiente dall’esposizione ai campi magnetici ed elettromagnetici.
Quale fondamento giuridico dell’obbligo di provvedere, la ricorrente richiama le seguenti fonti normative: l’art. 32
della Costituzione; la legge 13 marzo 1958 n. 296; gli artt. 1, 4, 10 e 12 della l. 22 febbraio 2001 n. 36 (legge quadro
sulla protezione dalle esposizioni ai campi elettrici, magnetici ed elettromagnetici), la direttiva 1999/5/CE; l’art. 2043
c.c.
Si sono costituite le Amministrazioni intimate, eccependo, in via preliminare, l’inammissibilità del ricorso sotto
diversi profili e contestando, nel merito, la fondatezza delle doglianze formulate dalla parte ricorrente.
Si è costituita in giudizio anche la società Brondi s.p.a., eccependo l’inammissibilità del ricorso per difetto di
giurisdizione del giudice adito, il difetto di legittimazione della ricorrente, l’insussistenza dell’obbligo di provvedere, il
difetto di integrità del contraddittorio, il difetto dei presupposti per la concessione della misura cautelare.
Con memoria depositata in data 13 ottobre 2018 la ricorrente, pur riconoscendo l’inammissibilità del rito del silenzio
nei confronti degli atti di natura normativa, si è soffermata a considerare la mancata attuazione della campagna di
informazione e di educazione ambientale, di cui all’art. 10 della l. n. 36/2001.
Nel corso del giudizio le parti costituite hanno avuto modo di rappresentare compiutamente le rispettive tesi
difensive.
All’udienza camerale del 13 novembre 2018, su richiesta delle parti, come da verbale, il ricorso è stato trattenuto in
decisione.
Preliminarmente, in accoglimento della eccezione sollevata dalle Amministrazioni resistenti, deve essere dichiarata
l’inammissibilità parziale del ricorso, per difetto assoluto di giurisdizione, in ordine al mancato esercizio da parte
delle Amministrazioni intimate di poteri di natura normativa.
In prima istanza, infatti, l’Associazione ricorrente si duole dell’inerzia delle Amministrazioni intimate rispetto alla
attuazione dell’art. 12, comma 1, della l. n. 36/2001, a norma della quale: “1. Con decreto del Ministro dell'ambiente,
di concerto con il Ministro della sanità, previo parere del Comitato e sentite le competenti Commissioni
parlamentari, sono stabilite, entro centoventi giorni dalla data di entrata in vigore della presente legge, tenendo conto
anche degli orientamenti e degli atti dell'Unione europea in materia di inquinamento elettromagnetico, tutela dei
consumatori e istruzioni per l'uso dei prodotti, le informazioni che i fabbricanti di apparecchi e dispositivi, in
particolare di uso domestico, individuale o lavorativo, generanti campi elettrici, magnetici ed elettromagnetici, sono
tenuti a fornire agli utenti, ai lavoratori e alle lavoratrici, mediante apposite etichettature o schede informative. Le
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informazioni devono riguardare, in particolare, i livelli di esposizione prodotti dall'apparecchio o dal dispositivo, la
distanza di utilizzo consigliata per ridurre l'esposizione al campo elettrico, magnetico ed elettromagnetico e le
principali prescrizioni di sicurezza. Con lo stesso decreto sono individuate le tipologie di apparecchi e dispositivi per
i quali non vi è emissione di campo elettrico, magnetico ed elettromagnetico, o per i quali tali emissioni sono da
ritenersi cosi basse da non richiedere alcuna precauzione”.
Orbene, risulta non controverso tra le parti che questa disposizione normativa non ha ancora trovato attuazione.
Sennonché il rito del silenzio – inadempimento non può essere utilizzato per costringere le Amministrazioni
intimate alla adozione del decreto ministeriale, cui fa riferimento la disposizione normativa sopra richiamata,
costituendo esso un atto di natura normativa (più precisamente, regolamentare).
Per pacifica giurisprudenza infatti, è esclusa, ai sensi dell’art. 7, co. 1, ultimo periodo, c.p.a., la possibilità di sindacare,
con lo speciale rito del silenzio, la mancata adozione, da parte degli organi titolari del relativo potere, di atti
normativi (leggi, atti aventi forza di legge, regolamenti), venendo in rilievo ambiti nei quali l'Amministrazione
esprime scelte di natura politica (Consiglio di Stato, sez. V, 22 gennaio 2015 n. 273).
Ne consegue che la domanda formulata dalla odierna ricorrente deve essere considerata in parte qua inammissibile,
per difetto assoluto di giurisdizione, dovendo ritenersi che la mancata adozione del decreto ministeriale, di cui all’art.
12 della l. n. 36/2001, assuma rilevanza solo sul piano della responsabilità politica degli organi di governo e,
comunque, non sia coercibile sul piano giuridico con il ricorso al rito del silenzio – inadempimento.
Sempre in via preliminare, deve essere esaminata l’eccezione di inammissibilità del ricorso, per difetto di
legittimazione attiva dell’Associazione ricorrente, sollevata dalle Amministrazioni resistenti. Queste ultime
sostengono che, non figurando tra le Associazioni di protezione ambientale individuate con decreto del Ministro
dell’Ambiente di cui all’art. 13 della l. n. 349/1986, l’Associazione ricorrente sarebbe priva di legittimazione ad agire.
L’eccezione è infondata.
Ritiene il Collegio di aderire a quell’orientamento giurisprudenziale secondo il quale l’esplicita legittimazione, ai sensi
degli artt. 13 e 18 della legge 8 luglio 1986, n. 349, delle Associazioni ambientalistiche di dimensione nazionale e
ultraregionale all'azione giudiziale non esclude, di per sé sola, analoga legittimazione ad agire in un ambito territoriale
ben circoscritto, e ciò anche per i comitati che si costituiscono al precipuo scopo di proteggere l'ambiente, la salute
e/o la qualità della vita delle popolazioni residenti su tale circoscritto territorio. Le previsioni normative citate hanno
introdotto un criterio di legittimazione "legale" "aggiuntivo", e non "sostitutivo", rispetto ai criteri elaborati
precedentemente dalla giurisprudenza per l'azionabilità in giudizio dei c.d. “interessi diffusi”. Ne consegue che il
giudice amministrativo può riconoscere, caso per caso, la legittimazione a impugnare atti amministrativi a tutela
dell'ambiente a favore di associazioni locali (indipendentemente dalla loro natura giuridica), purché le stesse a)
perseguano statutariamente in modo non occasionale obiettivi di tutela ambientale, b) abbiano un adeguato grado di
rappresentatività e stabilità e c) svolgano la propria attività in un'area di afferenza ricollegabile alla zona in cui è
situato il bene a fruizione collettiva che si assume leso (Consiglio di Stato, sez. V, 17 ottobre 2012 n. 5295; in senso
conforme, Consiglio di Stato, sez. VI, 12 giugno 2015 n. 2894).
Orbene, dagli atti depositati in giudizio emerge che:
- l’Associazione ricorrente è stata costituita ai sensi della l. 7 dicembre 2000 n. 383;
- lo Statuto dell’Associazione stabilisce, all’art. 5, che la durata dell’Associazione è illimitata, e all’art. 6, che lo scopo
principale dell’Associazione medesima è quello di “promuovere, attraverso l’azione dei suoi Soci, la tutela della salute
e della integrità degli esseri viventi e dell’ambiente dall’esposizione ai campi elettrici, magnetici ed elettromagnetici,
statici o variabili, generati artificialmente e da tutte le forme di inquinamento chimico, fisico, radioattivo e biologico”;
- l’ambito di operatività dell’Associazione è individuato nel territorio della Regione Veneto (art. 7 dello Statuto).
Ritiene conseguentemente il Collegio che conformemente all’orientamento giurisprudenziale sopra richiamato non
vi siano ragioni per denegare alla Associazione ricorrente la legittimazione ad agire per la tutela della salute e
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dell’ambiente dall’inquinamento elettromagnetico indotto dall’uso dei telefoni mobili (cellulari e cordless).
Il Collegio non ravvisa poi la necessità di disporre l’integrazione del contraddittorio, sulla base della eccezione
sollevata dalla società Brondi s.p.a., non venendo in rilievo rispetto alla fattispecie dedotta in giudizio
controinteressati in senso tecnico.
Nel merito, il Collegio rileva che, facendo seguito ad altre precedenti istanze, l’Associazione ricorrente, con istanza
del 28 giugno 2017, ha diffidato il Ministero della Salute, il Ministero dell’Ambiente e il Ministero dello Sviluppo
Economico ad adottare i seguenti atti:
a) ad emanare il decreto di cui all’art. 12 della l. n. 36/2001;
b) ad eseguire una campagna informativa rivolta alla intera popolazione, avente ad oggetto la indicazione delle
modalità d’uso e dei rischi per la salute e per l’ambiente connessi all’uso di telefoni cellulari e cordless.
Con il ricorso in esame, dopo essersi lungamente soffermata sui rischi per la salute e per l’ambiente derivanti da un
uso improprio degli apparecchi di telefonia mobile soprattutto per gli utenti più giovani di età, sulla base delle ultime
ricerche scientifiche, l’Associazione ricorrente ha chiesto l’annullamento del silenzio – inadempimento formatosi per
effetto dell’inerzia delle Amministrazioni intimate e che venga accertato l’obbligo delle predette Amministrazioni di
provvedere, entro un determinato termine.
Orbene, come sopra evidenziato, la domanda (processuale) dell’Associazione ricorrente diretta ad ottenere
l’emanazione del decreto ministeriale di cui all’art. 12 della l. n. 36/2001, è inammissibile per difetto assoluto di
giurisdizione, venendo in rilievo il mancato esercizio di poteri di natura normativa.
Rimane invece da scrutinare la fondatezza della domanda formulata dalla ricorrente con riferimento al mancato
avvio da parte dei Ministeri competenti ratione materiae di una campagna informativa rivolta alla intera popolazione,
avente ad oggetto l’indicazione delle modalità d’uso e dei rischi per la salute e per l’ambiente connessi all’uso degli
apparecchi di telefonia mobile (telefoni cellulari e cordless).
L’Associazione ricorrente individua il fondamento giuridico della predetta richiesta nell’art. 10 della l. n. 36/2001, a
norma del quale: “Il Ministro dell’ambiente, di concerto con i Ministri della sanità (ora Ministro della salute, n.d.r.),
dell’università e della ricerca scientifica e tecnologica e della pubblica istruzione (ora Ministro dell’Istruzione,
dell’Università e della Ricerca, n.d.r.), promuove lo svolgimento di campagne di informazione e di educazione
ambientale ai sensi della legge 8 luglio 1986 n. 349”.
Nel corso del giudizio, l’Associazione ricorrente ha prodotto alcuni documenti tratti dalla letteratura scientifica, dai
quali emerge che l’utilizzazione inadeguata dei telefoni cellulari o cordless, comportando l’esposizione di parti
sensibili del corpo umano ai campi elettromagnetici, può avere effetti nocivi per la salute umana, soprattutto con
riguardo ai soggetti più giovani e, quindi, più vulnerabili, potendo incidere negativamente sul loro sviluppo psico –
fisico.
Orbene, i rischi per la salute paventati dall’Associazione ricorrente non sono stati efficacemente contestati dalle
Amministrazioni resistenti, che si sono limitate ad invocare l’inammissibilità anche di questa seconda richiesta.
A tale riguardo, ritiene il Collegio che le campagne informative e di educazione ambientale di cui all’art. 10 della l. n.
36/2001 non possano essere sussunte nella categoria degli atti meramente materiali, come sostenuto dalle
Amministrazioni resistenti, ma debbano essere ascritte al genus degli atti amministrativi generali, in quanto sono
rivolte ad una pluralità indefinita di soggetti, trovano il fondamento giuridico in norme di rango legislativo,
presuppongono lo svolgimento di un’attività istruttoria finalizzata alla individuazione dei rischi connessi
all’esposizione del corpo umano ai campi elettromagnetici e alla individuazione delle precauzioni da adottare (sia da
parte degli utenti che dei produttori dei predetti apparecchi) per limitarne gli effetti potenzialmente nocivi per la
salute e hanno lo scopo di sensibilizzare gli utenti in merito ad un uso più consapevole degli apparecchi di telefonia
mobile, al fine di salvaguardare il diritto alla salute che è un diritto costituzionalmente tutelato (art. 32 della
Costituzione).
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Dagli atti depositati in giudizio risulta che già, con nota prot. n. 0001080 –P del 16 gennaio 2012, il Ministero della
Salute, in riscontro ad una precedente richiesta di uno dei procuratori della Associazione ricorrente, evidenziava:
“…. il tema dei possibili rischi per la salute conseguenti all’uso del cellulare è alla costante attenzione del Ministero
della Salute, in particolare a seguito della classificazione stabilita dall’Agenzia Internazionale per la Ricerca sul
Cancro nel 2011, di agente possibilmente cancerogeno per l’uomo (categoria 2B) per i campi elettromagnetici in
radiofrequenza”.
Nella medesima nota, il Ministero della Salute, ha evidenziato che il Consiglio Superiore di Sanità, nel parere del 15
novembre 2011, tenuto conto della posizione formalmente assunta dall’Istituto Superiore di Sanità, “… ha rilevato
che allo stato delle conoscenze scientifiche non è dimostrato alcun nesso di causalità tra esposizione a
radiofrequenze e patologie tumorali, rimarcando tuttavia come l’ipotesi di un rapporto causale non possa essere del
tutto esclusa in relazione ad un uso molto intenso del telefono cellulare…” e che lo stesso Consiglio Superiore di
Sanità “… ha quindi raccomandato di mantenere vivo l’interesse della ricerca e della sorveglianza sul tema, in attesa
che le nuove conoscenze risolvano le attuali aree di incertezza, suggerendo nel contempo l’avvio di una campagna
d’informazione al pubblico al fine di promuovere e incoraggiare un uso responsabile del telefono, soprattutto in
relazione ai bambini che tendono ad essere avvicinati all’uso del telefono cellulare in età sempre più precoce”,
precisando infine: “La campagna di informazione è in fase di preparazione e sarà basata sul quadro delle conoscenze
desumibili dalle più autorevoli fonti e organismi nazionali e internazionali”.
Nonostante il ragguardevole lasso di tempo intercorso, la preannunciata campagna informativa non risulta essere
stata ancora attuata.
Deve conseguentemente essere dichiarato l’obbligo del Ministero dell’Ambiente, del Ministero della Salute e del
Ministero dell’Istruzione, dell’Università e della Ricerca, ciascuno per il proprio ambito di competenza, di
provvedere, in attuazione di quanto disposto dall’art. 10 della l. n. 36/2001, ad adottare una campagna informativa,
rivolta alla intera popolazione, avente ad oggetto la individuazione delle corrette modalità d’uso degli apparecchi di
telefonia mobile (telefoni cellulari e cordless) e l’informazione dei rischi per la salute e per l’ambiente connessi ad un
uso improprio di tali apparecchi.
La predetta campagna di informazione e di educazione ambientale dovrà essere attuata nel termine di sei mesi dalla
notifica o, se anteriore, dalla comunicazione in via amministrativa della presente sentenza, avvalendosi dei mezzi di
comunicazione più idonei ad assicurare una diffusione capillare delle informazioni in essa contenute.
In ragione dell’accoglimento parziale delle domande formulate dall’Associazione ricorrente, ricorrono all’evidenza
valide ragioni per disporre l’equa compensazione delle spese di giudizio.
P.Q.M.
Il Tribunale Amministrativo Regionale per il Lazio (Sezione Terza Quater), definitivamente pronunciando sul
ricorso, come in epigrafe proposto, così dispone:
- dichiara inammissibile, per difetto assoluto di giurisdizione, la domanda di annullamento del silenzio –
inadempimento sulla istanza della ricorrente relativa alla emanazione del decreto ministeriale, di cui all’art. 12 della l.
n. 36/2001;
- accoglie la domanda di annullamento del silenzio – inadempimento sulla istanza presentata dalla ricorrente, sulla
base dell’art. 10 della l. n. 36/2001, e, per l’effetto, dichiara l’obbligo del Ministero dell’Ambiente, del Ministero della
Salute e del Ministero dell’Istruzione, dell’Università e della Ricerca, ciascuno per il proprio ambito di competenza,
di provvedere (nei termini e con le modalità indicate in motivazione) ad adottare una campagna informativa, rivolta
alla intera popolazione, avente ad oggetto l’individuazione delle corrette modalità d’uso degli apparecchi di telefonia
mobile (telefoni cellulari e cordless) e l’informazione dei rischi per la salute e per l’ambiente connessi ad un uso
improprio di tali apparecchi.
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Spese compensate.
Ordina che la presente sentenza sia eseguita dall'autorità amministrativa.
Così deciso in Roma nella camera di consiglio del giorno 13 novembre 2018 con l'intervento dei magistrati:
Giuseppe Sapone, Presidente
Pierina Biancofiore, Consigliere
Paolo Marotta, Consigliere, Estensore
L'ESTENSORE
Paolo Marotta
IL PRESIDENTE
Giuseppe Sapone
IL SEGRETARIO
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ONCOLOGY LETTERS 18: 5383-5391, 2019
Radiofrequency radiation from nearby mobile phone base
stations-a case comparison of one low and
one high exposure apartment
TARMO KOPPEL
1
, MIKKO AHONEN
2
, MICHAEL CARLBERG
3
,
LENA K. HEDENDAHL
3
and LENNART HARDELL
3
1
Department of Labour Environment and Safety, Tallinn University of Technology, Tallinn 19086;
2
Institute of Environmental Health and Safety, Tallinn 11615, Estonia;
3
The Environment and Cancer Research Foundation, SE-702 17 Örebro, Sweden
Received May 10, 2019; Accepted August 5, 2019
DOI: 10.3892/ol.2019.10899
Abstract.
Radiofrequency (RF) radiation in the frequency
range of 30-300 GHz has, since 2011, been classified as a
‘possible’ human carcinogen by Group 2B, International
Agency for Research on Cancer (IARC) at WHO. This was
based on a number of human epidemiology studies on increased
risk for glioma and acoustic neuroma. Based on further human
epidemiology studies and animal studies, the evidence on RF
radiation carcinogenesis has increased since 2011. In previous
measurement studies, it has been indicated that high envi-
ronmental RF radiation levels are present in certain areas of
Stockholm Sweden, including in one apartment. Field spatial
distribution measurements were performed in the previously
measured apartment in Stockholm, which exhibited high
RF radiation from nearby base stations. Based on the RF
broadband analyzer spot measurements, the maximum indoor
E‑field topped at 3 V m
-1
in the bedroom at the 7th
floor. The
maximum outdoor exposure level of 6 V m
-1
was encountered
at the 8th
floor balcony, located at the same elevation and only
6.16 m away from the base station antennas. For comparison,
a measurement was made in a low exposure apartment in
Stockholm. Here, the maximum indoor field 0.52 V m
-1
was
measured at the corner window, with direct line of sight to the
neighboring house with mobile phone base station antennas.
The maximum outdoor field of 0.75 V m
-1
was measured at
the balcony facing the same next-door building with mobile
phone base station antennas. The minimum field of 0.10 V m
-1
was registered on the apartment area closest to the center of
the building, demonstrating the shielding effects of the indoor
walls. Good mobile phone reception was achieved in both
apartments. Therefore, installation of base stations to risky
places cannot be justified using the good reception requirement
argument.
Introduction
Public exposure to radiofrequency (RF) electromagnetic fields
(EMF) in today's cities may be caused by a number of sources,
including mobile phone base stations, TV and radio towers,
wireless local area networks (WLAN), emergency services
radio network, RF‑identification systems, microwave ovens,
anti-theft gates etc. Additionally, individual's exposure may be
significantly elevated by personal usage of mobile and cordless
phones, 2-way radios, WLAN, Bluetooth and other wireless
devices. In this study we have focused on the exposure from
mobile phone base station antennas. Exposure in two apart-
ments positioned close to mobile phone base station antennas
is measured in detail.
Developments in telecommunications technologies have
led to widespread use of mobile devices connected to the
network in constantly increasing loads. This has resulted
also in the public's exposure to RF EMFs. Temporal trends
in RF EMF exposure in everyday environments were inves-
tigated across European cities of Basel, Ghent and Brussels
in 2011-2012 (1). Within a year total RF exposure levels in all
investigated outdoor locations combined raised 57.1%. The
increase in exposure was most notably observed in outdoor
locations due to mobile phone base stations (1).
In many European countries on-site RF exposure measure-
ments have been conducted since the 1990's. Most studies have
focused on the mobile communications' frequency bands. A
comparative analysis concluded that due to the developments
in telecommunications technology, the RF exposure is continu-
ously increasing and is estimated >65% of the total exposure (2).
Based on the personal exposure measurements in the EU, the
mean RF is generally from 0.10 to 0.26 V m
-1
; however most of
these studies are based on outdoor measurements.
RF field exposure literature in Europe was reviewed,
comparing indoor levels to outdoor levels (3). The mean RF
Correspondence to:
Professor Lennart Hardell, The Environment
and Cancer Research Foundation, Studievägen 35, SE-702 17 Örebro,
Sweden
E-mail: [email protected]
Key words:
radiofrequency radiation, microwaves, mobile phone,
base stations, exposure, health, building
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5384
KOPPEL
et al:
RF RADIATION AND BASE STATIONS
exposure from spot measurements in homes was determined
to be 0.29 V m
-1
and for outdoor 0.54 V m
-1
. In outdoor studies
the exposure levels rarely exceeded 1.0 V m
-1
, whereas the
highest exposure contributor was the downlink i.e., radiation
from mobile phone base station antenna. A finding of the
systematic review was that there was no distinct difference
in exposure levels between European countries. However,
studies done by different researchers across the Europe have
used different procedures limiting the comparability between
studies (3).
RF levels are exponentially higher when located closer
to the mobile phone base station antenna. Therefore, proper
safety measures must be applied when protecting public from
the excess RF radiation. One of the main safety principles is
creating sufficient distance between the public and the RF
sources. This requirement may not be met in certain housing
conditions. Mobile phone base stations installed on rooftops
may become very close to people in nearby apartments.
RF field exposure from a mobile phone base station antenna,
located at the rooftop showed that allowable maximum safety
levels were exceeded when being closer than 30 m to the base
station antenna (4). With the increasing distance, the RF power
density is increasingly affected by the landscape topography,
buildings, and trees that induce reflection and absorption. Also,
RF power density depends on the numbers of channels in use
by the base station antenna, the number of time intervals used
and other mobile communication specific factors. The base
station's maximum RF level varies across the day, which is an
indicator of the mobile communications' service load. Also,
RF power density distribution is greatly determined by the
antenna's directional pattern. Values were measured highest in
the balconies within the main radiation lobe of the antenna (4).
We have previously reported results from our measure-
ments of RF radiation levels at certain places in Stockholm,
Sweden such as at the Central Railway station (5), the Old
Town (6), and in the City (7). High radiation was measured at
a square, Järntorget, in the Old Town as further displayed in a
recent publication displaying RF E‑field distribution (8). Most
of the radiation was downlink.
Of special concern is our results of measurements in
a Stockholm apartment for everyday living purposes (9).
Two groups of base stations are located close to the apart-
ment. The total mean RF radiation level was 3,811 µW/m
2
(range 15.2-112,318 µW/m
2
) for the measurement of the whole
apartment, including balconies. Particularly high levels were
measured on three balconies and in 3 of 4 bedrooms. High
mean exposure levels in the bedrooms of growing children (one
at 2,531 µW/m
2
and the other at 1,471 µW/m
2
) with maximum
peaks at 11,803 and 13,739 µW/m
2
, respectively, may have
deleterious effects on their physical and mental health (9,10).
The aim of this study was to further investigate radiation
levels in the high exposure apartment (9) and to compare it
with a low exposure apartment showing RF E‑field distribu-
tion. This was a measurement study with no involvement of
test persons. Thus, no ethical permission was needed.
Materials and methods
In the present study RF field levels were investigated in two
apartments near mobile phone base station antennas. One
of the apartments represented a high exposure living area,
while the other was of low exposure area. Both of the apart-
ments were near to mobile phone base stations but located at
different city districts in Stockholm, Sweden. The locations of
the base stations close to the apartment with high RF radiation
exposure are shown in Figs. 1 and 2, whereas the base stations
relating to the low exposure apartment are shown in Fig. 3.
The high exposure apartment's outdoor areas were posi-
tioned close to the mobile phone base station antennas, being
as close as 6 m. The low exposure apartment's balcony was
about 40 m away from the base station antennas, since these
were installed on the neighboring building and significantly
higher on the roof.
Field spatial distribution measurements were conducted
in the investigated apartments. The following analyses bring
forth the low and high exposure determinant factors. RF
electric field was measured at each room of the apartments.
Depending on the room size, the room was divided into two to
ten quadrants (smaller imaginary squares). At each quadrant a
spot measurement was conducted. At each spot the field was
measured with slow circular movements to cover the area of
about 1 m² at heights of 0.7-2 m. At each spot, the average
and maximum electric field in Volts per meter (V m
-1
) was
recorded representing the measurement period of about 1 min.
The measurements were conducted on a working day
during business hours (afternoon) in January 2019.
Field perturbation by the measurer was minimized by
distancing the meter from the body-the meter was held at arm's
length, with the extending probe outward. The measurements
area was therefore at about 0.8-0.9 m from the investigator.
Spot distance to mobile phone base station antenna was
measured by targeting the closest antenna element. Distance
was measured by laser distance meter STABILA LE50, which
provides precise distance measurements up to 100 m with the
resolution of 0.001 m at the accuracy ±1.5 mm/m.
The measurements were conducted with a RF broad-
band analyzer, Narda NBM‑520, with a E‑field probe E0391
(Narda-Safety-Test-Solutions GmbH, Pfullingen, Germany).
The Narda NBM-series meter is capable of time and spatial
averaging and determining the maximum level during the period
monitored. Narda EF0391 probe is intended by the manufacturer
for base station measurements and has a frequency range from
100 kHz to 3 GHz.
The broadband meter Narda EF0391 covers a large range
of RF transmissions, including different telecommunications
protocols: frequency modulation (FM) radio broadcasting;
television (TV) broadcasting; TETRA emergency services
(police, rescue, etc.); global system for mobile communica-
tions (GSM) second generation mobile communications;
universal mobile telecommunications systems (UMTS) third
generation mobile communications, 3G; long-term evolution
(LTE) fourth generation mobile communications standard,
4G; digital European cordless telecommunications (DECT)
cordless telephone systems standard; Wi-Fi wireless local
area network protocol, 2.45 GHz; worldwide interoperability
for microwave access (WIMAX) wireless communication
standard for high speed voice, data and internet.
Mobile communications' service coverage reception level
was confirmed using an Android mobile phone, showing
service coverage in decibel milliwatts (dBm).
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Figure 1. A view from the high exposure apartment's balcony, this was one
of the highest exposure areas in the apartment's main floor with the RF field
topping at 5.1 V m
-1
, base station antenna as 11.87 m away from the fence.
RF, radiofrequency.
Figure 3. View to the low exposure apartment (rectangle). Mobile phone base
station antennas are visible on the neighboring building (circled); the highest
RF exposure level was on the balcony, which had the line of sight to both
of the antennas. However due to the elevation difference, the balcony had
highest electric field only 0.75 V m
-1
; based on spot measurements maximum
readings over 1-min period; base station antennas' sector include the inves-
tigated building. Rectangle, low exposure apartment; circle, neighboring
building. RF, radiofrequency.
Statistical methods.
The data was analyzed using the spread-
sheet software Microsoft Excel 2016, calculating mean,
median, minimum and maximum for the measured areas.
Mean (x
median, and minimum values were based on the
̄),
time averaging function of spot measurements; maximum
value was based on the maximum reading registered during
the spot measurement. Differences in field level across
different areas was compared in a table and illustrated in a box
plot and the factors determining the attenuation/elevation of
the field pointed out.
Figure 2. A view from the high exposure apartment's balcony, a set of mobile
phone base station antennas are 6 m away from the fence; this was the highest
radiation area, with the RF exposure topping at 6 V m
-1
, even though the
antennas sector was positioned away from the balcony. RF, radiofrequency.
Results
The field spatial distribution measurements conducted at the
apartments in Stockholm show great variation in the RF field
levels.
High exposure apartment.
As illustrated in Figs. 4-6, the
propagation of the field from the nearby mobile phone base
stations' several antennas in the high exposure apartment.
Based on the RF broadband analyzer spot measurements, the
maximum indoor E‑field topped at 3 V m
-1
at the bedroom on
the 7th
floor. The maximum outdoor exposure level of 6 V m
-1
was encountered on the 8th
floor balcony, located at the same
elevation and only 6.16 m away from the base station antennas.
Outdoor areas i.e. balconies have notably higher exposure,
indicated by the darker color.
High exposure levels were encountered also on the 6th
floor balcony with a direct line of sight to the mobile phone
base station antenna at 11.87 m distance. Since the base station
antenna was not aimed at the aforementioned area, hence even
higher exposure conditions are avoided. The lowest exposure
area is in the middle of the apartment (0.30 V m
-1
), which
is still twice as high as the mean exposure level of the low
exposure apartment (0.16 V m
-1
).
Low exposure apartment.
RF field in the low exposure apart-
ment is illustrated in Fig. 7. The field distribution in low
In the present study, measurement data are presented both
in tables and visual views. Spatial distribution of the RF levels
is presented in a heat map view. Heat map is possible only by a
volume of spatially scattered spot measurements. Heat map is
also seen by some other authors as a way to communicate the
measurements data in a comprehensible way to the public (11).
The measurement data, specifically average spot measure-
ment values, were entered to the contour map software
3DFIELD ver. 4.5.2.0 (by Vladimir Galouchko) and spatial
field distribution maps were drawn. Field distribution maps
were based on the spot measurements using 1 min time
averaging.
Conversion from V m
-1
, to
W/m², see also Table I. In most
of our earlier studies we have used the EME Spy 200 from
Satimo and preferred to show our results in power flux density
in W/m² and µW/m² for RF radiation. In the current measure-
ments the broadband analyzer Narda NBM‑520 measures in V
m
-1
and the contour map software 3DFIELD is also constructed
for measurements in V m
-1
.
To convert from electric field strength, E, in V m
-1
to power
flux density in W/m
2
, S, use the formula: S=0.002654 x E
2
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Table I. Conversion table from E, Electric field strength in
V m
-1
to S, power flux density in µW/m
2
.
E in V m
-1
3.3
3.0
2.7
2.4
2.1
1.8
1.7
1.6
1.5
1.4
1.3
1.2
1.1
1.0
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
S in µW/m
2
28,902
23,886
19,348
15,287
11,704
8,599
7,670
6,794
5,971
5,202
4,485
3,822
3,211
2,654
2,150
1,698
1,300
955
663
425
239
106
26
difference in mean outdoor exposure levels between the apart-
ments. Considering maximum readings, the outdoor exposure
difference was eight-fold.
Tables II and III presents the main statistics for the low
exposure and high exposure apartment, expressed in V m
-1
(Table II) and µW/m² (Table III). Tables II and III statistics are
based on 1-min averaged spot measurements. The maximum
indoor RF field was 0.52 V m
-1
and 3.00 V m
-1
respectively.
Maximum reading at the balcony outside the low exposure
apartment was 0.75 V m
-1
compared with 6.00 V m
-1
outside
the high exposure apartment.
Discussion
There are a limited number of studies of RF exposure levels
in Sweden. A car mounted measurement system was used to
map spatially some of rural, urban and city areas published in
2014 (12). Mean power density levels showed highest exposure
levels at Stockholm city (6,700 µW/m²), followed by city of
Solna (3,278 µW/m²) and then urban areas as represented by
Göteborg, Helsingborg, Jönköping and Ljungby (1,500 µW/m²)
and rural areas represented by Ryssby and Ekerö (230 µW/m²).
Their study clearly indicated that higher population density
results in higher RF exposure (12). They also noted that
power density can vary by >50 dB (100,000 times) over a
driving distance of 10 km, which supports the finding in our
study-high RF exposure is not required to have a good mobile
telephony service reception. Note that these measurements do
not represent current RF radiation due to the rapid increase of
deployment of the wireless communication (8).
A RF survey in Greece, found median urban electric field
(median 1.1 V m
-1
) to be significantly higher than rural levels
(median 0.3 V m
-1
). As the study utilized temporal measurements
with 6-min averaging from 90 installed measurements stations,
the data showed large diurnal variation for stations positioned
close to mobile phone base stations, with median diurnal
variation of 33.8% (13). These measurements are also old.
Baltrėnas
et al
(4) investigated a 10-story building neigh-
boring a mobile phone base station antenna, where the height
of the building was 30 m distanced 35 m from the base station.
These conditions are similar to our study. The base station
antenna was approximately on the same height as floor 6.
Consequently, the highest exposed floors were 5‑7, with floors
where the power density at the balcony was about three times
higher at 6th floor as compared to the 3rd floor. The difference
was about 15-times when comparing the RF power density at
the 1st floor to the 6th floor (4).
The present measurements with means of RF radiation up
to 1.3 V/m (4,485 µW/m²) at the windows in the bedrooms in the
high exposure apartment imply that this exposure may almost
be compared to the exposure from a mobile phone in calling
mode for many hours per day. A cohort study on Swiss adoles-
cents showed that there was an association between whole
body cumulative RF radiation dose from mobile phone talk,
internet use and sent SMS and symptoms like headache and
exhaustibility and also a decrease in figural memory (14,15).
Many research studies have shown effects from RF radiation
exposure on animals below current safety levels with opened
blood brain barrier and neuronal damage (16,17), oxidative stress
with increased production of reactive oxygen species (18,19),
exposure apartment shows much less variation in amplitude,
as the field is several times lower when compared to the high
exposure apartment. The maximum indoor field (0.52 V m
-1
)
was measured at the corner window, with direct line of sight
to the neighboring house with mobile phone base station
antennas. Maximum outdoor field of 0.75 V m
-1
was measured
at the balcony facing the same next-door building with mobile
phone base station antennas. The minimum field of 0.10 V m
-1
was registered on the apartment area closest to the center of
the building, hence demonstrating the shielding effects of the
indoor walls.
Spot measurements resulted both in time averaged and
maximum RF field levels. Pearson's product‑moment correla-
tion coefficient shows high correlation between the two sets of
values: r=0.95 in the high exposure apartment, and r=0.97 in
the low exposure apartment. In average, maximum values were
58% higher than time averaged values in the high exposure
apartment, and 87% higher in the low exposure apartment.
In Fig. 8 a boxplot is presented comparing the high expo-
sure apartment to the low exposure apartment (indoor areas)
based on 1-min spot measurements maximum reading.
Field increase from indoor to outdoor.
Comparison was also
made in both apartments between the outdoor area (staying
at the balcony) and the corresponding adjacent room area,
which had access to the balcony. There was about a five‑fold
difference in mean indoor exposure levels and about a six-fold
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Figure 4. Spatial field distribution map of the high exposure apartment on the 6th floor; time‑averaged RF electric field (V m
-1
). RF, radiofrequency.
Figure 5. Spatial field distribution map of the high exposure apartment, a
bedroom on the 7th floor; time‑averaged RF electric field (V m
-1
). RF, radio-
frequency.
Figure 6. Spatial field distribution map of the high exposure apartment, a
room on the 8th floor and on the same elevation with mobile phone base
station antennas; RF radiation from base station antennas indicated with
arrows; time‑averaged RF electric field (V m
-1
). RF, radiofrequency.
DNA-damage especially in the memory center hippocampus in
the brain and increase in pro‑inflammatory cytokines (20).
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Figure 7. Spatial field distribution map of the low exposure apartment; time‑averaged RF electric field (V m
-1
). RF, radiofrequency.
Figure 8. Box plot comparing indoor areas of the low exposure apartment to
the high exposure apartment (V m
-1
). For median RF electric field the differ-
ence is more than four times; based on spot measurements maximum readings
over 1‑min period. Whiskers plot depicts (from bottom up) minimum, first
quartile, median, third quartile and maximum of the sample containing all
the spot measurement values in the area. RF, radiofrequency.
Apart from animal studies research studies on people
living near mobile phone base station show augmented
indications on health risks. Adverse effects have been seen
on neurotransmitters in the brain (21), on hormones like
cortisol, ACTH and from the thyroid, decreased levels of
testosterone in men and prolactin in young women and also
increase in salivary cortisol (22,23). Other studies have shown
lowered antioxidant levels and induced DNA damage in blood
lymphocytes (10,24) as well as health complaints. Symptoms
like sleep disturbances, headache, fatigue, dizziness, cardio-
vascular symptoms depression and difficulties with memory
and concentration have been reported from people living near
mobile phone base stations (25,26).
Human exposure has increased rapidly in recent years and will
increase substantially with the introduction of the fifth genera-
tion (5G) for wireless communication (www.5gappeal.eu) (27,28)
and should now be regarded as an environmental pollutant. Of
special concern is that RF radiation in the frequency range
30 kHz to 300 GHz was in 2011 classified as a ‘possible human
carcinogen’ Group 2B by the International Agency for Research
on Cancer (IARC) (29,30). The carcinogenic evidence has by
now strengthened and RF radiation should be reclassified as a
known human carcinogen, Group 1 (27,28). Environmental RF
radiation is often involuntary with little possibilities to avoid,
especially since mostly nothing has been done to inform and
protect people from RF radiation (31,32).
Especially the two bedrooms for the children in this
apartment were exposed to high RF radiation, (mean 2,531
and 1,471 µW/m
2
) (9). Children will probably be exposed for
a whole lifetime in contrast to the present generation. They
also seem to be more sensitive for RF radiation with more
immature cells in their growing bodies (33,34).
A study from Taiwan calculated annual power density in
watt-year/km
2
to each township from all 71,185 mobile phone
base stations in service between 1998-2007. They found a
statistically significantly increased risk for all neoplasms in
children with higher-than-median exposure of RF radiation
from base stations during five years prior to their neoplams (35).
The Interphone study group calculated the estimated RF dose
from mobile phones in five of the participating countries. The
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5389
Table II. Statistics for the low and high exposure apartment. Radiofrequency field (V m
-1
). Mean, median and minimum values
are based on the average of 1 min spot measurements (calculated based on 1 min temporal monitoring sample). The maximum
is based on the same spot measurements maximum registered RF level.
Apartment
Low exposure
High exposure
Low exposure
High exposure
RF, radiofrequency.
Area
Indoor area
Indoor area
Outdoor area (balcony)
Outdoor area (balcony)
Number of
measured spots
20
72
2
10
Mean (x
̄)
-1
Vm
0.16
0.77
0.40
2.46
Median
(V m
-1
)
0.15
0.60
0.40
2.65
Minimum
(V m
-1
)
0.10
0.30
0.39
1.00
Maximum
(V m
-1
)
0.52
3.00
0.75
6.00
Table III. Statistics for the low and high exposure apartment. The radiofrequency field in power flow density in µW/m
2
. Mean,
median and minimum values are based on the average of 1 min spot measurements (calculated based on 1 min temporal sample
monitoring). Maximum is based on the same spot measurements maximum registered RF level.
Number of
measured spots
20
72
2
10
Mean (x
̄)
in µW/m
2
68
1,573
424
16,061
Median
(µW/m
2
)
60
955
424
18,638
Minimum
(µW/m
2
)
26
239
404
2,654
Maximum
(µW/m
2
)
718
23,886
1,492
95,544
Apartment
Low exposure
High exposure
Low exposure
High exposure
RF, radiofrequency.
Area
Indoor area
Indoor area
Outdoor area (balcony)
Outdoor area (balcony)
RF radiation dose was estimated as total cumulative specific
energy (TCSE) in J/kg absorbed at the tumor's estimated centre.
The risk for a glioma increased with increasing TSCE 7+ years
before diagnoses (36). Several studies have shown increasing
risks for brain tumors, especially glioblastoma multiforme,
with increasing years of mobile phone use, amount of calls and
calling time (29,30,37,38).
In comparing two Stockholm apartments, several factors
and exposure determinant could be pointed out. Both apart-
ments were located in the vicinity of the mobile phone base
station antenna, which allowed good mobile services reception
indoor. Measured RF field levels in the low exposure apart-
ment demonstrate that high exposure is not needed to provide
good mobile phone reception.
Two mobile phone base stations placed very near, less
than 20 m to an apartment may imply health risks for the
inhabitants.
The low exposure apartment exposure levels were lower
since the mobile phone base station was installed on top of the
neighboring building, whereas on the high exposure apartment
the base station was on top of the same building.
The high exposure apartment was on the top floor, with
the mobile phone base station antennas situated on the roof
above. The low exposure apartment was positioned seven
floors lower from the roof where the base station antennas
were located.
The low exposure apartment was located on the opposite
side of the building from the mobile phone base station, hence
Figure 9. Mobile phone base station antenna neighboring the low exposure
apartment; the buildings hinder the propagation of the RF field, especially
shielding the sides facing away from the radiofrequency source; mobile
phone base station antennas are sector antennas and radiate the micro-
waves into a direction (sector) these are aimed at. Rectangles, low exposure
apartment.
the building itself provided cover (Fig. 9). Building materials,
such as concrete and metal structures provide partial shielding
effect against inbound radio waves.
In both apartments, indoor RF levels were several folds
lower than outdoor levels of the corresponding room. Lower
levels were detected also in the vicinity of the windows. This
indicates a notable screening effect by the contemporary
heat‑reflecting windows.
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In both apartments the lowest exposure levels were regis-
tered within the center of the building, far away from the
windows, shielded by the concrete or brick walls.
Although the tin roof of the high exposure apartment
shields it from the majority of the inbound radio waves,
countless reflections and diffraction from the structures on
the roof and balconies provide the pathway to indoor. The RF
field penetrated the building's constructions, including the
windows and resulted in notably high exposure levels indoor.
Acknowledgements
The authors would like to thank Dr Jolanta Karpowicz, Head
of Department of Bioelectromagnetics, Central Institute for
Labour Protection-National Research Institute (CIOP-PIB) for
the discussion regarding exposure analysis.
Funding
The present study was supported by grants from Mr. Brian
Stein and Cancerhjälpen.
Availability of data and materials
The datasets generated and/or analyzed during the present
study are available from the corresponding author on reason-
able request.
Authors' contributions
All authors participated in the conception, design and writing
of the manuscript and have read and approved the final version.
TK, LH and MA conducted the measurements. MC and TK
performed the statistical analysis. MC checked the statistical
methods and results. LKH wrote the medical sections, contrib-
uted to the conclusions and conversion tables.
Ethics approval and consent to participate
Not applicable.
Patient consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
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25. Abdel-Rassoul G, El-Fateh OA, Salem MA, Michael A,
Farahat F, El-Batanouny M and Salem E: Neurobehavioral
effects among inhabitants around mobile phone base stations.
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Subjective symptoms related to GSM radiation from mobile phone
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27. Belpomme D, Hardell L, Belyaev I, Burgio E and Carpenter DO:
Thermal and non-thermal health effects of low intensity
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Baan R, Grosse Y, Lauby Secretan B, El Ghissassi F, Bouvard V,
Benbrahim-Tallaa L, Guha N, Islami F, Galichet L, Straif K and
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Working Group: Carcinogenicity of radiofrequency electromag-
netic fields. Lancet Oncol 12: 624‑626, 2011.
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to Humans, Non-Ionizing Radiation, Part 2: Radiofrequency
Electromagnetic Fields, vol. 102, International Agency for
Research on Cancer, Lyon, France (2013). Available at:
http://monographs.iarc.fr/ENG/Monographs/vol102/mono102.
pdf. Accessed on April 16, 2019.
31. Starkey SJ: Inaccurate official assessment of radiofrequency
safety by the advisory group on non-ionizing radiation. Rev
Environ Health 31: 493-503, 2016.
32. Hardell L: World health organization, radiofrequency radiation
and health-a hard nut to crack (review). Int J Oncol 51: 405-413,
2017.
33. Markovà E, Malmgren LO and Belyaev IY: Microwaves from
mobile phones inhibit 53BP1 focus formation in human stem
cells stronger than in differentiated cells: Possible mechanistic
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2010.
34. Morgan LL, Kesari S and Davis DL: Why children absorb more
microwave radiation than adults: The consequences. J Microsc
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tion-based case-control study of radiofrequency exposure in
relation to childhood neoplasm. Sci Total Environ 435-436:
472-478, 2012.
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Hours M, Krewski D, McBride M, Parent ME, Sadetzki S,
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This work is licensed under a Creative Commons
Attribution-NonCommercial-NoDerivatives 4.0
International (CC BY-NC-ND 4.0) License.
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News
Advisory Group recommendations on priorities for the IARC
Monographs
An Advisory Group of 29 scientists
from 18 countries met in March, 2019,
to recommend priorities for the
International Agency for Research
on Cancer (IARC) Monographs
programme during 2020–24. IARC
periodically convenes such advisory
groups to ensure that the Monographs
evaluations reflect the current state
of scientific evidence relevant to
carcinogenicity.
1
A detailed report of
the Advisory Group will be published
subsequently.
2
The Advisory Group assessed
the response to a public call for
nominations and considered more
than 170 unique candidate agents,
including the recommended priorities
remaining from a similar Advisory
Group meeting convened in 2014.
3
The expertise of the Advisory
Group covered multiple disciplines,
and the members appraised, on
an individual nomination basis,
the evidence according to human
exposure (including any evidence
of exposure in low-income and
medium-income countries), cancer
epidemiology, cancer bioassays
in experimental animals, and
carcinogen mechanisms, in line with
the evaluation methodology recently
refined in the Preamble to the IARC
Monographs.
1
A complementary
approach assessed all nominations
using a chemoinformatics, text
mining, and chemical similarity
analysis workflow;
4
this approach
helped to reveal coverage and gaps
in the extent of evidence across
data streams, supporting decisions
on individual agents and groups
of chemically related nominations.
The Advisory Group deliberated
on all nominated agents both by
evidence stream (ie, exposure,
human cancer, cancer bioassay, and
carcinogen mechanisms) and by type
of agent (eg, metals, fibres, chemicals,
biological agents, and complex
mixtures) to inform development of
priority recommendations.
The Advisory Group recommended
a broad range of agents with high
(table 1), medium, or low (table 2)
priority for evaluation. Priority was
assigned on the basis of evidence
Published
Online
April 17, 2019
http://dx.doi.org/10.1016/
S1470-2045(19)30246-3
For more on the
IARC
Monographs
see
http://monographs.iarc.fr/
Upcoming meetings
June 4–11, 2019, volume 124:
Shift work that involves circadian
disruption
Nov 5–11, 2019, volume 125:
Some industrial chemicals
March 24–31, 2020, volume 126:
Opium
IARC Monographs Advisory
Group Members
M M Marques (Portugal)—
Meeting Chair; A Berrington de
Gonzalez (USA)—Meeting Vice
Chair; F A Beland (USA);
P Browne (France); P A Demers
(Canada); D W Lachenmeier
(Germany)—Subgroup Meeting
Chairs; T Bahadori (USA);
D K Barupal (USA); F Belpoggi
(Italy); P Comba (Italy); M Dai
(China); R D Daniels (USA);
C Ferreccio (Chile); O A Grigoriev
(Russia); Y C Hong (South Korea);
R N Hoover (USA); J Kanno
(Japan); M Kogevinas (Spain);
G Lasfargues (France);
R Malekzadeh (Iran); S Masten
(USA); R Newton (Uganda and
UK); T Norat (UK); J J Pappas
(Canada); C Queiroz Moreira
(Brazil); T Rodriguez (Nicaragua);
J Rodríguez-Guzmán (USA);
V Sewram (South Africa); L Zeise
(USA)
Declaration of interests
All advisory group members
declare no competing interests
Invited Specialists
None
Representatives
R Corvi, for the Joint Research
Centre, European Commission,
Italy; B Kim, E Y Park, for the
National Cancer Center,
South Korea
Declaration of interests
All representatives declare no
competing interests
Observers
S Borghoff, for ToxStrategies,
USA
Declaration of interests
SB is sponsored by the American
Beverage Association
Rationale
Agents not previously evaluated by IARC Monographs
Haloacetic acids (and other disinfection byproducts)
Metalworking fluids
Cannabis smoking, fertility treatment, glucocorticoids,
Salmonella typhi,
sedentary
behaviour*, tetracyclines and other photosensitising drugs
Cupferron, gasoline oxygenated additives, gentian violet, glycidamide, malachite green
and leucomalachite green, oxymetholone, pentabromodiphenyl ethers, vinclozolin
Breast implants, dietary salt intake*, neonatal phototherapy*, poor oral hygiene*
Aspartame
Arecoline, carbon disulphide, electronic nicotine delivery systems and nicotine*,
human cytomegalovirus, parabens
Agents previously evaluated by IARC Monographs†
Automotive gasoline (leaded and unleaded), carbaryl, malaria
Acrylamide*, acrylonitrile, some anthracyclines, coal dust, combustion of biomass,
domestic talc products, firefighting exposure, metallic nickel, some pyrethroids (ie,
permethrin, cypermethrin, deltamethrin)
Aniline, acrolein, methyl eugenol and isoeugenol*, multi-walled carbon nanotubes*,
non-ionising radiation (radiofrequency)*, some perfluorinated compounds
(eg, perfluorooctanoic acid)
Ostrogen:oestradiol and oestrogen-progestogens‡, hydrochlorothiazide, Merkel cell
polyomavirus, perchloroethylene, very hot foods and beverages
1,1,1-trichloroethane, weapons-grade alloy (tungsten, nickel, and cobalt)
Acetaldehyde, bisphenol A*, cobalt and cobalt compounds, crotonaldehyde, cyclopeptide
cyanotoxins, fumonisin B
1
, inorganic lead compounds, isoprene, o-anisidine
New human cancer, bioassay, and mechanistic evidence to warrant
re-evaluation of the classification
New human cancer and mechanistic evidence to warrant
re-evaluation of the classification
New bioassay and mechanistic evidence to warrant re-evaluation
of the classification
New human cancer evidence to warrant re-evaluation of the
classification
New bioassay evidence to warrant re-evaluation of the classification
New mechanistic evidence to warrant re-evaluation of the
classification
Relevant human cancer, bioassay, and mechanistic evidence
Relevant human cancer and bioassay evidence
Relevant human cancer and mechanistic evidence
Relevant bioassay and mechanistic evidence
Relevant human cancer evidence
Relevant bioassay evidence
Relevant mechanistic evidence
Evidence of human exposure was identified for all agents. *Advised to conduct in latter half of 5-year period. †See current International Agency for Research on Cancer (IARC)
list of classifications, volumes 1–123. ‡Group 1 carcinogen; new evidence of cancer in humans indicates possible causal associations for additional tumour sites (see Section 3
of Preamble to the IARC Monographs
1
).
Table :
Agents recommended for evaluation by the IARC Monographs with high priority
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Vol 20 June 2019
763
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News
IARC/WHO Secretariat
L Benbrahim-Tallaa; V Bouvard;
I A Cree; F El Ghissassi; J Girschik;
Y Grosse; K Z Guyton; A L Hall;
M Kojenjak; V McCormack;
K Müller; M K Schubauer-Berigan;
J Schüz; K Straif; M C Turner;
C Vickers; J Zavadil
Declaration of interests
MCT received personal fees from
ICF Incorporated, LLC, outside
this work. All other secretariat
declare no competing interests.
For the
Preamble to the IARC
Monographs
see https://
monographs.iarc.fr/wp-content/
uploads/2019/01/
Preamble-2019.pdf
For
IARC declarations of
interests
see https://
monographs.iarc.fr/wp-content/
uploads/2018/07/priorities-doi.
pdf
For the
IARC list of
classifications, volumes 1–123
see https://monographs.iarc.fr/
list-of-classifications-volumes/
Previous evaluation status
Medium priority agents
2,3-butanedione (diacetyl), alachlor, biphenyl, chlorinated paraffins, chlorpyrifos, c.i. direct blue 218, diphenylamine,
hydrazobenzene, indole-3-carbinol, mancozeb, nanomaterials (eg, titanium dioxide or nanosilica), nitrogen dioxide,
o-benzyl-p-chlorophenol,
ozone, pendimethalin, sleep, styrene-acrylonitrile trimer, terbufos, tris(chloropropyl)phosphate
Aflatoxins†, anthracene, antimony trioxide, atrazine, bromate compounds, dimethyl hydrogen phosphite, furan,
N-methylolacrylamide, p-nitrotoluene, Schistosoma mansoni,
tris(2-chloroethyl) phosphate, tobacco smoking (including
second hand)†
Low priority agents
2-hydroxy-4-methoxybenzophenone, aluminium, androstenedione, butyl methacrylate, cinidon ethyl, dysbiotic
microbiota, fonofos, furmecyclox, isoflavones, isophorone, laboratory work and occupation as a chemist, methanol,
S-ethyl-N,N,-dipropylthiocarbamate,
semiconductor manufacturing, Sucralose
1,1-dimethylhydrazine, benzophenone-1, carbon black, catechol, chlordecone, cumene, dichloromethane, hepatitis D
virus, human papillomavirus (beta [cutaneous] and some alpha [mucosal] types),
Opisthorchis felineus,
outdoor air
pollution†, pyrrolizidine alkaloids, selenium and selenium compounds
Agents not previously evaluated
by the IARC Monographs
Agents previously evaluated by
the IARC Monographs*
Agents not previously evaluated
by the IARC Monographs
Agents previously evaluated by
the IARC Monographs*
Evidence of human exposure was identified for all agents. *See current International Agency for Research on Cancer (IARC) list of classifications, volumes 1–123. †Group 1
carcinogen; new evidence of cancer in humans indicates possible causal associations for additional tumour sites (see Section 3 of Preamble to the IARC Monographs
1
).
Table
2:
Agents recommended for evaluation by the IARC Monographs with medium and low priority
of human exposure and the extent
of available evidence for evaluating
carcinogenicity (ie, the availability of
relevant human cancer, experimental
animal bioassay, or mechanistic
evidence to support a new or updated
evaluation according to the Preamble
to the IARC Monographs
1
). Any of
the three evidence streams could
alone support prioritisation of agents
with no previous evaluation. For
previously evaluated agents, the
Advisory Group considered the basis
of the previous classification, as well
as the potential impact of the newly
available evidence during integration
across streams (see table 4 in
Preamble to the IARC Monographs
1
).
Agents without evidence of
human exposure or evidence for
evaluating carcinogenicity were
not recommended for further
consideration. The Advisory
Group recognised that agents
related to the identified priorities
might also warrant evaluation.
Furthermore, additional agents
might merit consideration if new
relevant evidence indicating an
emerging carcinogenic hazard
(eg, from cancer epidemiology
studies, cancer bioassays, or studies
on key characteristics of carcinogens)
becomes available in the next 5 years.
In line with the interim standard
operating procedure adopted by the
IARC Governing Council,
5
IARC will
consider this advice when selecting
agents for future Monograph
evaluations according to the
Preamble to the IARC Monographs.
1
The views expressed are those of the authors and do
not necessarily represent the decisions, policy, or
views of their respective institutions.
IARC Monographs Priorities Group
International Agency for Research on
Cancer, Lyon, France
All authors declare no competing interests.
1
International Agency for Research on Cancer.
Preamble to the IARC Monographs. 2019.
https://monographs.iarc.fr/wp-content/
uploads/2019/01/Preamble-2019.pdf
(accessed April 16, 2019).
International Agency for Research on Cancer.
Report of the Advisory Group to Recommend
Priorities for IARC Monographs during
2020–2024; 25–27 March, 2019. Lyon:
Monographs on the Evaluation of Carcinogenic
Risks to Humans, in press.
Straif K, Loomis D, Guyton K, et al.
Future priorities for the IARC Monographs.
Lancet Oncol
2014;
15:
683–84.
Guha N, Guyton KZ, Loomis D, Barupal DK.
Prioritizing chemicals for risk assessment using
chemoinformatics: examples from the IARC
Monographs on pesticides.
Environ Health Perspect
2016;
124:
1823–29.
International Agency for Research on Cancer.
Sixtieth Session of the IARC Governing Council,
GC/60/13. 2018. http://governance.iarc.fr/GC/
GC60/En/Docs/GC60_13_CoordinationWHO.
pdf (accessed April 12, 2019).
2
3
4
5
764
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Vol 20 June 2019
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Swiss Re SONAR
New emerging risk insights
May 2019
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What shapes the insurance industry?
Past experience and, importantly, new,
changing and not-yet envisioned risks.
We created this SONAR report to
inform and inspire conversations about
emerging risks, so we can continue to
build resilience together, in these
uncertain times.
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Contents
Overview
Foreword
Introduction
Macro trends
15 Emerging risk themes and 5 Trend spotlights
Societal environment
Vaccination – a shot worth more than politics and profitability
Retirement skills gap – accidents waiting to happen
Concussion injuries in sport – head on to more widespread claims
A celebrity body – the hazards of aesthetic surgery tourism
2
3
5
7
16
17
18
19
Political environment
Limits to tinkering – the fiscal and monetary policy balance at risk
Beggar thy neighbour? Global trade reordered
Conflicting interests – the widening urban-rural divide
Shifting litigation regimes –
Trend spotlight
22
23
24
25
Technological and natural environment
Teaching an old dog new tricks – digital tech meets legacy hardware
The surveillance economy –
Trend spotlight
Off the leash – 5G mobile networks
Smart construction –
Trend spotlight
Wiggle room – Artificial Intelligence and healthcare
The warehouse of the future –
Trend spotlight
Resilience at stake – forestsʼ vital functions under threat
Pervasive and toxic – chemicals in our bodies and environment
26
27
29
30
31
32
33
34
Competitive and business environment
Donʼt ask, donʼt tell – genetic testing and adverse selection
Risky bets? Insurance demand in an age of shifting markets
Financial services and the digital revolution –
Trend spotlight
Getting the balance right – technology regulation affecting the insurance industry
36
38
40
41
Special feature – Climate change and Life & Health
Climate change – from emerging risk to real-life danger
Itʼs existential – climate change and life & health
42
44
47
54
Appendix A: High impact emerging risk themes, 2015–2019
Appendix B: Terms and definitions
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Overview
Emerging risk themes by potential impact and timeframe
0–3 years
Teaching an old dog new
tricks – digital tech meets
legacy hardware
Donʼt ask, donʼt tell –
genetic testing and
adverse selection
Getting the balance
right – technology
regulation affecting the
insurance industry
Vaccination – a shot
worth more than politics
and profitability
Beggar thy neighbour? –
Global trade reordered
Resilience at stake –
forestsʼ vital functions
under threat
Wiggle room – Artificial
Intelligence and
healthcare
Pervasive and toxic –
chemicals in our bodies
and environment
Conflicting interests – the
widening urban-rural
divide
> 3 years
Off the leash – 5G mobile
networks
Limits to tinkering – the
fiscal and monetary
policy balance at risk
Itʼs existential – climate
change and life & health
(Special feature)
Risky bets? Insurance
demand in an age of
shifting markets
Retirement skills gap –
accidents waiting to
happen
Concussion injuries in
sport – head on to more
widespread claims
A celebrity body –the
hazards of aesthetic
surgery tourism
Most affected business areas
for
Property
for
Casualty
for
Life & Health
for
Financial markets
for
Operations
Potential impact
High
Medium
Low
2
Swiss Re
SONAR New emerging risk insights
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Foreword
In our annual SONAR report for 2019, we highlight the emerging risks
we have identified and assessed through the course of the last year.
The clash of new and legacy technologies, the fiscal and monetary
imbalance, and the retirement skills gap are just some of the risks we
feature in this study.
Many of these risks are entirely new, because they emerge from
innovations not seen before, or new developments in society
and/or in insurance framework conditions. The expected timeframe
for the maturation of the risks into real-life events with significant
loss-making potential is often short. However, we also cover
“slow-burner” emerging risks, where evolution of the exposure
to the point of potential for notable impact on the insurance industry
will be long-running.
A classic example is climate change. Swiss Re and the insurance
industry at large first flagged climate change as an emerging risk
many decades ago. The risk has now “emerged” but associated
(and challenging) uncertainties still remain. Such as, for example,
the implications of climate change on Life & Health insurance. We
devote a special feature chapter to this important topic in this report.
We hope this yearʼs SONAR report provokes new insights for you.
We look forward to engaging with you to discuss your thoughts and
the spectrum of emerging risks overall.
Patrick Raaflaub
Group Chief Risk Officer
Swiss Re
SONAR New emerging risk insights
3
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Failure of key infrastructure like power
distribution can significantly impact the
insurance industry.
4
Swiss Re
SONAR New emerging risk insights
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Introduction
We define emerging risks as newly developing or changing risks which are difficult
to quantify. The loss potential of these risks is currently difficult to estimate, but they
may have a major business impact on the insurance industry. Against the backdrop
of macro trends identified by Swiss Re, which are synthesized in overarching
perspectives (see macro trends environments and overarching topics, page 7),
this yearʼs SONAR report features 15 new emerging risk themes and five emerging
trend spotlights. It also includes a special feature on the implication of climate
change on Life & Health insurance.
To assess and underwrite risks, the insurance industry relies on experience (ie,
historical data for identified and insurable risks). However, historical data alone
cannot build understanding of the future risk landscape, which is forever changing
and presents new and previously unforeseen risks. Here, the insurance industry
needs to demonstrate foresight and make use of sound future intelligence.
Knowledge sharing through different forms of risk dialogue with all stakeholders
can help insurers manage emerging risks more effectively, for industry sustainability
and to improve societal resilience. Swiss Reʼs SONAR report, which has been
published annually since 2013, provides a forward-looking perspective, to further
promote and engage with such risk dialogue.
Swiss Re identifies emerging risks, first and foremost, through its proprietary
SONAR tool, an internal crowdsourcing platform that collects input and feedback
from underwriters, client managers, risk experts and others across Swiss Re. The
emerging risk themes outlined in this report are based on early signals collected
throughout the year. They neither reflect the entire emerging risk landscape of the
insurance industry nor that of Swiss Re. They have been categorised according
to their estimated impact and potential timeframe to materialise, and with respect
to the line of business (see figure page 2) where we expect the biggest exposure
will rest.
Per lines of business, the top emerging risk themes identified in this yearʼs edition are:
for
Property:
for
Casualty:
Retirement skills gap – accidents waiting to happen
Teaching an old dog new tricks – digital tech meets
legacy hardware
Donʼt ask, donʼt tell – genetic testing and adverse
selection
Limits to tinkering – the fiscal and monetary policy
balance at risk
Getting the balance right – technology regulation
affecting the insurance industry
for
Life & Health:
for
Financial Markets:
for
Operations:
Some of the emerging risk themes and trends presented in this and previous SONAR
reports may never materialise as exposures with loss-making potential. Others likely
will. The earlier the re/insurance industry starts adapting to new risks, the better
prepared it will be to successfully protect its bottom line, develop new products and
write profitable business.
In an appendix, emerging risks with highest impact are listed from past reports
dating back to 2015, with additional information about cross-cutting themes (see
Appendix A: Key emerging risks from SONAR reports 2015–2019).
Swiss Re
SONAR New emerging risk insights
5
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The low carbon economy calls
for new solutions such as high speed
trains or renewable energy
installations.
6
Swiss Re
SONAR New emerging risk insights
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Macro trends
Screening of interdependent macro trends
For todayʼs and tomorrowʼs risk landscape, Swiss Re has identified and assessed
23 macro trends. This is central to understanding the risk landscape of the future, to
make informed decisions and to create solutions for emerging risk pools. Swiss Re
assesses these trends and their interdependencies through discussions with experts,
in-depth reviews and by undertaking annual surveys.
The list of 23 macro trends for 2019 remains unchanged from the previous year,
when “Data as an asset” was added. We deem these trends as having the
potential to be decisive elements for the re/insurance industry within the next five
to ten years. The trends fall into four, interlinked “environment” categories, namely
(1) societal; (2) political; (3) competitive and business, and (4) technological and
natural environments.
In this section, we provide insights into the four environments and the respective
macro trends. We also highlight three overarching topics that feature strong
interdependencies between certain macro trends, are reflected in todayʼs reality,
and are expected to shape the future of our industry.
Societal environment
Growing middle class in HGM
Longevity & radical medical innovation
Connected & collaborative society
Mass migration & urbanisation
The future of work & talent gaps
Rising social inequality & unrest
Political environment
Public sector moving risk to private sector
Protectionism & fragmented regulation
Increasing nationalism
Instability of geopolitical & economic systems
Low yield environment & risk of inflation
Technological and natural environment
Climate change & resource scarcity
Structural change of energy production,
distribution & consumption
Massive expansion of digital & cyber risk
Data as an asset
Technology application as efficiency play
Disruptive digital technologies
Autonomous transportation & robotics
Competitive and business environment
Re/insurance value chain disaggregation
Rise of collateralised reinsurance
Strategic partnerships with non-insurance
companies & institutions
Regional champions going global
Increasing digital customer interaction
Swiss Re
SONAR New emerging risk insights
7
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Macro trends
environments
Societal environment
The economic relevance of the middle class remains all pervasive but increasingly,
the onus is shifting to the emerging economies, most notably Asia Pacific. A large
number of households in emerging markets have escaped poverty over the past
years, and growing household wealth has led to more consumption. Shift and overall
growth of insurance markets are to be expected, but they cannot be taken for
granted (see page 38 “Risky bets?”).
Escape from poverty has seen mass migration from rural areas to cities. The UN
Department of Economic and Social Affairs estimates that by 2030, the number of
people living in urban settings across the world will reach 5 billion, up from around
2.5 billion today. Over 90% of the increase will occur in high growth markets (HGM),
and most in China and India. Migration and urbanisation concentrate risk. For one,
large cities are more prone to health hazards, an important consideration for Life and
Health (L&H) insurers. And also, with an associated accumulation of economic
assets in urban areas, there is more potential for large financial losses in the event of
a major natural disaster, an opportunity for property lines of business. Serving as
powerhouses to national economies, cities also invite resentment from the rural
periphy. A number of recent democratic elections and votes, e.g. Brexit, have shown
signs for a growing divide between the populations of metropolitan centres and of
rural peripheries (see page 24 “Conflicting interests”).
In the mature economies, the post-World War II baby-boomers have mostly reached
retirement years (with regard to the skills gap opening and subsequent risk, see page
17 “Retirement skills gap”) with sufficient savings and asset gains accumulated from
the prosperity of the 20th century. The next generation is still strong in numbers, but
is accumulating less wealth and experiencing more pressure from globalisation and
automation. The pension systems in many mature markets is becoming increasingly
unsustainable for future retirees. This, and a shrinking middle class in some part of
the developed world, may deepen social inequality. As more people feel left behind,
a pool of dissatisfaction will likely build. In times of social media connectivity and of
traditional political parties disrupted by political entrepreneurship, channeled
resentment has become more decisive, and social unrest is on the rise. The “gilets
jaunes” (yellow vests) movement in France is a case in point.
Currently, this is mostly a mature markets’ problem, but it may also provide signals
for the fast changing demography of developing countries. For instance, Chinaʼs is
grappling with unintended effects of its population policies. Small family units after
decades of one-child policies will struggle to finance the retirement years of the
countryʼs already rapidly aging population. Restrictions on mobility are further
exacerbating inequality.
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Political environment
Globalisation momentum has slowed over the past decade. Relative to world GDP,
cross-border investment, trade, bank loans and supply chains have all been
shrinking or stagnating. This started well before US Donald Trumpʼs Presidency.
His anti-globalisation campaign, which has been a political success for his
administration, has since been copied around the world. Multilateralism is on the
back foot and global governance of commerce embodied by the World Trade
Organization (WTO) is at risk of collapse (see page 12 “Globalisation fragmented”
and page 23 “Beggar thy neighbor”).
Rules on privacy, data and espionage are splintering. Even accounting and
anti-trust regulations are fragmenting. Tax systems are being bent to patriotic
ends, including a strong trend of taxing corporates locally based on local revenues.
In this regard, the US is pressuring firms to repatriate capital, while Europe is
targeting Silicon Valley. Moreover, the US makes frequent use of the power it
derives from running the worldʼs dollar-payments system to curb the activities
of foreign companies. The old powers cling to what they still command, while
broader economic, political and cultural power continues to shift to Asia.
While the low yield environment persists, room for manoeuvre by central banks
has become increasingly limited. Long-term accommodative monetary policy
combined with weaker global coordination has led to growing inflation risk. Central
banks may lack the tools and independence to address inflation, resulting in a new
super-cycle dominated by fiscal policy (see page 22 “Limits to tinkering”).
Aging populations in richer countries put public finances, including pension and
health systems, under strain. As a consequence, public services and assets are
being outsourced to the private sector. One example is Haven, a joint venture by
Amazon, Berkshire and JP Morgan to improve access to primary care in the US,
simplify insurance and make transcription drugs more affordable for employees.
1
¹
Amazon, Berkshire, JPMorgan healthcare company to be called Haven,
Reuters, 6 March 2019,
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Macro trends
environments
Technological and natural
environment
The world is undergoing a shift in terms of who owns data, especially in regards to
individuals (see page 27 “The surveillance economy”). As social media and other
companies which have “control” over data begin shifting their approach – either
pre-actively or in response to regulatory pressure – data may increasingly come
back into the hands of the individual. Data has been and will continue to be a key
differentiator in business, including for re/insurers (see page 41 “Getting the
balance right”).
Technologies like Big Data and cloud computing can greatly increase the efficiency
of capturing, storing and computing data. The Fourth Industrial Revolution is
progressing full steam ahead including, among others, process automation,
Internet of Things (IoT) devices and digital analytics capable of rapid analysis of
massive amounts of un-/structured data (regarding speed of data transmission
through 5G also see page 29 “Off the leash“). The combination of more data and
better analytics can lead to better insurability of previously difficult-to-price
products, and also to new capabilities in fraud detection. All this, however, raises
privacy issues and trust concerns, and thus regulatory involvement. For insurers,
specifically, these developments also raise the spectre of adverse selection.
The rise of Artificial Intelligence (AI) will have a major impact on knowledge and
human capital-intensive businesses (for the realm of healthcare see page 31
“Wiggle room”), transforming existing employees into an “augmented” workforce.
This could lead to an increase in unemployment, initially among lesser-skilled
professions, and trigger social unrest.
The frequency and severity of risks resulting from cyber-attacks are expected to
grow significantly over the next years. Recent examples have revealed how
unprepared companies and government agencies are for such attacks. The need
for cyber resilience has become a main focus of attention among corporate clients
and insurance companies, triggering insurance demand. Cyber risk presents one
of the largest opportunities for the re/insurance industry, while simultaneously
also posing one of the biggest challenges. Keeping up with the changes in the
cyber and technology space, and developing solutions to cover the resulting and
ever-evolving risks is no mean feat.
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Competitive and business
environment
Primary insurers continue in their struggle to reshape their traditional systems and
processes to serve the consumer base with next-generation insurance solutions
(also see page 40 “Financial services and the digital revolution”). Reinsurers and
intermediaries seek access to distribution channels and risks outside the
traditional value chain. As international re/insurers face more restrictions with
respect to data privacy and operational issues with legacy systems, innovative
business models and digital eco-systems are likely to emerge, starting off in
HGMs. These will significantly impact the global re/insurance value chain.
Digital ecosystems present a great opportunity for insurers to interact with
potential customers. China is one of the fiercest Insurtech marketplaces in the
world, and e-commerce is transforming the way the population interacts with
industry. With the emergence of disruptive technology finding application in
many industries, strategic partnerships seem to be a key component of the
development of innovative insurance solutions. Investments in digital platforms
by tech giants and Insurtech start-ups have been on a continual upward path
since 2014.
With respect to the growing involvement of the emerging economies in global
development, on the re/insurance side, many of the emerging markets remain
dominated by national players. Some of these firms, for example from China and
Korea, are developing global ambitions, and this will impact the dynamics of
international re/insurance business in the years to come.
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Macro trends
overarching topics
Low-carbon economy
The low-carbon economy model is rapidly gaining traction, as societies and
enterprises explore and develop new solutions. The last decade has seen
exponential growth of solar and wind power installations. This was mainly driven by
large falls in production costs, initially due to innovation and then economies of scale.
Similarly, there has been significant progress in battery storage technology, critical
for the anticipated future dominance of the electric mobility. The official policy
stance has become more supportive of the low-carbon ideal. For instance in motor,
advanced countriesʼ regulatory measures on combustion engine are becoming ever
more demanding. And in China, the leadership has decided to clean up its cities. In
2018, the Ministry of Ecology and Environment was established with a mandate to
invigorate enforcement and conduct local inspections. Policy innovation in transport
means that today, China operates 99% of the worldʼs electric buses.
2
The current
policy priority is autonomous electric cars.
From an insurance perspective, the low-carbon economy is characterised by a range
of often competing technologies and business models. The lack of performance
history on these raises many uncertainties. A number of hypes in recent times turned
out to be dead-ends: biofuels for cars and carbon capture for coal-fired power
generation, to name a couple of examples. Thatʼs not say insurers should not remain
alert of new developments. While low-carbon energy generation models contains
inherently less property and casualty risk than high temperature/pressure
generation, they also entail new risk factors and insurability potential, such as
performance risk due to weather dependency. Insurers have already begun to
address exposures like this with innovative parametric-based products.
Less optimistic, technological progress and shifts in regulation and in social norms
are giving rise to the risk of stranded assets. These are unanticipated asset write-
downs, devaluations or conversion to liabilities in high-carbon sectors such as oil and
gas (including tar sands), utilities and basic materials. Nevertheless, despite such
challenges, opportunities abound. The low-carbon economy is growing broadly and
tangibly. Re/insurance can facilitate the introduction of low-carbon technologies by
assessing and underwriting new risks as they emerge and by partnering with
innovators across different industries, design new risk transfer solutions for the
exposures of the future.
Globalisation, fragmented
After eight decades of expansion, trade globalisation is facing a major test.
After World War II, the Western powers established an open and stable system
of multinational trade – centred on the General Agreement on Tariffs and Trade
(GATT), and the Soviets created an alternative trade network. After the end of the
Cold War, the Western system prevailed, leading to a “golden age” of globalisation
(1990–2007) powered by trade expansion, the rise of emerging markets and
differentiation of value chains according to comparative advantage. This was
facilitated by a period of (relative) US-led international political stability and
embedded in global formats such as the G7, G20, and WTO.
The global financial crisis of 2008–09 brought globalisation momentum to a halt. In
the decade before the financial crisis, world goods and services trade volumes
doubled. In the decade after, volumes have grown by less than half the pre-crisis
rate.
3
Cross-border investment, trade, bank loans and supply chains have all been
shrinking or stagnating relative to world GDP. The Trump administration
enthusiastically engages in trade wars. Geopolitical rivalry is gripping the tech
²
³
Electric Buses in Cities,
Bloomberg New Energy Finance, March 2018
The International Monetary Fundʼs (IMF)
World Economic Outlook Database
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industry, which accounts for about 20% of world stock markets. Rules on privacy,
data and espionage are splintering. Tax systems are being bent to patriotic ends. The
US and EU have new regimes for vetting foreign investment, while China has only
started to live up to its commitment to giving foreign firms a level-playing field.
All the while, the globalisation of world commerce continues, but patterns and
governance have changed markedly.
4
Global institutions have lost influence relative
to assertive nation states, which in turn are catering to the louder and more
idiosyncratic demands of their citizens. For multinationals, re/insurers included,
this represents a more demanding landscape with less predictable stakeholders.
Demography and health
The worldʼs population is growing. Average life expectancy at birth is expected to
rise from 71 years in 2010–2015 to 77 years in 2045–2050.
5
Demographic cohorts
differ in age structures, wealth and health. While longer lives are a positive social
outcome, they also pose a number of challenges.
First, the aging of societies, which we see in mature markets but also in emerging
economies. China, which is now the worldʼs second largest economy, is aging
rapidly due to the one-child policy in place from 1979 to 2015. The average age of
the Chinese population is increasing much faster than in other markets, the effects
being not only a shrinking productive workforce, but also significant shifts in the old
age dependency ratio. A resource gap widens quickly for the growing prevalence of
age-correlated health issues, chronic diseases, dementia and other problems that
require medical attention, caretakers and financial means. The accumulation of
resource strain on health systems are common to many economies, but are dealt
with quite differently. Immigration can be an important mitigating factor for
healthcare labour shortages, but only in societies that are open to foreigners.
Another way to tackle increasing health costs is through technological innovation –
from care robots to wearables monitoring health conditions. Face-to-face
patient/physician interaction is being increasingly supported (or replaced) by
telecommunications and digital means. Consequently, L&H insurance products
are increasingly digitalised, from consulting through to claims handling. The number
of digitally sold policies is growing exponentially, and the trend to more digital
interaction reflects both customer demand and efficiency gains. Advances in
diagnosis and testing hold equal promise and risks, including over-diagnosis and
subsequent unwarranted treatments, as well as adverse selection risk from genetic
tests cheaply available to consumers.
While medical innovation and the increasing awareness around lifestyle impacts
has increased longevity and life quality for many, we see significant counter trends.
In many emerging markets, with modernisation and changes in diets and physical
activity levels, there is increased obesity and diabetes. But even mature markets
show unexpected declines in mortality improvement. The longer trends and
underlying reasons warrant deeper analysis.
6
In the US opioid crisis, excessive
subscriptions for addictive painkillers has fuelled a fire of pre-existing social,
demographic and health problems that a struggling health system has failed to
cope with. Interconnections between demographics and health will remain an
important field to follow.
⁴
⁵
⁶
See risk theme “Beggar thy neighbour? - Global trade reordered”
World Population Prospects: The 2017 Revision, Key Findings and Advance Tables,
United Nations Department of Economic and Social Affairs, June 2017
sigma 6/2018 – Mortality improvement: understanding the past and framing the future,
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15 Emerging risk
themes and
5 Trend spotlights
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Societal environment
Vaccination – a shot worth more than politics and profitability
One of the blessings of modern medicine is vaccination. Immunisation is a
cost-effective way to keep many transmissible viral and bacterial diseases in
check and, according to estimates of the World Health Organization (WHO),
prevents 2–3 million deaths every year. But this achievement is under threat,
due to questions around the economic viability of vaccine production and
distribution and also what we see as weaponisation of vaccination in areas
of conflict and with growing impacts of anti-vaccination campaigns. Vaccine
shortages and refusal increase the likelihood of infection spread, which can
potentially balloon to pandemic proportions, most notably for highly
infectious diseases where herd immunity counts. The implications of a
pandemic are most severe for life and health insurers. There are indirect
implications for broader financial markets also.
Casualty
Impact:
medium
Most affected
L&H, FM
business areas
Time frame (years):
0–3
Property
Operations
Financial Markets
L&H
For profitability reasons, the large pharmaceutical companies in the West
are content to leave vaccine production to companies in new markets such
as China. Globally, more vaccines are needed to fight diseases like hepatitis
B or influenza and the supply chain has become increasingly based in
the East. This results in new dependencies and the possibility of vaccine
shortages in some locations, especially during periods of heightened
political tension and national economic rivalry. Another danger we see is a
lag in the development of new vaccines where the profit potential does not
make for an attractive business case for pharmaceutical companies.
The WHO lists “vaccine hesitancy” among the “Ten threats to global health
in 2019.”
7
This “reluctance or refusal to vaccinate despite the availability
of vaccines” is attributable, among others, to complacency, inconvenience
in accessing vaccines and lack of confidence, the report says. Whatever
the reasons, such attitudes risk the resurgence of otherwise avoidable
dangerous diseases. A very recent case in point, in the US, there were 465
confirmed cases of measles across 19 states in the first quarter of 2019,
the second largest outbreak since 2000 when measles were said to have
been eliminated.
8
The anti-vaccination movement derives legitimacy from cultural and/or
philosophical rejection of vaccines as a force for good. However, in our view
the politicisation of the anti-vaccination movement as a means of expressing
dissent against domestic authorities and international organisations only
heightens the risk of pandemics.
Potential impacts:
Vaccines shortages and refusals increases the likelihood that infections
will spread, increasing morbidity and mortality.
Life insurers are exposed to higher claims in the case of a severe
pandemic.
A large pandemic can have significant impact on the health system
and also mortality, with potential for large scale reduction of regional
populations.
A drop in productivity, due to many factors (eg, closed schools). Trade,
travel and tourism will be subdued and economic output will be reduced.
9
This affects financial markets and is therefore directly relevant for
re/insurersʼ balance sheets on both the asset and liability side.
⁷
⁸
⁹
Ten threats to global health in 2019,
World Health Organisation, 2019
Measles Cases and Outbreaks,
Center for Disease Control and Prevention
Epidemics and Economics,
Finance and Development, Vol 55, No. 2, IMF, June 2018
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Societal environment
Retirement skills gap – accidents waiting to happen
Almost one in five workers in the oil and gas industry is a baby boomer. This
generation will retire in the next few years, which may lead to an expected
shortage of 10 000 petro-technical professionals globally by 2025.
10
Combined with current layoffs and fewer students enrolling in university
courses as petro-technical professionals, this situation is threatening the safe
operation of hazardous oil and gas installations. Such circumstances are
troubling especially given that ageing facilities often run at peak capacity.
The same is true of healthcare. By 2030, thereʼs likely to be a shortage of
15 million healthcare professionals globally.
11
This is worrying since the
demand for healthcare services in developed markets will rise as the baby
boomers retire. These two sector-specific scenarios can be extrapolated to
developed economies as a whole. In all sectors, from manufacturing to
engineering to financial services, many people will be retiring in the coming
years, taking with them critical know-how and experience that technology
can only in part replace.
Research shows that professional experience is a very important element for
safety, and that an increase in workplace-related accidents in manufacturing
industries can come as a result of outsourcing.
12
The safety of individuals at
the workplace and general operational safety are closely related, and
workplace safety records will be a sentinel for things to come.
What does this mean for insurance? An uptick in P&C, professional
indemnity, medical malpractice as well as healthcare-related claims might
be among the consequences.
Potential impacts:
A growing skills gap might cause more frequent occurrence of major
accidents in hazardous industries and incidents in production and
construction industry.
Service industries could be exposed to more professional indemnity
claims.
A shortage of healthcare professionals might increases the risk of the
healthcare industry to medical malpractice claims.
A skills shortage in the healthcare sector will likely lead to increase costs
in the provision of healthcare services, something that advances in
technology will only in part offset.
Impact:
medium
Most affected
P&C
business areas
Time frame (years):
>3
Property
Operations
Casualty
Financial Markets
L&H
¹⁰
¹¹
¹²
Retirement Wave and Digital Reinvention Prompt Urgent Talent Reassessment,
www.rigzone.com, 29 December 2017, and
The Talent Well Has Run Dry,
Accenture, 2017
Global Health Workforce Labor Market Projections for 2030,
World Bank Group,
August 2016
Sanna Nenonen,
Fatal workplace accidents in outsourced operations in the manufacturing
industry,
Safety Science, Vol.49, Issue 10, December 2011
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Societal environment
Concussion injuries in sport – head on to more widespread
claims
Impact:
low
Most affected
Casualty
business areas
Time frame (years):
>3
Each year more than 42 million individuals are diagnosed with concussion,
often resulting from sports or recreational activity.
13
Millions more suffer
sub-concussive blows, where the intensity of impact is not sufficient to result
in a clinical diagnosis of concussion. Repetitive head trauma has been linked
to many conditions that have latency periods of years or even decades, such
as Parkinsonʼs disease, Amyotrophic Lateral Sclerosis (ALS), dementia and
Chronic Traumatic Encephalopathy (CTE), a progressive neurodegenerative
disease which currently can only be diagnosed post death. Researchers are
getting closer to being able to identify CTE in the living and this is expected
to significantly increase the number of diagnoses.
14
There is also increasing
evidence that even a single concussion experience may result in an
increased risk of Parkinsonʼs disease and dementia, or have lasting impact
on cognitive function.
15
Head trauma is not only a concern for professional athletes. CTE has been
discovered in individuals who only played youth or college sports, including
athletes and (American) football, soccer, rugby, basketball and baseball
players.
The discovery of the long-term risks of head trauma has sparked high-profile
litigations in the US, filed by athletes against professional sports
organisations such as the National Football League (NFL). That lawsuit was
settled for an uncapped amount, estimated to be well over USD 1 billion.
Hundreds of other suits remain pending, against collegiate sports governing
bodies, helmet manufacturers, youth sports organisations, and dozens of
individual colleges and universities.
The number of people potentially affected, the increased attention on head
trauma, and the size of the NFL settlement are just a few of the factors that
make this a true emerging risk.
Potential impacts:
Broader awareness of the issue will increase concussion diagnoses, as
more people seek medical attention. This will trigger liability insurance,
but also impact on life and health books.
Additional litigations are to be expected due to the size of the NFL
settlement and rising awareness of long-term risks increases.
Enactment of youth concussion laws and revised rules/guidelines by
sports organisations may increase requirements on standards of care
and potential liabilities.
Property
Operations
Casualty
Financial Markets
L&H
¹³
¹⁴
¹⁵
Kathryn L. Van Pelt et al.,
A cohort study to identify and evaluate concussion risk factors
across multiple injury settings: findings from the CARE Consortium,
Injury Epidemiology,
Vol. 6, No.1, 2019
Nadia Kuonang,
A study of NFL playersʼ brains might help diagnose CTE in the living,
CNN,
10 April 2019, and
Study suggests path to detecting CTE in the living,
Associated Press,
11 April 2019
Barlow et al.,
Investigation of the changes in oscillatory power during task switching after
mild traumatic brain injury,
European Journal of Neuroscience, Vol. 48, No. 12, 2018;
and Nina Bai,
With Dangers of Everyday Concussions Revealed, Scientists Race to Find
Solutions,
UCSF Research, October 17, 2018
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Societal environment
A celebrity body – the hazards of aesthetic surgery tourism
More people are travelling abroad for medical procedures such as plastic
surgery and dentistry. The reasons include lower costs, no coverage for
the treatment under home country healthcare plans, lack of access to
required treatment in the home country, better quality of treatment and
reduced waiting time. Travelling abroad for plastic surgery beauty
enhancement treatments not covered by healthcare insurance policies
is especially popular.
Experts have put the dramatic growth of plastic surgery down to a rise in
the number of celebrities promoting cosmetic procedures, cultivating a
consumer-base conditioned to desire new norms in body shapes and looks.
Researchers at the Boston Medical Center have found the kinds of facial
surgery people are requesting now include nasal and facial symmetry,
rhinoplasties, hair transplants and eyelid surgical procedures.
16
Cosmetic surgery poses pressing problems. A report by the Nuffield Council
on Bioethics outline the risks of this lucrative market in the UK.
17
The
absence of a coherent regulatory framework means that often non-specialist
or underqualified physicians perform aesthetic procedures without adequate
infrastructure, sometimes with devastating consequences. When
undertaking treatment abroad, the patient and physician may not speak the
same language fluently. this increases the risk of misunderstandings, wrong
treatments and undesired effects.
Itʼs not always clear if health insurance in the home country covers the
additional costs originating from planned procedures abroad. This relates
to rules on medical malpractice and its insurance, for example, regarding
whether insurers have to cover costs from unplanned procedures
abroad and if these costs can be recovered. Moreover, given difference in
regulatory practices by jurisdiction, it can be difficult to assign the weight
of responsibility. Given the high growth of cosmetic plastic surgery both
at home and abroad, itʼs likely that in the future answers to these questions
will more often come out of the courtroom.
Potential impacts:
An unclear situation about medical malpractice claims in this area could
trigger defense costs and later even the claims themselves.
Manufacturers of the products and equipment used in cosmetic
procedures are competing in a lucrative market, with different approval
and oversight processes in different jurisdictions. Product liability claims
for related implants could become an issue.
Medical standards – also for procedures and related care services – may
be of poor quality in some countries. If medical travelers do not research
their chosen medical centre, they may find themselves with unwanted
and potentially dangerous results.
Antibiotic resistance is a global problem. Resistant bacteria may be picked
up in countries with a high prevalence of superbugs in hospitals.
For operations abroad, flying after surgery can increase the risk of blood
clotting.
Impact:
low
Most affected
Casualty
business areas
Time frame (years):
>3
Property
Operations
Casualty
Financial Markets
L&H
¹⁶
¹⁷
Susruthi Rajanala, Mayra B.C. Maymone, Neelam A. Vashi,
Selfies — Living in the Era of
Filtered Photographs,
JAMA Facial Plastic Surgery, Vol. 20, No. 6, 2018
Cosmetic procedures: ethical issues,
Nuffield Council on Bioethics, 2017
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More people travel abroad
for plastic surgery. This raises
pressing questions – also for
the insurance industry.
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Political environment
Limits to tinkering – the fiscal and monetary policy balance
at risk
Impact:
high
Most affected
FM
business areas
Time frame (years):
>3
Since the global financial crisis, the worldʼs major central banks have
engaged in extraordinary policy measures resulting in massive expansion of
their balance sheets. With central banks running out of tools to stimulate the
economy, the growing consensus is that another economic downturn will
need a fiscal response. The key question is what form of fiscal activism we
might see. One idea – similar to the case of Japan – is to combine increased
fiscal spending with more ultra-accommodative monetary policy, such as
quantitative easing (QE) or yield curve control.
There are still more radical proposals. One example is outright “helicopter
money”, where central banks use their balance sheets to absorb the increase
in government borrowing. This would be different from QE in that central
banks would pledge to keep government bonds on their balance sheets
indefinitely. Another idea that has gained traction recently is Modern
Monetary Theory (MMT), which some argue is neither modern, monetary
nor a theory. Under MMT, fiscal rather than monetary policy acts as the main
stabilisation tool for the economy, while low interest rates are used to keep
public finances sustainable.
While officially central banks retain their independence, the closer
coordination with government raises questions about how true that is.
We think outright regime shift towards alternative monetary/fiscal
frameworks such as MMT is unlikely in the near-term. That said, we do
expect fiscal policy to play a significantly bigger role, this at a time when
global leverage is already close to historic highs, both to stimulate economic
growth and to reduce income and wealth inequality. The degree and
design of fiscal dominance will be important to monitor as it could have
significant consequences for the economy and financial markets, including
the insurance sector.
In a fairly benign scenario of closer policy coordination amid low inflation,
a prolonged period of low interest rates would be the most likely outcome.
By contrast, an outright regime change in the fiscal and monetary policy
framework, such as MMT, could notably increase uncertainty around the
inflation outlook and financial market stability. In the long-run, this could
result in much higher inflation and interest rates, with broad repercussions
on financial markets.
Potential impacts:
The economy and financial markets, including the re/insurance industry,
could benefit if changes to fiscal and monetary policy stimulate growth
and financial stability.
On the flipside, a policy shift could lead to a notable rise in uncertainty,
causing higher financial market volatility and significant declines in asset
valuations.
If central banks (are forced to) keep interest rates low to accommodate
increased fiscal spending, the insurance industry would suffer, in
particular life insurers.
Meanwhile, an unexpected and sustained increase in inflation – also a
potential consequence of a regime change – would be harmful for the
re/insurance industry, in particular for inflation-sensitive liability lines of
business. At the same time, however, life insurers would benefit from a
potential increase in interest rates as their liabilities typically have a longer
duration than their assets
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Political environment
Beggar thy neighbour? Global trade reordered
As with other multinational businesses, insurers have become used to basic
global rules that made global commerce more predictable. But the rules-
based trading system is now in crisis. The very existence of the World Trade
Organization (WTO) – which governs a thriving global commerce – is being
questioned, most notably by its architects. For international businesses, this
fundamental challenge is aggravated by regulatory fragmentation and shifts
to revenue-based local taxation.
The significance for re/insurers is that regulatory restrictions and capital
requirements may threaten business models based on global risk
diversification and efficient capital management
18
. The US – architect of the
current global trade order – no longer regards trade as the “tide that lifts all
boats”, but rather as a zero-sum game. The Trump administration questions
the WTOʼs dispute settlement system and favours new trade agreements,
based on bilateral relationships. There is now real danger of open trade
conflict between the worldʼs major trading blocs: the US, the European
Union and China. The named three are all shaping their own trade networks.
Further US disengagement from global geopolitical affairs and multilateral
institutions for example, as well as the pursuit of trade policy through
aggressive use of tariffs, withdrawal from existing agreements, and bilateral
renegotiations, will significantly reduce the odds of bilateral deals.
19
The Chinese approach differs, evolving around sweeping investments of
billions of dollars into infrastructure projects in 60 countries under the
umbrella of the Belt and Road Initiative. The goal is to create a network of
trade routes connecting east and west. It has attracted many cheerleaders
but also drawn harsh criticism. The European Commission now considers
China both a strategic partner and an economic competitor. It in turn is
showing a tendency to join the state mercantilist bandwagon by backing
national champions, restricting foreign direct investment in sensitive sectors,
and seeking trade deals in its favour.
As a result, multilateral trade liberalisation – a significant driver of
globalisation and prosperity during the past two decades – has come to a
halt. Trade architecture is no longer dominated by a Western alliance, but
by competing architects building their own systems and channels. These
competing trading blocs negotiate and revise agreements, putting greater
emphasis on immediate domestic priorities as well as special interests.
Multinational re/insurers will discover new opportunities but must also
navigate previously unseen risks.
Potential impacts:
Multinationals, including re/insurers and banks, risk getting caught
between competing spheres of power.
Regulatory restrictions and capital requirements may reduce market
access and threaten business models based on global risk diversification
and efficient capital management.
Local political events may have outsized consequences, including on
financial markets, if amplified by geopolitical dynamics (eg, elections in
the Maldives becoming a proxy contest between India and China )
Higher infrastructure project risk resulting from lower standards and less
scrutiny due to the absence of respected multilateral agencies
(Over)-sized projects – partly driven by short-term political interests –
increase the risks of unprofitable underwriting of white elephants, for
instance railroads without passengers.
Legal risk of any litigation in unchartered jurisdictions
¹⁸
¹⁹
OECD,
The Contribution of Reinsurance Markets to Managing Catastrophe Risk,
Dec. 2018.
B. Eichengreen, A Mehl and L Chiţu,
Mars or Mercury Redux: The Geopolitics of Bilateral
Trade Agreements,
ECB Working Paper No. 2246, February 2019
Impact:
medium
Most affected
FM
business areas
Time frame (years):
0–3
Property
Operations
Casualty
Financial Markets
L&H
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Political environment
Conflicting interests – the widening urban-rural divide
The world is urbanising rapidly. More than 50% of world population already
resides in cities. While Europe has 35 cities of a million people or more,
China will have an estimated 225 by 2025.
20
Cities host many of the worldʼs
top research institutions, and the presence of major international business
makes them ideal locations to bring together university, government, and
private R&D efforts. Capital, knowledge and creativity feed from one other
and turn cities into engines of growth, wealth and opportunity.
The flipside is the relative status loss of semi-urban and rural regions.
The widening gulf between empowered urban centres and disenfranchised
rural peripheries translates into contrasting economic and social realities.
In Latvia, for example, about half the countryʼs population lives in the
metropolitan area of its capital, Riga, which generates about 70% of the
countryʼs economic output. While Rigaʼs standard of living reaches the EU
average, in the poorest rural regions, the standard of living is just a third
of that average.
21
Such socio-economic contrast polarises cultural values and political
interests. It nurtures resentment and it divides public discourse. The growing
political opposition between urban centres and rural periphery is not
confined to Latvia. It reflects a broader global development: people who are
outward-looking, embrace globalisation and share “progressive” cultural
norms tend to live in cities; those rooted in local communities and uphold
traditional values tend to live in the rural periphery.
The electoral landscape offers some evidence that a growing cultural divide
and segregation between “city” and “countryside” can translate into different
political preferences and create unexpected outcomes. Examples include
the US presidential election of 2016 and the UKʼs referendum to leave the
EU. In both cases, the peripheral and rural areas outvoted the large cities and
metropolitan areas. With persistent division and growing alienation between
the poles, more “surprises” may well be forthcoming. For example in the EU,
there is evidence that population density is a powerful driver of anti-system
voting: regions and localities with lower density are more prone to support
anti-European integration parties.
22
Potential impacts:
The rapid growth of cities increases economic value concentration.
This offers opportunities for the insurance sector, but also accentuates
risk accumulation.
Rural-urban antagonisms could increase market uncertainties, curb
investments and endanger functioning supply chains. The cumulative
negative impact on financial markets would present challenges for
insurers.
A growing gap between urban centres and the rural periphery could
endanger the internal cohesion of territorial states, fan separatist
tendencies and make finding policy solutions acceptable to all national
socio-economic groups more challenging.
Economic development could slow if electoral choices and social protests
from rural communities prevent policies that enable cities to thrive.
The (perceived) alienation of geographies and specific regions or localities
could create resentments that bring more extremist parties into power,
making political and regulatory framework conditions more volatile and
detrimental for insurance business.
²⁰
²¹
²²
The Great Migration: Urban Aspirations,
Policy Research Working Paper 6879, The World
Bank, 2014.
Rudolf Hermann, “Riga und der Rest des Landes”,
Neue Zürcher Zeitung,
29 January 2019.
Lewis Dijkstra, Hugo Poelman, and Andrés Rodriguez-Pose,
The Geography of EU
Discontent,
European Commission Working Papers, Directorate-General for Regional and
Urban Policy, 2018
Impact:
low
Most affected
Operations
business areas
Time frame (years):
0–3
Property
Operations
Casualty
Financial Markets
L&H
24
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Political environment
Emerging trend
spotlight
Shifting litigation
regimes
Litigation funding and class actions, especially prevalent in the US, are
becoming increasingly popular in other parts of the world.
Litigation funding is the upfront payment by a third party of fees associated
with a litigation case – such as the plaintiffʼs own legal costs, or the Adverse
Cost Order in case the plaintiff loses – in return for a slice of the compensation
received as a result of the lawsuit filed. The ongoing low interest environment
makes litigation funding more lucrative to investors and thus drives propensity
to sue. In turn, this may lead to more successful – and expensive – insurance
claims and ballooning defence costs for the insurer. Well-known in the US,
recently the practice has become more prevalent in the APAC region, South
Africa and the UK. A landmark decision by the UK court of appeal concerning
Mastercard and its fees, greatly lowered the threshold for class actions to
proceed. The court also explicitly welcomes third-party funding for litigation.
While a further appeal is likely, it is an on-going case example that illustrates
that companies in the UK will be needing to spend significant amounts of
money to defend against an uptick of class actions. Some of the largest
funders, in some cases publicly-traded companies, have significant activities
outside the US.
For the insurance industry, the mechanism is a double-edged sword. On one
hand, it boosts opportunities to provide products and services to clients facing
growing need for liability and legal expenses covers. Stronger consumer
protection laws also drive pressure on producers to manage their liability risks
by way of product safety and adequate insurance cover. On the other hand,
the increased use of third-party funding can result in claims proliferation,
longer litigation, more exposure for insurers defending such claims and higher
settlement costs. Another worrying trend is the potential of governments to
sell its law enforcement authorities to private firms in exchange for a payout.
An example is the recent recruitment of external legal counsels by the Office
of Attorney General, D.C for climate change litigation. These external counsels
will be paid through the contingency fee arrangements in the event of
damages awarded by the court.
The other development – class actions – is focused in Europe. Influenced by
scandals such as “Dieselgate”, the European Commission has proposed a
“New Deal for Consumers.”
23
This would entail the introduction of a directive
on representative actions for the protection of the collective interests of
consumers. The core of the proposal is that a qualified entity would be able
to bring a representative action before a Member State court or other
administrative authority on behalf of classes of consumers. Where Member
States do not already allow class actions, they would be required to introduce
them. Nevertheless, while the above proposed directive provides progress,
a deluge of litigation may not yet be in the inevitable trend due to adverse
costs risks, as funders and insurers need to carry out significant due diligence
on the cases they may invest in.
The European Commission considers only litigation-based class or
representative actions, but these are not the only mechanisms for collective
redress nor the most efficient. Conceivable alternatives include “regulatory
redress” with regulatory authority intervention, which would be an agreement
or order for redress to be paid. If coupled with an ombudsman scheme, such
an alternative dispute resolution (ADR) could present a promising path.
24
The Commissionʼs “New deal” proposal is subject to political negotiations
between the European Parliament and the Council. The outcome will have
important consequences for the insurance industry.
²³
²⁴
Review of EU consumer law – New Deal for Consumers,
European Commission, 2017
Christopher Hodges,
Collective Redress: The Need for New Technologies,
Journal of
Consumer Policy, 2018
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Technological and natural environment
Teaching an old dog new tricks – digital tech meets legacy
hardware
Impact:
high
Most affected
P&C
business areas
Time frame (years):
0–3
Digital solutions and old hardware donʼt always harmonise. A prime and
real example happened on 13 July 2017 when thousands of commuters
were stranded during peak rush hour as the metro network in Melbourne
went into meltdown.
25
The reason was that a 40-year-old interface
board being used to connect to the new digitised software was not able
to handle the input to the systemʼs tracks and signals, which themselves
were also outdated.
This example illustrates the existing challenge. Standard procedure is
to seek to improve the operational efficiency of old assets with software
enhancements. Technological improvements on software are made on an
ongoing basis to keep pace with increasing capacity and complexity of
demands. Much hardware, though, is still of yesteryear.
We see an increasing dovetailing of old and new structures, often in areas
of critical infrastructure, including smart electric power grids or pipelines,
hospitals or cash points. New technology as part of industry 4.0 – a term
used to describe technologies like artificial intelligence, quantum computing,
3D printing and IoT in eg production processes – applied to legacy solutions
changes the existing risk landscape. While it reduces some old exposures,
it also gives rise to new risks. To this end, insurers need to continuously
re-evaluate their risks assessments and adapt their underwriting approach to
technological innovation as applied in complex, multi-stage, multi-party and
sometimes multinational nature construction projects, as well as in legacy
infrastructure.
26
Potential impacts:
Large infrastructure breakdowns or accidents triggered by new software
not working with old hardware can lead to property damage, bodily injury
and business interruption claims. There are also new forms of cyber risks
to date not priced for.
Large failures of key infrastructure like power or communications can also
impact operations of the insurance industry.
As technology increases connectivity, insurers face higher risk
accumulation and unexpected losses potential from the combination of
new software with old hardware.
While technological innovation can lead to reduced claims frequency in
certain areas (eg, advanced driver-assistance systems for vehicles), it may
also increase claims severity by introducing new exposures to an existing
risk landscape.
Property
Operations
Casualty
Financial Markets
L&H
²⁵
²⁶
Andie Noonan,
Melbourne suffers peak-hour train delays after computer fault
sigma 2/2018 – Constructing the future: recent developments in engineering insurance,
Swiss Re Institute
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Technological and natural environment
Emerging trend
spotlight
The surveillance
economy
Many of this publicationʼs readers probably have a social media account.
Whether used for professional purposes, to stay in touch with old friends,
or exchange views and perspectives, participants benefit from a network
of connections which they otherwise would not have access to. And all this
for free.
But … just as thereʼs no such thing as a free lunch, thereʼs no such thing as a
free internet platform. So how do we pay for these services? Weʼre told that
theyʼre funded by the ads that show next to the content weʼre consuming.
Weʼre not that interested in why and how the advertiser chooses to show us
that particular commercial at that particular time of day or period in our lives.
All the while, however, our online activity – our data – is being used to analyse
patterns and predict behaviours, for sale on to the highest bidder. Monetising
data is key for corporate profit. According to a recent study, a company is
2.6 times more likely to grow at more than 10% if it monetises data.
27
The most mundane activities may lead to surprising conclusions. For example,
the type of music we listen to online can be analysed for signs of depression,
and this information can be then sold for advertising purposes to a medical
company. Data on sleep patterns and activity from wearables can be used to
confirm the signs of depression gathered from the kind of music we listen to.
All this happens without our conscious knowledge and without recourse
because our cars, phones, and homes have an increasing number of sensors
that link our online and offline lives. Once this knowledge about us has been
created, thereʼs no easy way to change it.
For corporates as well as for consumers, todayʼs surveillance economy can
generate advantages. Individualsʼ willingness to “pay” with their data instead
of money may translate into competitive advantage and cheaper services.
It also helps link consumers with products and services best suited to their
needs. On the darker side, however, the surveillance economy can be
construed as intrusive and even Orwellian. The constant collection of our data
means we are constantly being observed, analysed, compared and rated.
And, by knowing what motivates us and understanding our belief systems,
corporates can manipulate us, distort the market economy with their
asymmetrical knowledge and even the democratic processes by manipulating
information flows.
So what are the implications for insurance? According to a recent study on
auto insurance, drivers participating in pay-as-you-drive programmes where
their driving is monitored and their insurance premiums adjusted based on the
data from the car, become 30% safer as a result.
28
This means that monitoring
results in safer behaviour, improving the quality of life for the driver and
lowering the claims for the insurance company. On the other hand, should
an insurance company also receive data from music streaming services
about our potential depression, it still may draw inadequate conclusions from
correlations, end up reserving excessive amounts for our future medical
treatment or face reputational risk and regulatory scrutiny.
²⁷
²⁸
The Dark Side of Data Commercialization,
Forrester Research, 19 April 2018
Yizhou Jin, Shoshana Vasserman,
Buying Data from Consumers – The impact of monitoring
programs in US auto insurance,
Harvard Business School, 21 January 2019
Swiss Re
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5G mobile networks will
enable wireless connectivity
in real time – a prerequisite for
broad use of autonomous cars.
28
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Technological and natural environment
Off the leash – 5G mobile networks
5G – short for fifth generation – is the latest standard for cellular mobile
communications. Providing ultrafast broadband connection with higher
capacity and lower latency, 5G is not only heaven for your smartphone.
It will enable wireless connectivity in real time for any device of the Internet
of things (IoT), whether that be autonomous cars or sensor-steered factory.
In doing so, it will allow decentralised seamless interconnectivity
between devices.
To allow for a functional network coverage and increased capacity overall,
more antennas will be needed, including acceptance of higher levels of
electromagnetic radiation. In some jurisdictions, the rise of threshold values
will require legal adaptation. Existing concerns regarding potential negative
health effects from electromagnetic fields (EMF) are only likely to increase.
An uptick in liability claims could be a potential long-term consequence.
Other concerns are focused on cyber exposures, which increase with the
wider scope of 5G wireless attack surfaces. Traditionally IoT devices have
poor security features. Moreover, hackers can also exploit 5G speed and
volume, meaning that more data can be stolen much quicker. A large-scale
breakthrough of autonomous cars and other IoT applications will mean
that security features need to be enhanced at the same pace. Without,
interruption and subversion of the 5G platform could trigger catastrophic,
cumulative damage. With a change to more automation facilitated by
new technology like 5G, we might see a further shift from motor to more
general and product liability insurance.
There are also worries about privacy issues (leading to increased litigation
risks), security breaches and espionage. The focus is not only on hacking
by third parties, but also potential breaches from built-in hard- or software
“backdoors.” In addition, the market for 5G infrastructure is currently
focussed on a couple of firms, and that raises the spectre of concentration
risk.
Potential impacts:
Cyber exposures are significantly increased with 5G, as attacks become
faster and higher in volume. This increases the challenge of defence.
Growing concerns of the health implications of 5G may lead to political
friction and delay of implementation, and to liability claims. The
introductions of 3G and 4G faced similar challenges.
Information security and national sovereignty concerns might delay
implementation of 5G further, increasing uncertainty for planning
authorities, investors, tech companies and insurers.
Heated international dispute over 5G contractors and potential for
espionage or sabotage could affect international cooperation, and impact
financial markets negatively.
As the biological effects of EMF in general and 5G in particular are still
being debated, potential claims for health impairments may come with a
long latency.
Impact:
high
Most affected
P&C
business areas
Time frame (years):
>3
Property
Operations
Casualty
Financial Markets
L&H
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Technological and natural environment
Emerging trend
spotlight
Smart construction
The building industry is under construction. Projects are getting more
complex, costs are rising and pressure to build quickly is increasing. Driving
this trend is growing populations, a global shift towards data-driven solutions,
and the increased costs of natural disasters. The last two years were the
costliest annual back-to-back period ever in terms of insurance industry losses
resulting from natural disasters. The natural catastrophe losses for 2017 and
2018 combined were USD 219 billion.
29
The above factors are driving change in construction, with greater use of new
technologies such as 3D printing, drones, wireless sensors, site automation
and prefabricated components. In essence, smart construction is a drive to
digitisation. From an insurance perspective, while more data can mean more
accurate pricing, there are also challenges regarding data quality and security.
Consequently, with increasing use of computer software and automation,
associated risks may shift from human error to mechanical malfunction. Risks
include cyber vulnerability, data corruption and loss, and inaccurate
predictions due to defective modelling.
In 2016, the Dubai government launched its 3D Printing Strategy, with the
aim of constructing 25% of buildings using 3D printing technology by 2030.
In 2015, a Chinese construction company built the Mini Sky City, a 57-storey
skyscraper in central China in 19 working days. The rapid build time was
achieved by having 90% of the structure prefabricated in a factory. In Japan,
machinery manufacturer Komatsu has been using smart construction
technologies since 2015 in over 3 300 sites across the country. This entails
using specialised drones to conduct survey work in under one hour, a process
that could typically keep many workers busy for several days. An added
benefit of such technology could be an increase in worker safety.
All told, traditionally the construction sector overall has been slow to innovate.
One factor holding back adoption of new technologies is lack of sufficient
data to substantiate the value of offsite manufactured assets across the
construction lifecycle. A number of governments, including in the UK,
Singapore and Finland, have been making steps towards a more data-driven
approach to construction. For instance, they now mandate use of Building
Information Modelling (BIM) for public projects to standardise the sharing and
exchange of information concerning the construction and post-construction
management of a building.
30
But BIM is far from being adopted by all players,
especially smaller construction companies. Driving more universal shift to
this technology remains a challenge.
As with many other trends in the digital age, to stay competitive insurers
must develop new ways to locate, manage and analyse data. At the same
time, of paramount importance is to strengthen industry oversight and not
overestimate the impacts of innovation. In our view, this will be the only
way to protect and advance the principles of sound construction methods.
²⁹
³⁰
sigma
2/2019 op. cit. Read more in
Natural catastrophes and man-made disasters in 2018:
“secondary” perils on the frontline,
Swiss Re Institute, 10 April 2019
sigma
2/2018, op. cit. Read more in
Digitalisation and its impact on the construction and
insurance industries,
Swiss Re Institute, 4 October 2018
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Technological and natural environment
Wiggle room – Artificial Intelligence and healthcare
Medical imaging and related diagnostics are being enhanced by Artificial
Intelligence (AI). The US Food and Drug Administration has already
approved AI software to support the detection of strokes and fractures based
on MRI images.
31
More will follow soon, with many applications beyond
imaging pending approval.
Investments in AI healthcare are surging globally. In places where healthcare
provision is practically non-existent, affordable AI-driven systems can make
treatments more accessible. And in developed countries, a shortage of
healthcare workers and instant accessibility and cost efficiency will help
build the value proposition and acceptance of AI-driven treatments.
A word of caution, however. Errors in healthcare can have big implications,
and longer-term trust in AI-assisted treatments could suffer. Currently, the
outcomes generated by AI lack a certain degree of transparency and, thus,
accountability. While black-box AI may be fine for shopping, thatʼs unlikely to
be the case where AI leads to a wrong decision being made in a healthcare
treatment scenario. Patients and insurers alike will need to understand how
AI is involved in a doctorʼs action, and who can be held liable.
32
Insurers of health-related products should continue to engage with
healthcare providers, regulators and customers to ensure proper review of
risks of AI in healthcare. Other aims of such dialogue should be to reduce
short-term costs and possible liabilities, create standards for explainability
and transparency, and shape public perception of AI as being innately
beneficial to the provision of healthcare services.
Premature adoption before issues around accuracy, explainability and
privacy issues are solved may do more damage than good. A careful,
progressive approach, adopting technology that is commensurate with the
risks and needs, and that complements human capabilities, is in the longer
term interest of patients, healthcare providers and insurers.
Potential impacts:
In many cases, diagnostics can become more accurate, especially
regarding medical imaging. The reverse is true if errors occur leading to
catastrophic personal outcomes. In most situations, human interpretation
of AI-assisted insights will be a key feature.
Data used for machine learning may enhance rather than reduce bias, so
explainability for ethical and regulatory purposes will be essential, as will
be scrutiny of the algorithms used and the decisions taken.
On the upside. AI in healthcare may enable around-the-clock availability
and low cost, thus increasing accessibility to more people.
Used in conjunction with devices, AI could monitor health 24/7, allowing
more rapid identification of problems and better outcomes.
AI applied to big and combined databases could enhance understanding
of health issues, and enhance diagnostics and treatment strategies.
However, issues around privacy, compatibility and security need to be
overcome first.
Impact:
low
Most affected
Casualty, L&H
business areas
Time frame (years):
0–3
Property
Operations
Casualty
Financial Markets
L&H
³¹
³²
FDA permits marketing of artificial intelligence algorithm for aiding providers in detecting
wrist fractures,
US Food & Drug Administration, 24 May 2018, and
FDA permits marketing
of clinical decision support software for alerting providers of a potential stroke
in patients,
US Food & Drug Administration, 13 February 2018
“Blame your robot – emerging artificial intelligence legislation”,
SONAR,
Swiss Re, 2017
Swiss Re
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Technological and natural environment
Emerging trend
spotlight
The warehouse
of the future
The warehouse is the backstage room in retail or department stores, where
customers are handed the product they came to the store to buy. If it canʼt be
found in the display, it may still sit in the warehouse. These repositories are the
logistical link between increasingly globalised supply chains and consumers
on the ground. Warehouses have been around for centuries, and now they are
undergoing a revolution.
Being relatively closed and controllable systems, warehouses are hotbeds for
automisation and robotics. In the warehouse of the future, robotic shelves will
move around at high speed. They will feed batches that leave the warehouse,
or feed from batches that restock it. Collaboration between humans and robots
will continue to be important in the fully automated warehouse. But where
humans are involved, theyʼll only interact from safe islands.
This system is already reality in retail, particularly in pharmacies. A pharmacist
feeds the name of a certain drug into the registry system, which is then
automatically retrieved from the repository without human involvement. The
system also automatically re-orders products, and controls the warehouse
according to demand and expiration dates. Informed by former sales,
predictive analytics enables optimisation.
On-the-spot 3D printing will gain prominence for certain trades to
accommodate demand for customisation and spare parts. Warehouse are set
to become much more dynamic, with extended functionalities. Online trade
has made front stores redundant: itʼs no wonder that companies like Amazon
are at the forefront of warehouse innovation.
With respect to insurance, we see new risks and opportunities emerging
from the more complex, automated and interdependent systems. First, the
new warehouses represent a new fire hazard, with high-value concentration
risk. If fire protection systems do not work, both the value of the content
and the whole supply chain are at risk. With fewer humans and more
technology, product liability and professional indemnity losses (for warehouse
consultants and engineers), as well as property business interruption losses
from flawed hardware and software will gain prominence, while single-loss
events from human failure will become more rare. That said, the increasing
interconnectivity could also mean a trend towards higher impact loss events,
with just one (human or technology) failure having greater consequences.
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Technological and natural environment
Resilience at stake – forestsʼ vital functions under threat
Almost a third of our planetʼs land surfaces is covered by forests. By storing
carbon and water, and helping regulate our climate, forests are of enormous
value to life.
33
Forests also provide important services like timber, drinking
water, food, land slide and storm surge protection, pollinators for agriculture
and with their biodiversity genetic resources for pharmacology.
Despite all this, survival of these natural resorts of resilience are coming
under ever-increasing pressure. So much so that the destruction of the
Amazon rainforest could reach a point where the ecosystem transforms
irreversibly into a savannah-like state, with the loss of current benefits
accumulating to USD 5 trillion.
34
The situation is just as bad in other parts
of the world, such as the Philippines or Indonesia. Key drivers of the
destruction of forests are land clearance for agriculture and illegal logging.
Another main concern is that deforestation is in itself a major contributor
to climate change, accounting for nearly 20% of global greenhouse gas
emissions, more than the whole global mobility sector.
35
This is a self-
perpetuating disaster scenario, as under drier and warmer conditions,
climate change has also led to increased frequency and intensity of forest
fires in Canada, for example. Furthermore, monoculture tree plantations such
as for paper are less resilient vis-à-vis natural perils like extreme weather
conditions/storms that are occurring more frequently as climates change.
36
Potential impacts:
The agriculture sector and associated insurance lines are impacted by
water scarcity in deforested areas and by loss of protection from floods,
landslides and avalanches.
Life and health insurance may be impacted via the spread of diseases
from cleared forests into cities, driven by increased road access to forests
where epidemics can spread from animals to people.
37
The biodiversity of forests is deteriorating, putting at risk the cheapest
source of clean drinking water, and also undermining the role of forests in
protecting us from landslides and storm surges.
38
The related economic
activities provide an important basis for forestry and agricultural risk
transfer to insurance companies.
There is a vast potential for insurance as todayʼs commercial forests
remain largely uninsured, while an increasing number of commercial
forest companies are looking for risk protection/transfer solutions.
Combined with effective forest management, forestry insurance can
strengthen the resilience of forests and reduce emissions from
degradation and deforestation.
39
Impact:
low
Most affected
Property
business areas
Time frame (years):
0–3
Property
Operations
Casualty
Financial Markets
L&H
³³
³⁴
³⁵
³⁶
³⁷
³⁸
³⁹
Climate Change 2014: Synthesis Report. Contribution of Working Groups I, II and III to the
Fifth Assessment Report of the Intergovernmental Panel on Climate Change, IPCC, 2014
Franklin, S and R Pindyck
Tropical forests, tipping points, and the social cost of
deforestation,
Ecological Economics, Vol. 153, 2018
https://www.ipcc.ch/site/assets/uploads/2018/02/SYR_AR5_FINAL_full.pdf
Adam Felton et al.,
Replacing monocultures with mixed-species stands: Ecosystem service
implications of two production forest alternatives in Sweden,
US National Library of
Medicine and National Institutes of Health, February 2016
Jim Robbins,
How Forest Loss Is Leading To a Rise in Human Disease,
Yale School of
Forestry & Environmental Studies, 23 February 2016
Winnie Hu,
A Billion-Dollar Investment in New Yorkʼs Water,
The New York Times, 18
January 2018; Brian Blankespoor, Susmita Dasgupta,Glenn-Marie Lange,
Mangroves as
a protection from storm surges in a changing climate,
US National Library of Medicine
and National Institutes of Health, May 2017;
The State of the Worldʼs Forests,
Food and
Agriculture Organisation of the United Nations, 2018
Forestry insurance; a largely untapped potential,
Swiss Re, 8 December 2015
Swiss Re
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Technological and natural environment
Pervasive and toxic – chemicals in our bodies and environment
The chemicals behind Teflon and many other materials used in cookware,
food packaging (food wrappers, pizza boxes etc), carpeting, upholstery,
fire-fighting foam, apparel, floor wax, textiles and sealants belong to a family
of substances known as PFAS (per- and polyfluoroalkyl substances).
40
They have achieved notoriety by showing up in the blood samples of 98%
of all Americans, not surprising given their ubiquitous presence in the
environment. It is equally not surprising that this finding has invited legal
actions. The most notable case currently is a 2018 class action lawsuit
brought against major producers on behalf of Americans who have been
exposed to PFAS chemicals.
41
PFAS are just one of a group of chemicals in widespread use and with
resulting persistence in the environment where the time between application
and first showing of potential negative side effects can be very long. Given
the potential dangers that these chemicals pose, regulators across the globe
are taking action. In 2007, the EU enacted the REACH legislation to improve
the protection of human health and the environment from the risks posed by
chemicals.
42
The law requires companies to demonstrate how the substance
can be used safely.
China, meanwhile, has introduced a similar law, and the US has overhauled
its chemical regulation TSCA.
43
There are differences between how the laws
regulate chemicals, but they all require more transparency with respect to
ensuring the safety of human life and the environment. Such transparency
will help make the world a safer place, but will also generate potential for
new lawsuits.
Potential impacts:
Product liability and recall claims are to be expected in case of known or
potentially negative side effects on human health from exposure to
chemicals.
Environmental release on a gradual or accidental basis could impact
environmental liability policies, including clean-up costs.
Employersʼ liability and workers compensation claims may be triggered
where a connection between workplace-related diseases and certain
chemicals is established.
Impact:
low
Most affected
Casualty
business areas
Time frame (years):
0–3
Property
Operations
Casualty
Financial Markets
L&H
⁴⁰
⁴¹
⁴²
⁴³
As according to
United States Environmental Protection Agency.
Sharon Lerner,
Nationwide Class Action Lawsuit Targets Dupont, Chemours, 3M,
and Other Makers of PFAS Chemicals,
The Intercept, 6 October 2018
REACH stands for Registration, Evaluation, Authorisation and Restriction of Chemicals.
See
Understanding REACH,
European Chemicals Agency
TSCA stands for Toxic Substances Control Act. See
TSCA Inventory,
US Environmental
Protection Agency. Also
China REACH (MEP 7),
www.chemsafetypro.com,
30 December 2015
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An often long time lag between
application and the first signs
of potential negative side
effects of chemicals make
protection challenging.
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Competitive and business environment
Donʼt ask, donʼt tell – genetic testing and adverse selection
Since publication of our 2017 SONAR report on cancer screening and liquid
biopsies, genetic testing has been widely adopted by public health systems
and individuals. This has significant implications for life insurers, not least in
respect to the regulatory constraints involved.
44
The major challenge for life insurers is to obtain adequate and risk-relevant
information during the underwriting process, since existing regulation was
mostly enacted before the widespread distribution of direct-to-consumer
(DTC) genetic tests. Generally, regulation disallows the use of genetic
information in underwriting life insurance. This raises the prospect of more
customers at higher risk of disease or mortality applying for life insurance,
leading to adverse selection. Customers in the know may also fear being
denied life cover due to some genetic conditions, leading the insured to
withhold such information from the insurer.
45
A new generation of predictive genetic tests based on polygenic risk scores
(which attempt to quantify the cumulative effects of a number of genetic
variants to display predisposition to a disease
46
) promoted by companies
such as 23andMe and YouSurance, is only likely to widen the information
gap between insurer and insured. Nevertheless, some insurance groups
have been looking at the upside potential.
47
Regulation that stimulates genetic information asymmetry will significantly
impact insurersʼ ability to offer attractively priced coverage, and may
challenge the way in which insurance risk is considered and managed.
Insurers must be able to evaluate relevant consumer information when
underwriting, and that includes risk-relevant data from genetic tests.
Currently, there seem to be three broad regulatory approaches to access and
use of genetic data for risk assessment: none/self-regulation, limitations by
law, and outright legal ban. This lack of uniform approach shows the need
for industry groups and regulators to work together to agree on reasonable
self-regulation, one that balances the interests of consumers while
maintaining the ability of insurers to underwrite sustainable products.
48
Potential impacts:
Loss developments can be worse than expected if those at increased risk
buy disproportionate insurance cover, while those not exposed to
genetically-triggered diseases stay away.
As with any new innovation, there will be a challenging transition period
in which insurers will need to develop the know-how of capturing and
managing the data, design systems to incorporate the data and
implement new underwriting approaches.
As the results yielded by genetic tests become more accurate and their
use becomes more widespread, the way insurers traditionally pool risk to
differentiate individual risks may no longer be suitable.
Allowing access to an insuredʼs genetic information would enable more
accurate risk assessment.
In addition, access to genetic information could improve customer
engagement and services. New value-added products to cover specific
diagnostics, or services tailored to the insuredʼs health goals, could create
an active partnership between life insurer and insured, vastly improving
customer retention.
⁴⁴
⁴⁵
⁴⁶
⁴⁷
⁴⁸
See
2017 SONAR
report, Swiss Re
Seeing the future? How genetic testing will impact life insurance,
Swiss Re Institute, 2017,
Polygenic risk scores: how useful are they?
Genomics Education Programme,
25 October 2018
The Risk of Anti-Selection in Protection Business from Advances in Statistical Genetics,
Reinsurance Group of America and Kings College London, August 2018
Can life insurance pass the genetic test?
Swiss Re Institute, 2019
Impact:
high
Most affected
L&H
business areas
Time frame (years):
0–3
Property
Operations
Casualty
Financial Markets
L&H
36
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Genetic testing can create an
information asymmetry between
customers and insurers.
Swiss Re
SONAR New emerging risk insights
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Competitive and business environment
Risky bets? Insurance demand in an age of shifting markets
Globally, too many people are un- or underinsured and not protected when
a catastrophe strikes. In 2018, the estimated worldwide protection gap for
global catastrophe risks stood at around USD 80 billion.
49
The mortality
protection gap is even larger. In the US alone, the mortality protection gap,
a measure of life underinsurance, was close to USD 25 trillion in 2016.
50
These numbers should be seen against the backdrop of shrinking middle
classes in developed markets, the primary target group for many insurance
products. The OECD defines middle class income as being between 70%
and up to 200% of the median income. While almost 70% of baby boomers
were part of middle-income households in their twenties, only 60% of
millennials are today.
51
In all OECD countries – except Switzerland, Ireland
and Spain – the income portion of the middle class is diminishing. According
to McKinsey Global Institute, 98% of all households in 25 developed
economies have seen their income rise between 1993 and 2005.
52
The
picture is very different for the years 2005 to 2014 when 70% of households
experienced flat or even falling income. Moodyʼs paints a similar picture for
the US, saying that rising prices and interest rates will erode disposable
income. Shrinking disposable incomes may put willingness to pay for
insurance coverage to the test. We already witnessed this in the US, after the
global financial crisis of 2008–09. There was a significant widening of the
mortality protection gap between 2007 and 2010 due to a large increase in
joblessness and decrease in household asset values and increase in debt.
When people were asked why they didnʼt buy life insurance even though
they knew about the gap, 61% said they have other financial priorities.
53
From an insurance industry standpoint, the hope – or wishful thinking – is
that any shortfalls in the West can be offset by gains in the East, especially
China. Indeed, China has already overtaken the US in respect to its global
GDP contribution, and is projected to remain the growth engine of the world
economy. But growth rates are slowing down. Although insurance potential
continues to move East driven by demand from the thriving middle classes
there, the risk of growing income inequality there is considerable, especially
in the longer run.
Potential impacts:
China has already overtaken the US in terms of contribution to global GDP
and is projected to remain the growth engine of the world economy. Even
so, its growth rates are slowing, and that could curb insurance demand.
Insurance potential continues to move East. The thriving middle classes
are to be found in Asia rather than in the West. However, there is risk in
the longer run that the middle classes do not grow as expected, which
could also lead to rising income inequality.
Middle income households experiencing relative status loss and financial
pressure tend to cut expenses deemed not essential, and insurance often
falls into this basket.
Whether real or just perceived – middle classes in the US and Europe are
claiming status loss, which often translates into resentment towards
“establishment” and “foreigners.” The populist behaviours at the ballot box
and social unrest on the street bring more uncertainty and volatility to
these market environments.
Impact:
medium
Most affected
P&C, L&H
business areas
Time frame (years):
>3
Property
Operations
Casualty
Financial Markets
L&H
29
27
25
23
21
19
2000
2004
2008
2012
2016
Life insurance has not recovered
since the financial crisis
(life insurance in trillions USD)
Source: Swiss Re Institute, Life underinsurance
in the US; bridging the USD 25 trillion mortality
protection gap, September 2018
⁴⁹
⁵⁰
⁵¹
⁵²
⁵³
sigma
2/2019 op. cit.
Life underinsurance in the US: bridging the USD 25 trillion mortality protection gap,
Swiss Re Institute, Expertise publication, Sept 2018
Under pressure: the squeezed middle class,
OECD, April 2019
Poorer than their parents? Flat or falling incomes in advanced economies,
McKinsey Global Institute, 2016
Life underinsurance in the US; bridging the USD 25 trillion mortality protection gap,
Swiss Re Institute, September 2018
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Globally, too many people
are un- or underinsured.
Swiss Re
SONAR New emerging risk insights
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Competitive and business environment
Emerging trend
spotlight
Financial services
and the digital
revolution
Digitisation is all the rage in financial services. This has been the case
for a long time already and everybody agrees itʼs happening. Ironic,
therefore, that there is little consensus about what it actually means,
how itʼs changing the industry, or what actually needs to be done.
The expected bitcoin upheaval, which started a couple of years ago
with calls to bring down the traditional banking system, failed to
materialise. On the other hand, smart contracts and the underlying
blockchain technology have been adopted by traditional players in
banking and insurance, although some critics claim that blockchain
itself still isnʼt living up to its promise.
54
Nevertheless, nervousness among large financial institutions
about innovative start-ups persists, both with regards to potential
competition and investment opportunities. There are daily reports
about digital disruption and how to survive. The consulting companies
in particular are eager to promote digital disruption, offering guidance
and a helping hand. Everyone wants to be a winner, but nobody
exactly knows what direction to take. Which element of the digital
revolution needs to be prioritised? How quickly do we need to adopt
new behaviours, and what skills are required? And for re/insurers,
what does this all mean?
The problem many institutions face is a clash of culture and hierarchy.
Technologically affine youngsters come up against experienced and
established caution, meaning their skills are not always deployed most
effectively. On the other hand, experience and tradition is not
necessarily a bad thing, not where it prevents companies from falling
for the wrong technical innovation. Tension between old tradition and
new ideas can be healthy. Smart digitisation strategies are not only
about how to be ahead of everyone else, but also about the traps and
risks to avoid. Too much haste may lead to costly mistakes, institutional
memory loss, mispricing, increased cyber vulnerability and a generally
bad risk culture. To consider trade-offs, to find the right balance, thatʼs
where the challenge lies. Finding a safe pathway through that digital
challenge looks set to keep financial services firms busy for a while yet.
⁵⁴
Blockchainʼs Occam problem,
McKinsey & Company, January 2019
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Competitive and business environment
Getting the balance right – technology regulation affecting the
insurance industry
Impact:
Most affected
business areas
Time frame (years):
medium
Operations
(incl. regulation)
0–3
As technological innovation advances, regulation follows on its heels. We are
now seeing a first wave of non-insurance tech regulation spilling over into
the insurance industry. Much of this is about access to and use of customer
data, such as the General Data Protection Regulation (GDPR) and ePrivacy
Regulation coming out of the European Union. These have created
momentum for similarly broad data protection regulation in other locations,
which are both expansive in how businesses collect, store and use customer
data, and come with cross-border implications. Even the passive storage of
cloud-based data in an overseas jurisdiction entails regulatory, political and
business risks. Microsoftʼs jurisdictional battle with US law enforcement over
customer data stored in its Ireland data centre is a case in point.
Excessive data protection requirements like limitations on cross-border data
sharing can hinder the ability of insurers to utilise data in meaningful ways,
including developing more personalised solutions and more frequent and
meaningful interactions with clients. To ensure fair treatment of end users
and avoid discrimination, re/insurers have to take a responsible approach.
Increasingly in the spotlight are the potential risks arising from the
operational aspects of tech innovation such as cloud services, outsourcing
and cybersecurity. The consequent general lack of global harmonisation
means thereʼs a risk of conflicting laws.
In addition, global fragmentation of cybersecurity laws could increase
operational costs and compliance risks. This could impact companiesʼ future
use of data-linked technologies. Outsourcing IT infrastructure to the cloud
offers access to innovative services in many areas such as robotics, mobility
and Big Data. New regulatory requirements that limit the use of cloud
computing could hinder the development of a compelling digital service
portfolio for a customer base, one thatʼs increasingly asking for digital
experience in service delivery.
The lack of global harmonisation means risk of conflicting laws. For this
reason, it is important that regulator efforts be well coordinated between
jurisdictions. Technological development in an increasingly interconnected
digital environment underscores the need for collaboration between
regulators. Sound international standards are a prerequisite to optimise the
insurance value chain from end-to-end.
Potential impacts:
Laws and regulations relating to technological developments need to be
well balanced and internationally coordinated. Otherwise, they could
greatly increase a multinational insurersʼ legal, compliance and regulatory
risks.
Specific insurance regulation and general regulation eg data protection
might not be aligned and cause friction.
Legacy regulation and/or regulatory roadblocks limit timely utilisation of
new technologies and hinder meaningful strategic partnerships.
New data protection regulation might make the use of data for insurance
purposes more difficult, thus obstructing fair risk assessment and forcing
cross subsidisation.
Digital transformation is necessary to stay competitive. Regulators should
not restrict the use of cloud services but rather ensure that insurers have
processes in place to identify, manage and mitigate the risks that cloud
usage presents.
Property
Operations
Casualty
Financial Markets
L&H
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Special feature – Climate change in Life & Health
Climate change – from emerging
risk to real-life danger
Climate change was on Swiss Re‘s emerging
risk agenda in 1989 already, long before the
term “emerging risk” was coined. Since then,
climate change has fully emerged as a real and
present-day problem. First impacts such as the
greater frequency and severity of wildfire events
are already showing. As the following infographic
depicts, however, climate change risks extend
to a wide-reaching scope of threats that society,
and the insurance industry, are exposed to today.
While many areas of climate change have been
researched extensively, one risk area that has
not, to date, been afforded the same degree of
investigation is the impact of climate change on
human life and health. We expect the impacts
here to also be significant and therefore in the
following section, bring the focus to exploring
how societies and healthcare systems will
need to adapt to a warmer world.
Property insurance
Potential impacts
of climate change
Supply-chain
interruption insurance
Marine insurance
Glacial melting
Sea leve
Weather
changes
Altered rainfall patterns
Permafrost melting
Climate
change
Heat days
Sea ice decline
Ocean
changes
This graphic is intended to foster the risk dialogue and
tries to explain complex interactions and interconnections
in a simplified way. The graphic does not pretend to be
comprehensive or complete. Please also take a look at the
interactive version on swissre.com/SONAR2019
Acidity changes
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Agriculture insurance
Fishery insurance
Casualty insurance
Workplace accidents insurance
Life insurance
Health insurance
Trigger
Economy/financial markets
Potential main outcome
el rise
Storm surges
Floods
Migration
Thunderstorms/hail
Reduced agricultural
output/famine
Poverty
Droughts/water scarcity
Wildfires
Respiratory diseases
Soil subsidence
Permafrost virus/
bacteria release
Vector-borne diseases
Epidemics/pandemics
Cardiovascular diseases
Reduced physical
work capacity
New offshore exploration
Accidents
New shipping routes
Hurricanes/typhoons/storms
Power supply
interruption
Coral reef/biodiversity
damage
Tourism decline
Swiss Re
SONAR New emerging risk insights
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Special feature – Climate change in Life & Health
Itʼs existential – climate change and life & health
While not all the threats of climate change are fully understood, it fully emerged
as a present real life risk. The most pronounced risks from climate change affecting
human health stem from heatwaves, floods, droughts, fires and vector-borne
diseases. Millions of lives can be saved and the burden on healthcare services
reduced if we pay more heed to changing climates. Without action, mortality rates
and healthcare costs could soar,
55
and this would have significant consequences
for the health, workersʼ compensation and life insurance lines of business.
56
Changes in mortality will be driven by several changes occurring simultaneously.
First, we expect that heatwaves will become more severe and extend to areas
previously not impacted. This includes in the temperate zone, where a large
proportion of the worldʼs population lives. The 2003 heat wave in France was a
first taste of things to come. It caused 70 000 deaths – mainly among the elderly.
57
With no mitigation, and with rapidly ageing populations in many countries, a future
event will have an even bigger impact because the share of vulnerable older
populations in the affected regions is rising fast.
58
Increasing temperatures and high humidity due to climate change is another area
of concern, in that this combination enables vector-borne diseases to conquer
new ground. The West Nile and Zika epidemics were first warning signs.
59
Climate
change will extend the transmission season and geographical range for many
infectious diseases.
60
For example Lyme disease, avian influenza, meningitis, dengue
fever and tropical bacterial and viral infections are projected to increase with climate
warming, including potential shifts in their geographic range.
61
Severe drought
conditions can lead to increased wildfires, which in turn lead to air pollution. This is
even in areas far away from any conflagration, as the California wildfires of 2018
showed.
62
Knock-on effects
The secondary impact of climate change will amplify the above. In focus here are
migration, urbanisation, food security & nutrition, and water scarcity. Already today,
more than 2 billion people live in areas of water stress,
63
areas where access to clean
water for drinking, sanitation and personal hygiene – all pre-requisites for public
health – is limited.
64
The number of regions affected by water stress will increase as
temperatures rise. Public health could be further compromised by the expected
increase of, for example, extreme heat, droughts and floods affecting agriculture.
This will diminish or destroy the nutritional supply chains that help people withstand
health threats.
65
Nor will fishery compensate because rising sea temperatures and
ocean acidification will likely mean lower catches.
66
⁵⁵
⁵⁶
⁵⁷
⁵⁸
⁵⁹
⁶⁰
⁶¹
⁶²
⁶³
⁶⁴
⁶⁵
⁶⁶
COP24 Special Report: Health and Climate Change,
World Health Organisation, 2018
sigma 6/2018, op. cit.
Death toll exceeded 70 000 in Europe during the summer of 2003,
Comptes Rendus Biologies,
Vol. 331, No, 2, February 2018
The 2018 report of the Lancet Countdown on health and climate change: shaping the health of
nations for centuries to come,
The Lancet, 8 December 2018
Impacts of 1.5C of Global Warming on Natural and Human Systems,
IPCC, 2018
Human health and adaptation: understanding climate impacts on health and opportunities for action.
Synthesis paper by the secretariat,
United Nations, March 2017
Impacts of 1.5C of Global Warming on Natural and Human Systems,
op. cit.
ʼNo
fresh airʼ: wildfire smoke sets apocalyptic haze over San Francisco,
The Guardian,
13 November 2018
SDG 6 Synthesis Report 2018 on Water and Sanitation,
United Nations, 28 June 2018
Human health and adaptation: understanding climate impacts on health and opportunities for action.
Synthesis paper by the secretariat,
op. cit.
The State of Food Security and Nutrition in the World,
Food and Agriculture Organisation of the
United Nations, 2018
Heatwaves take their toll on the high seas,
Nature: international journal of science, 4 March 2019
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Extreme weather events will not only impact agriculture. With continued sea level
rise,
67
storm surges may reach further inland. With increased value concentration
in mega-cities exposed to storm surges, economic and insured losses are likely to
increase further. So too will the risk of epidemics. Migration to urban centres is
concentrating an ever larger share of the worldʼs population in a small areas. As has
happened many times before, storms and floods that destroy infrastructure can
trigger significant epidemics. And, once the flood water recedes, toxic mould may
remain in buildings, posing yet another threat to public health.
In polar and other regions were permafrost has long been the environment norm,
another possible consequence of warmer temperatures could be the release of older
bacteria and viruses as ice thaws. Having not been exposed to these strains for
thousands of years, the immunity of the worldʼs population to such threats will be
low. The building of new harbours to accommodate increasing marine traffic with
the opening up of the arctic sea route, will make it more likely viruses or bacteria will
be able to travel to far distant locations, triggering an epidemic or pandemic. Such
outbreaks could be especially serious if the bacteria prove resistant to antibiotics
(see section in the 2017 SONAR report on antibiotic resistance).
Becoming climate resilient in public health
The world community has acknowledged the imperative with the “Paris agreement
on climate change” which aims to keep global warming well below 2 degrees
Celsius in the long-term. In addition, it outlined in the WHO COP 24 special report on
Health & Climate change what to do to save lives, reduce epidemics and make public
health climate resilient.
68
The immediate public health activities necessary to meet the challenge of climate
change are to strengthen the prevention of climate-sensitive health risks and to build
an adaptive skill set to absorb the changing, increasing risks presented by climate
change described before. This also involves related sectors like food security and
safety or sanitation. Additionally, however, there are other specific risks the health
sector must address to achieve resilience in the face of climate change.
Health care facilities are the operational heart of service delivery, protecting health
and treating patients, both during and after weather and climate-related events
(such as heat stroke during heatwaves and injuries during cyclones) and in response
to other environmental risks to health (such as asthma due to poor air quality). Health
care facilities in poor and rich countries alike must be able to deliver in changing
climate conditions, such as during extreme weather events. Cooling systems during
heat days, flood security, emergency power and water supplies must become
standard in health care facilities worldwide.
⁶⁷
⁶⁸
Impacts of 1.5C of Global Warming on Natural and Human Systems,
op. cit.
COP24 Special Report: Health and Climate Change,
op. cit.
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Many workers in the
oil and gas industry
will retire in the next
few years: This will
create a skills gap.
46
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Appendix A: High impact emerging risk themes, 2015–2019
Every year Swiss Re publishes new emerging risks in its SONAR report. Occasionally,
an emerging risk is reported again in a later report in case new aspects emerge or if
the risk persists with increased urgency. Some overarching themes and common
aspects are usually reflected in every report, often in the list of emerging risks ranked
with highest impacts. For 2015–2019, here we list the top risks of each year and
discuss how the overarching concerns regarding market dynamics, cyber risks and
climate change have been profiled in specific high impact emerging risk themes over
the years.
Market dynamics
As a key sector of the financial industry, the insurance industry is exposed to market
dynamics. In 2015, the euro zone crises and expansive monetary policies were
in the foreground, as were concerns over domestic populist movements fostering
de-globalisation. While uncertainties from central bank quantitative easing
continued in 2016, a potential slow-down of emerging market growth was added
to the top emerging risks list. International regulatory fragmentation and protective
trade barriers where each flagged as top risks in 2017, next to a return of inflation.
Then, in 2018 national protectionism and regulatory fragmentation to hamper
diversification for international re/insurers were synthesised into a top risk under the
theme “A brave new world?” Heightened geopolitical tensions and trade conflicts are
further confirming ongoing concern about the volatile global business environment
for insurers.
Cyber risks
Cyber risk presents one of the largest opportunities for the re/insurance industry,
while simultaneously presenting one of the largest challenges. The frequency and
severity of risks resulting from cyber-attacks and their changing nature, are expected
to grow significantly over the next years. The need for cyber resilience has become
a main focus of attention among corporate clients and insurance companies,
triggering insurance demand. The SONAR report has flagged the evolving aspects
of technological change and uncertainty in a series of cyber risk themes over the
past years. This includes a focus on vulnerabilities from the IoT (2015), the challenges
from increased internet fragmentation (2016), accumulation risks from cloud
solutions (2017) and lurking cyber risk from end-of-life software and hardware still
in use (2018). In this yearʼs report, we focus on exposures from 5G mobile and where
software enhancements are applied to existing legacy hardware, particularly in the
case of large infrastructure facilities.
Climate change
Swiss Re identified climate change as an emerging risk 30 years ago. Three decades
on, we continue to flag the impact of climate change on specific risk factors and
pools. For example, in 2015 we highlighted the associated theme of potential super
natural catastrophes from “atmospheric rivers” affecting the US West Coast. We
then raised a closer connection to climate change in the form of growing water
stress and drought potential in our 2017 SONAR report, in our exposé on “The big
drying”. Today, climate change has become a fully-emerged risk, and in this yearʼs
report we have a dedicated section on its impact on life & health insurance.
Swiss Re
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Appendix A: High impact emerging risk themes, 2015–2019
2015
De-globalisation
2016
The great monetary
experiment (cont.)
2017
Bugs on the march –
underestimated
infectious diseases
2018
Asbestos reloaded –
USD 100 billion in
losses and counting
2019
Limits to tinkering –
the fiscal and
monetary policy
balance at risk
Teaching an old dog
new tricks – digital
tech meets legacy
hardware
Off the leash – 5G
mobile networks
The great monetary
experiment
Internet
fragmentation
Reduced market
access – protecting
your own backyard
A brave new
world? – emerging
geopolitical risk
Super nat cats
Emerging market
crises 2.0
The perfect storm –
cloud risk
accumulation
Algorithms are only
human too –
opaque, biased,
misled
Coming back to bite
us – lurking cyber
risks
Challenges of the
Internet of Things
The big drying –
growing water stress
Itʼs existential –
climate change and
life & health
(Special feature)
Donʼt ask, donʼt tell –
genetic testing and
adverse selection
Societal environment
Political environment
Technological and natural environment
Competitive and business environment
The return of
inflation – the effect
on insurance
business
Island solutions –
regulatory
fragmentation
A slow poison – the
erosion of risk
diversification
Listed above are our risk themes from the SONAR reports 2015–2019 with high impact potential. Risks with medium and
low impact potentials are not listed. These high impact risks are colour-coded according to their respective macro trend
environments. Together with the following descriptions per risk, the synopsis reflects a “high priority portfolio” of emerging risk,
as it develops over time. It also allows “to keep track” of older emerging risks and reflect that some of the risks are
reported once only, others reappear, and some overarching concerns (see page 47) are monitored throughout the years.
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Summary of high impact emerging risk themes (2015–2019)
2015
De-globalisation:
Political conflicts have been intensifying over the last few years in
many regions including Eastern Europe, the Middle East and East Asia. Sanctions
and other interventionist policy tools have led to economic distress, driving an
upsurge in populist and nationalist sentiment. In Europe, this could trigger territorial
separatism (eg, Scotland or Catalonia) and eventually undermine integration projects
such as the European Union.
The great monetary experiment:
The euro area debt crisis lingers on, with only
modest growth, high unemployment and unsustainable debt levels in some
countries. Traditional policy tools, including expansionary fiscal policy and monetary
easing, are no longer feasible. Nevertheless, extremely accommodative monetary
policies continue and even intensify. Short- to mid-term consequences include
extremely low interest rates, distortions of risk-return profiles, potential asset price
bubbles, and increasing economic inequality. Longer-term consequences include
potential for higher inflation and reputational damage for central banks.
Super nat cats:
The US Geological Service published a study on a winter storm
scenario, looking at the impact of an “atmospheric river” event with a return period
of 1 000 years. Findings indicate that flooding would overwhelm flood protections
in many areas, resulting in the evacuation of more than a million residents, direct
property damage of nearly USD 400 billion and business interruption costs of about
USD 325 billion. The risk of volcanic eruptions might also be underestimated as no
large eruption has occurred since 1815. However, eruptions can have a devastating
impact if they occur close to population centres. They can also impact global travel,
as illustrated by the eruption of Icelandʼs Eyjafjallajökull volcano in 2010.
Challenges of the Internet of Things:
The IoT will revolutionise the digital world.
Increased connectivity and reliance on digital processes raises questions about
network and data security, resilience and long-term maintenance and software
updates. Losses could occur from system malfunction and malicious attacks from
hackers and criminals. There may also be legal and compliance risks due to the lack
of consistent regulatory standards across countries.
2016
The great monetary experiment (cont.):
Quantitative easing continues, resulting
in a low to negative interest rate environment. Economic growth and inflation
remains tepid in the euro area and Japan, triggering discussions about additional
monetary policy stimulus. Negative interest rates will further undermine the
conventional insurance business model, particularly for life insurers and pension
funds.
Internet fragmentation:
Cyber crime and espionage have grown strongly, making
the internet less safe. Governments urge more effective protection of online assets
and consider isolating critical IT infrastructure from global networks. Disconnected
national/regional nets will become more common. Technology companies risk
disruption to their business model and might face liability suits if no longer able to
access data stored on cross-border servers.
Emerging market crises 2.0
– Amid rising US interest rates, economic growth in
China has continued to slow, with knock-on impact on commodity prices leading to
net capital outflows from emerging markets. Emerging market turmoil could hurt
insurersʼ balance sheets and may trigger detrimental regulatory consequences.
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Appendix A: High impact emerging risk themes, 2015–2019
2017
Bugs on the march – underestimated infectious diseases:
The risk factors
associated with infectious diseases, even known ones, are changing (eg, climate
change, animal husbandry, land use, and poor health in areas connected with the
world economy). These factors could facilitate outbreak and proliferation of
infectious diseases.
Reduced market access – protecting your own backyard:
Free trade, open
markets and globalisation are coming under increasing pressure, with governments
favouring local markets and national champions. Protectionism is no longer an
emerging market phenomenon.
The perfect storm – cloud risk accumulation:
Ever more widespread use of
cloud and cloud-of-clouds solutions comes with a variety of risks: cyber attack,
technical failure, prolonged outage and data inaccessibility. The data volumes
involved and service interruption potential pose significant and catastrophic risk
to system resilience.
The big drying – growing water stress:
Farming, industrial use and household
consumption are exacerbating water shortages in a growing number of regions
(eg, California, US mid-West, southern Europe, the Mediterranean, South Africa).
Severe water shortages also have an adverse impact on food production and can
undercut oil and gas production.
The return of inflation – the effect on insurance business:
Inflation is picking
up in US and UK (not yet Europe and Japan). A sudden increase in inflation can
adversely impact insurer profits. The long-term effect of accommodative monetary
policy of recent years remain unclear.
Island solutions – regulatory fragmentation:
International regulatory
coordination activities among G20 are increasingly stalling, diminishing the chance
for international standards and norms, and leaving an uneven playing field.
Regulatory island solutions increase coordination and operational costs, and
compliance burden to multinational insurers.
2018
Asbestos reloaded – USD 100 billion in losses and counting:
Millions of metric
tons of asbestos are still being processed in many countries. A UN report showed
that over 300 million people in Europe and Central Asia are potentially exposed.
Latin America and other regions are at risk also.
A brave new world? – emerging geopolitical risk:
The global political and
economic balance has become multi-polar. Global institutions lack mitigating power
in circumstances of conflict. Aggressive propaganda, cyber-attacks and other means
of “hybrid war” between nation states increase uncertainty.
Algorithms are only human too – opaque, biased, misled:
Algorithms are
susceptible to discriminatory bias. Black-boxed workings of algorithmic calculations
can conceal and perpetuate mistakes. Whatʼs lacking is governance around
development and application of algorithms.
Coming back to bite us – lurking cyber risks:
Flaws and vulnerabilities in
hardware (chips) and software may remain undetected for a long time (eg, “sleeper”
cyber risk played out in recent WannaCry-attack). The risk is mispricing in cyber-
covers, which may in turn impact operations.
A slow poison – the erosion of risk diversification:
Re/insurance provides
financial protection from risks by deploying capital across borders and lines of
business. National protectionism and regulatory fragmentation are jeopardizing
the benefits of international diversification.
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2019
Limits to tinkering – the fiscal and monetary policy balance at risk:
There is
a growing consensus that another economic downturn will need a fiscal response.
Potential responses include quantitative easing, “helicopter money” or modern
monetary theory. The re/insurance industry could benefit if changes to policy bring
growth and financial stability. The possible flipside is a rise in uncertainty, causing
higher financial market volatility and declines in asset valuations.
Teaching an old dog new tricks – digital tech meets legacy hardware:
Technological improvements are ongoing. Hardware in areas of critical
infrastructure, including smart electric power grids or pipelines, hospitals or cash
points, however, is often out dated. As a consequence, insurers face higher risk
accumulation unexpected loss potential in the areas of property damage, bodily
injury, business interruption and cyber risk.
Off the leash – 5G mobile networks:
5G will enable wireless connectivity in real
time for any device of the IoT, such as autonomous cars or sensor-steered factory.
Current concerns regarding potential negative health effects from electromagnetic
fields are likely to increase. Hackers can also exploit 5G speed and volume to acquire
(or steal) more data faster. Major concerns are possible privacy and security
breaches, and espionage.
Itʼs existential – climate change and life & health:
The most pronounced risks
from climate change affecting human health stem from heatwaves, floods, droughts,
fires and vector-borne diseases. Millions of lives and healthcare services could be at
risk. Without action, mortality rates and healthcare costs could soar, and this would
have significant consequences for the health, workersʼ compensation and life
insurance lines of business.
Donʼt ask, donʼt tell – genetic testing and adverse selection:
Over the past
years, the cost of genetic testing has declined significantly and, with direct-to-
consumer (DTC) testing kits, genetic tests are now available and affordable for
individual use. It has been widely adopted by public health systems and individuals.
This has significant implications for life insurers, not least in respect to the regulatory
constraints involved.
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Appendix B: Terms and definitions
What is SONAR?
SONAR stands for Systematic Observation of Notions Associated with Risk. It is
Swiss Reʼs tool for identifying, assessing and managing emerging risks. Experts
across the company use a web-based platform to collect early signals of emerging
risks. All signals are assessed and prioritised by an emerging risk management team
which closely interacts with topic experts from Swiss Reʼs business areas. The team
serves as a catalyst for risk identification and assessment to define and implement
recommendations in collaboration with the business. The findings are regularly
shared internally and summarised for external audiences here.
What are emerging risks?
We define emerging risks as newly developing or changing risks that are difficult to
quantify and could have a major impact on society and industry.
What are emerging risk themes?
Emerging risk themes illustrate potential new or changing risk developments for the
insurance industry. They are mainly derived from SONAR but also draw on other
sources. All themes have been assessed and edited by Swiss Reʼs emerging risk
management experts. This report only features new emerging risk themes (ie, topics
covered in previous editions are not listed again). You can retrieve prior reports from
our webpage: www.swissre.com/sonar
What is meant by overall impact?
The overall impact is an indicator of the potential financial, reputational and/or
regulatory impact associated with an emerging risk topic. It is assessed on a scale
from high to low:
HIGH
Potentially high financial, reputational and/or regulatory impact
or significant stakeholder concern
Potentially medium financial, reputational and/or regulatory impact or
moderate stakeholder concern
Potentially low financial, reputational and/or regulatory impact,
or low stakeholder concern
MEDIUM
LOW
What is meant by time frame?
We divide themes into those likely to occur in less than 3 years and those likely to
occur over a longer time horizon. This assessment should not be used as an indicator
of when action is needed, as some themes likely to occur in the more distant future
may, nonetheless, require immediate action to prepare.
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What is meant by impact per business area?
Spider graph indicating the potential impact on major insurance business areas on a
scale from 0 (= no impact) to 4 (=significant impact).
What are trend spotlights?
Boxes throughout the text provide selective spotlights on emerging trends which
could become relevant for the re/insurance industry and its clients. The selection of
topics is non-exhaustive, and descriptions are intended as food for thought and
discussion starters rather than comprehensive reviews.
What are macro trends?
Swiss Re has identified a set of macro trends assumed to have a high impact on the
re/insurance industry within the next 5 to ten years. The macro trends featured in
this report have been selected independently through expert discussions and
surveys. They provide context to the emerging risk insights from the SONAR process.
Swiss Re
SONAR New emerging risk insights
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Title
Swiss Re SONAR – New emerging risk insights
May 2019
Authors
Sustainability, Emerging and Political Risk
Management, Swiss Re Institute, Strategy
Development & Performance Management
Acknowledgments
We would like to thank all Swiss Re employees who
post risk notions and contributed to this publication,
as well as the SONAR officers who provided input and
feedback to the content of this report, and build bridges
to their respective business areas.
Editing and realization
Group Communications, Swiss Re Institute
Layout
Swiss Re Corporate Real Estate & Services /
Media Production, Zurich
Photographs
Getty images, iStockphoto
Printing
Multicolor Print AG, Baar
Disclaimer
The content of this report is subject to copyright
with all rights reserved. The information may be
used for private or internal purposes, provided that
any copyright or other proprietary notices are not
removed. Electronic reuse of the content of this
brochure is prohibited. Reproduction in whole or in
part or use for any public purpose is only permitted
with the prior written approval of Swiss Re, and if the
source reference is indicated. Courtesy copies are
appreciated. Although all the information discussed
herein was taken from reliable sources, Swiss Re
does not accept any responsibility for the accuracy
or comprehensiveness of the information given or
forward looking statements made. The information
provided and forward looking statements made are for
informational purposes only and in no way constitute
or should be taken to reflect Swiss Reʼs position, in
particular in relation to any ongoing or future dispute.
In no event shall Swiss Re be liable for any financial or
consequential loss or damage arising in connection
with the use of this information and readers are
cautioned not to place undue reliance on forward-
looking statements. Swiss Re undertakes no obligation
to publicly revise or update any forward-looking
statements, whether as a result of new information,
future events or otherwise.
Visit www.swissre.com to download or to order
additional copies of Swiss Re publications.
05/19, 1507585_19_EN
©2019 Swiss Re. All rights reserved.
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Swiss Re Institute
Mythenquai 50 /60
P.O. Box
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Telephone + 41 43 285 2551
Fax +41 43 282 0075
[email protected]
institute.swissre.com
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Toprådgiver i Holland advarer mod ukritisk 5G-udrulning
https://tabttraad.home.blog/2020/03/24/topraadgiver-i-holland-advarer-...
Toprådgiver i Holland advarer mod ukritisk
5G-udrulning
Author: Tabt Tråd
NYHED / UDLAND:
Formanden for
strålingskomitéen
i Hollands nationale
sundhedsråd,
Hans Kromhout,
advarer nu landets beslutningstagere mod ukritisk
5G-udrulning.
Den nederlandske professor mener, at alle herlighederne ved 5G skal holdes nøje op
imod de risici for folkesundheden, som samfundet løber.
Det skriver det nederlandske dagblad,
De Telegraaf.
Hans Kromhout mener ikke, at forsigtigheden med mobilstråling lever op til de
standarder, man anvender til at beskytte befolkningen mod andre risici som
kemikalier, pesticider og medicin, hvor kravene ifølge Hans Kromhout er strenge.
Hans Kromhout kritiserer især, at autoriteterne på strålingsområdet ignorerer klare
forskningsresultater som det amerikanske NTP-projekt, der varede i 19 år og som
sluttede med en klar konklusion af kræftfund i forsøgsrotter.
“Den amerikanske NTP-undersøgelse, som leverede klare beviser for sammenhæng
mellem kræft og eksponering for EMR (red. elektromagnetisk stråling) – var godt
udført og repræsenterede et stort gennembrud. Alligevel forsøger visse grupper at
1 af 2
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Toprådgiver i Holland advarer mod ukritisk 5G-udrulning
https://tabttraad.home.blog/2020/03/24/topraadgiver-i-holland-advarer-...
bortforklare”, siger han til avisen.
Mistillid til ICNIRP
Hans Kromhout kritiserer, at en lang række lande ret ukritisk adopterer deres
grænseværdier fra det private forskerselskab ICNIRP og kalder det “ganske
usædvanligt”, at et selskab som ICNIRP kan opnå så stor en indflydelse.
“Det er lidt af en uigennemsigtig klub, hvor det er uklart, hvordan medlemmerne
vælges. Kald det som selvbestaltet. I den forstand kan man ikke tillægge
organisationen en uafhængig status”, siger han til avisen.
To af verdens nøgleposter på området er besat af hollændere. I ICNIRP er
nederlandske Eric van Rongen formand, indtil han træder et skridt tilbage og bliver
næstformand i maj 2020.
Siden 2006 har nederlandske Emilie van Deventer været leder af WHO-kontoret
The International EMF Project i Geneve, som siden oprettelsen i 1996 har arbejdet
meget tæt med ICNIRP.
ICNIRP’s hovedstifter og første formand, Michael Repacholi, forlod ICNIRP i 1996
for at blive leder i det nyoprettede WHO-kontor, som i betydelig grad har fungeret
for teleindustriens sponsormidler.
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REPUBBLICA ITALIANA
IN NOME DEL POPOLO ITALIANO
LA CORTE D’APPELLO DI TORINO
SEZIONE LAVORO
Composta da:
Dott.ssa Rita MANCUSO
Dott.ssa Caterina BAISI
Dott.ssa Silvia CASARINO
ha pronunciato la seguente
SENTENZA
nella causa di lavoro iscritta al n.
721/2017
R.G.L. promossa da:
ISTITUTO
NAZIONALE
PER
L’ASSICURAZIONE
CONTRO GLI INFORTUNI SUL LAVORO
–
I.N.A.I.L. -,
con sede in Roma, Via IV Novembre n. 144, in persona del
Direttore Regionale pro-tempore del Piemonte, rappresentato e
difeso per procura generale alle liti Notaio Romano di Chivasso
del 07.08.2013 rep. N. 55082 Raccolta 16699 dagli Avv.ti
Loretta Clerico ed Elia Pagliarulo, ed elettivamente domiciliato
in Torino, Corso Galileo Ferraris n. 1 presso l’Avvocatura
Regionale INAIL
APPELLANTE
CONTRO
ROMEO ROBERTO,
residente a Leinì (TO), Via Lamarmora
PRESIDENTE
CONSIGLIERE
CONSIGLIERE Rel.
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n. 11, rappresentato e difeso per procura in calce al ricorso
introduttivo del giudizio di primo grado, congiuntamente e
disgiuntamente, dagli Avv.ti Renato Ambrosio, Stefano Bertone
e Chiara Ghibaudo, ed elettivamente domiciliato presso il loro
studio in Torino, Via Bertola n. 2
APPELLATO
oggetto: malattia professionale
CONCLUSIONI
Per l’appellante:
come da ricorso depositato in data 31.8.2017
Per l'appellato:
come da memoria difensiva depositata in data 22.10.2018
FATTI DI CAUSA
Il sig. Roberto Romeo ha chiamato l’INAIL davanti al Tribunale
di Ivrea, deducendo la natura professionale del neurinoma
dell’acustico destro
di cui è affetto, in quanto patologia contratta
per l’uso abnorme di telefoni cellulari nel
periodo 1995-2010, in
cui ha lavorato alle dipendenze di Telecom s.p.a., e chiedendo
quindi la condanna dell’Istituto convenuto a pagargli la
prestazione dovuta per legge, commisurata alla percentuale di
invalidità, indicata in misura pari ad almeno il 37%.
L’INAIL ha contestato la domanda attorea e ne ha chiesto il
rigetto.
Istruita la causa mediante escussione di alcuni testimoni e con
due c.t.u. medico-legali (una sul nesso causale
e l’altra sulla
quantificazione dei postumi permanenti), con sentenza n.
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96/2017 pubblicata il 21.4.2017, il Tribunale, in accoglimento
del ricorso, ha condannato l’INAIL a corrispondere al ricorrente
la prestazione spettante con riferimento alla percentuale di
invalidità del 23%, con condanna a rimborsare al ricorrente le
spese di lite e a pagare le spese di c.t.u..
Propone appello l’INAIL; resiste l’appellato.
Disposta nuova c.t.u. medico-legale (affidata congiuntamente
alla dott.ssa Carolina Marino
e al dott. Angelo D’Errico,
specialisti rispettivamente la prima in medicina-legale e il
secondo in medicina del lavoro, dirigente medico del Servizio
Sovrazonale di Edipemiologia ASL TO3),
all’udienza del
3.12.2019, all’esito della discussione,
la Corte ha deciso la causa
come da separato dispositivo.
RAGIONI DELLA DECISIONE
Il Tribunale ha accolto il ricorso osservando che:
-il ricorrente, quale referente/coordinatore di altri dipendenti
Telecom, ha utilizzato in maniera abnorme telefoni cellulari nel
periodo 1995-2010,
come dimostrato dall’istruttoria testimoniale
(testi Musso, Nani, Bilucaglia);
-in base ad essa si deve infatti ritenere che il ricorrente,
coordinando una quindicina di colleghi,
nell’ipotesi più prudente
utilizzasse con loro il telefono per almeno due ore e mezza al
giorno (2 telefonate x 5 minuti x 15 colleghi), e che,
nell’ipotesi
maggiore, le ore al telefono diventassero oltre sette (3 telefonate
x 10 minuti x 15 colleghi), a cui si aggiunge il tempo trascorso al
telefono per riferire ai propri superiori e per coordinarsi con il
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direttore dei lavori degli enti e con le imprese esterne che
collaboravano nei lavori, nonché durante il fine settimana, come
confermato dal teste Romeo, figlio del ricorrente;
-inoltre,
all’epoca non esistevano
strumenti per attenuare
l’esposizione alle radiofrequenze e
questa era aggravata dal tipo
di tecnologia utilizzata per i primi telefoni cellulari (tecnologia
ETACS), e dal fatto che spesso
l’utilizzo avveniva all’interno
dell’abitacolo di un’autovettura;
-la letteratura scientifica è divisa in merito alle conseguenze
nocive dell’uso dei telefoni cellulari: da una parte l’Agenzia
Internazionale per la Ricerca sul Cancro (IARC), facente parte
dell’Organizzazione Mondiale della Sanità
(ente imparziale ed
autorevole a livello mondiale) il 31.5.2011 ha reso nota una
valutazione
dell’esposizione
a campi elettromagnetici ad alta
frequenza, definendoli come “cancerogeni possibili per l’uomo”
(categoria 2B);
dall’altra
lo studio Interphone individua un
rischio del 40% superiore per i glioma (famiglia di tumori cui
appartiene anche quello che ha colpito il ricorrente) negli
individui che abbiano usato il cellulare molto a lungo e per molto
tempo; gli unici studiosi che con fermezza escludono qualsiasi
nesso causale tra utilizzo di cellulari e tumori encefalici sono i
proff. Ahlbom e Repacholi, ma detti autori si trovano in
posizione di conflitto di interessi, essendo il primo consulente di
gestori di telefonia cellulare ed il secondo di industrie elettriche;
-ai risultati a cui sono pervenuti gli studi finanziati dalle aziende
produttrici di telefoni cellulari non può essere attribuita
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particolare attendibilità in considerazione della posizione di
conflitto di interessi degli autori, come ritenuto dalla S.C. nella
sentenza n. 17438/2012 in un caso relativo ad altro tumore
encefalico (neurinoma del ganglio di Gasser);
-la c.t.u. ha accertato la sussistenza del nesso causale;
-pertanto, e considerate le peculiarità del caso concreto
(associazione tra tumore raro ed esposizione rara per durata ed
intensità; periodo di latenza congruo con i valori relativi ai
tumori non epiteliali; il fatto che la patologia sia insorta nella
parte destra del capo del ricorrente, soggetto destrimane;
mancanza di altra plausibile spiegazione della malattia), deve
ritenersi provato un nesso causale, o quantomeno concausale, tra
tecnopatia ed esposizione, sulla base della regola del “più
probabile che non”;
-i postumi permanenti debbono essere riconosciuti nella misura
del 23%, come da conclusioni del c.t.u., non contestate da alcuna
delle parti.
Con il primo motivo di gravame l’INAIL lamenta che il
Tribunale abbia omesso di pronunciarsi sull’eccezione di
inammissibilità del ricorso, ai sensi dell’art. 152 disp. att. c.p.c.,
per mancanza della dichiarazione di valore della prestazione
richiesta.
Il motivo è infondato, avendo la Corte Costituzionale, con
sentenza 20.11.2017 n. 241, dichiarato l’incostituzionalità di
detta norma.
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Con il secondo motivo, l’Istituto sostiene che il Tribunale abbia
erroneamente ritenuto provato un uso abnorme per 15 anni del
telefono
cellulare
per
esigenze
lavorative,
essendo
le
testimonianze sul punto contraddittorie: in particolare, secondo
la deposizione del teste Bilucaglia la durata delle telefonate (e
quindi l’esposizione
alle radiofrequenze)
era di un’ora e quaranta
minuti al giorno, mentre secondo quanto riferito dal teste Musso
essa arrivava fino a 10 ore, durata inverosimile in quanto
superiore alla stessa durata della giornata lavorativa. Inoltre,
secondo quanto
emerso dall’istruttoria testimoniale, le telefonate
tra l’appellato e i colleghi avvenivano anche mediante telefono
fisso,
e, d’altra parte, il figlio dell’appellato non è stato in grado
di quantificare le telefonate ricevute dal padre fuori dell’orario di
lavoro quando egli era reperibile. Né in base alle deposizioni dei
testimoni è possibile determinare la quantità e la durata delle
telefonate all’interno dell’abitacolo dell’autovettura.
Pur non potendosi ritenere, diversamente da quanto sostenuto
dall’appellato,
che
le circostanze storiche relative all’esposizione
siano provate per non essere state
contestate dall’INAIL ex artt.
115 e
416 comma 3 c.p.c., trattandosi di fatti non noti all’Istituto
e che quindi esso non è in grado di contestare o meno, il motivo
è comunque infondato.
L’istruttoria testimoniale ha infatti confermato la notevolissima
esposizione del sig. Romeo alle radiofrequenze
per l’uso del
telefono cellulare nel periodo 1995-2010.
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Infatti, il
teste Musso, collega dell’appellato dal 1990 al
2010, ha
riferito che l’appellato coordinava la sua attività e quella degli
altri tecnici esterni (di cui
l’appellato
era superiore gerarchico),
pari complessivamente a 15-20 persone; il teste ha dichiarato che
si sentiva con l’appellato quotidianamente più
volte al giorno,
circa 2-3 volte al giorno o anche di più, con chiamate della
durata di 5-10 minuti ciascuna.
Il teste Nani, collega dell’appellato dal 2000 al 2011, ha
dichiarato di essersi sentito con lui molto spesso, anche un paio
di volte all’ora,
e che le telefonate duravano 5 minuti, ma anche
di meno.
Il teste Bilucaglia, che ha lavorato con
l’appellato dai primi anni
‘90
al 1996,
ha dichiarato che quest’ultimo coordinava circa 10-
12 colleghi; e di avere contattato
l’appellato almeno 2-3
volte in
un giorno, con telefonate di circa 5-10 minuti ciascuna.
Come rilevato dal Tribunale, le telefonate dell’appellato
intercorrevano anche con il direttore dei lavori, con le imprese
esterne e con i superiori (v. testi Musso e Bilucaglia).
Escludendo quindi i valori massimi (che si ottengono
considerando il numero più elevato di telefonate effettuate dai
tecnici all’appellato e la durata
massima di esse, come indicati
dai testi) e prendendo perciò in considerazione il numero minimo
e
il
numero
medio
di
telefonate
di
ciascun
tecnico
(rispettivamente 2 e 2,5) per il numero di essi (l5-20 secondo
Musso, 10-12 secondo Bilucaglia),
si ottiene un’esposizione,
secondo le testimonianze di Musso e Nani, da un minimo di 3,30
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ore al giorno (200 minuti) a un medio di 5 ore al giorno (300
minuti), e, secondo la testimonianza di Bilucaglia, da un minimo
di 1 ore e 40 minuti (100 minuti) a un medio di 3 ore e 50 minuti
(230 minuti).
Pertanto, pur con il grado di precisione compatibile con il fatto
di riferirsi a circostanze che, anche a distanza notevole di tempo,
si ripetono durante un periodo lungo, anche con un inevitabile
grado di variabilità, il quadro istruttorio consente, a parere della
Corte, di ritenere provata un’esposizione a radiofrequenze molto
elevata, che, in via del tutto prudenziale, va quantificata in circa
4 ore al giorno per tutto il periodo dedotto nel ricorso.
All’epoca non esistevano strumenti che consentissero di evitare
il contatto diretto del telefono cellulare con il viso, come
cuffiette o auricolari (v. teste Musso, e v. teste Nani, secondo cui
le cuffiette, peraltro acquistate personalmente dai tecnici
Telecom, avevano iniziato ad essere utilizzate a partire
dall’inizio
del 2000,
e, nello stesso senso, v. teste Bilucaglia).
E’ vero, come osservato dall’INAIL, che l’appellato disponeva
di un ufficio dotato di un telefono fisso (v. teste Musso), ma i
testi hanno riferito che lo contattavano sul telefono cellulare in
quanto era più facile reperirlo, considerato che sovente si
spostava fuori dell’ufficio
e che era meno agevole rintracciarlo
sul telefono fisso, in quanto in tal caso occorreva passare per il
centralino (v. testi Musso, Nani, Bilucaglia).
E’ poi emerso che la tecnologia ETACS
(che, come si dirà più
oltre con riferimento alla c.t.u. svolta nel presente grado,
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emetteva radiofrequenze molto più potenti di quelle utilizzate
attualmente dai telefoni cellulari) è durata circa 7 anni (teste
Musso, v. anche teste Nani, che ha dichiarato che a partire dal
2000 prevaleva la tecnologia GSM; nello stesso senso, v. teste
Bilucaglia).
Queste circostanze hanno reso l’esposizione, già di per sé
prolungata, particolarmente intensa.
Il figlio dell’appellato, sentito come teste, ha
poi confermato che
il padre è destrimane.
Con il terzo motivo di gravame,
l’INAIL deduce l’erroneità della
conclusione del Tribunale in ordine all’esistenza
del
nesso
eziologico tra la patologia e l’esposizione lavorativa a
radiofrequenze.
In particolare:
-osserva in primo luogo che il neurinoma del nervo acustico non
è una malattia tabellata,
sicché l’onere di provare la natura
professionale della patologia incombe sul ricorrente;
-critica la c.t.u. disposta dal Tribunale, evidenziando gli errori
materiali ivi contenuti e sostenendo che essa perviene a
conclusioni errate, poiché non suffragate da una legge scientifica
generale di copertura o quantomeno da una legge scientifica che
abbia un preponderante consenso;
-deduce che la c.t.u., le cui conclusioni sono state recepite dal
Tribunale, si è basata sulla classificazione IARC del 2013, senza
dare adeguatamente conto di studi successivi, e non ha
correttamente valutato il significato della classificazione delle
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radiofrequenze in relazione all’evidenza cancerogena, ossia
come categoria 2B (“possibilmente cancerogeno per l’uomo”), e
quindi
la più debole tra quelle utilizzate dall’Agenzia per
classificare
agenti
che
presentino
evidenze
positive
di
cancerogenicità (a fronte della categoria 2A, “probabilmente
cancerogeno per l’uomo” e della categoria 1, “cancerogeno per
l’uomo”);
-sostiene che lo studio Interphone deve ritenersi attendibile, in
quanto studio caso-controllo indipendente, pur a fronte di un
solo parziale finanziamento da parte di industrie di telefoni
cellulari e operatori di telefonia mobile, come pure devono
ritenersi attendibili gli studi di Hardell; detti studi e gli ulteriori,
pur con i limiti evidenziati dalla relazione del dott. Grandi
(ricercatore del Dipartimento di Medicina, Epidemiologia, Igiene
del Lavoro e Ambientale INAIL), prodotta nel presente grado,
non supportano
l’associazione tra utilizzo del telefono cellulare e
l’insorgenza del tumore;
-deduce che, diversamente da quanto sostenuto dal c.t.u. (e
condiviso dal Tribunale), non sono conosciuti i meccanismi di
azione delle radiofrequenze;
-sostiene che non è provato
che l’appellato (soggetto destrimane)
usasse il telefono cellulare appoggiandolo sempre all’orecchio
destro;
-deduce inoltre che non è corretto, come ha fatto il Tribunale,
inferire dalla coesistenza di due fenomeni rari (nel caso di
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specie, tumore raro ed esposizione rara a radiofrequenze) un
nesso di causa-effetto tra di essi;
-sostiene infine che erroneamente è stato ritenuto un periodo di
latenza del tumore (secondo la dottrina scientifica, almeno 10
anni) compatibile con l’esposizione a radiofrequenze
sin dal
1995, considerato che il tumore (a lentissima crescita), si è
manifestato già nel dicembre 2009, e, pertanto, non risulta
applicabile il rischio individuale pari a 1,44, riportato invece dal
c.t.u..
Alla luce della c.t.u. disposta nel presente grado anche questo
motivo di gravame è infondato.
I Consulenti d’Ufficio si sono correttamente attenuti al quesito
formulato dalla Corte con ordinanza del 16.1.2019, in cui era
richiesto di svolgere gli accertamenti peritali basandosi su
un’esposizione pari a 4 ore al
giorno (come dimostrata
dall’istruttoria testimoniale
di cui si è già detto), seppure per
mero errore, nel verbale di conferimento incarico del 19.3.2019,
si sia fatto riferimento al quesito formulato nel primo grado, che
non precisava la durata dell’esposizione.
Pertanto, in conformità
ai tempi di esposizione indicati nel quesito conferito, è stato
stimato un tempo di utilizzo lavorativo del telefono cellulare pari
a 840 ore/anno (4 ore x 210 giorni lavorativi), con un tempo
stimato complessivo di utilizzo
nell’intervallo di 15 anni
intercorso tra il 1995 ed il 2010 pari a 12.600 ore (840 ore/anno
x 15 anni) (v. pag. 51 c.t.u.).
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I
periti
hanno
inoltre
considerato
che,
come
emerso
dall’istruttoria, i telefoni cellulari utilizzati dall’appellato sino
alla fine del 1999 erano analogici (utilizzavano la tecnologia
ETACS) e quindi, dal 2000, erano digitali (utilizzavano la
tecnologia GSM),
evidenziando che “I
telefoni analogici e quelli
digitali basati su tecnologia GSM 2G erano caratterizzati da
emissioni di radiofrequenze (RF) molto superiori rispetto a
quelli digitali attuali 3G e 4G, con livelli di intensità di
emissioni di RF di quasi due ordini di grandezza superiori
(IARC, 2013), ovvero quasi 100 volte superiori”
(v. pagg. 51-52
c.t.u., affermazione tratta dalla Monografia IARC (2013) sulle
radiofrequenze, come precisato dai Consulenti d’Ufficio a pag.
121 della relazione).
Premesso che il neurinoma acustico (o schwannoma vestibolare,
indicato per brevità
nella c.t.u. come “NA”),
tumore cerebrale
benigno, raro e a crescita lenta, è caratterizzato da un periodo di
latenza dall’inizio dell’esposizione ad un fattore di rischio fino al
momento della diagnosi di malattia pari a non meno di 10-15
anni (v. pag. 54 e segg.), i Consulenti d’Ufficio hanno citato i
numerosi studi sulla materia, dando atto che la maggior parte di
essi sono studi caso-controllo che sono stati condotti dal gruppo
di lavoro Interphone
e dal gruppo di ricerca dell’Università di
Orebro, Svezia, guidato dal prof. Hardell, evidenziandone le
caratteristiche e le metodologie, nonché i limiti e le critiche
svolte su di essi dalla letteratura scientifica (v. pag. 58 e segg.).
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Dopo lo studio Interphone pubblicato nel 2010 sulla relazione tra
esposizione a TC (telefono cellulare) e gliomi e meningiomi (tra
cui non era quindi incluso il NA),
“Nel
2011 il gruppo di studio
INTERPHONE pubblicava, in un altro articolo, i risultati dello
studio internazionale caso-controllo su uso di telefoni cellulari e
rischio di sviluppare neurinomi dell’acustico, che comprendeva
più di 1.000 casi e oltre 2.000 controlli arruolati tra il 2000 e il
2004 (INTERPHONE,
2011).
Questo studio non ha riscontrato differenze nell’esposizione
pregressa a TC in casi e controlli per “utilizzo regolare”
definito sulla base di almeno una chiamata alla settimana.
Al contrario, ha osservato un
eccesso di rischio statisticamente
significativo di sviluppare NA
(di quasi 3 volte nei soggetti
esposti, rispetto ai non esposti),
nei soggetti
classificati nella
classe più alta di esposizione, corrispondente ad un
utilizzo
complessivo di TC superiore a 1.640 ore
(traducibili in durate
medie di esposizione di 1 ora al giorno per 4 anni, o di 2 ore al
giorno per 2 anni, o di mezz’ora al giorno per 8 anni)”,
evidenziando inoltre che i risultati dello studio mostravano nella
classe con più alta esposizione cumulativa (utilizzo complessivo
di telefono cellulare maggiore o uguale a 1640 ore)
un’associazione statisticamente significativa del NA solo
con
l’uso ipsilaterale di telefono cellulare
(OR, o
Odds Ratio
= 3.74),
sicchè
“Dal
momento che, come anche osservato da Cardis
(Cardis,
2008),
le
emesse
radiofrequenze
dai
telefoni
(RF)/emissioni
portatili
vengono
elettromagnetiche
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assorbite soprattutto dal lato del capo al quale viene accostato
l’apparecchio
telefonico
durante
l’utilizzo
(c.d.
utilizzo
ipsilaterale)
e che con l’aumentare della distanza del telefono
dal capo la dose di radiazioni elettromagnetiche assorbita dai
tessuti diminuisce bruscamente,
il riscontro di un’associazione
statisticamente significativa del NA solo con
l’uso ipsilaterale di
TC supporta l’ipotesi che le RF emesse dai TC svolgano un
ruolo causale nell’induzione/sviluppo di NA”.
Con riferimento ad una delle osservazioni dell’appellante sopra
riportate, rileva la Corte che, non contestato e confermato dalla
testimonianza del
figlio dell’appellato che quest’ultimo
è
destrimane, il fatto che si tenda ad usare il telefono,
esclusivamente o quasi, appoggiandolo all’orecchio del lato del
corpo “dominante”, rientra nel
fatto notorio essendo usualmente
riscontrabile
nell’esperienza comune.
I Consulenti d’Ufficio hanno poi citato la classificazione dello
IARC (Agenzia Internazionale per la Ricerca sul Cancro) del
2011, secondo cui le radiofrequenze sono
“possibilmente
cancerogene
monografia
per
del
l’uomo”,
2013
valutazione
radiazioni
confermata
non
nella
sulle
ionizzanti,
evidenziando
che nell’aprile 2019
un Advisory Group della
IARC, composto da 29 ricercatori provenienti da 19 paesi, ha
inserito le radiofrequenze tra gli agenti per cui è ritenuta
prioritaria una rivalutazione di cancerogenicità da parte della
IARC nel periodo 2020-2024 (IARC Monographs Priorities
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Group, 2019). Hanno quindi menzionato gli studi successivi (v.
pagg. 68-69).
Nella tabella redatta dai Consulenti d’Ufficio alle pagg. 70 e 71
della perizia sono riportate le caratteristiche e i risultati degli
studi epidemiologici pubblicati sull’associazione
tra utilizzo di
TC e NA, relativi al rischio di NA stimato per i soggetti con la
più alta esposizione cumulativa in ciascuno studio, in termini di
durata dell’esposizione,
di durata cumulativa del tempo di
esposizione o della durata dell’abbonamento telefonico, divisi
anche
per
utilizzo
ipsilaterale
e
controlaterale
rispetto
all’insorgenza del tumore.
Come rilevato dai Consulenti d’Ufficio,
dall’esame della tabella
emerge che la maggioranza degli studi mostra eccessi di rischio
associati ad elevata durata di utilizzo o esposizione cumulativa a
TC, che in vari studi sono statisticamente significativi, con più
alti rischi associati all’utilizzo ipsilaterale di TC.
Nella perizia è evidenziato
“il
fatto che negli studi in cui il
rischio di NA è stimato sulla base del numero di ore cumulative
di utilizzo, la categoria con la più alta esposizione cumulativa
stimata (che trova il monte ore più alto di 1640 ore nello studio
INTERPHONE 2011) ha un limite che è almeno circa 8 volte più
basso del numero di ore (12.600 ore circa) di utilizzo di TC
stimato nel caso del Sig. Romeo”
(v. pag. 69 c.t.u.).
I Consulenti d’Ufficio hanno poi esaminato le evidenze da studi
sperimentali
su
animali, pubblicati successivamente alla
monografia IARC del 2013,
di cui uno condotto dall’Istituto
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Ramazzini e l’altro dal National Toxicology
Program (NTP)
statunitense: il primo ha osservato un incremento statisticamente
significativo di Schwannoma delle cellule cardiache di Schwann
a carico dei ratti maschi, anche se stimato su un numero limitato
di casi (3 casi nel gruppo a più alta esposizione vs. 0 casi nel
gruppo non esposto), ed un incremento non statisticamente
significativo di iperplasia delle cellule cardiache di Schwann,
che costituisce una lesione pre-tumorale, in entrambi i sessi
(Falcioni et al., 2018); e anche il secondo ha mostrato, per i ratti
maschi, un incrementato numero di casi di Schwannoma
cardiaco, rispetto ai ratti maschi non esposti, che era
statisticamente significativo sia per esposizione a radiofrequenze
CDMA (3 casi nel gruppo con esposizione intermedia, 6 casi nel
gruppo con la più alta esposizione e 0 casi tra i non esposti) che
per esposizione a quelle da GSM (5 casi nel gruppo più esposto e
0 casi tra i non esposti) (NTP, 2018).
I Consulenti d’Ufficio hanno precisato
che “gli
Schwannomi
cardiaci sono dello stesso tipo istologico dei neurinomi del
nervo acustico (che, infatti, sono denominati anche Schwannomi
vestibolari), cosa che supporta una relazione causale tra
esposizione a radiofrequenze e incidenza di NA”
(v. c.t.u. pag.
76).
In base a tutti questi elementi, i Consulenti d’Ufficio hanno
concluso che
“Nel
caso concreto specifico in esame, il rischio
derivante dall’utilizzo professionale di telefono cellulare risulta
decisamente aggravato in relazione principalmente al lungo
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periodo di esposizione (15 anni) ed all’elevata intensità
dell’esposizione stessa, quest’ultima dovuta sia alla tipologia di
apparecchi telefonici cellulari utilizzati (ETACS e quindi GSM
2G, con livelli di emissione quasi 100 volte superiori rispetto ai
più moderni telefoni cellulari), che all’elevato numero di ore di
utilizzo dell’apparecchio telefonico stesso (con un’esposizione
media
di
840
ore/anno,
con
conseguente
esposizione
complessiva in 15 anni
stimata nell’ordine di 12.600 ore).
Pertanto, anche alla luce delle risultanze dei più recenti studi
sugli animali condotti da NTP e dall’Istituto Ramazzini (che
mostrano eccessi di tumori dello stesso tipo istologico del NA,
anche se in altra sede) e
dalle recenti indicazioni dell’Advisory
Group
della
IARC
sulla
necessità
di
una
prioritaria
rivalutazione da parte della IARC della cancerogenicità delle
radiofrequenze,
considerando
le
risultanze
degli
studi
epidemiologici disponibili che, per quanto non del tutto
concordanti, mostrano comunque frequentemente un eccesso di
casi di NA in presenza di prolungata esposizione o di esposizioni
intense,
è dato ritenere che, nello specifico caso in esame, con
criterio di elevata probabilità logica, si possa ammettere un
nesso eziologico tra la prolungata e cospicua esposizione
lavorativa a radiofrequenze emesse da telefono cellulare e la
malattia denunciata dal periziato all’INAIL (neurinoma
dell’ottavo nervo cranico destro)”
(v. conclusioni preliminari a
pagg. 77-78, ribadite a pagg. 123-124 nelle conclusioni e
risposte ai quesiti).
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Le conclusioni sono fondate su un accurato ed aggiornatissimo
esame delle fonti della letteratura scientifica, applicata alle
peculiarità
del
caso
concreto
(per
quantità
e
durata
dell’esposizione),
in assenza di fattori alternativi di rischio,
secondo standard di certezza probabilistica (“più probabile che
non”).
Rispetto alle conclusioni del Consulenti d’Ufficio, i Consulenti
INAIL hanno svolto articolate osservazioni (riportate a pagg. 79-
84 della relazione), mentre i difensori dell’appellato hanno
sottolineato la posizione di conflitto di interesse di alcuni autori
di
studi
che
hanno
negato
la
cancerogenicità
delle
radiofrequenze (v. pagg. 84-97 c.t.u.),
in particolare nell’ambito
della
letteratura citata dall’INAIL (v. pagg. 94-95).
Ritiene la Corte che i Consulenti d’Ufficio abbiano fornito
esaustive risposte in merito alle osservazioni dei Consulenti di
parte appellante.
In particolare:
1)
i dati relativi all’esposizione su cui si sono basati i
Consulenti
d’Ufficio non sono, come sostenuto dai Consulenti INAIL, tratti
“sostanzialmente
dalle informazioni anamnestiche riferite
dall’assicurato”,
bensì, come già osservato, oggetto del quesito
formulato
dal
Collegio
avuto riguardo alle circostanze
comprovate all’istruttoria
testimoniale già sopra descritta;
2)
con riferimento alle critiche sull’attendibilità degli studi
secondo cui sussiste un nesso eziologico tra esposizione a
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radiofrequenze e il neurinoma dell’acustico, i
Consulenti
d’Ufficio hanno svolto le seguenti articolate repliche:
a)
quanto alle possibili distorsioni (“bias”),
i Consulenti
d’Ufficio hanno illustrato le differenze tra gli studi caso-
controllo e gli studi di coorte, precisando che nella materia in
esame la letteratura è quasi interamente costituita da studi caso-
controllo. In questo tipo di studio (a differenza degli studi di
coorte,
da cui si ricava il rapporto tra l’incidenza della malattia
nella popolazione esposta al fattore di rischio e l’incidenza della
stessa malattia nella popolazione non esposta), il rischio relativo
(RR) è approssimato da un altro indicatore di rischio, ovvero
l’Odds Ratio (OR), che viene calcolato sulla base del rapporto
tra la frequenza di esposizione al fattore di rischio tra i casi
(malati) rispetto alla frequenza di esposizione al fattore di rischio
tra i controlli (non malati).
Ciò rende possibili misclassificazioni non differenziali (che
interessano sia i casi che i controlli nella stessa misura), le quali,
come evidenziato dai Consulenti d’Ufficio, determinano sempre
una sottostima del rischio rispetto al rischio reale, e
misclassificazioni
differenziali
dell’esposizione
(errori
di
classificazione che interessano in diversa entità i casi rispetto ai
controlli), le quali possono condurre sia ad una sovrastima che
ad una sottostima del reale rischio di malattia dovuto
all’esposizione,
e la più seria minaccia alla validità dei risultati è
costituita da una forma di misclassificazione differenziale
dell’esposizione denominata “recall
bias”,
dovuta alla possibilità
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che i soggetti che risultano affetti da malattia tumorale ricerchino
nella propria memoria dei dati relativi alla propria pregressa
esposizione a possibili fattori di rischio per la salute che possano
avere determinato tale malattia.
Tuttavia i risultati degli studi disponibili (lo studio di Vrijheid et
al., 2009, lo studio di Aydin et al., 2011, e lo studio di Petterson
et al., 2015) indicano che è improbabile che gli studi su
esposizione a TC e rischio di NA siano stati affetti da una
misclassificazione differenziale dell’esposizione a RF da
TC,
tale da determinare una sovrastima dell’esposizione tra i casi
rispetto ai controlli e, pertanto, una conseguente sovrastima del
rischio di NA associato
all’esposizione a RF da TC; al
contrario,
sia i risultati di detti studi, che quelli di altri studi che hanno
valutato, in soggetti sani, la validità dell’esposizione a TC
“autoriferita” (ovvero riferita dagli stessi soggetti inclusi nello
studio e rilevata per mezzo di questionario o intervista ad essi
somministrati),
misclassificazione
indicano
non
la
presenza
di
una
forte
differenziale
dell’esposizione
(Samkange-Zeeb et al., 2004; Toledano et al., 2014; Vanden
Abeele et al., 2013), con conseguente sottostima della forza
dell’associazione tra esposizione a TC e rischio di
NA, rispetto
al rischio reale, sicché le stime di rischio (O.R.) ottenute nei
diversi studi sarebbero fortemente sottostimate e il rischio reale
di sviluppare NA sarebbe molto più alto di quello osservato negli
studi stessi (v. pagg 99-103 c.t.u.);
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b) anche quanto alla ipsilateralità
dell’utilizzo del telefono
cellulare rispetto al lato di comparsa del tumore gli studi
disponibili (Shimizu e Yamaguchi, 2012) evidenziano la
possibilità di una forte misclassificazione non differenziale, con
conseguente sottostima (v. pag. 103 c.t.u.);
c) a differenza di quanto sostenuto dai Consulenti di parte
INAIL, un effetto dose-risposta, cioè un significativo aumento
del rischio di sviluppare la malattia tumorale (NA) all’aumentare
della dose cumulativa di esposizione a RF da TC, è presente nei
risultati della pooled analysis di Hardell et al. (2013), come da
tabella riportata a pag. 104 della relazione, che mostra un rischio
di NA associato all’uso di telefoni wireless progressivamente
crescente all’aumentare della dose cumulativa di esposizione a
TC (calcolata in base alle ore di utilizzo di TC): v. pagg. 103-
105 c.t.u.;
d) un possibile motivo della mancanza di un effetto dose-risposta
nello studio Interphone (2011) e in altri studi è che le categorie
di esposizione cumulativa utilizzate fossero troppo basse: per
esempio, nello studio Interphone il limite inferiore per la
categoria di esposizione cumulativa più alta era posto a sole
1.640 ore di utilizzo di TC, corrispondenti a meno di
mezz’ora al
giorno per 10 anni. Come osservato nella relazione peritale, una
dose di esposizione al di sotto di questo limite potrebbe essere
non sufficiente a determinare lo sviluppo di NA (v. pag. 105
c.t.u.).
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Si tratta peraltro di una dose di esposizione, come emerge dalla
perizia, assolutamente non confrontabile con la massiccia e
prolungata esposizione a radiofrequenze
subita dall’appellato per
ben 15 anni;
e)
l’affermazione
dei Consulenti INAIL secondo cui soggetti
audiolesi protesizzati, che possiedono sussidi uditivi che
utilizzano quotidianamente per l’intera giornata con
annessa
funzione bluetooth, non hanno mai fatto riscontrare casi di
neurinomi dell’acustico,
non è supportata da alcun riferimento
bibliografico (v. pag. 107 c.t.u.);
f) diversamente da quanto sostenuto dai Consulenti INAIL, il
trend della patologia per cui è causa
(schwannoma dell’VIII
nervo cranico) mostra un aumento, in coincidenza con la
diffusione della telefonia cellulare, di detta malattia nel corso
degli ultimi decenni. I Consulenti d’Ufficio hanno indicato, nelle
pagg. 55-57 della relazione, i diversi studi sulla questione,
rilevando che, secondo alcuni di essi, l’aumento di incidenza
della malattia sarebbe attribuibile al miglioramento delle
tecniche strumentali - basata sulla diffusione di nuove
tecnologie, ad esempio TAC e RMN - utilizzate per pervenire
alla diagnosi di tale tumore; ma osservando tuttavia che studi
basati sui dati più recenti mostrano un ulteriore incremento di
incidenza di NA, anche riferito a periodi in cui la diffusione dei
migliori strumenti di diagnostica di questi tumori era già
avvenuto (Kleijwegt et al., 2016: aumento nella regione di
Leyden dell’incidenza di NA di oltre 3 volte in un arco
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temporale di 11 anni intercorrente tra il 2001 al 2012; Marinelli
et al., 2018: aumento dell’incidenza di NA in Minnesota, USA,
di oltre 2 volte in un arco temporale di 11 anni intercorrente tra il
1995 al 2016; sempre negli USA, il Central Brain Tumor
Registry, CBTRUS, ha pubblicato report annuali dal 2007 al
2016 con dati registrati dal 2004 al 2013 che evidenziano un
raddoppio dell’incidenza annuale
di NA: da 0,88 a 1,73 x
100.000); a pag. 108 della relazione hanno richiamato i dati del
registro
tumori
danese
che
evidenziano
un
incremento
nell’incidenza di tumori cerebrali, con un aumento del 40% tra
gli uomini e del 29% tra le donne tra il 2001 e il 2010
(Sundhedsstyrelsen, 2010).
E’ quindi condivisibile la conclusione dei
Consulenti d’Ufficio
secondo cui è
improbabile che l’incremento di incidenza di NA
sia
attribuibile
unicamente
alla
possibilità,
derivante
dell’affinamento delle metodiche diagnostiche
di tale tumore o
anche da una maggiore accessibilità della popolazione alle
strutture sanitarie, di ottenere più diagnosi di NA.
3)
Con riferimento agli studi di NTP e dell’Istituto Ramazzini,
alle osservazioni critiche dei Consulenti INAIL sulla loro
validità scientifica, anche mediante richiamo al recentissimo
articolo
pubblicato dall’International Commission on Non
Ionizing Radiation Protection (ICNIRP) su Health Physics, i
Consulenti d’Ufficio (v. pagg. 108-113 della relazione) hanno
esaustivamente replicato che:
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- si tratta dei più grandi studi sperimentali su animali condotti
finora e sono caratterizzati da elevata standardizzazione dei
protocolli di ricerca e da alta qualità dei metodi utilizzati;
- lo scopo principale degli studi sperimentali sui tumori condotti
sugli animali è quello di valutare se l’esposizione ad un sospetto
agente cancerogeno provochi o meno eccessi di tumori nei
gruppi di animali esposti. Pertanto il fatto che, per gli animali
oggetto di studio, possano essere previsti tempi e modalità di
esposizione differenti rispetto a quelli degli esseri umani (per i
roditori, a differenza che per l’uomo, “total
body”
e per l’intera
vita), non rende i risultati degli studi meno validi.
Inoltre, con riferimento
all’osservazione della difesa dell’INAIL,
nel corso della discussione orale,
circa l’inattendibilità di questi
studi in quanto non effettuati sull’uomo,
la Corte ritiene
esaustiva e condivisibile la replica dei Consulenti d’Ufficio
(anche mediante richiamo a fonti di letteratura scientifica sullo
studio del NTP) secondo cui il criterio razionale per condurre
studi di cancerogenicità in modelli animali
“si
basa su dati
sperimentali che mostrano che ogni agente noto come
cancerogeno nell’uomo, quando adeguatamente testato, ha
mostrato di essere cancerogeno negli animali (IARC, 2006) e
che quasi un terzo dei cancerogeni umani sono stati identificati
dopo che effetti cancerogeni sono stati trovati in studi ben
condotti sugli animali (Huff, 1993). Non c’è ragione di credere
che un agente fisico come le radiofrequenze possa danneggiare i
tessuti animali, ma non i tessuti umani”
(Melnick, 2019, citato
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alle pagg. 76-77 e 109 della relazione). Le sperimentazioni sulla
cancerogenicità di agenti o sostanze vengono usualmente
eseguite su animali, quali i roditori, che presentano elementi di
similitudine con gli uomini, sicché non si può negare
pregiudizialmente valore scientifico ai risultati di detti studi;
-
il fatto che l’eccesso di tumore sia stato riscontrato soltanto nei
ratti (e quasi esclusivamente di sesso maschile) non inficia la
validità dello studio, considerato che lo schwannoma cardiaco
insorge in diverse varietà di ceppi di ratti (e con maggior
frequenza nei maschi), ma non è mai stato osservato nei topi;
-
nonostante, nello studio dell’Istituto Ramazzini, l’esposizione
dei ratti sia avvenuta alla dose massima testata, il tasso di
assorbimento specifico conseguente all’esposizione era di poco
superiore al limite massimo per irradiazione al corpo intero per
l’uomo;
mentre, quanto allo studio del NTP, pur essendo la dose
di esposizione molto superiore al limite massimo di esposizione
ammissibile per irradiazione al corpo intero per l’uomo, la dose
assorbita a livello locale è solo una piccola parte della dose
somministrata a tutto il corpo, e, in particolare, per il cervello, la
dose assorbita è stata stimata in circa il 10% della dose totale
somministrata a tutto il corpo;
- il numero di casi di tumore riscontrato negli animali è
statisticamente significativo: nello studio di NTP, 6 casi nel
gruppo a più alta esposizione a RF da CDMA e 5 casi in quello
con più alta esposizione a RF da GSM, mentre nessun caso si è
verificato nel gruppo non esposto; nello
studio dell’Istituto
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Ramazzini, 3 casi osservati nel gruppo a più alta esposizione e
nessuno nel gruppo non esposto;
- in merito alla diversa localizzazione degli schwannomi
riscontrati nei ratti esposti negli studi dell’NTP e dell’Istituto
Ramazzini (localizzazione a livello cardiaco invece che a livello
cerebrale), appare probabile che la modalità di irradiazione degli
animali abbia influito nel determinare questo risultato, in quanto
la somministrazione di RF è stata indirizzata a tutto il corpo e
non concentrata solo sulla testa degli animali da esperimento,
come invece avviene per l’esposizione a RF negli utilizzatori
di
TC;
- gli schwannomi cardiaci sono dello stesso tipo istologico dei
neurinomi del nervo acustico (che, infatti, sono denominati
anche schwannomi vestibolari), cosa che supporta una relazione
causale tra esposizione a radiofrequenze e incidenza di NA.
Pertanto, il fatto che i NA siano tumori benigni, al contrario
degli schwannomi cardiaci maligni osservati nei ratti negli studi
del NTP e dell’Istituto Ramazzini, appare irrilevante, considerato
che questi studi dimostrano che l’esposizione a RF può
determinare una trasformazione neoplastica delle cellule di
Schwann, processo che sia i tumori benigni che i tumori maligni
hanno in comune;
- lo studio del NTP ha concluso affermando che i risultati
dimostrano una chiara evidenza di attività cancerogena delle RF
(NTP, 2018);
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-
l’effettuazione di confronti multipli nelle analisi condotte nei
due studi del NTP e dell’Istituto Ramazzini ha
sicuramente
aumentato il rischio che si verificassero associazioni spurie in
questi due studi, ma la probabilità che tre analisi indipendenti
abbiano trovato solo per caso un incremento significativo di
sviluppare tumori dello stesso tipo istologico e nella stessa sede
anatomica è bassissima, anche considerando i molti confronti
effettuati in analisi, ciò che supporta in maniera inequivocabile
l’effetto cancerogeno delle RF;
- la presenza di un effetto cancerogeno è supportata anche
dall’osservazione di un significativo aumento del danno al DNA,
valutato per mezzo della presenza di rotture del DNA con la
metodica Comet assay, in vari organi, tra cui soprattutto il
cervello, sia in ratti che in topi (Wyde, 2016);
- diversamente da quanto sostenuto dai Consulenti INAIL, le
analisi sono state condotte
“in
cieco” (v. articolo di Melnick del
2019, in risposta alle critiche
dell’INCIRP riguardo
allo studio
del NTP);
4) In merito alla
motivazione per la quale l’Advisory Group della
IARC ha inserito le radiofrequenze tra gli agenti per cui è
ritenuta prioritaria una rivalutazione di cancerogenicità da parte
della IARC nel periodo 2020-2024 (secondo i Consulenti INAIL
non per motivi di particolare allarme, ma in quanto rivalutazione
rientrante nelle normali procedure di aggiornamento periodico
delle
valutazioni
di
evidenza
cancerogena
promosse
dall’Agenzia),
nella relazione peritale è trascritta la tabella
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riportata nell’articolo,
dalla quale si ricava che le radiazioni non
ionizzanti (radiofrequenze) sono tra gli agenti per i quali è
raccomandata una rivalutazione urgente (“high
priority”)
della
cancerogenicità per l’uomo,
indicazione, specificata nella tabella
stessa, motivata dal fatto che le nuove evidenze derivanti da test
biologici e meccanicistici
“richiedono
una rivalutazione della
classificazione”.
Nell’articolo dell’Advisory Group è inoltre
specificato che la priorità per la rivalutazione è stata assegnata
sulla base di evidenze sull’esposizione umana e in base al grado
di evidenza disponibile per valutare la cancerogenicità (v. pagg.
113-115 c.t.u.);
5) Quanto alle osservazioni dei Consulenti INAIL circa
l’incompatibilità dell’evoluzione della patologia dell’appellato
(essendo il tumore, già nel 2010, di dimensioni pari a 2,6 cm, a
fronte di un ritmo di crescita di circa 1,5 mm all’anno) e i periodi
di latenza della stessa (oltre 15-20 anni, non meno di 10-15
anni), i Consulenti d’Ufficio hanno osservato che, secondo
l’autore citato dai
Consulenti INAIL (Dott. P. Ferroli, Istituto
Besta di Milano), il ritmo di crescita del tumore, di circa 1,5 mm
all’anno,
si riferisce a circa
il 75% dei neurinomi dell’acustico,
mentre un quarto di essi ha tendenza a crescere più rapidamente
e in maniera più aggressiva (v. pag. 116 c.t.u.). Inoltre, i
Consulenti d’Ufficio, alle pagg. 116-117 della relazione, hanno
citato ampia letteratura scientifica da cui risultano tassi di
crescita del neurinoma dell’acustico piuttosto variabili.
In
particolare, in caso di NA caratterizzati da fenomeni cistici ed
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2259378_1520.png
emorragici (come quello dell’appellato), sono stati osservati tassi
di crescita di oltre 4 mm/anno (Paldor et al., 2016), e nella
revisione di Paldor vengono citati anche alcuni case reports nei
quali sono stati descritti casi di NA con tassi di crescita fino a 25
mm/anno (Fayad et al, 2014).
Appare dunque condivisibile la conclusione sul punto dei
Consulenti d’Ufficio
secondo cui “I
tassi di crescita del NA
osservati nella letteratura scientifica, la presenza nel caso in
esame di fenomeni cistico-necrotici (anche citati dai CTP
INAIL) e il lungo periodo intercorso tra la prima esposizione e
la diagnosi di NA (15 anni), rappresentano elementi certamente
non idonei a giustificare una esclusione del nesso causale tra
esposizione a RF da TC e insorgenza di NA, così come sostenuto
dai CTP INAIL.
Al contrario, tali dati rappresentano elementi assolutamente
compatibili con la sussistenza, nel caso in esame, del riscontro
di un NA delle dimensioni di 2.6 cm al momento della diagnosi,
in soggetto esposto da 15 anni a RF da TC”
(v. pag. 117).
6)
Pertanto, considerato il periodo di esposizione dell’appellato
alle radiofrequenze (dal 1995 al 2010, anno in cui gli è stato
diagnosticato
il
NA),
il
tempo
intercorso
tra
l’inizio
dell’esposizione e la comparsa del tumore
(pari a15 anni, e non a
4 anni come sostenuto dai Consulenti INAIL) è assolutamente
compatibile con l’induzione e lo sviluppo del NA sulla base dei
dati di letteratura, anche considerando 5 anni per l’iniziazione
del tumore e 10 anni per il suo sviluppo.
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Inoltre,
diversamente
da
quanto
sostenuto
dalla
difesa
dell’appellante nel corso della discussione orale, non vi è
contraddizione tra quanto argomentato dai Consulenti d’Ufficio
alle pagg. 115-118 in merito alla latenza della malattia, al suo
sviluppo e alle dimensioni del tumore al momento della diagnosi
nel 2010 (2,6 cm), e quanto scritto alle pagg. 57-58 della
relazione sul periodo di latenza riconosciuto nella letteratura
scientifica (almeno 10-15 anni), avendo i Consulenti d’Ufficio
motivato sulla compatibilità tra il periodo di latenza della
malattia e le dimensioni del tumore, menzionando (a differenza
dei
Consulenti
INAIL)
copiosa
letteratura
scientifica
sull’estrema variabilità della crescita media del tumore, che
ha
registrato anche casi di valori massimi pari a 17 mm/anno e
addirittura fino a 25 mm/anno (v. pagg. 116-117 c.t.u.).
7)
Non vi è contraddizione tra l’affermazione dei
Consulenti
d’Ufficio (v. nota 25 a pag. 70 della relazione) secondo cui
«Appare
quindi improbabile che si possano vedere gli eventuali
effetti dell’uso di TC sull’incidenza dei NA, almeno sui dati fino
al 2010, data la diffusione relativamente recente dei TC e il
lungo periodo di induzione di questi tumori»
e l’affermazione
dell’esistenza del nesso eziologico
nel caso di specie, poiché la
frase di cui sopra è evidentemente riferita al fatto che appare
improbabile che negli studi epidemiologici si potessero vedere
eventuali effetti dell’uso di
telefono cellulare, in quanto nelle
popolazioni esaminate da tali studi
l’inizio dell’esposizione, per
la gran parte dei soggetti, era troppo recente, mentre, nel caso
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concreto in esame,
l’esposizione dell’appellato
ha avuto inizio
nel 1995, ovvero 15 anni prima della diagnosi del tumore (NA)
ed in un periodo storico in cui i TC erano ancora poco diffusi
nella maggior parte dei paesi europei (v. pagg. 118-119 c.t.u.).
I Consulenti d’Ufficio hanno pertanto ravvisato il nesso causale
tenendo correttamente in considerazione la concreta esposizione
dell’appellato alle radiofrequenze, che,
per le sue peculiarità
(durata ed intensità
conseguente all’uso abnorme del telefono
cellulare), presenta caratteristiche del tutto diverse da quelle
medie riscontrate in generale dalla popolazione nel periodo per
cui è causa;
8) con riferimento alle conclusioni dei Consulenti INAIL, che, al
fine di escludere il nesso causale, richiamano il documento
dell’ISS, rapporto ISTISAN 19/11,
i Consulenti d’Ufficio hanno
esaustivamente replicato che:
“il
rapporto ISTISAN su RF e
tumori è stato criticato dall’associazione Medici per l’Ambiente
(ISDE, acronimo di International Society of Doctors for
Environment) per varie ragioni (Di Ciaula, 2019), tra cui: la
selezione degli studi inclusi nelle meta-analisi presentate;
l’interpretazione delle associazioni osservate tra RF e tumori
intracranici; l’uso inappropriato dei dati sull’andamento
dell’incidenza dei tumori cerebrali per confutare l’associazione
tra RF e tumori cerebrali; il non aver tenuto conto nella loro
valutazione dei risultati di recenti studi sperimentali su animali,
…,
che hanno mostrato effetti cancerogeni su ratti (NTP, 2018;
Falcioni et al., 2018) e, soprattutto, per non avere fatto
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conseguire alla dichiarata incertezza sugli effetti associati ad un
uso intenso e prolungato di TC raccomandazioni più stringenti
sui limiti di esposizione a RF, in particolare per i bambini e gli
adolescenti, che potrebbero essere maggiormente suscettibili a
tali effetti (Di Ciaula, 2019)”
(v. pag. 119 c.t.u.).
I Consulenti d’Ufficio hanno poi menzionato il rapporto della
ANSES (Agenzia Nazionale Francese per la Sicurezza Sanitaria
per Alimentazione Ambiente e Lavoro) sugli effetti delle onde
emesse dai telefoni mobili sulla salute, che conclude segnalando
che gli studi scientifici pubblicati sino ad oggi non permettono di
escludere la comparsa di
effetti biologici per l’uomo oltre certe
soglie di esposizione a RF da TC, evidenziando inoltre che il
76% dei telefoni cellulari esaminati emette radiofrequenze
superiori al limite massimo raccomandato dall’ICNIRP per
esposizione di testa e tronco (v. pagg. 119-121 c.t.u.).
I Consulenti d’Ufficio, a parere della Corte, hanno replicato
punto per punto alle osservazioni dei Consulenti INAIL,
menzionando copiosa letteratura scientifica a supporto delle
proprie argomentazioni, e fornendo, in conclusione, solidi
elementi per affermare
un ruolo causale tra l’esposizione
dell’appellato alle radiofrequenze
da telefono cellulare e la
patologia per cui è causa.
I dati epidemiologici, i risultati delle sperimentazioni sugli
animali (non contraddetti, allo stato, da altre sperimentazioni
dello stesso tipo),
la durata e l’intensità dell’esposizione
(assolutamente peculiari per la loro abnormità) che assumono
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particolare rilievo considerata
l’accertata –
a livello scientifico
–
relazione dose-risposta tra esposizione a radiofrequenze da
telefono cellulare e rischio di neurinoma dell’acustico,
unitamente alla mancanza di un altro fattore che possa avere
cagionato la patologia, complessivamente valutati, consentono di
ritenere che, caso specifico, sussista una legge scientifica di
copertura che supporta l’affermazione
del nesso causale
secondo
criteri probabilistici (“più probabile che non”).
In effetti, buona parte della letteratura scientifica che esclude la
cancerogenicità dell’esposizione
a radiofrequenze,
o che
quantomeno sostiene che le ricerche giunte ad opposte
conclusioni non possano essere considerate conclusive, come
evidenziato anche dai Consulenti d’Ufficio a commento delle
osservazioni della difesa dell’appellato (riportate alle pagg. 84-
97 della relazione), versa in posizione di conflitto di interessi,
peraltro non sempre dichiarato: si veda in particolare, a pag. 94
della relazione, l’osservazione della difesa dell’appellato
(in
alcun modo contestata dalla controparte) secondo cui gli autori
degli studi indicati dall’INAIL, nominativamente
elencati, sono
membri di ICNIRP e/o di SCENIHR, che hanno ricevuto,
direttamente o indirettamente, finanziamenti dall’industria.
I Consulenti d’Ufficio
hanno al riguardo osservato: “Inoltre,
anche alla luce dell’ampia documentazione sui conflitti di
interesse
di
diversi
ricercatori
coinvolti
nello
studio
INTERPHONE, pure prodotta dai consulenti dell’appellante, si
ritiene che debba essere dato minor peso agli studi pubblicati da
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autori che non hanno dichiarato l’esistenza di conflitti di
interesse invece sussistenti e che debba essere dato maggior
peso ai risultati di studi condotti da ricercatori esenti da tali
conflitti, come ad esempio gli studi effettuati da Hardell e
collaboratori.
Nel caso in esame, possono concretizzare situazioni di conflitto
di interesse
rispetto alla valutazione dell’effetto sulla salute
delle RF, ad esempio, quei casi in cui l’autore dello studio ha
effettuato consulenze per l’industria telefonica o ha ricevuto
finanziamenti per la realizzazione di studi dall’industria
telefonica oppure (come anche stabilito anche dal Karolinska
Institutet di Stoccolma, in relazione all’esposto presentato
contro il prof. Ahlbom, poi destituito dalla presidenza del
gruppo di lavoro IARC sulle RF proprio a causa della sua
appartenenza all’ICNIRP) nel caso in cui l’autore stesso sia
membro dell’ICNIRP (International Commission on Non-
Ionizing Radiation). Infatti l’ICNIRP è un’organizzazione
privata, le cui linee guida sulle RF hanno una grande
importanza economica e strategica per l’industria delle
telecomunicazioni, con la quale peraltro diversi membri
dell’ICNIRP hanno legami attraverso rapporti di consulenza …
A parte possibili legami con l’industria, appare evidente che i
membri dell’ICNIRP dovrebbero astenersi dal valutare l’effetto
sulla salute di livelli
di RF che l’ICNIRP stesso ha già
dichiarato sicuri e quindi non nocivi per la salute (Hardell,
2017)”
(v.
pag. 107 relazione).
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L’impostazione
dei
Consulenti
d’Ufficio
è
del
tutto
condivisibile, essendo evidente
che l’indagine,
e le conclusioni,
di autori indipendenti diano maggiori garanzie di attendibilità
rispetto a quelle commissionate, gestite o finanziate almeno in
parte, da soggetti interessati
all’esito degli studi.
L’ampia letteratura scientifica citata ed applicata dai
Consulenti
d’Ufficio, del tutto indipendente, deve quindi ritenersi affidabile,
così come le conclusioni, a livello epidemiologico, a cui essa è
pervenuta.
Del resto, proprio in una controversia nei confronti dell’INAIL
relativa a malattia professionale (tumore intracranico) per
esposizione a radiofrequenze da telefono cellulare, la S.C. ha
ritenuto che “L’ulteriore
rilievo circa la maggiore attendibilità
proprio di tali studi, stante la loro posizione di indipendenza,
ossia per non essere stati cofinanziati, a differenza di altri,
anche dalle stesse ditte produttrici di cellulari, costituisce
ulteriore e non illogico fondamento delle conclusioni accolte”
(v. Cass. 12.10.2012 n. 17438).
Trattandosi di malattia professionale non tabellata e ad eziologia
multifattoriale, la prova della causa di lavoro, indubbiamente
gravante sul lavoratore, per costante giurisprudenza di legittimità
deve essere valutata in termini di ragionevole certezza, e quindi,
esclusa
la
rilevanza
della
mera
possibilità
dell’origine
professionale, essa può essere ravvisata in presenza di un
rilevante grado di probabilità (cfr., tra le molte, Cass. 10.4.2018
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n. 8773 ), grado che, per le ragioni illustrate, è emerso dalla c.t.u.
disposta nel presente grado.
La percentuale di invalidità nella misura del 23%, già
riconosciuta nella c.t.u. disposta dal Tribunale e ribadita dalla
consulenza espletata nel presente grado, è stata espressamente
accettata dall’appellato
(v. pag. 3, punto a, memoria appellato).
In conclusione, l’appello dev’essere respinto.
Le spese del grado seguono la soccombenza e si liquidano in
dispositivo in conformità ai parametri vigenti, tenuto conto del
valore della causa e dell’attività difensiva svolta,
con distrazione
in favore dei difensori.
Le spese di c.t.u., viste le conclusioni a cui essa è pervenuta,
vanno poste a
carico definitivo dell’INAIL.
Al rigetto dell’appello consegue
ex lege
(art. 1, commi 17-18, l.
228/2012) la dichiarazione che sussistono i presupposti per
l’ulteriore pagamento, a carico dell’appellante, di un importo
pari a quello del contributo unificato
dovuto per l’impugnazione.
P.Q.M.
Visto l’art. 437 c.p.c.,
respinge l’appello;
condanna
l’Inail a rimborsare all’appellato le spese del grado,
liquidate in euro 10.000,00, oltre rimborso forfettario, Iva e Cpa,
con distrazione in favore dei difensori;
pone a carico dell’appellante gli oneri di CTU, liquidati come da
separato decreto;
dichiara la sussistenza delle condizioni per l'ulteriore pagamento,
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a carico dell'appellante, di un importo pari a quello del
contributo unificato dovuto per l'impugnazione.
Così deciso all’udienza del
3.12.2019
IL CONSIGLIERE Est.
Dott.ssa Silvia CASARINO
LA PRESIDENTE
Dott.ssa Rita MANCUSO
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VERIZON COMMUNICATIONS INC
FORM
Report)
10-K
(Annual
Filed 02/21/20 for the Period Ending 12/31/19
Address
Telephone
CIK
Symbol
SIC Code
Industry
Sector
Fiscal Year
1095 AVENUE OF THE AMERICAS
NEW YORK, NY, 10036
212-395-1000
0000732712
VZ
4813 - Telephone Communications (No Radiotelephone)
Integrated Telecommunications Services
Telecommunication Services
12/31
http://www.edgar-online.com
© Copyright 2020, EDGAR Online, a division of Donnelley Financial Solutions. All Rights Reserved.
Distribution and use of this document restricted under EDGAR Online, a division of Donnelley Financial Solutions, Terms of Use.
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UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549
FORM 10-K
(Mark one)
☒
ANNUAL REPORT PURSUANT TO SECTION 13 OR 15(d)
OF THE SECURITIES EXCHANGE ACT OF 1934
For the fiscal year ended December 31, 2019
OR
☐
TRANSITION REPORT PURSUANT TO SECTION 13 OR 15(d)
OF THE SECURITIES EXCHANGE ACT OF 1934
For the transition period from
to
Verizon Communications Inc.
(Exact name of registrant as specified in its charter)
Commission file number: 1-8606
Delaware
(State or other jurisdiction
of incorporation or organization)
23-2259884
(I.R.S. Employer Identification No.)
1095 Avenue of the Americas
New York, New York
(Address of principal executive offices)
10036
(Zip Code)
Registrant’s telephone number, including area code: (212) 395-1000
Securities registered pursuant to Section 12(b) of the Act:
Title of Each Class
Common Stock, par value $0.10
Common Stock, par value $0.10
2.375% Notes due 2022
0.500% Notes due 2022
1.625% Notes due 2024
4.073% Notes due 2024
0.875% Notes due 2025
3.250% Notes due 2026
1.375% Notes due 2026
0.875% Notes due 2027
1.375% Notes due 2028
1.875% Notes due 2029
1.250% Notes due 2030
1.875% Notes due 2030
2.625% Notes due 2031
2.500% Notes due 2031
0.875% Notes due 2032
4.750% Notes due 2034
3.125% Notes due 2035
3.375% Notes due 2036
2.875% Notes due 2038
1.500% Notes due 2039
Securities registered pursuant to Section 12(g) of the Act:
None
Indicate by check mark if the registrant is a well-known seasoned issuer, as defined in Rule 405 of the Securities Act.
☒
Yes
☐
No
Indicate by check mark if the registrant is not required to file reports pursuant to Section 13 or Section 15(d) of the Act.
☐
Yes
☒
No
Trading Symbol(s)
VZ
VZ
VZ22A
VZ22B
VZ24B
VZ24C
VZ25
VZ26
VZ26B
VZ27E
VZ28
VZ29B
VZ30
VZ30A
VZ31
VZ31A
VZ32
VZ34
VZ35
VZ36A
VZ38B
VZ39C
Name of Each Exchange on Which Registered
New York Stock Exchange
The NASDAQ Global Select Market
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
New York Stock Exchange
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2259378_1531.png
Indicate by check mark whether the registrant (1) has filed all reports required to be filed by Section 13 or 15(d) of the Securities Exchange Act of 1934 during the preceding 12
months (or for such shorter period that the registrant was required to file such reports), and (2) has been subject to such filing requirements for the past 90 days.
☒
Yes
☐
No
Indicate by check mark whether the registrant has submitted electronically every Interactive Data File required to be submitted pursuant to Rule 405 of Regulation S-T (§232.405
of this chapter) during the preceding 12 months (or for such shorter period that the registrant was required to submit such files).
☒
Yes
☐
No
Indicate by check mark whether the registrant is a large accelerated filer, an accelerated filer, a non-accelerated filer, a smaller reporting company, or an emerging growth
company. See the definitions of "large accelerated filer," "accelerated filer," "smaller reporting company," and "emerging growth company" in Rule 12b-2 of the Exchange Act.
(Check one):
Large accelerated filer
Non-accelerated filer
☒
☐
Accelerated filer
Smaller reporting company
Emerging growth company
☐
☐
☐
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial
accounting standards provided pursuant to Section 13(a) of the Exchange Act.
☐
Indicate by check mark whether the registrant is a shell company (as defined in Rule 12b-2 of the Act).
☐
Yes
☒
No
At June 30, 2019, the aggregate market value of the registrant’s voting stock held by non-affiliates was approximately $236,226,048,492.
At January 31, 2020, 4,135,863,778 shares of the registrant’s common stock were outstanding, after deducting 155,569,868 shares held in treasury.
Documents Incorporated By Reference:
Portions of the registrant’s Annual Report to Shareholders for the year ended December 31, 2019 (Parts I and II).
Portions of the registrant’s definitive Proxy Statement to be delivered to shareholders in connection with the registrant’s 2020 Annual Meeting of Shareholders (Part III).
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Table of Contents
TABLE OF CONTENTS
Item No.
PART I
Item 1.
Item 1A.
Item 1B.
Item 2.
Item 3.
Item 4.
PART II
Item 5.
Item 6.
Item 7.
Item 7A.
Item 8.
Item 9.
Item 9A.
Item 9B.
PART III
Item 10.
Item 11.
Item 12.
Item 13.
Item 14.
PART IV
Item 15.
Item 16.
Signatures
Certifications
Exhibits, Financial Statement Schedules
Form 10-K Summary
22
27
27
Directors, Executive Officers and Corporate Governance
Executive Compensation
Security Ownership of Certain Beneficial Owners and Management and Related Stockholder Matters
Certain Relationships and Related Transactions, and Director Independence
Principal Accounting Fees and Services
20
21
21
21
21
Market for Registrant’s Common Equity, Related Stockholder Matters and Issuer Purchases of Equity Securities
Selected Financial Data
Management’s Discussion and Analysis of Financial Condition and Results of Operations
Quantitative and Qualitative Disclosures About Market Risk
Financial Statements and Supplementary Data
Changes in and Disagreements with Accountants on Accounting and Financial Disclosure
Controls and Procedures
Other Information
19
19
19
19
19
19
19
20
Business
Risk Factors
Unresolved Staff Comments
Properties
Legal Proceedings
Mine Safety Disclosures
4
15
18
18
18
18
Page
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Table of Contents
PART I
Item 1. Business
General
Verizon Communications Inc. (Verizon or the Company) is a holding company that, acting through its subsidiaries, is one of the world’s leading providers of communications,
information and entertainment products and services to consumers, businesses and government entities. With a presence around the world, we offer voice, data and video
services and solutions on our networks that are designed to meet customers’ demand for mobility, reliable network connectivity, security and control. Formerly known as Bell
Atlantic Corporation (Bell Atlantic), we were incorporated in 1983 under the laws of the State of Delaware. We began doing business as Verizon on June 30, 2000 following our
merger with GTE Corporation. We have a highly diverse workforce of approximately 135,000 employees as of December 31, 2019.
Our principal executive offices are located at 1095 Avenue of the Americas, New York, New York 10036 (telephone number 212-395-1000).
In November 2018, we announced a strategic reorganization of our business. Under the new structure, effective April 1, 2019, there are two reportable segments that we operate
and manage as strategic business units - Verizon Consumer Group (Consumer) and Verizon Business Group (Business).
Verizon Consumer Group
Our Consumer segment provides consumer-focused wireless and wireline communications services and products. Our wireless services are provided across one of the most
extensive wireless networks in the United States (U.S.) under the Verizon brand and through wholesale and other arrangements. Our wireline services are provided in nine states
in the Mid-Atlantic and Northeastern U.S., as well as Washington D.C., over our 100% fiber-optic network under the Fios brand and over a traditional copper-based network to
customers who are not served by Fios. In 2019, the Consumer segment’s revenues were $91.1 billion, representing approximately 69% of Verizon’s consolidated revenues. As of
December 31, 2019, Consumer had approximately 95 million wireless retail connections, 6 million broadband connections and 4 million Fios video connections.
Verizon Business Group
Our Business segment provides wireless and wireline communications services and products, video and data services, corporate networking solutions, security and managed
network services, local and long distance voice services and network access to deliver various Internet of Things (IoT) services and products. We provide these products and
services to businesses, government customers and wireless and wireline carriers across the U.S. and select products and services to customers around the world. In 2019, the
Business segment's revenues were $31.4 billion, representing approximately 24% of Verizon’s consolidated revenues. As of December 31, 2019, Business had approximately
25 million wireless retail postpaid connections and approximately 489 thousand broadband connections.
Additional discussion of our reportable segments is included in the 2019 Verizon Annual Report to Shareholders under the headings "Management’s Discussion and Analysis of
Financial Condition and Results of Operations - Overview" and - "Segment Results of Operations" and in Note 13 to the consolidated financial statements of Verizon
Communications Inc. and Subsidiaries, which are incorporated by reference into this report.
Service and Product Offerings
Our Consumer segment's wireless and wireline products and services are available to our retail customers, as well as resellers that purchase wireless network access from us on a
wholesale basis. Our Business segment’s wireless and wireline products and services are organized by the primary customer groups targeted by these offerings: Global
Enterprise, Small and Medium Business, Public Sector and Other, and Wholesale.
Wireless
We offer wireless services and equipment to customers of both Consumer and Business.
Wireless Services
Our Consumer and Business segments provide a wide variety of wireless services accessible on a broad range of devices. Customers can obtain our wireless services on a
postpaid or prepaid basis. Retail (non-wholesale) postpaid accounts primarily represent retail customers that are directly served and managed by Verizon and use Verizon
branded services. A single account may include monthly wireless services for a variety of connected devices. A retail postpaid connection represents an individual line of service
for a wireless device for which a customer is generally billed one month in advance for a monthly access charge in return for access to and usage of network services. Our
prepaid service is offered only to Consumer customers and enables individuals to obtain wireless services without credit verification by paying for all services in advance.
Approximately 96% of our Consumer retail connections were postpaid connections as of December 31, 2019.
4
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Table of Contents
We offer various postpaid and prepaid service plans tailored to the needs of our customers. Depending on those needs at a particular time, our plans may include features related
to, among other things: unlimited or metered domestic and/or international voice, data, and texting; the ability to share data allowances and/or use data allowances in different
periods; high definition voice and video features; the ability to use a device as a Wi-Fi hotspot; and varying data rates depending on the plan and usage on that plan. Our service
offerings vary from time to time based on customer needs, technology changes and market conditions and may be provided as standard plans or as part of limited time
promotional offers.
Access to the Internet is available on all smartphones and nearly all basic phones. In addition, our customers can access the Internet at broadband speeds on notebook computers
and tablets that are either wireless-enabled or that are used in conjunction with separate dedicated devices that provide a mobile Wi-Fi connection.
As of January 2017, we no longer offer Consumer customers new fixed-term, subsidized service plans for phones; however, we continue to offer subsidized plans to our
Business customers. We also continue to service existing plans for customers who have not yet purchased and activated devices under the Verizon device payment program.
Wireless Equipment
Consumer and Business offer several categories of wireless equipment to customers, including a variety of smartphones and other handsets, wireless-enabled Internet devices,
such as tablets, laptop computers and netbooks, and other wireless-enabled connected devices, such as smart watches and other wearables. In certain cases, we permit customers
to acquire equipment from us using device payment plans, which permit the customer to pay for the device in installments over time.
Verizon Consumer Group
In addition to the wireless services and equipment discussed above, Consumer sells residential fixed connectivity solutions, including Internet, video and voice services, and
wireless network access to resellers on a wholesale basis.
Residential Fixed Services.
We provide residential fixed connectivity solutions to customers over our 100% fiber-optic network under the Fios brand, and over a traditional
copper-based network to customers who are not served by Fios. During 2018, we commercially launched fifth-generation (5G) wireless technology for the home (5G Home) on
proprietary standards in four U.S. markets and on global standards in a fifth market in 2019.
We offer residential fixed services tailored to the needs of our customers. Depending on those needs at a particular time, our services may include features related to, among
other things: Internet access at different speed tiers using fiber-optic, copper or wireless technology; video services that may feature a variety of channel options, video on
demand products, cloud-based services and digital video recording capabilities; over-the-top video services; and voice services.
Network Access Services.
We sell network access to mobile virtual network operators (MVNOs) on a wholesale basis, who in turn resell wireless service under their own
brand(s) to consumers.
Verizon Business Group
In addition to the wireless services and equipment discussed above, our Business segment provides communications products and enhanced services, including video and data
services, corporate networking solutions, security and managed network services, local and long distance voice services and network access to deliver various IoT products and
services.
Global Enterprise
Global Enterprise offers services to large businesses, which are identified based on their size and volume of business with Verizon, as well as non-U.S. public sector customers.
In 2019, Global Enterprise revenues were $10.8 billion, representing approximately 34% of Business’s total revenues.
Global Enterprise offers a broad portfolio of connectivity, security and professional services designed to enable our customers to optimize their business operations, mitigate
business risks and capitalize on data. These services include the following:
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Network Services.
We offer a portfolio of network connectivity products to help our customers connect with their employees, partners, vendors, and customers. These
products include private networking services, private cloud connectivity services, virtual and software defined networking services, and Internet access services.
Advanced Communications Services.
We offer a suite of services to our customers to help them communicate with their employees, partners, vendors, constituents and
customers. These products include Internet Protocol (IP)-based voice services, unified communications and collaboration tools and customer contact center solutions.
Security services.
We offer a suite of management and data security services that help our customers protect, detect and respond to security threats to their networks,
data, applications and infrastructure.
Core services.
We provide a portfolio of domestic and global voice and data solutions utilizing traditional telecommunications technology, including voice calling,
messaging services, conferencing, contact center solutions and private line and data access networks. Core services also include the provision of customer premises
equipment, and installation, maintenance and site services.
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IoT services.
We provide the network access required to deliver various IoT products and services. We work with companies that purchase network access from us to
connect their Open Development-certified devices, bundled together with their own solutions, which they sell to end users. We are building IoT capabilities by
leveraging business models that monetize usage on our networks at the connectivity, platform and solution layers.
Small and Medium Business
Small and Medium Business offers wireless services and equipment, tailored voice and networking products, Fios services, IP networking, advanced voice solutions, security and
managed information technology (IT) services to our U.S.-based customers that do not meet the requirements to be categorized as Global Enterprise. In 2019, Small and Medium
Business revenues were $11.5 billion, representing approximately 36% of Business’s total revenues.
In addition to the wireless services and equipment discussed above, Small and Medium Business provides fixed connectivity solutions comparable to the residential fixed
services provided by Consumer, as well as business services and connectivity similar to the products and services offered by Global Enterprise, in each case with features and
pricing designed to address the needs of small and medium businesses.
Public Sector and Other
Public Sector and Other offers wireless products and services as well as wireline connectivity and managed solutions to U.S. federal, state and local governments and educational
institutions. These services include the business services and connectivity similar to the products and services offered by Global Enterprise, in each case, with features and
pricing designed to address the needs of governments and educational institutions. In 2019, Public Sector and Other revenues were $5.9 billion, representing approximately 19%
of Business’s total revenues.
Public Sector and Other also includes solutions that support fleet tracking management, compliance management, field service management, asset tracking and other types of
mobile resource management in the United States and around the world.
Wholesale
Wholesale offers wireline communications services including data, voice, local dial tone and broadband services primarily to local, long distance, and wireless carriers that use
our facilities to provide services to their customers. In 2019, Wholesale revenues were $3.2 billion, representing approximately 10% of Business’s total revenues. A portion of
Wholesale revenues are generated by a few large telecommunications companies, most of which compete directly with us. Wholesale's services include:
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Data services.
We offer a portfolio of data services with varying speeds and options to enhance our Wholesale customers’ networks and provide connections to their
end-users and subscribers.
Voice services.
We provide switched access services that allow carriers to complete their end-user calls that originate or terminate within our territory. In addition, we
provide originating and terminating voice services throughout the U.S. and globally utilizing our TDM and VoIP networks.
Local services.
We offer an array of local dial tone and broadband services to competitive local exchange carriers, some of which are offered to comply with
telecommunications regulations. In addition, we offer services such as colocation, resale and unbundled network elements in compliance with applicable regulations.
Distribution
We use a combination of direct, indirect and alternative distribution channels to market and distribute our products and services to Consumer customers.
Our direct channel, including our company-operated stores, is a core component of our distribution strategy. Our sales and service centers also represent a significant distribution
channel for our services.
Our indirect/digital partners channel includes agents that sell our wireless and wireline products and services at retail locations throughout the U.S., as well as through the
Internet. The majority of these sales are made under exclusive selling arrangements with us. We also have relationships with high-profile national retailers that sell our wireless
and wireline products and services, as well as convenience store chains that sell our wireless prepaid products and services. In 2019, we grew our digital channel and expanded
omni channel experiences for our customers to offer choice and convenience.
In addition to our direct channel, our Business segment has additional distribution channels that include business solution fulfillment provided by resellers, non-stocked device
fulfillment performed by distributors and integrated mobility services provided by system integrators and resellers.
Competition and Related Trends
The telecommunications industry is highly competitive. We expect competition to remain intense as traditional and non-traditional participants seek increased market share.
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With respect to our wireless connectivity products and services, we compete against other national wireless service providers, including AT&T Inc., Sprint Corporation and T-
Mobile USA, Inc., as well as various regional wireless service providers. We also compete for retail activations with resellers that buy bulk wholesale service from wireless
service providers, including Verizon, and resell it to their customers. Resellers may include cable companies. Competition remains intense as a result of high rates of smartphone
penetration in the wireless market, increased network investment by our competitors, the development and deployment of new technologies, such as 5G, the introduction of new
products and services, offerings that include additional premium content, new market entrants, the availability of additional licensed and unlicensed spectrum, and regulatory
changes. In 2019, we began offering Apple Music and Disney+ to customers as part of their Unlimited plans. Competition may also increase as smaller, stand-alone wireless
service providers merge or transfer licenses to larger, better capitalized wireless service providers and as MVNOs resell wireless communication services.
We also face competition from other communications and technology companies seeking to increase their brand recognition and capture customer revenue with respect to the
provision of wireless products and services, in addition to non-traditional offerings in mobile data. For example, Microsoft Corporation, Alphabet Inc., Apple Inc. and others are
offering alternative means for making wireless voice calls that, in certain cases, can be used in lieu of the wireless provider’s voice service, as well as alternative means of
accessing video content.
With respect to our wireline connectivity services, we compete against cable companies, wireless service providers, domestic and foreign telecommunications providers, satellite
television companies, Internet service providers, over-the-top (OTT) providers and other companies that offer network services and managed enterprise solutions. Cable
operators have increased the size and capacity of their networks in order to deliver digital products and services. We introduced offerings that provide customized Internet and
video packages. Several major cable operators also offer bundles with wireless services through strategic relationships. Customers have more choices for obtaining video content
from various online services. We expect the market will continue to shift from traditional linear video to OTT offerings. We expect customer migration from traditional voice
services to wireless services to continue as a growing number of customers place greater value on mobility and wireless companies position their services as a landline
alternative. We also face increasing competition from cable operators and other providers of VoIP services, as well as Internet portal providers.
We believe that the following are the most important competitive factors and trends in the telecommunications industry:
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Network reliability, speed and coverage.
We consider networks that consistently provide high-quality, fast and reliable service to be a key differentiator in the market
and driver of customer satisfaction. Lower prices, improved service quality and new service offerings, which in many cases include video content, have led to
increased customer usage of connectivity services. We and other network-based providers must ensure that our networks can meet these increasing capacity usage
requirements and offer highly reliable national coverage.
Pricing.
With respect to wireless services and equipment, pricing plays an important role in the wireless competitive landscape. As the demand for wireless services
continues to grow, wireless service providers are offering a range of service plans at competitive prices. Many wireless service providers also bundle wireless service
offerings with other products and offer promotional pricing and incentives, some of which may be targeted specifically to customers of Verizon. We and other wireless
service providers, as well as equipment manufacturers, offer device payment options, which provide customers with the ability to pay for their device over a period of
time, and some providers offer device leasing arrangements. In addition, aggressive device promotions have become more common in an effort to gain a greater share
of subscribers interested in changing carriers. With respect to wireline services, pricing is used by competitors to capture market share from incumbents, and it is a
significant factor as non-traditional modes of providing communication services emerge and new entrants compete for customers. For example, VoIP and portal-based
voice and video calling is often free or nearly free to customers and is often supported by advertising revenues.
Customer service.
We believe that high-quality customer service is a key factor in retaining customers and attracting new customers, including those of other providers.
Our customer service, retention and satisfaction programs are based on providing customers with convenient and easy-to-use products and services and focusing on
their needs in order to promote long-term relationships and minimize churn. The Verizon Up program, for example, was launched to promote long-term relationships
with our Consumer customers. The program offers a variety of rewards to customers in exchange for points in connection with their account-related transactions.
Customer service is highly valued by our Business customers. We provide Global Enterprise and Public Sector and Other customers with ready access to their system
and performance information, and we conduct proactive testing of our networks to identify issues before they affect our customers. We service our Small and Medium
Business customers through service representatives and online support, as well as through store-based representatives for small business customers. For Wholesale
customers, we pursue service improvement through continued system automation initiatives.
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Product differentiation.
Customer and revenue growth are increasingly dependent on the development of new and enhanced products and services, as the delivery of
new and innovative products and services has been accelerating. Customers are shifting their focus from access to applications and are seeking ways to leverage their
broadband, video and wireless connections. To compete effectively, providers need to continuously review, improve and refine their product portfolio and develop and
rapidly deploy new products and services tailored to the needs of customers. We continue to pursue the development and rapid deployment of new and innovative
products and services, both independently and in collaboration with application providers, content providers and device manufacturers. Features such as wireless and
wireline inter-operability are becoming increasingly important, driven by both customer demand and technological advancement.
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Sales and distribution.
A key to achieving sales success in the consumer and small and medium business sectors of the wireless industry is the reach and quality of
sales channels and distribution points. We seek to optimally vary distribution channels among our company-operated stores selling wireless products and services,
outside sales teams and telemarketing, web-based sales and fulfillment capabilities, our extensive indirect distribution network of retail outlets and our sale of wireless
service to resellers, which resell wireless services to their end-users.
In addition to these competitive factors and trends, companies with a global presence are increasingly competing with us in our Business segment. A relatively small number of
telecommunications and integrated service providers with global operations serve customers in the global enterprise market and, to a lesser extent, the global wholesale market.
We compete with these providers for large contracts to provide integrated solutions to global enterprises. Many of these companies have strong market presence, brand
recognition and existing customer relationships, all of which contribute to intensifying competition that may affect our future revenue growth.
In the Global Enterprise and Public Sector and Other markets, competition remains high, primarily as a result of increased industry focus on technology convergence. We
compete in this area with system integrators, carriers, and hardware and software providers. In addition, some of the largest information technology services companies are
making strategic acquisitions, divesting non-strategic assets and forging new alliances to improve their cost structure. Many new alliances and acquisitions have focused on
emerging fields, such as cloud computing, software defined network, communication applications and other computing tasks via networks, rather than by the use of in-house
machines.
In the Small and Medium Business market, customer purchasing behaviors and preferences continue to evolve. Solution speed and simplicity with user interfaces that have a
consumer-like "look and feel" are becoming key differentiators for customers who are seeking full life-cycle offers that simplify the process of starting, running and growing
their businesses. Several major cable operators also offer bundles with wireless services through strategic relationships.
Our Wholesale business competes with traditional carriers for long-haul, voice and IP services. In addition, mobile video and data needs are driving a greater need for wireless
backhaul. Network providers, cable companies and niche players are competitors for this business opportunity.
Verizon Media
Our media business, Verizon Media, includes diverse media and technology brands that serve both consumers and businesses. Verizon Media provides consumers with owned
and operated and third-party search properties as well as mail, news, finance, sports and entertainment offerings, and provides other businesses and partners access to consumers
through digital advertising, content delivery and video streaming platforms. In 2019, Verizon Media's revenues were $7.5 billion.
Verizon Media Products and Solutions
Ad Platform
Our Verizon Media Ad Platform provides advertisers and publishers with a simplified suite of intelligent advertising solutions across desktop, mobile and television devices.
Verizon Media's business is comprised primarily of search advertising, display advertising, Ecommerce and subscriptions.
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Search advertising.
Our search properties serve as a guide for users to discover information on the Internet. Verizon Media serves click-based search advertisements
generated by proprietary algorithmic technology, as well as advertisements from partners. Verizon Media provides the underlying search products that facilitate user
searches within Verizon Media and third-party partner properties.
Display advertising.
Display advertising is made up of both graphical and performance-based advertising and takes the form of impression-based contracts, time-based
contracts and performance-based contracts. Verizon Media display ads leverage proprietary data signals to identify and engage users on Verizon Media properties and
across the web. Through Verizon Media Ad Platform, we provide customers the ability to buy advertising inventory, measure campaigns across screens and advertising
formats using self-serve technology or our managed services. We also provide publishers with the ability to monetize their ad inventory.
Ecommerce.
Our Ecommerce offering includes different types of business models, including facilitating transactions between businesses and consumers, enabling
businesses that facilitate transactions for other businesses, and facilitating transactions between consumers.
Subscription memberships.
Our paid subscription offerings include premium content and services across our mail, news, finance, sports and entertainment properties,
privacy and security solutions and computer protection.
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Verizon Media Platform
As the digital platform reshapes the delivery of media and entertainment content, there is an increasing need for stable, high-quality video delivery platforms. Our Media
Platform offers a scalable platform for delivering content, including live broadcasts, video on demand, games, software and websites to our customers on their devices at any
time. This platform is targeted at media and entertainment companies and other businesses that deliver their digital products and services through the Internet.
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Global Network and Technology
Our global network architecture is used by both Consumer and Business. Our network technology platforms include both wireless and wireline technologies.
Network Evolution
We are evolving the architecture of our networks to a next-generation multi-use platform, providing improved efficiency and virtualization, increased automation and
opportunities for edge computing services that will support both our fiber-based and radio access network technologies. We call this the Intelligent Edge Network. We expect
that this new architecture will simplify operations by eliminating legacy network elements, improve our fourth-generation (4G) Long-Term Evolution (LTE) wireless coverage,
speed the deployment of 5G wireless technology and create new opportunities in the business market.
5G Deployment
Over the past several years, we have been leading the development of 5G wireless technology industry standards and the ecosystems for fixed and mobile 5G wireless services.
We believe 5G technology will be able to provide users with eight capabilities, or currencies. The eight currencies are peak data rates, mobile data volumes, mobility, number of
connected devices, energy efficiency of connected devices, service deployment, reduced latency and improved reliability. We expect that 5G technology will provide higher
throughput and lower latency than the current 4G LTE technology and enable our networks to handle more traffic as the number of Internet-connected devices grows. During
2018, we commercially launched 5G Home on proprietary standards in four U.S. markets and on global standards in a fifth U.S. market in 2019. We also launched our 5G Ultra
Wideband Network in 31 U.S. markets in 2019, as well as several 5G-compatible smartphones.
4G LTE
Our primary wireless network technology platform is 4G LTE, which provides higher data throughput performance for data services at a lower cost compared to that offered by
3G technology. As of December 31, 2019, our 4G LTE network is available in over 700 markets covering approximately 327 million people, including those in areas served by
our LTE in Rural America partners. Under this program, we have collaborated with wireless carriers in rural areas to build and operate a 4G LTE network using each carrier’s
network assets and our core 4G LTE equipment and 700 Megahertz (MHz) C Block and Advanced Wireless Services (AWS) spectrum.
Wireless Network Reliability and Build-Out
We consider the reliability, coverage and speed of our wireless network as key factors for our continued success. We believe that steady and consistent network and platform
investments provide the foundation for innovative products and services. As we design and deploy our network, we focus on the number of successful data sessions the network
enables, delivering on our advertised throughput speeds, and the number of calls that are connected on the first attempt and completed without being dropped. We utilize three
strategies to maintain the quality of our network: increasing the density of our network elements, deploying new technologies as they are developed and putting additional
wireless spectrum into service. We choose among these strategies based on the circumstances present at different times in each of our service areas.
We have been densifying our network by utilizing small cell technology, in-building solutions and distributed antenna systems. Network densification enables us to add capacity
to address increasing mobile video consumption and the growing demand for IoT products and services on our 4G LTE and 5G networks. We are also utilizing existing network
capabilities to handle increased traffic without interrupting the quality of the customer experience. We continue to deploy advanced technologies to increase both network
capacity and data rates.
In order to build and upgrade our existing 4G LTE network and deploy our 5G network, we must complete a variety of steps, which can include securing rights to a large number
of sites as well as obtaining zoning and other governmental approvals and fiber facilities, for our macro and small cells, in-building systems and antennas and related radio
equipment that comprise distributed antenna systems. We have relationships with a wide variety of vendors that supply various products and services that support our wireless
network operations. We utilize tower site management firms as lessors or managers of a portion of our existing leased and owned tower sites.
Our networks include various elements of redundancy designed to enhance the reliability of the services provided to our customers. To mitigate the impact of power disruptions
on our operations, we have battery backup at every switch and every macro cell. We also utilize backup generators at a majority of our macro cells and at every switch location.
In addition, we have a fleet of portable backup generators that can be deployed, if needed. We further enhance reliability by using a fully redundant Multiprotocol Label
Switching backbone network in critical locations.
In addition to our own network coverage, we have roaming agreements with a number of wireless service providers to enable our customers to receive wireless service in nearly
all other areas in the U.S. where wireless service is available. We also offer a variety of international wireless voice and data services to our customers through roaming
arrangements with wireless service providers outside the U.S.
Fios
Residential broadband service has seen significant growth in bandwidth demand over the past several years, and we believe that demand will continue to grow. We expect the
continued emergence of new video services, new data applications and the proliferation of IP devices in the home will continue to drive new network requirements for increased
data speeds and throughput. We believe that the Passive Optical Network (PON) technology underpinning Fios positions us well to meet these demands in a cost-effective and
efficient manner.
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While deployed initially as a consumer broadband network, our PON infrastructure is also experiencing more widespread application in the Business segment, especially as
businesses increasingly migrate to Ethernet-based access services.
Global IP
Verizon owns and operates one of the largest global fiber-optic networks in the world, providing connectivity to Business customers in more than 150 countries. Our global IP
network includes long-haul, metro and submarine assets that span over 1 million route miles and enable and support international operations.
Global business is rapidly evolving to an "everything-as-a-service" model in which Business customers seek cloud-based, converged enterprise solutions delivered securely via
managed and professional services. We are continuing to deploy packet optical transport technology in order to create a global network platform to meet this demand.
Spectrum
The spectrum licenses we hold can be used for mobile wireless voice, video and data communications services. We are licensed by the Federal Communications Commission
(FCC) to provide these wireless services on portions of the 800 MHz band, also known as cellular spectrum, the 1800-1900 MHz band, also known as Personal Communication
Services (PCS) spectrum, portions of the 700 MHz upper C band and AWS 1 and 3 spectrum in the 1700 and 2100 MHz bands, in areas that, collectively, cover nearly all of the
population of the U.S. This spectrum is collectively called low and mid-band spectrum. We are using our low and mid-band spectrum to provide both 3G and 4G LTE wireless
services. However, we are increasingly reallocating spectrum previously used for 3G service to provide 4G LTE service. We are also repurposing low and mid-band spectrum to
complement our spectrum licenses in the 28 and 39 Gigahertz (GHz) band, collectively called millimeter wave spectrum.
Millimeter wave spectrum is being used for our 5G technology deployment. We anticipate that we will need additional spectrum to meet future demand. This increasing demand
is driven by growth in customer connections and the increased usage of wireless broadband services that use more bandwidth and require faster rates of speed, as well as the
wider deployment of 5G mobile and fixed services. We can meet our future 4G and 5G spectrum needs by acquiring licenses or leasing spectrum from other licensees, or by
acquiring new spectrum licenses from the FCC, if and when future FCC spectrum auctions occur.
From time to time we have exchanged spectrum licenses with other wireless service providers through secondary market swap transactions. We expect to continue to pursue
similar opportunities to trade spectrum licenses in order to meet capacity and expansion needs in the future. In certain cases, we have entered into intra-market spectrum swaps
designed to increase the amount of contiguous spectrum within frequency bands in a specific market. Contiguous spectrum improves network performance and efficiency. These
swaps, as well as any spectrum purchases, require us to obtain governmental approvals.
Information regarding spectrum license transactions is included in the 2019 Verizon Annual Report to Shareholders in Note 3 to the consolidated financial statements of Verizon
Communications Inc. and Subsidiaries, which is incorporated by reference into this report.
Strategic Transactions
During March 2015, we completed a transaction with American Tower Corporation (American Tower) pursuant to which American Tower acquired the exclusive rights to lease
and operate approximately 11,300 of our wireless towers and corresponding ground leases for an upfront payment of $5.0 billion. We have subleased capacity on the towers from
American Tower for a minimum of 10 years at current market rates, with options to renew. Under the terms of the lease agreements, American Tower has exclusive rights to
lease and operate towers over an average term of approximately 28 years. As the leases expire, American Tower has fixed-price purchase options to acquire these towers based
on their anticipated fair market values at the end of the lease terms. As part of this transaction, we also sold 162 towers for $71 million.
In June 2015, we completed our acquisition of AOL Inc. (AOL), a leader in digital content and advertising. The aggregate cash consideration paid by Verizon at the closing was
approximately $3.8 billion.
In April 2016, we completed the sale (Access Line Sale) of our local exchange business and related landline activities in California, Florida and Texas, including Fios Internet
and video customers, switched and special access lines and high-speed Internet service and long distance voice accounts in these three states to Frontier Communications
Corporation (Frontier) for approximately $10.5 billion (approximately $7.3 billion net of income taxes), subject to certain adjustments and including the assumption of $612
million of indebtedness from Verizon by Frontier. The transaction included the acquisition by Frontier of the equity interests of Verizon’s incumbent local exchange carriers
(ILECs) in California, Florida and Texas.
The transaction resulted in Frontier acquiring approximately 3.3 million voice connections, 1.6 million Fios Internet subscribers, 1.2 million Fios video subscribers and the
related ILEC businesses from Verizon. Approximately 9,300 Verizon employees who served customers in California, Florida and Texas continued employment with Frontier.
In July 2016, we acquired Telogis, Inc., a global, cloud-based mobile enterprise management software business, for $877 million of cash consideration.
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In November 2016, we completed the acquisition of Fleetmatics Group PLC, a global provider of fleet and mobile workforce management solutions, for $60.00 per ordinary
share in cash. The aggregate merger consideration was approximately $2.5 billion, including cash acquired of $112 million.
In December 2016, we entered into a definitive agreement, which was subsequently amended in March 2017, with Equinix, Inc. (Equinix) pursuant to which we agreed to sell 23
customer-facing data center sites in the U.S. and Latin America for approximately $3.6 billion, subject to certain adjustments (Data Center Sale). The transaction closed in May
2017.
In February 2016, we entered into a purchase agreement to acquire XO Holdings' wireline business (XO), which owned and operated one of the largest fiber-based IP and
Ethernet networks in the U.S. Concurrently, we entered into a separate agreement to utilize certain wireless spectrum from a wholly-owned subsidiary of XO Holdings,
NextLink, that held XO's millimeter-wave wireless spectrum. The agreement included an option, subject to certain conditions, to acquire NextLink. In February 2017, we
completed our acquisition of XO for total cash consideration of approximately $1.5 billion, of which $100 million was paid in 2015.
In April 2017, we exercised our option to buy NextLink for approximately $493 million, subject to certain adjustments, of which $320 million was prepaid in the first quarter of
2017. The transaction closed in January 2018. The acquisition of NextLink was accounted for as an asset acquisition, as substantially all of the value related to the acquired
spectrum. Upon closing, we recorded approximately $657 million of wireless licenses, $110 million of a deferred tax liability and $58 million of other liabilities.
In June 2017, we completed our acquisition of the operating business of Yahoo! Inc. (Yahoo), a leader in search, communications, digital content and advertising. Pursuant to the
Purchase Agreement, upon the terms and subject to the conditions thereof, we agreed to acquire the stock of one or more subsidiaries of Yahoo holding all of Yahoo’s operating
business for approximately $4.83 billion in cash, subject to certain adjustments. In February 2017, Verizon and Yahoo entered into an amendment to the Purchase Agreement,
pursuant to which the Transaction purchase price was reduced by $350 million to approximately $4.48 billion in cash, subject to certain adjustments.
In August 2017, we entered into a definitive agreement to purchase certain fiber-optic network assets in the Chicago market from WideOpenWest, Inc. (WOW!), a leading
provider of communications services. The transaction closed in December 2017. In addition, the parties entered into a separate agreement pursuant to which WOW! was to
complete the build-out of the network assets in 2019. This build-out was completed in 2019. The total cash consideration for the transactions was approximately $275 million, of
which $226 million was paid in December 2017. During 2019 and 2018, the remaining cash consideration was paid.
In 2017, we entered into a transaction to acquire Straight Path Communications Inc., which held certain millimeter-wave spectrum licenses. The transaction closed in February
2018 for total consideration reflecting an enterprise value of approximately $3.1 billion. We are using the spectrum acquired for our 5G technology deployment.
Additional information regarding certain of these strategic transactions is included in the 2019 Verizon Annual Report to Shareholders in Note 3 to the consolidated financial
statements of Verizon Communications Inc. and Subsidiaries, which is incorporated by reference into this report.
Patents, Trademarks and Licenses
We own or have licenses to various patents, copyrights, trademarks, domain names and other intellectual property rights necessary to conduct our business. We actively pursue
the filing and registration of patents, copyrights, domain names, trademarks and service marks to protect our intellectual property rights within the United States and abroad. We
also actively grant licenses, in exchange for appropriate fees or other consideration and subject to appropriate safeguards and restrictions, to other companies that enable them to
utilize certain of our intellectual property rights and proprietary technology as part of their products and services. Such licenses enable the licensees to take advantage of the
results of Verizon’s research and development efforts. While these licenses result in valuable consideration for Verizon, we do not believe that the loss of such consideration, or
the expiration of any of our intellectual property rights, would have a material effect on our results of operations.
We periodically receive offers from third parties to purchase or obtain licenses for patents and other intellectual property rights in exchange for royalties or other payments. We
also periodically receive notices alleging that our products or services infringe on third-party patents or other intellectual property rights. These claims, whether against us
directly or against third-party suppliers of products or services that we sell to our customers, if successful, could require us to pay damages or royalties, or cease offering the
relevant products or services.
Acquisitions and Divestitures
Information about our acquisitions and divestitures is included in the 2019 Verizon Annual Report to Shareholders under the heading "Management’s Discussion and Analysis of
Financial Condition and Results of Operations - Acquisitions and Divestitures" and in Note 3 to the consolidated financial statements of Verizon Communications Inc. and
subsidiaries, which is incorporated by reference into this report.
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Regulatory and Competitive Trends
Regulatory and Competitive Landscape
Verizon operates in a regulated and highly competitive market. Current and potential competitors include other voice and data service providers, such as other wireless
companies, traditional telephone companies, cable companies, Internet service providers, software and application providers and other non-traditional competitors. Many of these
companies have strong market presence, brand recognition and existing customer relationships, all of which contribute to a highly competitive market that may affect our future
revenue growth. Some of our competitors also are subject to fewer regulatory constraints than Verizon. For many services offered by Verizon, the FCC is our primary regulator.
The FCC has jurisdiction over interstate telecommunications services and other matters under the Communications Act of 1934, as amended (Communications Act or Act).
Other Verizon services are subject to state and local regulation.
Federal, State and Local Regulation
Wireless Services
The FCC regulates several aspects of our wireless operations. Generally, the FCC has jurisdiction over the construction, operation, acquisition and transfer of wireless
communications systems. All wireless services require use of radio frequency spectrum, the assignment and distribution of which is subject to FCC oversight. Verizon
anticipates that it will need additional spectrum to meet future demand. We can meet our needs for licensed spectrum by purchasing licenses or leasing spectrum from others, or
by participating in a competitive bidding process to acquire new spectrum from the FCC. Those processes are subject to certain reviews, approvals and potential conditions.
Today, Verizon holds FCC spectrum licenses that allow it to provide a wide range of mobile and fixed communications services, including both voice and data services. FCC
spectrum licenses typically have a term of 10 years, at which time they are subject to renewal. While the FCC has routinely renewed all of Verizon’s wireless licenses, challenges
could be raised in the future. If a wireless license was revoked or not renewed, Verizon would not be permitted to provide services on the spectrum covered by that license. Some
of our licenses require us to comply with so-called "open access" FCC regulations, which generally require licensees of particular spectrum to allow customers to use devices and
applications of their choice, subject to certain technical limitations. The FCC has also imposed certain specific mandates on wireless carriers, including construction and
geographic coverage requirements, technical operating standards, provision of enhanced 911 services, roaming obligations and requirements for wireless tower and antenna
facilities.
The Act generally preempts regulation by state and local governments of the entry of, or the rates charged by, wireless carriers. The Act does not prohibit states from regulating
the other "terms and conditions" of wireless service. For example, some states attempt to regulate wireless customer billing matters and impose reporting requirements. Several
states also have laws or regulations that address safety issues (e.g., use of wireless handsets while driving) and taxation matters. In addition, wireless tower and antenna facilities
are often subject to state and local zoning and land use regulation, and securing approvals for new or modified facilities is often a lengthy and expensive process.
Broadband
Verizon offers many different broadband services. Traditionally, the FCC recognized broadband Internet access services as "information services" subject to a "light touch"
regulatory approach rather than to the traditional, utilities-style regulations. In 2015, the FCC declared that broadband Internet access services are "telecommunications services"
subject to common carriage regulation under Title II of the Communications Act. In December 2017, the FCC adopted an order reversing the 2015 Title II Order to return to
"light touch" regulation of broadband Internet access services. The "light touch" portions of this order have been upheld by the U.S. Court of Appeals for the D.C. Circuit but
further appeals are likely. The part of the FCC order automatically preempting state action on the subject was vacated, and a number of states are likely to join those that have
taken steps to regulate broadband. Regardless of regulation, Verizon remains committed to the open Internet, which provides consumers with competitive choices and unblocked
access to lawful websites and content, and our commitment to our customers can be found on our website at http://responsibility.verizon.com/broadband-commitment.
Wireline Voice
Verizon offers many different wireline voice services, including traditional telephone service and other services that rely on technologies such as VoIP. For regulatory purposes,
legacy telephone services are generally considered to be "common carrier" services. Common carrier services are subject to heightened regulatory oversight with respect to rates,
terms and conditions and other aspects of the services. The FCC has not decided the regulatory classification of VoIP but has said VoIP service providers must comply with
certain rules, such as 911 capabilities and law enforcement assistance requirements.
State public utility commissions regulate Verizon’s telephone operations with respect to certain telecommunications intrastate matters. Verizon operates as an "incumbent local
exchange carrier" in nine states and the District of Columbia. These incumbent operations are subject to various levels of pricing flexibility and other state oversight and
requirements. Verizon also has other wireline operations that are more lightly regulated.
Video
Verizon offers a multichannel video service that is regulated like traditional cable service. The FCC has a body of rules that apply to cable operators, and these rules also
generally apply to Verizon. In areas where Verizon offers its facilities-based multichannel video services, Verizon has been required to obtain a cable franchise from local
government entities, or in some cases a state-wide franchise, and comply with certain one-time and ongoing obligations as a result.
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Privacy and Data Security
We are subject to federal, state and international laws and regulations relating to privacy and data security that impact all parts of our business, including wireline, wireless,
broadband and the development and roll out of new products, such as those in the media and IoT space. At the federal level, our voice business is subject to the FCC's privacy
requirements. Oversight of broadband Internet access privacy and data security is governed by the Federal Trade Commission (FTC). Generally, attention to privacy and data
security requirements is increasing at both the state and federal level, and several privacy-related bills have been introduced or are under considerations at each level. Europe's
General Data Protection Regulation, which went into effect in May 2018, includes significant penalties for non-compliance. In addition, a new privacy law took effect in
California at the beginning of 2020, an additional privacy law is scheduled to take effect in Maine in 2020, and other states are considering additional regulations. These
regulations could have a significant impact on our businesses.
Public Safety and Cybersecurity
The FCC plays a role in addressing public safety concerns by regulating emergency communications services and mandating widespread availability of both media
(broadcast/cable) and wireless emergency alerting services. In response to cyber attacks that have occurred or could occur in the future, however, the FCC or other regulators
may attempt to increase regulation of the cybersecurity practices of providers. The FCC is also addressing the use by American companies of equipment produced by companies
imposing potential national security risks, but Verizon does not use such equipment in its network. In addition, due to recent natural disasters, federal and state agencies may
attempt to impose regulations to ensure continuity of service during disasters.
Intercarrier Compensation and Network Access
The FCC regulates some of the rates that carriers pay each other for the exchange of voice traffic (particularly traditional wireline traffic) over different networks and other
aspects of interconnection for some voice services. The FCC also regulates some of the rates and terms and conditions for certain wireline "business data services" and other
services and network facilities. Verizon is both a seller and a buyer of these services, and both makes and receives interconnection payments. The FCC has focused in recent
years on whether changes in the rates, terms and conditions for both the exchange of traffic and for business data services may be appropriate.
Information About Our Executive Officers
See Part III, Item 10. "Directors, Executive Officers and Corporate Governance" of this Annual Report on Form 10-K for information about our executive officers.
Employees
As of December 31, 2019, Verizon and its subsidiaries had approximately 135,000 employees. Labor unions represent approximately 23% of our employees.
Information on Our Internet Website
We make available, free of charge on our website, our annual reports on Form 10-K, quarterly reports on Form 10-Q, current reports on Form 8-K, and all amendments to those
reports at http://www.verizon.com/about/investors as soon as reasonably practicable after such reports are electronically filed with the Securities and Exchange Commission
(SEC). These reports and other information are also available on the SEC's website at www.sec.gov. We periodically provide other information for investors on this website, as
well, including news and announcements regarding our financial performance, information on corporate governance and details related to our annual meeting of shareholders.
We encourage investors, the media, our customers, business partners and other stakeholders to review the information we post on this channel. Website references in this report
are provided as a convenience and do not constitute, and should not be viewed as, incorporation by reference of the information contained on, or available through, the websites.
Therefore, such information should not be considered part of this report.
Cautionary Statement Concerning Forward-Looking Statements
In this report we have made forward-looking statements. These statements are based on our estimates and assumptions and are subject to risks and uncertainties. Forward-
looking statements include the information concerning our possible or assumed future results of operations. Forward-looking statements also include those preceded or followed
by the words "anticipates," "believes," "estimates," "expects," "hopes" or similar expressions. For those statements, we claim the protection of the safe harbor for forward-
looking statements contained in the Private Securities Litigation Reform Act of 1995. We undertake no obligation to revise or publicly release the results of any revision to these
forward-looking statements, except as required by law. Given these risks and uncertainties, readers are cautioned not to place undue reliance on such forward-looking statements.
The following important factors, along with those discussed elsewhere in this report and in other filings with the SEC, could affect future results and could cause those results to
differ materially from those expressed in the forward-looking statements:
•
•
•
•
cyber attacks impacting our networks or systems and any resulting financial or reputational impact;
natural disasters, terrorist attacks or acts of war or significant litigation and any resulting financial or reputational impact;
disruption of our key suppliers’ or vendors' provisioning of products or services;
material adverse changes in labor matters and any resulting financial or operational impact;
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•
•
•
•
•
•
•
•
•
•
•
the effects of competition in the markets in which we operate;
failure to take advantage of developments in technology and address changes in consumer demand;
performance issues or delays in the deployment of our 5G network resulting in significant costs or a reduction in the anticipated benefits of the enhancement to our
networks;
the inability to implement our business strategy;
adverse conditions in the U.S. and international economies;
changes in the regulatory environment in which we operate, including any increase in restrictions on our ability to operate our networks;
our high level of indebtedness;
an adverse change in the ratings afforded our debt securities by nationally accredited ratings organizations or adverse conditions in the credit markets affecting the cost,
including interest rates, and/or availability of further financing;
significant increases in benefit plan costs or lower investment returns on plan assets;
changes in tax laws or treaties, or in their interpretation; and
changes in accounting assumptions that regulatory agencies, including the SEC, may require or that result from changes in the accounting rules or their application,
which could result in an impact on earnings.
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Item 1A. Risk Factors
The following discussion of "Risk Factors" identifies the most significant factors that may adversely affect our business, operations, financial condition or future performance.
This information should be read in conjunction with "Management’s Discussion and Analysis of Financial Condition and Result of Operations" and the consolidated financial
statements and related notes. The following discussion of risks is not all-inclusive but is designed to highlight what we believe are important factors to consider when evaluating
our business and expectations. These factors could cause our future results to differ materially from our historical results and from expectations reflected in forward-looking
statements.
Operational Risks
Cyber attacks impacting our networks or systems could have an adverse effect on our business.
Cyber attacks, including through the use of malware, computer viruses, dedicated denial of services attacks, credential harvesting, social engineering and other means for
obtaining unauthorized access to or disrupting the operation of our networks and systems and those of our suppliers, vendors and other service providers, could have an adverse
effect on our business. Cyber attacks may cause equipment failures, loss of information, including sensitive personal information of customers or employees or valuable
technical and marketing information, as well as disruptions to our or our customers’ operations. Cyber attacks against companies, including Verizon, have increased in
frequency, scope and potential harm in recent years. They may occur alone or in conjunction with physical attacks, especially where disruption of service is an objective of the
attacker. The development and maintenance of systems to prevent such attacks is costly and requires ongoing monitoring and updating to address their increasing prevalence and
sophistication. While, to date, we have not been subject to cyber attacks that, individually or in the aggregate, have been material to Verizon's operations or financial condition,
the preventive actions we take to reduce the risks associated with cyber attacks, including protection of our systems and networks, may be insufficient to repel or mitigate the
effects of a major cyber attack in the future.
The inability to operate or use our networks and systems or those of our suppliers, vendors and other service providers as a result of cyber attacks, even for a limited period of
time, may result in significant expenses to Verizon and/or a loss of market share to other communications providers. The costs associated with a major cyber attack on Verizon
could include expensive incentives offered to existing customers and business partners to retain their business, increased expenditures on cybersecurity measures and the use of
alternate resources, lost revenues from business interruption and litigation. Further, certain of Verizon’s businesses, such as those offering security solutions and infrastructure
and cloud services to business customers, could be negatively affected if our ability to protect our own networks and systems is called into question as a result of a cyber attack.
Our presence in the IoT industry, which includes offerings of telematics products and services, could also increase our exposure to potential costs and expenses and reputational
harm in the event of cyber attacks impacting these products or services. In addition, a compromise of security or a theft or other compromise of valuable information, such as
financial data and sensitive or private personal information, could result in lawsuits and government claims, investigations or proceedings. Any of these occurrences could
damage our reputation, adversely impact customer and investor confidence and result in a material adverse effect on Verizon’s results of operation or financial condition.
Natural disasters, terrorist acts or acts of war could cause damage to our infrastructure and result in significant disruptions to our operations.
Our business operations are subject to interruption by power outages, terrorist attacks, other hostile acts and natural disasters, including an increasing prevalence of wildfires and
intensified storm activities. Such events could cause significant damage to our infrastructure upon which our business operations rely, resulting in degradation or disruption of
service to our customers, as well as significant recovery time and expenditures to resume operations. Our system redundancy may be ineffective or inadequate to sustain our
operations through all such events. We are implementing, and will continue to implement, measures to protect our infrastructure and operations from the impacts of these events
in the future, but these measures and our overall disaster recovery planning may not be sufficient for all eventualities. These events could also damage the infrastructure of the
suppliers that provide us with the equipment and services that we need to operate our business and provide products to our customers. These occurrences could result in lost
revenues from business interruption, damage to our reputation and reduced profits.
We depend on key suppliers and vendors to provide equipment that we need to operate our business.
We depend on various key suppliers and vendors to provide us, directly or through other suppliers, with equipment and services, such as fiber, switch and network equipment,
smartphones and other wireless devices that we need in order to operate our business and provide products to our customers. For example, our smartphone and other device
suppliers often rely on one vendor for the manufacture and supply of critical components, such as chipsets, used in their devices, and there are a limited number of companies
capable of supplying the network infrastructure equipment on which we depend. These suppliers or vendors could fail to provide equipment or service on a timely basis, or fail to
meet our performance expectations, for a number of reasons, including, for example, disruption to the global supply chain as a result of the coronavirus. If such failures occur,
we may be unable to provide products and services as and when requested by our customers, or we may be unable to continue to maintain or upgrade our networks. Because of
the cost and time lag that can be associated with transitioning from one supplier to another, our business could be substantially disrupted if we were required to, or chose to,
replace the products or services of one or more major suppliers with products or services from another source, especially if the replacement became necessary on short notice.
Any such disruption could increase our costs, decrease our operating efficiencies and have a material adverse effect on our business, results of operations and financial condition.
The suppliers and vendors on which we rely may also be subject to litigation with respect to technology on which we depend, including litigation involving claims of patent
infringement. Such claims are frequently made in the communications industry. We are unable to predict whether our
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business will be affected by any such litigation. We expect our dependence on key suppliers to continue as we develop and introduce more advanced generations of technology.
A significant portion of our workforce is represented by labor unions, and we could incur additional costs or experience work stoppages as a result of the renegotiation
of our labor contracts.
As of December 31, 2019, approximately 23% of our workforce was represented by labor unions. While we have labor contracts in place with these unions, with subsequent
negotiations we could incur additional costs and/or experience work stoppages, which could adversely affect our business operations. In addition, while a small percentage of the
workforce of our wireless and other businesses outside of wireline is represented by unions, we cannot predict what level of success unions may have in further organizing this
workforce or the potentially negative impact it would have on our operations.
Economic and Strategic Risks
We face significant competition that may reduce our profits.
We face significant competition in our industries. The rapid development of new technologies, services and products have eliminated many of the traditional distinctions among
wireless, cable, Internet and local and long distance communication services and brought new competitors to our markets, including other telephone companies, cable companies,
wireless service providers, satellite providers and application and device providers. While these changes have enabled us to offer new types of products and services, they have
also allowed other providers to broaden the scope of their own competitive offerings. If we are unable to compete effectively, we could experience lower than expected revenues
and earnings. A projected sustained decline in any of our reporting units' revenues and earnings could have a significant impact on its fair value and has caused us in the past, and
may cause us in the future, to record goodwill impairment charges. The amount of any impairment charge could be significant and could have a material adverse impact on our
results of operations for the period in which the charge is taken. In addition, wireless service providers are significantly altering the financial relationships with their customers
through commercial offers that vary service and device pricing, promotions, incentives and levels of service provided – in some cases specifically targeting our customers. Our
ability to compete effectively will depend on, among other things, our network quality, capacity and coverage, the pricing of our products and services, the quality of our
customer service, our development of new and enhanced products and services, the reach and quality of our sales and distribution channels and our capital resources. It will also
depend on how successfully we anticipate and respond to various factors affecting our industries, including new technologies and business models, changes in consumer
preferences and demand for existing services, demographic trends and economic conditions. If we are not able to respond successfully to these competitive challenges, we could
experience reduced profits.
If we are not able to take advantage of developments in technology and address changing consumer demand on a timely basis, we may experience a decline in the
demand for our services, be unable to implement our business strategy and experience reduced profits.
Our industries are rapidly changing as new technologies are developed that offer consumers an array of choices for their communications needs and allow new entrants into the
markets we serve. In order to grow and remain competitive, we will need to adapt to future changes in technology, enhance our existing offerings and introduce new offerings to
address our customers’ changing demands. If we are unable to meet future challenges from competing technologies on a timely basis or at an acceptable cost, we could lose
customers to our competitors. We may not be able to accurately predict technological trends or the success of new services in the market.
The deployment of our 5G network is subject to a variety of risks, including those related to equipment availability, unexpected costs, and regulatory permitting requirements
that could cause deployment delays or network performance issues. These issues could result in significant costs or reduce the anticipated benefits of the enhancements to our
networks. If our services fail to gain acceptance in the marketplace, or if costs associated with the implementation and introduction of these services materially increase, our
ability to retain and attract customers could be adversely affected.
In addition to introducing new offerings and technologies, such as 5G technology, we must phase out outdated and unprofitable technologies and services. If we are unable to do
so on a cost-effective basis, we could experience reduced profits. In addition, there could be legal or regulatory restraints on our ability to phase out current services.
Adverse conditions in the U.S. and international economies could impact our results of operations.
Unfavorable economic conditions, such as a recession or economic slowdown in the U.S. or elsewhere, could negatively affect the affordability of and demand for some of our
products and services. In difficult economic conditions, consumers may seek to reduce discretionary spending by forgoing purchases of our products, electing to use fewer higher
margin services, dropping down in price plans or obtaining lower-cost products and services offered by other companies. Similarly, under these conditions, the business
customers that we serve may delay purchasing decisions, delay full implementation of service offerings or reduce their use of services. In addition, adverse economic conditions
may lead to an increased number of our consumer and business customers that are unable to pay for services. If these events were to occur, it could have a material adverse effect
on our results of operations.
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Regulatory and Legal Risks
Changes in the regulatory framework under which we operate could adversely affect our business prospects or results of operations.
Our domestic operations are subject to regulation by the FCC and other federal, state and local agencies, and our international operations are regulated by various foreign
governments and international bodies. These regulatory regimes frequently restrict or impose conditions on our ability to operate in designated areas and provide specified
products or services. We are frequently required to maintain licenses for our operations and conduct our operations in accordance with prescribed standards. We are often
involved in regulatory and other governmental proceedings or inquiries related to the application of these requirements. It is impossible to predict with any certainty the outcome
of pending federal and state regulatory proceedings relating to our operations, or the reviews by federal or state courts of regulatory rulings. Without relief, existing laws and
regulations may inhibit our ability to expand our business and introduce new products and services. Similarly, we cannot guarantee that we will be successful in obtaining the
licenses needed to carry out our business plan or in maintaining our existing licenses. For example, the FCC grants wireless licenses for terms generally lasting 10 years, subject
to renewal. The loss of, or a material limitation on, certain of our licenses could have a material adverse effect on our business, results of operations and financial condition.
New laws or regulations or changes to the existing regulatory framework at the federal, state and local, or international level, such as those described below, or new laws or
regulations enacted to address the potential impacts of climate change, could restrict the ways in which we manage our wireline and wireless networks and operate our Media
business, impose additional costs, impair revenue opportunities and potentially impede our ability to provide services in a manner that would be attractive to us and our
customers.
•
Privacy and data protection
- we are subject to federal, state and international laws related to privacy and data protection. Europe's General Data Protection Regulation,
which went into effect in May 2018, includes significant penalties for non-compliance. In addition, a new privacy law took effect in California at the beginning of
2020, an additional privacy law is scheduled to take effect in Maine in 2020, and other states are considering additional regulations. These regulations could have a
significant impact on our businesses.
Regulation of broadband Internet access services
- In its 2015 Title II Order, the FCC nullified its longstanding "light touch" approach to regulating broadband Internet
access services and "reclassified" these services as telecommunications services subject to utilities-style common carriage regulation. The FCC repealed the 2015 Title
II Order in December 2017, and returned to its traditional light-touch approach for these services. The 2017 order has been affirmed in part by the D.C. Circuit, but
further appeals and challenges are possible; the outcome and timing of these or any other challenge remains uncertain. Several states have also adopted or are
considering adopting laws or executive orders that would impose net neutrality and other requirements on some of our services (in some cases different from the FCC’s
2015 rules). The enforceability and effect of these state rules is uncertain.
"Open Access"
- we hold certain wireless licenses that require us to comply with so-called "open access" FCC regulations, which generally require licensees of
particular spectrum to allow customers to use devices and applications of their choice. Moreover, certain services could be subject to conflicting regulation by the FCC
and/or various state and local authorities, which could significantly increase the cost of implementing and introducing new services.
•
•
The further regulation of broadband, wireless and our other activities and any related court decisions could restrict our ability to compete in the marketplace and limit the return
we can expect to achieve on past and future investments in our networks.
We are subject to a significant amount of litigation, which could require us to pay significant damages or settlements.
We are subject to a substantial amount of litigation, including, from time to time, shareholder derivative suits, patent infringement lawsuits, antitrust class actions, wage and hour
class actions, personal injury claims, property claims, and lawsuits relating to our advertising, sales, billing and collection practices. In addition, our wireless business also faces
personal injury and wrongful death lawsuits relating to alleged health effects of wireless phones or radio frequency transmitters. We may incur significant expenses in defending
these lawsuits. In addition, we may be required to pay significant awards or settlements.
Financial Risks
Verizon has significant debt, which could increase further if Verizon incurs additional debt in the future and does not retire existing debt.
As of December 31, 2019, Verizon had approximately $99.1 billion of outstanding unsecured indebtedness, $9.4 billion of unused borrowing capacity under its existing
revolving credit facility and $12.4 billion of outstanding secured indebtedness. Verizon’s debt level and related debt service obligations could have negative consequences,
including:
•
•
•
•
requiring Verizon to dedicate significant cash flow from operations to the payment of principal, interest and other amounts payable on its debt, which would reduce the
funds Verizon has available for other purposes, such as working capital, capital expenditures, dividend payments and acquisitions;
making it more difficult or expensive for Verizon to obtain any necessary future financing for working capital, capital expenditures, debt service requirements, debt
refinancing, acquisitions or other purposes;
reducing Verizon’s flexibility in planning for or reacting to changes in its industries and market conditions;
making Verizon more vulnerable in the event of a downturn in its business; and
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•
exposing Verizon to increased interest rate risk to the extent that its debt obligations are at variable interest rates.
Adverse changes in the credit markets and other factors could increase our borrowing costs and the availability of financing.
We require a significant amount of capital to operate and grow our business. We fund our capital needs in part through borrowings in the public and private credit markets.
Adverse changes in the credit markets, including increases in interest rates, could increase our cost of borrowing and/or make it more difficult for us to obtain financing for our
operations or refinance existing indebtedness. In addition, our ability to obtain funding under asset-backed debt transactions is subject to our ability to continue to originate a
sufficient amount of assets eligible to be securitized. Our borrowing costs also can be affected by short- and long-term debt ratings assigned by independent rating agencies,
which are based, in significant part, on our performance as measured by customary credit metrics. A decrease in these ratings would likely increase our cost of borrowing and/or
make it more difficult for us to obtain financing. A severe disruption in the global financial markets could impact some of the financial institutions with which we do business,
and such instability could also affect our access to financing.
Increases in costs for pension benefits and active and retiree healthcare benefits may reduce our profitability and increase our funding commitments.
With approximately 135,000 employees and approximately 191,000 retirees as of December 31, 2019 eligible to participate in Verizon’s benefit plans, the costs of pension
benefits and active and retiree healthcare benefits have a significant impact on our profitability. Our costs of maintaining these plans, and the future funding requirements for
these plans, are affected by several factors, including the legislative and regulatory uncertainty regarding the potential modification of the Patient Protection and Affordable Care
Act, increases in healthcare costs, decreases in investment returns on funds held by our pension and other benefit plan trusts and changes in the discount rate and mortality
assumptions used to calculate pension and other postretirement expenses. If we are unable to limit future increases in the costs of our benefit plans, those costs could reduce our
profitability and increase our funding commitments.
Item 1B. Unresolved Staff Comments
None.
Item 2. Properties
Our principal properties do not lend themselves to simple description by character and location. Our total gross investment in property, plant and equipment was approximately
$266 billion at December 31, 2019 and $253 billion at December 31, 2018, including the effect of retirements, but before deducting accumulated depreciation. Our gross
investment in property, plant and equipment consisted of the following:
At December 31,
Network equipment
Land, buildings and building equipment
Furniture and other
2019
77.3%
12.0%
10.7%
100.0%
2018
78.0%
12.4%
9.6%
100.0%
Network equipment consists primarily of cable (aerial, buried, underground or undersea) and the related support structures of poles and conduit, wireless plant, switching
equipment, network software, transmission equipment and related facilities. Land, buildings and building equipment consists of land and land improvements, central office
buildings or any other buildings that house network equipment, and buildings that are used for administrative and other purposes. Substantially all the switching centers are
located on land and in buildings we own due to their critical role in the networks and high set-up and relocation costs. We also maintain facilities throughout the U.S. comprised
of administrative and sales offices, customer care centers, retail sales locations, garage work centers, switching centers, cell sites and data centers. Furniture and other consists of
telephone equipment, furniture, data processing equipment, office equipment, motor vehicles, plant under construction and leasehold improvements.
Item 3. Legal Proceedings
In October 2013, the California Attorney General’s Office notified certain Verizon companies of potential violations of California state hazardous waste statutes primarily arising
from the disposal of electronic components, batteries and aerosol cans at certain California facilities. We are cooperating with this investigation and continue to review our
operations relating to the management of hazardous waste. While penalties relating to the alleged violations could exceed $100,000, we do not expect that any penalties
ultimately incurred will be material.
Item 4. Mine Safety Disclosures
None.
PART II
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Item 5. Market for Registrant’s Common Equity, Related Stockholder Matters and Issuer Purchases of Equity Securities
The principal market for trading in the common stock of Verizon is the New York Stock Exchange under the symbol "VZ". As of December 31, 2019, there were 605,414
shareholders of record.
Stock Repurchases
In February 2020, the Verizon Board of Directors authorized a share buyback program to repurchase up to 100 million shares of the Company's common stock. The program will
terminate when the aggregate number of shares purchased reaches 100 million, or a new share repurchase plan superseding the current plan is authorized, whichever is sooner.
Under the program, shares may be repurchased in privately negotiated transactions, on the open market, or otherwise, including through plans complying with Rule 10b5-1 under
the Exchange Act. The timing and number of shares purchased under the program, if any, will depend on market conditions and the Company's capital allocation priorities.
During the years ended December 31, 2019 and 2018, Verizon did not repurchase any shares of Verizon’s common stock under our previously authorized share buyback
program. At December 31, 2019, the maximum number of shares that could be purchased by or on behalf of Verizon under our share buyback program was 100 million.
For other information required by this item, see the section entitled "Stock Performance Graph" in the 2019 Verizon Annual Report to Shareholders, which is incorporated herein
by reference.
Item 6. Selected Financial Data
Information required by this item is included in the 2019 Verizon Annual Report to Shareholders under the heading "Selected Financial Data," which is incorporated herein by
reference.
Item 7. Management’s Discussion and Analysis of Financial Condition and Results of Operations
Information required by this item is included in the 2019 Verizon Annual Report to Shareholders under the heading "Management’s Discussion and Analysis of Financial
Condition and Results of Operations," which is incorporated herein by reference.
Item 7A. Quantitative and Qualitative Disclosures About Market Risk
Information required by this item is included in the 2019 Verizon Annual Report to Shareholders under the heading "Management’s Discussion and Analysis of Financial
Condition and Results of Operations - Market Risk," which is incorporated herein by reference.
Item 8. Financial Statements and Supplementary Data
Information required by this item is included in the consolidated financial statements and related notes of Verizon Communications Inc. and Subsidiaries in the 2019 Verizon
Annual Report to Shareholders, which is incorporated herein by reference.
Item 9. Changes in and Disagreements with Accountants on Accounting and Financial Disclosure
None.
Item 9A. Controls and Procedures
Our Chief Executive Officer and Chief Financial Officer have evaluated the effectiveness of the registrant’s disclosure controls and procedures (as defined in Rules 13a-15(e)
and 15d-15(e) of the Securities Exchange Act of 1934), as of the end of the period covered by this Annual Report, that ensure that information relating to the registrant which is
required to be disclosed in this report is recorded, processed, summarized and reported within required time periods using the criteria for effective internal control established in
Internal Control–Integrated Framework issued by the Committee of Sponsoring Organizations of the Treadway Commission in 2013. Based on this evaluation, our Chief
Executive Officer and Chief Financial Officer have concluded that the registrant’s disclosure controls and procedures were effective as of December 31, 2019.
In the ordinary course of business, we routinely review our system of internal control over financial reporting and make changes to our systems and processes that are intended to
ensure an effective internal control environment. There were no changes in the Company’s internal control over financial reporting during the fourth quarter of 2019 that have
materially affected, or are reasonably likely to materially affect, our internal control over financial reporting.
Management’s report on internal control over financial reporting and the attestation report of Verizon’s independent registered public accounting firm are included in the 2019
Verizon Annual Report to Shareholders and are incorporated herein by reference.
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Item 9B. Other Information
None.
PART III
Item 10. Directors, Executive Officers and Corporate Governance
Set forth below is information with respect to our executive officers.
Name
Hans Vestberg
Ronan Dunne
Matthew D. Ellis
Tami A. Erwin
K. Guru Gowrappan
Kyle Malady
Christine Pambianchi
Rima Qureshi
Craig L. Silliman
Anthony T. Skiadas
Age
54
56
48
55
39
52
51
55
52
51
Office
Chairman and Chief Executive Officer
Executive Vice President and Group CEO - Verizon Consumer
Executive Vice President and Chief Financial Officer
Executive Vice President and Group CEO - Verizon Business
Executive Vice President and Group CEO - Verizon Media
Executive Vice President and Chief Technology Officer
Executive Vice President and Chief Human Resources Officer
Executive Vice President and Chief Strategy Officer
Executive Vice President and Chief Administrative, Legal and Public Policy Officer
Senior Vice President and Controller
Held Since
2019
2019
2016
2019
2019
2019
2019
2017
2019
2013
Prior to serving as an executive officer, each of the above officers has held high-level managerial positions with the Company or one of its subsidiaries for at least five years,
with the exception of Hans Vestberg, who has been with the Company since 2017, Ronan Dunne, who has been with the Company since 2016, K. Guru Gowrappan, who has
been with the Company since 2018, Christine Pambianchi, who has been with the Company since 2019 and Rima Qureshi, who has been with the Company since 2017. Officers
are not elected for a fixed term of office and may be removed from office at any time at the discretion of the Board of Directors.
Hans Vestberg is the Chairman and Chief Executive Officer of Verizon. Mr. Vestberg joined the Company in April 2017 as Executive Vice President and President - Global
Networks and Technology. He began serving in his current role of Chief Executive Officer in August 2018 and was elected Chairman in March 2019. Prior to joining Verizon,
Mr. Vestberg served for six years as President and Chief Executive Officer of Ericsson, a multinational networking and telecommunications equipment and services company
headquartered in Sweden.
Ronan Dunne is the Executive Vice President and Group CEO - Verizon Consumer. Mr. Dunne joined the Company in September 2016 as Executive Vice President and
President of Verizon Wireless. Prior to joining Verizon, Mr. Dunne served for eight years as Chief Executive Officer of Telefónica UK Limited (O2), the second largest wireless
operator in the United Kingdom.
K. Guru Gowrappan is the Executive Vice President and Group CEO - Verizon Media. Mr. Gowrappan joined the Company in April 2018 as the President and Chief Operating
Officer of Oath. He began serving in his current role in October 2018. Prior to joining Verizon, Mr. Gowrappan served as the Global Managing Director of Alibaba Inc. from
2015 to 2018 and as the Chief Operating Officer for Quixey, a mobile search engine, from 2012 to 2015.
Christine Pambianchi is the Executive Vice President and Chief Human Resources Officer. Ms. Pambianchi joined the Company in July 2019. Prior to joining Verizon, Ms.
Pambianchi led the Human Resources function at Corning Incorporated, a leading innovator in materials science, where she served as Executive Vice President, People and
Digital, from 2018 to 2019 and as Senior Vice President, Human Resources, from 2010 to 2018.
Rima Qureshi is Executive Vice President and Chief Strategy Officer of Verizon. Ms. Qureshi joined the Company in November 2017. Prior to joining Verizon, Ms. Qureshi
served as President and Chief Executive Officer of Ericsson North America from 2016 to 2017 and as Senior Vice President and Chief Strategy Officer and head of mergers and
acquisitions of Ericsson from 2014 to 2016. Ms. Qureshi also served as Vice President of Ericsson’s CDMA Mobile Systems Group, Senior Vice President of Strategic Projects,
Chairman of Ericsson’s Northern Europe, Russia and Central Asia Group and Chairman of Ericsson’s Modem division before becoming Chief Strategy Officer.
For other information required by this item, see the sections entitled "Governance — Item 1: Election of Directors — Nominees for Election and — Election Process, — Our
Approach to Governance — Where to Find More Information on Governance at Verizon, — Our Board Composition and Structure — Board Committees — Audit Committee
and — Our Approach to Strategy and Risk Oversight — Other Risk-Related Matters — Business Conduct and Ethics” in our definitive Proxy Statement to be filed with the
Securities and Exchange Commission and delivered to shareholders in connection with our 2020 Annual Meeting of Shareholders, which are incorporated herein by reference.
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Item 11. Executive Compensation
For information with respect to executive compensation, see the sections entitled "Governance — Non-Employee Director Compensation" and "Executive Compensation —
Compensation Discussion and Analysis, — Compensation Committee Report and — Compensation Tables" in our definitive Proxy Statement to be filed with the Securities and
Exchange Commission and delivered to shareholders in connection with our 2020 Annual Meeting of Shareholders, which are incorporated by reference herein. There were no
relationships to be disclosed under paragraph (e)(4) of Item 407 of Regulation S-K.
Item 12. Security Ownership of Certain Beneficial Owners and Management and Related Stockholder Matters
For information with respect to the security ownership of the Directors and Executive Officers, see the section entitled "Stock Ownership —Security Ownership of Certain
Beneficial Owners and Management" in our definitive Proxy Statement to be filed with the SEC and delivered to shareholders in connection with our 2020 Annual Meeting of
Shareholders, which is incorporated herein by reference. In addition, the following table provides other equity compensation plan information:
The following table provides information as of December 31, 2019 for (i) all equity compensation plans previously approved by the Company’s shareholders, and (ii) all equity
compensation plans not previously approved by the Company’s shareholders. From May 9, 2009 until May 4, 2017, the Company only issued awards under the 2009 Verizon
Communications Inc. Long-Term Incentive Plan and, after May 4, 2017, the Company only issued awards under the 2017 Verizon Communications. Inc. Long-Term Incentive
Plan (2017 LTIP). Each of these plans provides for awards of stock options, restricted stock, restricted stock units, performance stock units and other equity-based hypothetical
stock units to employees of Verizon and its subsidiaries. No new awards are permitted to be issued under any equity compensation plan other than the 2017 LTIP. In accordance
with SEC rules, the table does not include outstanding awards that are payable solely in cash by the terms of the award, and such awards do not reduce the number of shares
remaining for issuance under the 2017 LTIP.
Weighted-average
exercise price of
outstanding options,
warrants and rights
(b)
(1)
Plan Category
Number of securities to
be issued upon exercise
of outstanding options,
warrants and rights (a)
Number of securities remaining
available for future issuance under
equity compensation plans
(excluding securities reflected in
column (a)) (c)
(2)
Equity compensation plans approved by security holders
Equity compensation plans not approved by security holders
Total
(1)
7,259,237
120,272
7,379,509
$
—
—
88,717,670
—
88,717,670
(3)
(4)
$
—
This amount includes: 7,259,237 of common stock subject to outstanding restricted stock units and performance stock units, including dividend equivalents accrued on such
awards through December 31, 2019. This does not include performance stock units, deferred stock units and deferred share equivalents payable solely in cash.
Verizon’s outstanding restricted stock units, performance stock units and deferred stock units do not have exercise prices associated with the settlement of these awards.
This number reflects the number of shares of common stock that remained available for future issuance under the 2017 LTIP.
This number reflects shares subject to deferred stock units credited to the Verizon Income Deferral Plan, which were awarded in 2002 under the Verizon Communications
Broad-Based Incentive Plan. No new awards are permitted to be issued under this plan.
(2)
(3)
(4)
Item 13. Certain Relationships and Related Transactions, and Director Independence
For information with respect to certain relationships and related transactions and Director independence, see the sections entitled "Governance — Our Approach to Governance
— Our Approach to Strategy and Risk Oversight — Other Risk-Related Matters — Related Person Transactions and — Our Board Composition and Structure — Our Board's
Independence" in our definitive Proxy Statement to be filed with the Securities and Exchange Commission and delivered to shareholders in connection with our 2020 Annual
Meeting of Shareholders, which are incorporated by reference.
Item 14. Principal Accounting Fees and Services
For information with respect to principal accounting fees and services, see the section entitled "Audit Matters — Item 3: Ratification of Appointment of Independent Registered
Public Accounting Firm" in our definitive Proxy Statement to be filed with the Securities and Exchange Commission and delivered to shareholders in connection with our 2020
Annual Meeting of Shareholders, which are incorporated by reference.
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PART IV
Item 15. Exhibits, Financial Statement Schedules
(a) Documents filed as part of this report:
Page
(1)
(2)
(3)
Report of Management on Internal Control Over Financial Reporting
Report of Independent Registered Public Accounting Firm on Internal Control Over Financial Reporting
Report of Independent Registered Public Accounting Firm on Financial Statements
Financial Statements covered by Report of Independent Registered Public Accounting Firm:
Consolidated Statements of Income
Consolidated Statements of Comprehensive Income
Consolidated Balance Sheets
Consolidated Statements of Cash Flows
Consolidated Statements of Changes in Equity
Notes to Consolidated Financial Statements
* Incorporated herein by reference to the appropriate portions of the registrant’s Annual Report to Shareholders for the fiscal year ended
December 31, 2019. (See Part II.)
(4)
Financial Statement Schedule
II – Valuation and Qualifying Accounts
(5)
Exhibits
Exhibits identified in parentheses below, on file with the SEC, are incorporated herein by reference as exhibits hereto. Unless otherwise indicated,
all exhibits so incorporated are from File No. 1-8606.
26
*
*
*
*
*
*
*
*
*
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Exhibit
Number
3a
3b
4a
Description
Restated Certificate of Incorporation of Verizon Communications Inc. (Verizon) (filed as Exhibit 3a to Form 10-Q for the period ended June 30, 2014 and
incorporated herein by reference).
Bylaws of Verizon, as amended and restated, effective as of December 5, 2019 (filed as Exhibit 3b to Form 8-K filed on December 5, 2019 and incorporated
herein by reference).
Indenture between Verizon, both individually and as successor in interest to Verizon Global Funding Corp., and U.S. Bank National Association, as successor
trustee to Wachovia Bank, National Association, formerly known as First Union National Bank, as Trustee, dated as of December 1, 2000 (incorporated by
reference to Verizon Global Funding Corp.’s Registration Statement on Form S-4, Registration No. 333-64792, Exhibit 4.1).
First Supplemental Indenture between Verizon, both individually and as successor in interest to Verizon Global Funding Corp., and U.S. Bank National
Association, as successor trustee to Wachovia Bank, National Association, formerly known as First Union National Bank, as Trustee, dated as of May 15, 2001
(incorporated by reference to Verizon Global Funding Corp.’s Registration Statement on Form S-3, Registration No. 333-67412, Exhibit 4.2).
Second Supplemental Indenture between Verizon, both individually and as successor in interest to Verizon Global Funding Corp., and U.S. Bank National
Association, as successor trustee to Wachovia Bank, National Association, formerly known as First Union National Bank, as Trustee, dated as of September 29,
2004 (incorporated by reference to Form 8-K filed on February 9, 2006, Exhibit 4.1).
Third Supplemental Indenture between Verizon, both individually and as successor in interest to Verizon Global Funding Corp., and U.S. Bank National
Association, as successor trustee to Wachovia Bank, National Association, formerly known as First Union National Bank, as Trustee, dated as of February 1,
2006 (incorporated by reference to Form 8-K filed on February 9, 2006, Exhibit 4.2).
Fourth Supplemental Indenture between Verizon, both individually and as successor in interest to Verizon Global Funding Corp., and U.S. Bank National
Association, as successor trustee to Wachovia Bank, National Association, formerly known as First Union National Bank, as Trustee, dated as of April 4, 2016
(incorporated by reference to Verizon Communications Inc.’s Registration Statement on Form S-4, Registration No. 333-212307, Exhibit 4.5).
Except for Exhibits 4a – 4e above, no other instrument which defines the rights of holders of long-term debt of Verizon and its consolidated subsidiaries is filed
herewith pursuant to Regulation S-K, Item 601(b)(4)(iii)(A). Pursuant to this regulation, Verizon hereby agrees to furnish a copy of any such instrument to the
SEC upon request.
4b
4c
4d
4e
4f
10a
10b
Description of Verizon's Securities Registered Pursuant to Section 12 of the Securities and Exchange Act of 1934, filed herewith.
NYNEX Directors’ Charitable Award Program (filed as Exhibit 10i to Form 10-K for the year ended December 31, 2000 and incorporated herein by reference).**
2009 Verizon Long-Term Incentive Plan, As Amended and Restated (incorporated by reference to Appendix D of the Registrant’s Proxy Statement included in
Schedule 14A filed on March 18, 2013).**
10b(i)
10b(ii)
10b(iii)
10b(iv)
10b(v)
Form of Performance Stock Unit Agreement 2016-2018 Award Cycle (filed as Exhibit 10a to Form 10-Q for the period ended March 31, 2016
and incorporated herein by reference).**
Form of Restricted Stock Unit Agreement 2016-2018 Award Cycle (filed as Exhibit 10b to Form 10-Q for the period ended March 31, 2016 and
incorporated herein by reference).**
Form of 2017 Performance Stock Unit Agreement pursuant to the 2009 Verizon Communications Inc. Long-Term Incentive Plan. (filed as
Exhibit 10a to Form 10-Q for the period ended March 31, 2017 and incorporated herein by reference).**
Form of 2017 Restricted Stock Unit Agreement pursuant to the 2009 Verizon Communications Inc. Long-Term Incentive Plan (filed as Exhibit
10b to Form 10-Q for the period ended March 31, 2017 and incorporated herein by reference).**
2017 Special Performance Stock Unit Agreement pursuant to the 2009 Verizon Communications Inc. Long-Term Incentive Plan for J. Stratton
(filed as Exhibit 10c to Form 10-Q for the period ended March 31, 2017 and incorporated herein by reference).**
10c
2017 Verizon Communications Inc. Long-Term Incentive Plan (incorporated by reference to Appendix B of the Registrant’s Proxy Statement included in
Schedule 14A filed on March 20, 2017).**
10c(i)
10c(ii)
10c(iii)
Form of 2017 Performance Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan. (filed as
Exhibit 10a to Form 10-Q for the period ended June 30, 2017 and incorporated herein by reference).**
Form of 2017 Restricted Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan (filed as Exhibit
10b to Form 10-Q for the period ended June 30, 2017 and incorporated herein by reference).**
2017 Special Restricted Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan (filed as Exhibit
10c to Form 10-Q for the period ended June 30, 2017 and incorporated herein by reference).**
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10c(iv)
Form of 2017 Restricted Stock Unit Agreement (cash-settled) pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan
(filed as Exhibit 10c(iv) to Form 10-K for period ended December 31, 2017 and incorporated herein by reference).**
Form of 2018 Performance Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan (filed as Exhibit
10a to Form 10-Q for the period ended March 31, 2018 and incorporated herein by reference).**
Form of 2018 Restricted Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term
Incentive Plan. (filed as Exhibit 10b to Form 10-Q for the period ended March 31, 2018 and incorporated herein by reference).**
2018 Special Performance Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan for H. Vestberg
(filed as Exhibit 10 to Form 10-Q for the period ended September 30, 2018 and incorporated herein by reference).**
2018 Restricted Stock Unit Agreement for G. Gowrappan pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan (filed as
Exhibit 10c(viii) to Form 10-K for the period ended December 31, 2018 and incorporated herein by reference).**
Special Performance Restricted Stock Unit Agreement for R. Dunne pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive
Plan (filed as Exhibit 10c(ix) to Form 10-K for the period ended December 31, 2018 and incorporated herein by reference).**
Special Performance Restricted Stock Unit Agreement for G. Gowrappan pursuant to the 2017 Verizon Communications Inc. Long-Term
Incentive Plan (filed as Exhibit 10c(x) to Form 10-K for the period ended December 31, 2018 and incorporated herein by reference).**
Amendment to Special Performance Restricted Stock Unit Agreement for G. Gowrappan pursuant to the 2017 Verizon Communications Inc.
Long-Term Incentive Plan (filed as Exhibit 10c(x)(i) to Form 10-K for the period ended December 31, 2018 and incorporated herein by
reference).**
Form of 2019 Performance Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term Incentive Plan (filed as Exhibit
10b to Form 10-Q for the period ended March 31, 2019 and incorporated herein by reference).**
Form of 2019 Restricted Stock Unit Agreement pursuant to the 2017 Verizon Communications Inc. Long-Term
Incentive Plan (filed as Exhibit 10c to Form 10-Q for the period ended March 31, 2019 and incorporated herein by reference).**
10c(v)
10c(vi)
10c(vii)
10c(viii)
10c(ix)
10c(x)
10c(x)(i)
10c(xii)
10c(xiii)
10d
10e
10f
Verizon Communications Inc. Short-Term Incentive Plan (filed as Exhibit 10a to Form 10-Q for the period ended March 31, 2019 and incorporated herein by
reference).**
Verizon Executive Deferral Plan (filed as Exhibit 10e to Form 10-K for the period ended December 31, 2017 and incorporated herein by reference).**
Verizon Income Deferral Plan (filed as Exhibit 10f to Form 10-Q for the period ended June 30, 2002 and incorporated herein by reference).**
10f(i)
Description of Amendment to Plan (filed as Exhibit 10o(i) to Form 10-K for the year ended December 31, 2004 and incorporated herein by
reference).**
10g
Verizon Excess Pension Plan (filed as Exhibit 10p to Form 10-K for the year ended December 31, 2004 and incorporated herein by reference).**
10g(i)
Description of Amendment to Plan (filed as Exhibit 10p(i) to Form 10-K for the year ended December 31, 2004 and incorporated herein by
reference).**
10h
10i
10j
10k
10l
10m
GTE’s Executive Salary Deferral Plan, as amended (filed as Exhibit 10.10 to GTE’s Form 10-K for the year ended December 31, 1998, File No. 1-2755 and
incorporated herein by reference).**
Bell Atlantic Senior Management Long-Term Disability and Survivor Protection Plan, as amended (filed as Exhibit 10h to Form SE filed on March 27, 1986 and
Exhibit 10b(ii) to Form 10-K for the year ended December 31, 1997 and incorporated herein by reference).**
GTE Executive Retiree Life Insurance Plan (filed as Exhibit 10q to Form 10-K for the year ended December 31, 2010 and incorporated herein by reference).**
Verizon Executive Life Insurance Plan, As Amended and Restated September 2009 (filed as Exhibit 10s to Form 10-K for the year ended December 31, 2010 and
incorporated herein by reference).**
Form of Aircraft Time Sharing Agreement (filed as Exhibit 10l to Form 10-K for year ended December 31, 2017 and incorporated herein by reference).**
NYNEX Deferred Compensation Plan for Non-Employee Directors (filed as Exhibit 10iii 5a to NYNEX’s Quarterly Report on Form 10-Q for the period ended
June 30, 1996, File No. 1-8608 and incorporated herein by reference).**
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10n
10o
Verizon Senior Manager Severance Plan (filed as Exhibit 10d to Form 10-Q for the period ended March 31, 2010 and incorporated herein by reference).**
AOL Inc. Long-Term Incentive Plan (filed as Exhibit 10o to Form 10-K for the period ended December 31, 2018 and incorporated herein by reference).**
10o(i)
Founders’ Grant Unit Agreement for T. Armstrong pursuant to the AOL Inc. Long-Term Incentive Plan (filed as Exhibit 10o(i) to Form 10-K for
the period ended December 31, 2018 and incorporated herein by reference).**
13
21
23
24
31.1
31.2
32.1
32.2
101.INS
101.SCH
101.PRE
101.CAL
101.LAB
101.DEF
104
**
Portions of Verizon’s Annual Report to Shareholders for the fiscal year ended December 31, 2019 filed herewith. Only the information incorporated by reference
into this Form 10-K is included in the exhibit.
List of principal subsidiaries of Verizon, filed herewith.
Consent of Ernst & Young LLP, filed herewith.
Powers of Attorney, filed herewith.
Certification of Chief Executive Officer pursuant to Section 302 of the Sarbanes-Oxley Act of 2002, filed herewith.
Certification of Chief Financial Officer pursuant to Section 302 of the Sarbanes-Oxley Act of 2002, filed herewith.
Certification of Chief Executive Officer pursuant to Section 906 of the Sarbanes-Oxley Act of 2002, filed herewith.
Certification of Chief Financial Officer pursuant to Section 906 of the Sarbanes-Oxley Act of 2002, filed herewith.
XBRL Instance Document - the instance document does not appear in the interactive data file because its XBRL tags are embedded within the inline XBRL
document.
XBRL Taxonomy Extension Schema Document.
XBRL Taxonomy Presentation Linkbase Document.
XBRL Taxonomy Calculation Linkbase Document.
XBRL Taxonomy Label Linkbase Document.
XBRL Taxonomy Extension Definition Linkbase Document.
Cover Page Interactive Data File (formatted as inline XBRL with applicable taxonomy extension information contained in Exhibits 101).
Indicates management contract or compensatory plan or arrangement.
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Schedule II - Valuation and Qualifying Accounts
Verizon Communications Inc. and Subsidiaries
For the Years Ended December 31, 2019, 2018 and 2017
(dollars in millions)
Additions
Balance at
Beginning of
Period
$
930
1,199
1,146
$
Charged to
Expenses
1,441
776
1,167
Additions
Balance at
Beginning of
Period
$
2,741
3,293
2,473
$
Charged to
Expenses
402
251
765
$
Charged to
Other Accounts
(d)
8
112
273
$
Balance at End
of Period
$
2,260
2,741
3,293
$
Charged to
Other Accounts
(a)
133
216
205
$
Balance at End
of Period
(c)
$
860
930
1,199
Description
Allowance for Uncollectible Accounts Receivable:
Year 2019
Year 2018
Year 2017
Deductions
(b)
1,644
1,261
1,319
Description
Valuation Allowance for Deferred Tax Assets:
Year 2019
Year 2018
Year 2017
(a)
(b)
(c)
(d)
(e)
Deductions
(e)
891
915
218
Charged to Other Accounts primarily includes amounts previously written off which were credited directly to this account when recovered.
Deductions primarily include amounts written off as uncollectible or transferred to other accounts or utilized.
Allowance for Uncollectible Accounts Receivable includes approximately $127 million, $165 million and $260 million at December 31, 2019, 2018, and 2017, respectively,
related to long-term device payment plan receivables.
Charged to Other Accounts includes current year increase to valuation allowance charged to equity and reclassifications from other balance sheet accounts.
Reductions to valuation allowances related to deferred tax assets.
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Item 16. Form 10-K Summary
None.
Signatures
Pursuant to the requirements of Section 13 or 15(d) of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the
undersigned, thereunto duly authorized.
VERIZON COMMUNICATIONS INC.
By:
/s/ Anthony T. Skiadas
Anthony T. Skiadas
Senior Vice President and Controller
Pursuant to the requirements of the Securities Exchange Act of 1934, this report has been signed below by the following persons on behalf of the registrant and in the capacities
and on the dates indicated.
Principal Executive Officer:
/s/ Hans E. Vestberg
Hans E. Vestberg
Principal Financial Officer:
/s/ Matthew D. Ellis
Matthew D. Ellis
Principal Accounting Officer:
/s/ Anthony T. Skiadas
Anthony T. Skiadas
Senior Vice President and
Controller
February 21, 2020
Executive Vice President and
Chief Financial Officer
February 21, 2020
Chairman and
Chief Executive Officer
February 21, 2020
Date: February 21, 2020
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*
Hans E. Vestberg
*
Shellye L. Archambeau
*
Mark T. Bertolini
*
Vittorio Colao
*
Melanie L. Healey
*
Clarence Otis, Jr.
*
Daniel H. Schulman
*
Rodney E. Slater
*
Kathryn A. Tesija
*
Carol B. Tomé
*
Gregory G. Weaver
* By: /s/ Anthony T. Skiadas
Anthony T. Skiadas
(as attorney-in-fact)
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
Director
February 21, 2020
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DESCRIPTION OF VERIZON’S SECURITIES
REGISTERED PURSUANT TO SECTION 12 OF
THE SECURITIES EXCHANGE ACT OF 1934
EXHIBIT 4f
As of December 31, 2019, Verizon Communications Inc. had the following twenty-one classes of securities registered under Section 12 of the Securities Exchange Act
of 1934, as amended: (i) common stock, $.0.10 par value per share (“Common Stock”), (ii) 2.375% Notes due 2022 (the “2.375% 2022 Notes”), (iii) 0.500% Notes due 2022 (the
“0.500% 2022 Notes”), (iv) 1.625% Notes due 2024 (the “1.625% 2024 Notes”), (v) 4.073% Notes due 2024 (the “4.073% 2024 Notes”), (vi) 0.875% Notes due 2025 (the “2025
Notes”), (vii) 3.250% Notes due 2026 (the “3.250% 2026 Notes”), (viii) 1.375% Notes due 2026 (the “1.375% 2026 Notes”), (ix) 0.875% Notes due 2027 (the “2027 Notes”),
(x) 1.375% Notes due 2028 (the “2028 Notes”), (xi) 1.875% Notes due 2029 (the “2029 Notes”), (xii) 1.250% Notes due 2030 (the “1.250% 2030 Notes”), (xiii)1.875% Notes
due 2030 (the “1.875% 2030 Notes”), (xiv) 2.625% Notes due 2031 (the “2.625% 2031 Notes”), (xv) 2.500% Notes due 2031 (the “2.500% 2031 Notes”), (xvi) 0.875% Notes
due 2032 (the “2032 Notes”), (xvii) 4.750% Notes due 2034 (the “2034 Notes”), (xviii) 3.125% Notes due 2035 (the “2035 Notes”), (xix) 3.375% Notes due 2036 (the “2036
Notes”), (xx) 2.875% Notes due 2038 (the “2038 Notes”) and (xxi) 1.500% Notes due 2039 (the “2039 Notes,” and together with the 2.375% 2022 Notes, the 0.500% 2022
Notes, the 1.625% 2024 Notes, the 4.073% 2024 Notes, the 2025 Notes, the 3.250% 2026 Notes, the 1.375% 2026 Notes, the 2027 Notes, the 2028 Notes, the 2029 Notes, the
1.250% 2030 Notes, the 1.875% 2030 Notes, the 2.625% 2031 Notes, the 2.500% 2031 Notes, the 2032 Notes, the 2034 Notes, the 2035 Notes, the 2036 Notes and the 2038
Notes, the “Notes”). In this exhibit, “we,” “our,” “us” and “Verizon Communications” refer to Verizon Communications Inc.
COMMON STOCK
Our restated certificate of incorporation provides authority to issue up to 6,500,000,000 shares of stock of all classes, of which 6,250,000,000 are shares of Common
Stock, and 250,000,000 are shares of preferred stock, $0.10 par value per share.
Subject to any preferential rights of the preferred stock, holders of shares of our Common Stock are entitled to receive dividends on that stock out of assets legally
available for distribution when, as and if authorized and declared by the board of directors and to share ratably in assets legally available for distribution to our shareholders in
the event of our liquidation, dissolution or winding-up. We may not pay any dividend or make any distribution of assets on shares of Common Stock until cumulative dividends
on shares of preferred stock then outstanding, if any, having dividend or distribution rights senior to the Common Stock have been paid.
Holders of Common Stock are entitled to one vote per share on all matters voted on generally by the shareholders, including the election of directors. In addition, the
holders of Common Stock possess all voting power except as otherwise required by law or except as provided for by any series of preferred stock. Our restated certificate of
incorporation does not provide for cumulative voting for the election of directors.
No holder of any shares of Common Stock has any preemptive or preferential right to acquire or subscribe for any unissued shares of any class of stock or any
authorized securities convertible into or carrying any right, option or warrant to subscribe for or acquire shares of any class of stock.
The Common Stock is listed on the New York Stock Exchange and the NASDAQ Global Select Market under the symbol “VZ.”
Our board of directors is authorized at any time to provide for the issuance of all or any shares of our preferred stock in one or more classes or series, and to fix for
each class or series voting powers, full or limited, or no voting powers, and distinctive designations, preferences and relative, participating, optional or other special rights and
any qualifications, limitations or restrictions, as shall be stated and expressed in the resolution or resolutions adopted by the board of directors providing for the issuance of the
preferred stock and to the fullest extent as may be permitted by Delaware law. This authority includes, but is not limited to, the authority to provide that any class or series be:
•
•
subject to redemption at a specified time or times and at a specified price or prices;
entitled to receive dividends (which may be cumulative or non-cumulative) at specified rates, on specified conditions and at specified times, and payable in preference
to, or in relation to, the dividends payable on any other class or classes or any other series;
entitled to rights upon the dissolution of, or upon any distribution of the assets of, Verizon Communications; or
convertible into, or exchangeable for, shares of any class or classes of our stock, or our other securities or property, at a specified price or prices or at specified rates of
exchange and with any specified adjustments.
•
•
Although no shares of preferred stock are outstanding as of December 31, 2019, in the event of the issuance of any shares of preferred stock, the rights evidenced by, or
amounts payable with respect to, the Common Stock may be materially limited or qualified by the terms of such preferred stock.
NOTES
The following description of the Notes is a summary and does not purport to be complete. This description is qualified in its entirety by reference to the indenture
between the Company and U.S. Bank National Association (as successor to Wachovia Bank, National Association,
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formerly known as First Union National Bank), as trustee, dated as of December 1, 2000, as amended (the “Indenture”) and the terms of the global securities representing the
Notes.
Principal Amount, Maturity, Interest and Listing
The following table sets forth for each series of Notes the applicable date of initial issuance, principal amount initially issued, principal amount outstanding as of
December 31, 2019, maturity date, interest rate per annum, interest payment and record dates, and New York Stock Exchange listing symbol:
Principal Amount
Outstanding as of
12/31/2019
€935,347,000
€453,963,000
€684,827,000
£412,534,000
€1,000,000,000
€1,250,000,000
€1,250,000,000
€1,250,000,000
€1,250,000,000
€750,000,000
€1,250,000,000
£550,000,000
€1,000,000,000
£500,000,000
€800,000,000
£456,624,000
£450,000,000
£1,000,000,000
€1,500,000,000
€500,000,000
NYSE
Listing
Symbol
VZ22A
VZ22B
VZ24B
VZ24C
VZ25
VZ26
VZ26B
VZ27E
VZ28
VZ29B
VZ30
VZ30A
VZ31
VZ31A
VZ32
VZ34
VZ35
VZ36A
VZ38B
VZ39C
Notes
2.375% 2022
Notes
0.500% 2022
Notes
1.625% 2024
Notes
4.073% 2024
Notes
2025 Notes
3.250% 2026
Notes
1.375% 2026
Notes
2027 Notes
2028 Notes
2029 Notes
1.250% 2030
Notes
1.875% 2030
Notes
2.625% 2031
Notes
2.500% 2031
Notes
2032 Notes
2034 Notes
2035 Notes
2036 Notes
2038 Notes
2039 Notes
Date of Initial
Issuance
February 12,
2014
November 2,
2016
December 1,
2014
June 18, 2014
November 2,
2016
February 12,
2014
October 27,
2017
April 8, 2019
November 2,
2016
October 27,
2017
April 8, 2019
September 19,
2019
December 1,
2014
April 8, 2019
September 19,
2019
February 12,
2014
November 2,
2016
October 27,
2017
October 27,
2017
September 19,
2019
Principal Amount
Initially Issued
€1,750,000,000
€1,000,000,000
€1,400,000,000
£694,804,000
€1,000,000,000
€1,250,000,000
€1,250,000,000
€1,250,000,000
€1,250,000,000
€750,000,000
€1,250,000,000
£550,000,000
€1,000,000,000
£500,000,000
€800,000,000
£850,000,000
£450,000,000
£1,000,000,000
€1,500,000,000
€500,000,000
Maturity Date
Interest Rate
Per Annum
Interest
Payment Date
February 17
June 2
March 1
June 18
April 2
February 17
October 27
April 8
November 2
October 26
April 8
September 19
December 1
April 8
March 19
February 17
November 2
October 27
January 15
September 19
Record Date
February 3
May 19
February 15
June 4
March 19
February 3
October 12
March 24
October 19
October 11
March 24
September 4
November 15
March 24
March 4
February 3
October 19
October 12
January 1
September 4
February 17, 2022 2.375%
June 2, 2022
March 1, 2024
June 18, 2024
April 2, 2025
0.500%
1.625%
4.073%
0.875%
February 17, 2026 3.250%
October 27, 2026 1.375%
April 8, 2027
November 2,
2028
0.875%
1.375%
October 26, 2029 1.875%
April 8, 2030
September 19,
2030
1.250%
1.875%
December 1, 2031 2.625%
April 8, 2031
March 19, 2032
2.500%
0.875%
February 17, 2034 4.750%
November 2,
2035
3.125%
October 27, 2036 3.375%
January 15, 2038 2.875%
September 19,
2039
1.500%
Interest on each series of Notes is payable annually in arrears and will be computed on the basis of the actual number of days in the period for which interest is being
calculated and the actual number of days from and including the last date on which interest was paid on such series (or the date of initial issuance of such series, if no interest has
been paid on such series), to but excluding the next scheduled interest payment date. This payment convention is referred to as ACTUAL/ACTUAL (ICMA) as defined by the
rulebook of the International Capital Market Association.
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If interest or principal on any of the 2.375% 2022 Notes, 0.500% 2022 Notes, 1.625% 2024 Notes, 2025 Notes, 3.250% 2026 Notes, 1.375% 2026 Notes, 2027 Notes,
2028 Notes, 2029 Notes, 1.250% 2030 Notes, 2.625% 2031 Notes, 2032 Notes, 2038 Notes and 2039 Notes (collectively, the “Euro Notes”) is payable on a Saturday, Sunday or
any other day when commercial banks are not open for business in The City of New York or London or any day on which the Trans- European Automated Real-time Gross
settlement Express Transfer payment system or any successor thereto is not open for transfer of payments, we will make the payment on the next succeeding business day in such
locations, and no additional interest will accrue as a result of the delay in payment. If interest or principal on any of the
4.073% 2024 Notes, 1.875% 2030 Notes, 2.500% 2031
Notes, 2034 Notes, 2035 Notes and 2036 Notes (collectively, the “Sterling Notes”)
is payable on a Saturday, Sunday or any other day when commercial banks are not open for
business in The City of New York or London, we will make the payment on the next business day in such locations, and no additional interest will accrue as a result of the delay
in payment.
We may issue additional Notes of any series in the future.
Ranking
Each series of Notes is unsecured and ranks equally with all of our unsecured and unsubordinated indebtedness.
Currency Conversion
All payments of principal, interest and additional amounts, if any, including any payments made upon any redemption, on the Euro Notes will be payable in euro.
All payments of principal, interest and additional amounts, if any, including any payments made upon any redemption, on the Sterling Notes will be payable in GBP.
If either euro or GBP, as applicable, is unavailable to us due to the imposition of exchange controls or other circumstances beyond our control (including the
dissolution of the euro), then all payments in respect of the relevant Notes will be made in U.S. dollars until euro or GBP, as the case may be, is again available to us. The
amount payable on any date in euro or GBP, as applicable, will be converted into U.S. dollars at a rate mandated by the U.S. Federal Reserve Board as of the close of business on
the second business day prior to the relevant payment date or, in the event the U.S. Federal Reserve Board has not mandated a rate of conversion, on the basis of the latest U.S.
dollar/euro exchange rate or U.S. dollar/GBP exchange rate, as applicable, available on or prior to the second business day prior to the relevant payment date as determined by us
in our sole discretion. Any payment in respect of the Notes alternatively made in U.S. dollars will not constitute an event of default under the Notes or the Indenture.
Optional Redemption
2.375% 2022 Notes, 0.500% 2022 Notes, 1.625% 2024 Notes, 4.073% 2024 Notes, 2025 Notes, 3.250% 2026 Notes, 1.375% 2026 Notes, 2028 Notes, 2029 Notes, 2.625% 2031
Notes, 2034 Notes, 2035 Notes, 2036 Notes and 2038 Notes
We have the option to redeem each of the 2.375% 2022 Notes, 0.500% 2022 Notes, 1.625% 2024 Notes, 4.073% 2024 Notes, 2025 Notes, 3.250% 2026 Notes, 1.375%
2026 Notes, 2028 Notes, 2029 Notes, 2.625% 2031 Notes, 2034 Notes, 2035 Notes, 2036 Notes and 2038 Notes on not less than 30 nor more than 60 days’ notice, in whole or in
part, at any time prior to maturity, at a redemption price equal to the greater of:
100% of the principal amount of the Notes of such series being redeemed, or
the sum of the present values of the remaining scheduled payments of principal and interest on the Notes of such series being redeemed (exclusive of interest
accrued to the date of redemption), as the case may be, discounted to the date of redemption on an annual basis (ACTUAL/ACTUAL (ICMA)) at (A) the
Comparable Government Bond Rate plus 20 basis points for the 2.375% due 2022 Notes, (B) the Comparable Government Bond Rate plus 15 basis points
for the 0.500% 2022 Notes, (C) the Comparable Government Bond Rate plus 15 basis points for the 1.625% 2024 Notes, (D) the Comparable Government
Bond Rate plus 25 basis points for the 4.073% 2024 Notes, (E) the Comparable Government Bond Rate plus 20 basis points for the 2025 Notes, (F) the
Comparable Government Bond Rate plus 25 basis points for the 3.250% 2026 Notes, (G) the Comparable Government Bond Rate plus 20 basis points for the
1.375% 2026 Notes, (H) the Comparable Government Bond Rate plus 20 basis points for the 2028 Notes, (I) the Comparable Government Bond Rate plus 25
basis points for the 2029 Notes, (J) the Comparable Government Bond Rate plus 25 basis points for the 2.625% 2031 Notes, (K) the Comparable
Government Bond Rate plus 25 basis points for the 2034 Notes, (L) the Comparable Government Bond Rate plus 25 basis points for the 2035 Notes, (M) the
Comparable Government Bond Rate plus 25 basis points for the 2036 Notes and (N) the Comparable Government Bond Rate plus 30 basis points for the
2038 Notes,
plus, in each case, accrued and unpaid interest on the principal amount being redeemed to, but excluding, the date of redemption.
2027 Notes, 1.250% 2030 Notes, 1.875% 2030 Notes, 2.500% 2031 Notes, 2032 Notes and 2039 Notes
We have the option to redeem the 2027 Notes, 1.250% 2030 Notes, 1.875% 2030 Notes, 2.500% 2031 Notes, 2032 Notes and 2039 Notes on not less than 10 nor more
than 60 days’ notice, in whole or in part,
(i)
at any time prior to (A) January 8, 2027 (three months prior to the maturity date of the 2027 Notes) (the “2027 Notes par call date”) with respect to the 2027
Notes, (B) January 8, 2030 (three months prior to the maturity date of the 1.250% 2030 Notes) (the “1.250% 2030 Notes par call date”) with respect to the
1.250% 2030 Notes (C) June 19, 2030 (three months prior to the maturity date of the 1.875% 2030 Notes) (the “1.875% 2030 Notes par call date”) with
respect to the 1.875% 2030 Notes (D) January 8, 2031 (three months prior to the maturity date of the 2.500% 2031 Notes) (the “2.500% 2031
(i)
(ii)
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Notes par call date”) with respect to the 2.500% 2031 Notes, (E) December 19, 2031 (three months prior to the maturity date of the 2032 Notes) (the “2032
Notes par call date”) with respect to the 2032 Notes and (F) March 19, 2039 (six months prior to the maturity date of the 2039 Notes) (the “2039 Notes par
call date”) with respect to the 2039 Notes, at a redemption price equal to the greater of:
(a) 100% of the principal amount of the Notes of such series being redeemed, or
(b) the sum of the present values of the remaining scheduled payments of principal and interest on the Notes of such series being redeemed
(exclusive of interest accrued to the date of redemption), assuming for such purpose that the (A) 2027 Notes matured on the 2027 Notes par call
date, (B) 1.250% 2030 Notes matured on the 1.250% 2030 Notes par call date, (C) 1.875% 2030 Notes matured on the 1.875% 2030 Notes par call
date, (D) 2.500% 2031 Notes matured on the 2.500% 2031 par call date, (E) 2032 Notes matured on the 2032 Notes par call date and (F) 2039
Notes matured on the 2039 Notes par call date, discounted to the date of redemption on an annual basis (ACTUAL/ACTUAL (ICMA)) at (AA) the
Comparable Government Bond Rate plus 20 basis points for the 2027 Notes, (BB) the Comparable Government Bond Rate plus 25 basis points for
the 1.250% 2030 Notes, (CC) the Comparable Government Bond Rate plus 25 basis points for the 1.875% 2030 Notes, (DD) the Comparable
Government Bond Rate plus 25 basis points for the 2.500% 2031 Notes, (EE) at the Comparable Government Bond Rate plus 25 basis points for
the 2032 Notes and (FF) the Comparable Government Bond Rate plus 30 basis points for the 2039 Notes; and
(ii)
at any time on or after (A) the 2027 Notes par call date with respect to the 2027 Notes, (B) the 1.250% 2030 Notes par call date with respect to the 1.250%
2030 Notes, (C) the 1.875% 2030 Notes par call date with respect to the 1.875% 2030 Notes, (D) the 2.500% 2031 Notes par call date with respect to the
2.500% 2031 Notes (E) the 2032 Notes par call date with respect to the 2032 Notes and (F) the 2039 Notes par call date with respect to the 2039 Notes, at a
redemption price equal to 100% of the principal amount of the Notes of such series being redeemed,
plus, in each case, accrued and unpaid interest on the principal amount of such series being redeemed to, but excluding, the date of redemption.
Defined Terms
The “Comparable Government Bond Rate” will be determined on the third business day preceding the redemption date and means, with respect to any date of
redemption, the rate per annum equal to the yield to maturity calculated in accordance with customary financial practice in pricing new issues of comparable corporate debt
securities paying interest on an annual basis (ACTUAL/ACTUAL (ICMA)) of the applicable Comparable Government Bond, assuming a price for the applicable Comparable
Government Bond (expressed as a percentage of its principal amount) equal to the applicable Comparable Government Bond Price for such date of redemption.
“Calculation Agent” means an independent investment banking or commercial banking institution of international standing appointed by us.
“Comparable Government Bond” means (i) with respect to any series of Euro Notes, the Federal Republic of Germany government security or securities selected by
one of the Reference Government Bond Dealers appointed by us as having an actual or interpolated maturity comparable with the remaining term of such series of Euro Notes
that would be utilized, at the time of selection and in accordance with customary financial practice, in pricing new issues of euro-denominated corporate debt securities of a
maturity comparable to the remaining term of such series of Euro Notes and (ii) with respect to any series of Sterling Notes, the United Kingdom government security or
securities selected by one of the Reference Government Bond Dealers appointed by us as having an actual or interpolated maturity comparable with the remaining term of such
series of Sterling Notes that would be utilized, at the time of selection and in accordance with customary financial practice, in pricing new issues of sterling-denominated
corporate debt securities of a maturity comparable to the remaining term of such series of Sterling Notes.
“Comparable Government Bond Price” means, with respect to any redemption date, (A) the arithmetic average of the Reference Government Bond Dealer Quotations
for such redemption date, after excluding the highest and lowest such Reference Government Bond Dealer Quotations, or (B) if the Calculation Agent obtains fewer than four
such Reference Government Bond Dealer Quotations, the arithmetic average of all such quotations.
“Reference Government Bond Dealer” means each of five banks selected by us, which are (A) primary European government securities dealers, and their respective
successors, or (B) market makers in pricing corporate bond issues.
“Reference Government Bond Dealer Quotations” means, with respect to each Reference Government Bond Dealer and any redemption date, the arithmetic average, as
determined by the Calculation Agent, of the bid and offered prices for the applicable Comparable Government Bond (expressed in each case as a percentage of its principal
amount) at 11:00 a.m., Central European Time (or in the case of the 4.073% 2024 Notes, London Time), on the third business day preceding such date for redemption quoted in
writing to the Calculation Agent by such Reference Government Bond Dealer.
Tax Redemption
2.375% 2022 Notes, 1.625% 2024 Notes, 4.073% 2024 Notes, 3.250% 2026 Notes, 2.625% 2031 Notes and 2034 Notes
Each of the 2.375% 2022 Notes, 1.625% 2024 Notes, 4.073% 2024 Notes, 3.250% 2026 Notes, 2.625% 2031 Notes and 2034 Notes may be redeemed at our option, in
whole but not in part, at any time on giving not less than 30 nor more than 60 days’ notice to the noteholders (which notice shall be irrevocable), at their principal amount,
together with interest accrued to, but excluding, the date fixed for redemption, if:
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(i)
we have or will become obliged to pay additional amounts with respect to such series of Notes as provided or referred to under “-Withholding Taxes-2.375%
2022 Notes, 4.073% 2024 Notes, 3.250% 2026 Notes and 2034 Notes”
below in the case of the 2.375% 2022 Notes, 1.625% 2024 Notes, 4.073% 2024
Notes, 3.250% 2026 Notes, 2.625% 2031 Notes and 2034 Notes, or under “-Withholding Taxes-1.625%
2024 Notes and 2.625% 2031 Notes”
below in the
case of the 1.625% 2024 Notes and 2.625% 2031 Notes, as a result of any change in, or amendment to, the laws, treaties, or rulings of the United States or
any political subdivision or any authority thereof or therein having the power to tax, or any change in the application or official interpretation of such laws or
regulations or rulings (including a holding by a court of competent jurisdiction in the United States), which change or amendment is enacted or adopted on or
after the issue date of such series of Notes; provided that, prior to the publication of any notice of redemption pursuant to this paragraph, we have delivered to
the trustee a certificate signed by one of our officers stating that we are entitled to effect such redemption and setting forth a statement of facts showing that
the conditions precedent to our right so to redeem have occurred; or
on or after the issue date of such series of Notes, any action is taken by a taxing authority of, or any decision has been rendered by a court of competent
jurisdiction in, the United States or any political subdivision of or in the United States or any authority thereof or therein having the power to tax, including
any of those actions specified in clause (i) above, whether or not such action was taken or decision was rendered with respect to us, or any change,
amendment, application or interpretation is officially proposed, which, in any such case, in the written opinion of independent tax counsel of nationally
recognized standing, will result in a material probability that we will become obliged to pay additional amounts with respect to such series of Notes; provided
that, prior to the publication of any notice of redemption pursuant to this paragraph, we have delivered to the trustee a certificate signed by one of our officers
stating that we are entitled to effect such redemption and setting forth a statement of facts showing that the conditions precedent to our right so to redeem
have occurred. However, no such notice of redemption shall be given less than 30 or more than 90 days prior to the earliest date on which we would be
obliged to pay such additional amounts if a payment in respect of such series of Notes were then due.
(ii)
0.500% 2022 Notes, 2025 Notes, 1.375% 2026 Notes, 2027 Notes, 2028 Notes, 2029 Notes, 1.250% 2030 Notes, 1.875% 2030 Notes, 2.500% 2031 Notes, 2032 Notes, 2035
Notes, 2036 Notes, 2038 Notes and 2039 Notes
Each of the 0.500% 2022 Notes, 2025 Notes, 1.375% 2026 Notes, 2027 Notes, 2028 Notes, 2029 Notes, 1.250% 2030 Notes, 1.875% 2030 Notes, 2.500% 2031 Notes,
2032 Notes, 2035 Notes, 2036 Notes, 2038 Notes and 2039 Notes may be redeemed at our option, in whole but not in part, at any time on giving not less than 30 nor more than
90 days’ notice to the noteholders (which notice shall be irrevocable), at their principal amount, together with interest accrued to the date fixed for redemption, if:
(i)
we have or will become obliged to pay additional amounts with respect to such series of Notes as provided or referred to under “-Withholding Taxes-0.500%
2022 Notes, 2025 Notes, 1.375% 2026 Notes, 2027 Notes, 2028 Notes, 2029 Notes, 1.250% 2030 Notes, 1.875% 2030 Notes, 2.500% 2031 Notes, 2032
Notes, 2035 Notes, 2036 Notes, 2038 Notes and 2039 Notes”
below as a result of any change in, or amendment to, the laws, treaties, or rulings of the United
States or any political subdivision or any authority thereof or therein having the power to tax, or any change in the application or official interpretation of
such laws or regulations or rulings (including a holding by a court of competent jurisdiction in the United States), which change or amendment is enacted or
adopted on or after the issue date of such series of Notes; or
on or after the issue date of such series of Notes, any action is taken by a taxing authority of, or any decision has been rendered by a court of competent
jurisdiction in, the United States or any political subdivision of or in the United States or any authority thereof or therein having the power to tax, including
any of those actions specified in clause (i) above, whether or not such action was taken or decision was rendered with respect to us, or any change,
amendment, application or interpretation is officially proposed, which, in any such case, will result in a material probability that we will become obliged to
pay additional amounts with respect to such series of Notes; provided that, prior to the publication of any notice of redemption pursuant to this paragraph, we
have delivered to the trustee a certificate signed by one of our officers stating that we are entitled to effect such redemption and setting forth a statement of
facts showing that the conditions precedent to our right so to redeem have occurred and a copy of an opinion of a reputable independent counsel of our
choosing to that effect based on that statement of facts. However no such notice of redemption shall be given less than 30 nor more than 90 days prior to the
earliest date on which we would be obliged to pay such additional amounts if a payment in respect of such series of Notes were then due.
(ii)
Withholding Taxes
For purposes of all clauses described under “-Withholding Taxes”, references to the holder or beneficial owner of a Note include a fiduciary, settlor, beneficiary or
person holding power over such holder or beneficial owner, if such holder or beneficial owner is an estate or trust, or a partner, member or shareholder of such holder or
beneficial owner, if such holder or beneficial owner is a partnership, limited liability company or corporation. In addition, we will not pay additional amounts to the holder of a
Note if such holder or the beneficial owner of such Note is a fiduciary, partnership, limited liability company or other fiscally transparent entity, or if the holder of such Note is
not the sole beneficial owner of such Note, as the case may be, to the extent that a beneficiary or settlor with respect to the fiduciary, or a beneficiary, partner or member of the
partnership, limited liability company or other fiscally transparent entity, or a beneficial owner would not have been entitled to the payment of an additional amount had the
beneficiary, settlor, beneficial owner, partner or member received directly its beneficial or distributive share of the payment. For purposes of “-Withholding Taxes,” the term
“Non-U.S. Person” means any person that is, for U.S. federal income tax purposes, a foreign corporation, nonresident alien individual, a nonresident fiduciary of a foreign estate
or foreign trust or a foreign partnership one or more of the partners of which is such a foreign corporation, nonresident alien individual or nonresident fiduciary.
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Any additional amounts paid pursuant to any clause described under “-Withholding Taxes” on the Euro Notes or the Sterling Notes will be paid in euro or GBP,
respectively.
2.375% 2022 Notes, 4.073% 2024 Notes, 3.250% 2026 Notes and 2034 Notes
All payments of principal, interest and premium (if any) in respect of the 2.375% 2022 Notes, 4.073% 2024 Notes, 3.250% 2026 Notes and 2034 Notes by us or a
paying agent on our behalf shall be made without withholding or deduction for or on account of any present or future taxes, duties, assessments or other governmental charges
(“Taxes”) imposed by or on behalf of the United States or any political subdivision thereof or any authority therein or thereof having the power to tax, unless the withholding or
deduction of such Taxes is required by law. In that event, we shall pay to a holder that is a Non-U.S. Person such additional amounts as may be necessary to ensure that the net
amount received by such holder, after withholding or deduction for or on account of such Taxes, will be equal to the amount such holder would have received in the absence of
such withholding or deduction. However, no additional amounts shall be payable with respect to any Note if the beneficial owner is subject to taxation solely for reasons other
than its ownership of Notes, nor shall additional amounts be payable for or on account of:
(i)
any Tax that would not have been imposed, withheld or deducted but for any present or former connection (other than the mere fact of being a holder or
beneficial owner of such Note) between the holder or the beneficial owner of such Note and the United States or the applicable political subdivision or
authority, including, without limitation, such holder or beneficial owner being or having been a citizen or resident of the United States or the applicable
political subdivision or authority or treated as being or having been a resident thereof;
any Tax that would not have been imposed, withheld or deducted but for the holder or beneficial owner of such Note being or having been with respect to the
United States a personal holding company, a controlled foreign corporation, a passive foreign investment company, a foreign private foundation or other
foreign tax-exempt organization, or a corporation that accumulates earnings to avoid U.S. federal income tax;
any Tax that is payable other than by withholding or deduction by us or a paying agent from payments in respect of such Note;
any gift, estate, inheritance, sales, transfer, personal property, excise or similar Tax;
any Tax that would not have been imposed, withheld or deducted but for a change in any law, treaty, regulation, or administrative or judicial interpretation
that becomes effective after the applicable payment becomes due or is duly provided for, whichever occurs later, to the extent such change in law, treaty,
regulation or administrative interpretation would apply retroactively to such payment;
any Tax that would not have been imposed, withheld or deducted but for the presentation of such Note more than 30 days after the applicable payment
becomes due or is duly provided for, whichever occurs later, except to the extent that such holder would have been entitled to such additional amounts on
presenting such Note for payment on the last date of such period of 30 days;
any Tax that would not have been imposed, withheld or deducted but for the failure of a direct or indirect holder or beneficial owner of such Note to comply
with applicable certification, information, documentation or other reporting requirements concerning the nationality, residence, identity or connection with
the United States of such holder or beneficial owner;
any Tax that would not have been imposed, withheld or deducted but for the failure of the holder or beneficial owner of such Note to meet the requirements
(including the statement requirements) of Section 871(h) or Section 881(c) of the Internal Revenue Code of 1986, as amended (the “Code”); or
any combination of items (i)-(viii).
(ii)
(iii)
(iv)
(v)
(vi)
(vii)
(viii)
(ix)
1.625% 2024 Notes and 2.625% 2031 Notes
All payments of principal, interest and premium (if any) in respect of the 1.625% 2024 Notes and 2.625% 2031 Notes by us or a paying agent on our behalf shall be
made without withholding or deduction for or on account of any Taxes imposed by or on behalf of the United States or any political subdivision thereof or any authority therein
or thereof having the power to tax, unless the withholding or deduction of such Taxes is required by law. In that event, we shall pay to a holder that is a Non-U.S. Person such
additional amounts as may be necessary to ensure that the net amount received by such holder, after withholding or deduction for or on account of such Taxes, will be equal to
the amount such holder would have received in the absence of such withholding or deduction. However, no additional amounts shall be payable with respect to any Note if the
beneficial owner is subject to taxation solely for reasons other than its ownership of Notes, nor shall additional amounts be payable for or on account of:
(i)
any Tax that would not have been imposed, withheld or deducted but for any present or former connection (other than the mere fact of being a holder or
beneficial owner of such Note) between the holder or the beneficial owner of such Note and the United States or the applicable political subdivision or
authority, including, without limitation, such holder or beneficial owner being or having been a citizen or resident of the United States or the applicable
political subdivision or authority or treated as being or having been a resident thereof;
any Tax that would not have been imposed, withheld or deducted but for the holder or beneficial owner of such Note being or having been with respect to the
United States a personal holding company, a controlled foreign corporation, a passive
(ii)
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foreign investment company, a foreign private foundation or other foreign tax-exempt organization, or a corporation that accumulates earnings to avoid U.S.
federal income tax;
(iii)
(iv)
(v)
any Tax that is payable other than by withholding or deduction by us or a paying agent from payments in respect of such Note;
any gift, estate, inheritance, sales, transfer, personal property, excise or similar Tax;
any Tax that would not have been imposed, withheld or deducted but for a change in any law, treaty, regulation, or administrative or judicial interpretation
that becomes effective after the applicable payment becomes due or is duly provided for, whichever occurs later, to the extent such change in law, treaty,
regulation or administrative interpretation would apply retroactively to such payment;
any Tax that would not have been imposed, withheld or deducted but for the presentation of such Note more than 30 days after the applicable payment
becomes due or is duly provided for, whichever occurs later, except to the extent that such holder would have been entitled to such additional amounts on
presenting such Note for payment on the last date of such period of 30 days;
any Tax that would not have been imposed, withheld or deducted but for the failure of a direct or indirect holder or beneficial owner of such Note to comply
with applicable certification, information, documentation or other reporting requirements concerning the nationality, residence, identity or connection with
the United States of such holder or beneficial owner;
any Tax that would not have been imposed, withheld or deducted but for the failure of the holder or beneficial owner of such Note to meet the requirements
(including the statement requirements) of Section 871(h) or Section 881(c) of the Code; or
any Tax imposed pursuant to Sections 1471 through 1474 of the Code, any current or future regulations or official interpretations thereof, any agreements
entered pursuant to Section 1471(b) of the Code and any intergovernmental agreements (and related legislation or official administrative guidance)
implementing the foregoing; or
any combination of items (i)-(ix).
(vi)
(vii)
(viii)
(ix)
(x)
0.500% 2022 Notes, 2025 Notes, 1.375% 2026 Notes, 2027 Notes, 2028 Notes, 2029 Notes, 1.250% 2030 Notes, 1.875% 2030 Notes, 2.500% 2031 Notes, 2032 Notes, 2035
Notes, 2036 Notes, 2038 Notes and 2039 Notes
All payments of principal, interest and premium (if any) in respect of the 0.500% 2022 Notes, 2025 Notes, 1.375% 2026 Notes, 2027 Notes, 2028 Notes, 2029 Notes,
1.250% 2030 Notes, 1.875% 2030 Notes, 2.500% 2031 Notes, 2032 Notes, 2035 Notes, 2036 Notes, 2038 Notes and 2039 Notes by us or a paying agent on our behalf shall be
made without withholding or deduction for or on account of any Taxes imposed by or on behalf of the United States or any political subdivision thereof or any authority therein
or thereof having the power to tax, unless the withholding or deduction of such Taxes is required by law. In that event, we shall pay to a holder that is a Non-U.S. Person such
additional amounts as may be necessary to ensure that the net amount received by such holder, after withholding or deduction for or on account of such Taxes, will be equal to
the amount such holder would have received in the absence of such withholding or deduction. However, no additional amounts shall be payable with respect to any Note if the
beneficial owner is subject to taxation solely for reasons other than its ownership of Notes, nor shall additional amounts be payable for or on account of:
(i)
any Tax that would not have been imposed, withheld or deducted but for any present or former connection (other than the mere fact of being a holder or
beneficial owner of such Note) between the holder or the beneficial owner of such Note and the United States or the applicable political subdivision or
authority, including, without limitation, such holder or beneficial owner being or having been a citizen or resident of the United States or the applicable
political subdivision or authority or treated as being or having been a resident thereof;
any Tax that would not have been imposed, withheld or deducted but for the holder or beneficial owner of such Note being or having been with respect to the
United States a personal holding company, a controlled foreign corporation, a passive foreign investment company, a foreign private foundation or other
foreign tax-exempt organization, or a corporation that accumulates earnings to avoid U.S. federal income tax;
any Tax that is payable other than by withholding or deduction by us or a paying agent from payments in respect of such Note;
any gift, estate, inheritance, sales, transfer, value added, personal property, excise or similar Tax;
any Tax that would not have been imposed, withheld or deducted but for a change in any law, treaty, regulation, or administrative or judicial interpretation
that becomes effective after the applicable payment becomes due or is duly provided for, whichever occurs later;
any Tax that would not have been imposed, withheld or deducted but for the presentation of such Note for payment more than 30 days after the applicable
payment becomes due or is duly provided for, whichever occurs later, except to the extent
(ii)
(iii)
(iv)
(v)
(vi)
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that such holder would have been entitled to such additional amounts on presenting such Note for payment on the last date of such period of 30 days;
(vii)
any Tax that would not have been imposed, withheld or deducted but for the failure of the holder or beneficial owner of such Note to comply with applicable
certification, information, documentation or other reporting requirements concerning the nationality, residence, identity or connection with the United States
of such holder or beneficial owner;
any Tax that would not have been imposed, withheld or deducted but for the failure of the holder or beneficial owner (or any financial institution or other
person through which the holder or beneficial owner holds any Notes) to comply with any certification, information, identification, documentation or other
reporting requirements with respect to itself or any beneficial owner or account holders thereof;
any Tax that would not have been imposed, withheld or deducted but for the failure of the holder or beneficial owner of such Note to meet the requirements
(including the statement requirements) of Section 871(h) or Section 881(c) of the Code;
any Tax imposed by the Foreign Account Tax Compliance Act pursuant to Sections 1471 through 1474 of the Code, any current or future regulations or
official interpretations thereof, any agreements entered into pursuant to Section 1471(b) of the Code and any intergovernmental agreements (and related
legislation or official administrative guidance) implementing the foregoing; or
any combination of items (i)-(x).
(viii)
(ix)
(x)
(xi)
Book-Entry Only Form
Each series of Notes was issued in book-entry only form, which means that it is represented by one or more permanent global securities registered in the name of The
Depository Trust Company, New York, New York (“DTC”), or its nominee. We refer to this form as “book-entry only.”
For debt securities issued in book-entry only form, DTC keeps a computerized record of its participants (for example, a broker) whose clients have purchased the
securities. Each participant then keeps a record of its clients who purchased the securities. A global security may not be transferred, except that DTC, its nominees and their
successors may transfer an entire global security to one another.
For book-entry only debt securities, we wire principal and interest payments to DTC’s nominee. We and the trustee treat DTC’s nominee as the owner of the global
securities for all purposes. Accordingly, neither we nor the trustee have any direct responsibility or liability to pay amounts due on the debt securities issued under the Indenture
to owners of beneficial interests in the global securities.
Under book-entry only form, we have not issued physical certificates representing beneficial interests in the global securities to individual holders of the debt
securities. Beneficial interests in global securities will be shown on, and transfers of global securities will be made only through, records maintained by DTC and its participants
and will be exchangeable for debt securities in certificated form with the same terms in authorized denominations only if:
•
•
•
Defeasance
The Indenture permits us to discharge or defease certain of our obligations on any series of debt securities issued under the Indenture at any time. We may defease such
obligations relating to a series of debt securities by depositing with the trustee sufficient cash or government securities to pay all sums due on that series of debt securities.
Liens on Assets
The Notes and other debt securities will not be secured. However, if at any time we mortgage, pledge or subject to any lien any of our property or assets, the Indenture
requires us to secure the Notes and other debt securities issued under the Indenture equally and ratably with the debt or obligations secured by such mortgage, pledge or lien for
as long as such debt or obligations remain secured. Exceptions to this requirement include the following:
•
•
•
•
purchase-money mortgages or liens;
liens on any property or asset that existed at the time when we acquired that property or asset;
any deposit or pledge to secure public or statutory obligations;
any deposit or pledge with any governmental agency required to qualify us to conduct any part of our business, to entitle us to maintain self-insurance or to
obtain the benefits of any law relating to workmen’s compensation, unemployment insurance, old age pensions or other social security; or
DTC notifies us that it is unwilling or unable to continue as depository;
DTC ceases to be a clearing agency registered under applicable law and a successor depository is not appointed by us within 90 days; or
We instruct the trustee that the global security is exchangeable for debt securities in certificated form.
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•
any deposit or pledge with any court, board, commission or governmental agency as security for the proper conduct of any proceeding before it.
The Indenture does not prevent any of our affiliates from mortgaging, pledging or subjecting to any lien, any property or asset, even if the affiliate acquired that
property or asset from us.
We may issue or assume an unlimited amount of debt under the Indenture.
Changes to the Indenture
The Indenture may be changed with the consent of holders owning more than 50% of the principal amount of the outstanding debt securities of each series affected by
the change. However, we may not change principal or interest payment terms of the Notes or the percentage required to change other terms of the Indenture without consent of
the holders of the Notes and the consent of others similarly affected.
We may enter into supplemental indentures for other specified purposes, including the creation of any new series of debt securities, without the consent of any holder
of debt securities issued under the Indenture.
Consolidation, Merger or Sale
The Indenture provides that we may not merge with another company or sell, transfer or lease all or substantially all of our property to another company unless:
•
•
•
•
•
•
Events of Default
An event of default means, for any series of debt securities issued under the Indenture, any of the following:
•
•
•
•
•
failure to pay interest on that series of debt securities for 90 days after payment is due;
failure to pay principal or any premium on that series of debt securities when due;
failure to perform any other covenant relating to that series of debt securities for 90 days after notice to us;
certain events of bankruptcy, insolvency and reorganization; and
any other event of default provided for in the supplement to the Indenture, board resolution or officers’ certificate designating the specific terms of such
series of debt securities.
the successor corporation expressly assumes:
payment of principal, interest and any premium on the debt securities issued under the Indenture; and
performance and observance of all covenants and conditions in the Indenture;
after giving effect to the transaction, there is no default under the Indenture;
we have delivered to the trustee an officers’ certificate and opinion of counsel stating that such transaction complies with the conditions set forth in the
Indenture; and
if as a result of the transaction, our property would become subject to a lien that would not be permitted by the asset lien restriction, we secure the debt
securities Issued under the Indenture equally and ratably with, or prior to, all indebtedness secured by that lien.
An event of default for a particular series of debt securities does not necessarily impact any other series of debt securities issued under the Indenture.
If an event of default for any series of debt securities occurs and continues, the trustee or the holders of at least 25% of the outstanding principal amount of the debt
securities of such series may declare the entire principal of all the debt securities of that series to be due and payable immediately. If this happens, subject to certain conditions,
the holders of a majority of the outstanding principal amount of the debt securities of that series can rescind the declaration if there has been deposited with the trustee a sum
sufficient to pay all matured installments of interest, principal and any premium.
The holders of more than 50% of the outstanding principal amount of any series of the debt securities, may, on behalf of the holders of all of the debt securities of that
series, control any proceedings resulting from an event of default or waive any past default except a default in the payment of principal, interest or any premium. We are required
to file an annual certificate with the trustee stating whether we are in compliance with all of the conditions and covenants under the Indenture.
Concerning the Trustee
Within 90 days after a default occurs with respect to a particular series of Notes, the trustee must notify the holders of such series of Notes of all defaults known to the
trustee if we have not remedied them (default is defined to mean any event which is, or after notice or lapse of time or both would become, an event of default with respect to
such series of Notes as specified above under “-Events of Default”). If a default described in the third bullet point under “-Events of Default” occurs, the trustee will not give
notice to the holders of the series until at
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least 60 days after the occurrence of that default. The trustee may withhold notice to the holders of the Notes of any default (except in the payment of principal, interest or any
premium) if it in good faith believes that withholding this notice is in the interest of the holders.
Prior to an event of default, the trustee is required to perform only the specific duties stated in the Indenture, and after an event of default, must exercise the same
degree of care as a prudent individual would exercise in the conduct of his or her own affairs. The trustee is not required to take any action permitted by the Indenture at the
request of holders of the debt securities, unless those holders protect the trustee against costs, expenses and liabilities. The trustee is not required to spend its own funds or
become financially liable when performing its duties if it reasonably believes that it will not be adequately protected financially.
U.S. Bank National Association, the trustee for the Notes, and its affiliates have commercial banking relationships with us and some of our affiliates and serves as
trustee or paying agent under indentures relating to debt securities issued by us and some of our affiliates.
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EXHIBIT 13
Selected Financial Data Verizon Communications Inc. and Subsidiaries
(dollars in millions, except per share amounts)
2019
Results of Operations
Operating revenues
Operating income
Net income attributable to Verizon
Per common share – basic
Per common share – diluted
Cash dividends declared per common share
Net income attributable to noncontrolling interests
Financial Position
Total assets
Debt maturing within one year
Long-term debt
Employee benefit obligations
Noncontrolling interests
Equity attributable to Verizon
$
291,727
10,777
100,712
17,952
1,440
$
264,829
7,190
105,873
18,599
1,565
$
257,143
3,453
113,642
22,112
1,591
$
244,180
2,645
105,433
26,166
1,508
$
244,175
6,489
103,240
29,957
1,414
$
131,868
30,378
19,265
4.66
4.65
2.435
523
$
130,863
22,278
15,528
3.76
3.76
2.385
511
$
126,034
27,425
30,101
7.37
7.36
2.335
449
$
125,980
29,249
13,127
3.22
3.21
2.285
481
$
131,620
30,615
17,879
4.38
4.37
2.230
496
2018
2017
2016
2015
53,145
43,096
22,524
16,428
61,395
• Significant events affecting our historical earnings trends in 2018 through 2019 are described in "Special Items" in the "Management’s Discussion and Analysis of Financial
Condition and Results of Operations" section.
• 2017 data includes severance, pension and benefit charges, gain on spectrum license transactions, acquisition and integration related charges, product realignment charges, net
gain on sale of divested businesses and early debt redemption costs. 2016 data includes severance, pension and benefit charges, gain on spectrum license transactions, net gain
on sale of divested businesses and early debt redemption costs. 2015 data includes severance, pension and benefit credits and gain on spectrum license transactions.
• On January 1, 2019, we adopted several Accounting Standards Updates (ASUs) that were issued by the Financial Accounting Standards Board (FASB) using the modified
retrospective basis. On January 1, 2018, we adopted several ASUs that were issued by the FASB. These standards were adopted on different bases, including: (1) prospective;
(2) full retrospective; and (3) modified retrospective. Based on the method of adoption, certain figures are not comparable, with full retrospective reflected in all periods. See
Note 1 to the consolidated financial statements for additional information.
Stock Performance Graph
2014
Verizon
S&P 500
$
100.0 $
100.0
2015
103.6 $
103.4
2016
125.1 $
127.7
2017
130.1 $
126.1
2018
144.7
$
110.3
2019
164.8
146.3
S&P 500 Telecom Services
100.0
101.4
113.5
138.3
132.2
173.8
The graph compares the cumulative total returns of Verizon, the S&P 500 Stock Index and the S&P 500 Telecommunications Services Index over a five-year period. It assumes
$100 was invested on December 31, 2014 with dividends being reinvested.
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Management’s Discussion and Analysis of Financial Condition and Results of Operations
Overview
Verizon Communications Inc. (Verizon or the Company) is a holding company that, acting through its subsidiaries, is one of the world’s leading providers of communications,
information and entertainment products and services to consumers, businesses and government entities. With a presence around the world, we offer voice, data and video
services and solutions on our networks that are designed to meet customers’ demand for mobility, reliable network connectivity, security and control. We have a highly diverse
workforce of approximately 135,000 employees as of December 31, 2019.
To compete effectively in today’s dynamic marketplace, we are focused on the capabilities of our high-performing networks to drive growth based on delivering what customers
want and need in the new digital world. During 2019, we focused on leveraging our network leadership; retaining and growing our high-quality customer base while balancing
profitability; enhancing ecosystems in growth businesses; and driving monetization of our networks and solutions. We are creating business value by earning customers',
employees' and shareholders' trust, limiting our environmental impact and continuing our customer growth while creating social benefit through our products and services. Our
strategy requires significant capital investments primarily to acquire wireless spectrum, put the spectrum into service, provide additional capacity for growth in our networks,
invest in the fiber that supports our businesses, evolve and maintain our networks and develop and maintain significant advanced information technology systems and data
system capabilities. We believe that steady and consistent investments in our networks and platforms will drive innovative products and services and fuel our growth.
We are consistently deploying new network architecture and technologies to extend our leadership in both fourth-generation (4G) and fifth-generation (5G) wireless networks.
We expect that our next-generation multi-use platform, which we call the Intelligent Edge Network, will simplify operations by eliminating legacy network elements, improve
4G Long-Term Evolution (LTE) wireless coverage, speed the deployment of 5G wireless technology and create new opportunities in the business market. Our network
leadership is the hallmark of our brand and the foundation for the connectivity, platform and solutions upon which we build our competitive advantage.
Highlights of Our 2019 Financial Results
(dollars in millions)
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Business Overview
In November 2018, we announced a strategic reorganization of our business. Under the new structure, effective April 1, 2019, there are two reportable segments that we operate
and manage as strategic business units - Verizon Consumer Group (Consumer) and Verizon Business Group (Business).
Revenue by Segment
———
Note: Excludes eliminations.
Verizon Consumer Group
Our Consumer segment provides consumer-focused wireless and wireline communications services and products. Our wireless services are provided across one of the most
extensive wireless networks in the United States (U.S.) under the Verizon brand and through wholesale and other arrangements. Our wireline services are provided in nine states
in the Mid-Atlantic and Northeastern U.S., as well as Washington D.C., over our 100% fiber-optic network under the Fios brand and over a traditional copper-based network to
customers who are not served by Fios. Our Consumer segment's wireless and wireline products and services are available to our retail customers, as well as resellers that
purchase wireless network access from us on a wholesale basis.
Customers can obtain our wireless services on a postpaid or prepaid basis. A retail postpaid connection represents an individual line of service for a wireless device for which a
customer is generally billed one month in advance for a monthly access charge in return for access to and usage of network services. Our prepaid service is offered only to
Consumer customers and enables individuals to obtain wireless services without credit verification by paying for all services in advance. The Consumer segment also offers
several categories of wireless equipment to customers, including a variety of smartphones and other handsets, wireless-enabled Internet devices, such as tablets, laptop computers
and netbooks, and other wireless-enabled connected devices, such as smart watches and other wearables.
In addition to the wireless services and equipment discussed above, Consumer sells residential fixed connectivity solutions, including Internet, video and voice services, and
wireless network access to resellers on a wholesale basis. The Consumer segment's operating revenues for the year ended December 31, 2019 totaled $91.1 billion, an increase of
$1.3 billion, or 1.4%, compared to the year ended December 31, 2018. As of December 31, 2019, Consumer had approximately 95 million wireless retail connections, 6 million
broadband connections and 4 million Fios video connections.
Verizon Business Group
Our Business segment provides wireless and wireline communications services and products, video and data services, corporate networking solutions, security and managed
network services, local and long distance voice services and network access to deliver various Internet of Things (IoT) services and products, including solutions that support
fleet tracking management, compliance management, field service management, asset tracking and other types of mobile resource management. We provide these products and
services to businesses, government customers and wireless and wireline carriers across the U.S. and select products and services to customers around the world. The Business
segment's operating revenues for the year ended December 31, 2019 totaled $31.4 billion, a decrease of $91 million, or 0.3%, compared to the year ended December 31, 2018.
As of December 31, 2019, Business had approximately 25 million wireless retail postpaid connections and 489 thousand broadband connections.
Corporate and Other
Corporate and other includes the results of our media business, Verizon Media, and other businesses, investments in unconsolidated businesses, insurance captives, unallocated
corporate expenses, certain pension and other employee benefit related costs and interest and financing expenses. Corporate and other also includes the historical results of
divested businesses and other adjustments and gains and losses that are not allocated in assessing segment performance due to their nature. Although such transactions are
excluded from the business segment results, they are included in reported consolidated earnings. Gains and losses from transactions that are not individually significant are
included in segment results as these items are included in the chief operating decision maker’s assessment of segment performance.
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Verizon Media includes diverse media and technology brands that serve both consumers and businesses. Verizon Media provides consumers with owned and operated and third-
party search properties as well as mail, news, finance, sports and entertainment offerings, and provides other businesses and partners access to consumers through digital
advertising, content delivery and video streaming platforms. Verizon Media's total operating revenues were $7.5 billion for the year ended December 31, 2019. This was a
decrease of 3.0% from the year ended December 31, 2018.
Capital Expenditures and Investments
We continue to invest in our wireless networks, high-speed fiber and other advanced technologies to position ourselves at the center of growth trends for the future. During the
year ended December 31, 2019, these investments included $17.9 billion for capital expenditures. See "Cash Flows Used in Investing Activities" and "Operating Environment
and Trends" for additional information. We believe that our investments aimed at expanding our portfolio of products and services will provide our customers with an efficient,
reliable infrastructure for competing in the information economy.
Global Network and Technology
We are focusing our capital spending on adding capacity and density to our 4G LTE network, while also building our next generation 5G network. We are densifying our
network by utilizing small cell technology, in-building solutions and distributed antenna systems. Network densification enables us to add capacity to address increasing mobile
video consumption and the growing demand for IoT products and services on our 4G LTE and 5G networks. Over the past several years, we have been leading the development
of 5G wireless technology industry standards and the ecosystems for fixed and mobile 5G wireless services. We believe 5G technology will be able to provide users with eight
capabilities, or currencies. The eight currencies are peak data rates, mobile data volumes, mobility, number of connected devices, energy efficiency of connected devices, service
deployment, reduced latency and improved reliability. We expect that 5G technology will provide higher throughput and lower latency than the current 4G LTE technology and
enable our networks to handle more traffic as the number of Internet-connected devices grows. During 2018, we commercially launched 5G Home on proprietary standards in
four U.S. markets and on global standards in a fifth U.S. market in 2019. We also launched our 5G Ultra Wideband Network in 31 U.S. markets in 2019, as well as several 5G-
compatible smartphones.
To compensate for the shrinking market for traditional copper-based products, we continue to build our wireline business around fiber-based networks supporting data, video and
advanced business services - areas where demand for reliable high-speed connections is growing. We are evolving the architecture of our networks to a next-generation multi-use
platform, providing improved efficiency and virtualization, increased automation and opportunities for edge computing services that will support both our fiber-based and radio
access network technologies. We call this the Intelligent Edge Network. We expect that this new architecture will simplify operations by eliminating legacy network elements,
improve our 4G LTE wireless coverage, speed the deployment of 5G wireless technology and create new opportunities in the business market.
Recent Developments
In 2019, the Federal Communications Commission (FCC) completed two millimeter wave spectrum license auctions. Verizon participated in these auctions and was the high
bidder on 9 and 1,066 licenses, respectively, in the 24 Gigahertz (GHz) and 28 GHz bands. We submitted an application to the FCC and paid cash of approximately $521 million
for the licenses. We received the licenses during the fourth quarter of 2019.
In December 2019, the FCC incentive auction for spectrum licenses in the upper 37 GHz, 39 GHz, and 47 GHz bands commenced. As an incumbent licensee, Verizon received
vouchers related to our existing 39 GHz licenses. These vouchers can be converted into cash, the amount of which will not be known until the conclusion of the auction, or
applied toward the purchase price of spectrum in the auction. At the conclusion of the auction, all existing licenses will be cancelled and new reconfigured licenses or cash will
be distributed depending on the results of the auction. Due to the FCC's rules restricting communications regarding the auction, we will not disclose our financial plans for the
auction during the quiet period for this auction unless legally required. In addition, as of this time, until the completion of the auction process, we cannot determine the resulting
financial outcome, including a potential gain or loss. Such gain or loss, if any, may be material.
Consolidated Results of Operations
In this section, we discuss our overall results of operations and highlight special items that are not included in our segment results. In "Segment Results of Operations," we
review the performance of our two reportable segments in more detail. A detailed discussion of 2017 items and year-over-year comparisons between 2018 and 2017 that are not
included in this Form 10-K can be found in the "Management's Discussion and Analysis of Financial Condition and Results of Operations" for the year ended December 31,
2018 filed with our most recent financial statements and included in the Company's Current Report on Form 8-K dated August 8, 2019.
Consolidated Revenues
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Consumer
Business
Corporate and other
Eliminations
Consolidated Revenues
$
$
2019
91,056
31,443
9,812
(443)
131,868
$
$
2018
89,762
31,534
9,936
(369)
130,863
$
$
2019 vs. 2018
1,294
(91)
(124)
(74)
1,005
1.4 %
(0.3)
(1.2)
20.1
0.8
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Consolidated revenues increased $1.0 billion, or 0.8%, during 2019 compared to 2018, primarily due to an increase in revenues at our Consumer segment, partially offset by
decreases in revenues at our Business segment and Corporate and other.
Revenues for our segments are discussed separately below under the heading "Segment Results of Operations."
Corporate and other revenues decreased $124 million, or 1.2%, during 2019 compared to 2018, primarily due to a decrease of $232 million in revenues within Verizon Media.
Consolidated Operating Expenses
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Cost of services
Cost of wireless equipment
Selling, general and administrative expense
Depreciation and amortization expense
Media goodwill impairment
Consolidated Operating Expenses
$
$
2019
31,772
22,954
29,896
16,682
186
101,490
$
$
2018
32,185
23,323
31,083
17,403
4,591
108,585
$
$
2019 vs. 2018
(413)
(369)
(1,187)
(721)
(4,405)
(7,095)
(1.3)%
(1.6)
(3.8)
(4.1)
(95.9)
(6.5)
Operating expenses for our segments are discussed separately below under the heading "Segment Results of Operations."
Cost of Services
Cost of services includes the following costs directly attributable to a service: salaries and wages, benefits, materials and supplies, content costs, contracted services, network
access and transport costs, customer provisioning costs, computer systems support, and costs to support our outsourcing contracts and technical facilities. Aggregate customer
care costs, which include billing and service provisioning, are allocated between Cost of services and Selling, general and administrative expense.
Cost of services decreased $413 million, or 1.3%, during 2019 compared to 2018, primarily due to decreases in network access costs, a product realignment charge in 2018 (see
"Special Items"), decreases in employee-related costs resulting from the Voluntary Separation Program and decreases in digital content costs. These decreases were partially
offset by increases in rent expense as a result of adding capacity to the networks to support demand and the adoption of the new lease accounting standard in 2019, regulatory
fees, and costs related to the device protection package offered to our wireless retail postpaid customers.
Cost of Wireless Equipment
Cost of wireless equipment decreased $369 million, or 1.6%, during 2019 compared to 2018, primarily as a result of declines in the number of wireless devices sold as a result of
an elongation of the handset upgrade cycle, partially offset by a shift to higher priced devices in the mix of wireless devices sold.
Selling, General and Administrative Expense
Selling, general and administrative expense includes salaries and wages and benefits not directly attributable to a service or product, bad debt charges, taxes other than income
taxes, advertising and sales commission costs, call center and information technology costs, regulatory fees, professional service fees, and rent and utilities for administrative
space. Also included is a portion of the aggregate customer care costs as discussed above in "Cost of Services."
Selling, general and administrative expense decreased $1.2 billion, or 3.8%, during 2019 compared to 2018, primarily due to decreases in employee-related costs primarily due to
the Voluntary Separation Program, a decrease in severance, pension and benefits charges (see "Special Items"), the acquisition and integration related charges in 2018 primarily
related to the acquisition of Yahoo's operating business (see "Special Items") and a net gain from dispositions of assets and businesses in 2019 (see "Special Items"), partially
offset by increases in advertising expenses, sales commission and bad debt expense. The increase in sales commission expense during 2019 compared to 2018, was primarily due
to a lower net deferral of commission costs as a result of the adoption of Topic 606 on January 1, 2018, using a modified retrospective approach.
Depreciation and Amortization Expense
Depreciation and amortization expense decreased $721 million, or 4.1%, during 2019 compared to 2018, primarily due to the change in the mix of net depreciable assets.
Media Goodwill Impairment
The goodwill impairment charges recorded in 2019 and 2018 for Verizon Media were a result of the Company's annual impairment test performed in the fourth quarter (see
"Critical Accounting Estimates").
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Other Consolidated Results
Other Income (Expense), Net
Additional information relating to Other income (expense), net is as follows:
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Interest income
Other components of net periodic benefit cost
Early debt extinguishment costs
Other, net
Total
nm - not meaningful
The change in Other income (expense), net during the year ended December 31, 2019, compared to the similar period in 2018, was primarily driven by early debt redemption
costs of $3.6 billion recorded during 2019, compared to $725 million recorded during 2018 (see "Special Items") as well as pension and benefit charges of $126 million recorded
in 2019, compared with pension and benefit credits of $2.1 billion recorded in 2018 (see "Special Items").
Interest Expense
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Total interest costs on debt balances
Less capitalized interest costs
Total
Average debt outstanding
Effective interest rate
Total interest costs on debt balances decreased during 2019 primarily due to lower average debt balances.
Provision for Income Taxes
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Provision for income taxes
Effective income tax rate
$
2019
2,945
13.0%
$
2018
3,584
18.3%
$
2019 vs. 2018
(639)
(17.8)%
$
$
$
2019
5,386
656
4,730
112,901
4.8%
$
$
$
2018
5,573
740
4,833
115,858
4.8%
$
$
2019 vs. 2018
(187)
(84)
(103)
(3.4)%
(11.4)
(2.1)
$
$
2019
121
627
(3,604)
(44)
(2,900)
$
$
2018
94
3,068
(725)
(73)
2,364
$
$
2019 vs. 2018
27
(2,441)
(2,879)
29
(5,264)
28.7 %
(79.6)
nm
39.7
nm
The effective income tax rate is calculated by dividing the provision for income taxes by income before income taxes. The effective income tax rate for 2019 was 13.0%
compared to 18.3% for 2018. The decrease in the effective income tax rate and the provision for income taxes was primarily due to the recognition of approximately $2.2 billion
of a non-recurring tax benefit in connection with the disposition of preferred stock, representing a minority interest in a foreign affiliate in 2019 compared to the non-recurring
deferred tax benefit of approximately $2.1 billion as a result of an internal reorganization of legal entities within the historical Wireless business, which was offset by a goodwill
charge that is not deductible for tax purposes in 2018.
A reconciliation of the statutory federal income tax rate to the effective income tax rate for each period is included in Note 12 to the consolidated financial statements.
Consolidated Net Income, Consolidated EBITDA and Consolidated Adjusted EBITDA
Consolidated earnings before interest, taxes, depreciation and amortization expenses (Consolidated EBITDA) and Consolidated Adjusted EBITDA, which are presented below,
are non-generally accepted accounting principles (GAAP) measures that we believe are useful to management, investors and other users of our financial information in
evaluating operating profitability on a more variable cost basis as they exclude the depreciation and amortization expense related primarily to capital expenditures and
acquisitions that occurred in prior years, as well as in evaluating operating performance in relation to Verizon’s competitors. Consolidated EBITDA is calculated by adding back
interest, taxes, and depreciation and amortization expenses to net income.
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Consolidated Adjusted EBITDA is calculated by excluding from Consolidated EBITDA the effect of the following non-operational items: equity in losses of unconsolidated
businesses and other income and expense, net, as well as the effect of special items. We believe that this measure is useful to management, investors and other users of our
financial information in evaluating the effectiveness of our operations and underlying business trends in a manner that is consistent with management’s evaluation of business
performance. We believe that Consolidated Adjusted EBITDA is widely used by investors to compare a company’s operating performance to its competitors by minimizing
impacts caused by differences in capital structure, taxes and depreciation policies. Further, the exclusion of non-operational items and special items enables comparability to
prior period performance and trend analysis. See "Special Items" for additional information.
It is management’s intent to provide non-GAAP financial information to enhance the understanding of Verizon’s GAAP financial information, and it should be considered by the
reader in addition to, but not instead of, the financial statements prepared in accordance with GAAP. Each non-GAAP financial measure is presented along with the
corresponding GAAP measure so as not to imply that more emphasis should be placed on the non-GAAP measure. We believe that non-GAAP measures provide relevant and
useful information, which is used by management, investors and other users of our financial information, as well as by our management in assessing both consolidated and
segment performance. The non-GAAP financial information presented may be determined or calculated differently by other companies and may not be directly comparable to
that of other companies.
(dollars in millions)
Years Ended December 31,
Consolidated Net Income
Add:
Provision for income taxes
Interest expense
Depreciation and amortization expense
Consolidated EBITDA
Add (Less):
Other (income) expense, net†
Equity in losses of unconsolidated businesses‡
Severance charges
Acquisition and integration related charges§
Product realignment charges§
Impairment charges
Net gain from dispositions of assets and businesses
Consolidated Adjusted EBITDA
† Includes Pension and benefits mark-to-market adjustments and early debt redemption costs, where applicable.
‡ Includes Product realignment charges and impairment charges, where applicable.
§ Excludes depreciation and amortization expense.
The changes in Consolidated Net Income, Consolidated EBITDA and Consolidated Adjusted EBITDA in the table above were primarily a result of the factors described in
connection with operating revenues and operating expenses.
$
2,900
15
204
—
—
186
(261)
47,189
$
(2,364)
186
2,157
531
450
4,591
—
47,410
2,945
4,730
16,682
44,145
3,584
4,833
17,403
41,859
$
2019
19,788
$
2018
16,039
Segment Results of Operations
We have two reportable segments that we operate and manage as strategic business units, Consumer and Business. We measure and evaluate our reportable segments based on
segment operating income. The use of segment operating income is consistent with the chief operating decision maker’s assessment of segment performance.
To aid in the understanding of segment performance as it relates to segment operating income, we use the following operating statistics to evaluate the overall effectiveness of
our segments:
Wireless retail connections
are retail customer device postpaid and prepaid connections. Retail connections under an account may include those from smartphones and basic
phones (collectively, phones) as well as tablets and other Internet devices, including wearables and retail IoT devices.
Wireless retail postpaid connections
are retail postpaid customer device connections. Retail connections under an account may include those from phones, as well as tablets and
other Internet devices, including wearables and retail IoT devices.
Fios Internet connections
are the total number of connections to the Internet using Fios Internet services.
Fios video connections
are the total number of connections to traditional linear video programming using Fios video services.
Broadband connections
are the total number of connections to the Internet using Digital Subscriber Line (DSL) and Fios Internet services.
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Voice connections
are the total number of traditional switched access lines in service and Fios digital voice connections.
Wireless retail connections, net additions
are the total number of additional retail customer device postpaid and prepaid connections, less the number of device disconnects
within the current period.
Wireless retail postpaid connections, net additions
are the total number of additional retail customer device postpaid connections, less the number of device disconnects within
the current period.
Churn
is the rate at which service to either retail or postpaid retail connections is terminated on a monthly basis.
Wireless retail postpaid ARPA
is the calculated average service revenue per account (ARPA) from retail postpaid accounts, which does not include recurring device payment
plan billings related to the Verizon device payment program, plan billings related to total mobile protection packages or regulatory fees.
Wireless retail postpaid accounts
are retail customers that are directly served and managed under the Verizon brand and use its services. Accounts include unlimited plans,
shared data plans and corporate accounts, as well as legacy single connection plans and family plans. A single account may include monthly wireless services for a variety of
connected devices.
Wireless retail postpaid connections per account
is calculated by dividing the total number of retail postpaid connections by the number of retail postpaid accounts as of the end
of the period.
Segment earnings before interest, taxes, depreciation and amortization (Segment EBITDA), which is presented below, is a non-GAAP measure and does not purport to be an
alternative to operating income as a measure of operating performance. We believe this measure is useful to management, investors and other users of our financial information
in evaluating operating profitability on a more variable cost basis as it excludes the depreciation and amortization expenses related primarily to capital expenditures and
acquisitions that occurred in prior years, as well as in evaluating operating performance in relation to our competitors. Segment EBITDA is calculated by adding back
depreciation and amortization expense to segment operating income. Segment EBITDA margin is calculated by dividing Segment EBITDA by total segment operating revenues.
You can find additional information about our segments in Note 13 to the consolidated financial statements.
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Verizon Consumer Group
Our Consumer segment provides consumer-focused wireless and wireline communications services and products. Our wireless services are provided across one of the most
extensive wireless networks in the United States under the Verizon brand and through wholesale and other arrangements. Our wireline services are provided in nine states in the
Mid-Atlantic and Northeastern U.S., as well as Washington D.C., over our 100% fiber-optic network under the Fios brand and over a traditional copper-based network to
customers who are not served by Fios.
Operating Revenues and Selected Operating Statistics
(dollars in millions, except
ARPA)
Increase/(Decrease)
Years Ended December 31,
Service
Wireless equipment
Other
Total Operating Revenues
Connections (‘000):
(1)
Wireless retail connections
Wireless retail postpaid connections
Fios Internet connections
Fios video connections
Broadband connections
Voice connections
Net Additions in Period (‘000):
(2)
Wireless retail
Wireless retail postpaid
Wireless retail postpaid phones
Churn Rate:
Wireless retail
Wireless retail postpaid
Wireless retail postpaid phones
Account Statistics:
Wireless retail postpaid ARPA
Wireless retail postpaid accounts (‘000)
(1)
Wireless retail postpaid connections per account
(1)
(2)
(1)
2019
$
65,383
18,048
7,625
$
91,056
$
$
2018
64,223
18,875
6,664
89,762
$
$
2019 vs. 2018
1,160
(827)
961
1,294
1.8 %
(4.4)
14.4
1.4
94,544
90,481
5,902
4,152
6,467
5,754
94,507
89,861
5,760
4,377
6,460
6,332
37
620
142
(225)
7
(578)
—
0.7
2.5
(5.1)
0.1
(9.1)
379
970
737
372
1,129
498
7
(159)
239
1.9
(14.1)
48.0
1.28%
1.05%
0.79%
1.25%
1.00%
0.76%
$
118.13
33,875
2.67
$
115.48
34,086
2.64
$
2.65
(211)
0.03
2.3
(0.6)
1.1
As of end of period
Excluding acquisitions and adjustments
Consumer's total operating revenues increased $1.3 billion, or 1.4%, during 2019 compared to 2018, primarily as a result of increases in Service and Other revenues, partially
offset by a decrease in Wireless equipment revenue.
Service Revenue
Service revenue increased $1.2 billion, or 1.8%, during 2019 compared to 2018, primarily due to increases in wireless service and Fios revenues, partially offset by decreases in
wireline voice and DSL services.
Wireless service revenue increased $1.3 billion, or 2.5%, during 2019 compared to 2018, due to increases in wireless access revenue, driven by customers shifting to higher
access plans including unlimited plans and increases in the number of devices per account, the declining fixed-term subsidized plan base and growth from reseller accounts.
Wireless retail postpaid ARPA increased 2.3%.
For the year ended December 31, 2019, Fios revenues totaled $10.4 billion and increased $92 million, or 0.9%, compared to 2018. This increase was due to a 2.5% increase in
Fios Internet connections, reflecting increased demand in higher broadband speeds, partially offset by a 5.1% decrease in Fios video connections, reflecting the ongoing shift
from traditional linear video to over-the-top (OTT) offerings.
Service revenue attributable to wireline voice and DSL broadband services declined during 2019, compared to 2018. The declines are primarily due to a decrease of 9.1% in
voice connections resulting primarily from competition and technology substitution with wireless and competing Voice over Internet Protocol (VoIP) and cable telephony
services.
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Wireless Equipment Revenue
Wireless equipment revenue decreased $827 million, or 4.4%, during 2019 compared to 2018, as a result of declines in wireless device sales primarily due to an elongation of the
handset upgrade cycle and increased promotions. These decreases were partially offset by a shift to higher priced units in the mix of wireless devices sold.
Other Revenue
Other revenue includes non-service revenues such as regulatory fees, cost recovery surcharges, revenues associated with our device protection package, leasing and interest on
equipment financed under a device payment plan agreement when sold to the customer by an authorized agent.
Other revenue increased $1.0 billion, or 14.4%, during 2019 compared to 2018, primarily due to pricing increases related to our wireless device protection plans, as well as
regulatory fees.
Operating Expenses
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Cost of services
Cost of wireless equipment
Selling, general and administrative expense
Depreciation and amortization expense
Total Operating Expenses
Cost of Services
Cost of services increased $549 million, or 3.6%, during 2019 compared to 2018, primarily due to increases in rent expense as a result of adding capacity to the networks to
support demand as well as an increase due to the adoption of the new lease accounting standard in 2019, increases in costs related to the device protection package offered to our
wireless retail postpaid customers, as well as regulatory fees. These increases were partially offset by decreases in employee-related costs primarily due to the Voluntary
Separation Program, as well as decreases in access costs and roaming.
Cost of Wireless Equipment
Cost of wireless equipment decreased $544 million, or 2.9%, during 2019 compared to 2018, primarily as a result of declines in the number of wireless devices sold as a result of
an elongation of the handset upgrade cycle. These decrease were partially offset by a shift to higher priced devices in the mix of wireless devices sold.
Selling, General and Administrative Expense
Selling, general and administrative expense increased $938 million, or 6.0%, during 2019 compared to 2018, primarily due to increases in sales commission and bad debt
expense, and an increase in advertising costs. The increase in sales commission expense during 2019 compared to 2018 was primarily due to a lower net deferral of commission
costs as a result of the adoption of Topic 606 on January 1, 2018 using a modified retrospective approach. These increases were partially offset by decreases in employee-related
costs primarily due to the Voluntary Separation Program.
Depreciation and Amortization Expense
Depreciation and amortization expense decreased $599 million, or 5.0%, during 2019 compared to 2018, driven by the change in the mix of total Verizon depreciable assets and
Consumer's usage of those assets.
Segment Operating Income and EBITDA
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Segment Operating Income
Add Depreciation and amortization expense
Segment EBITDA
Segment operating income margin
Segment EBITDA margin
$
$
2019
28,961
11,353
40,314
31.8%
44.3%
$
$
2018
28,011
11,952
39,963
31.2%
44.5%
$
$
2019 vs. 2018
950
(599)
351
3.4 %
(5.0)
0.9
$
$
2019
15,884
18,219
16,639
11,353
62,095
$
$
2018
15,335
18,763
15,701
11,952
61,751
$
$
2019 vs. 2018
549
(544)
938
(599)
344
3.6 %
(2.9)
6.0
(5.0)
0.6
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The changes in the table above during the periods presented were primarily a result of the factors described in connection with operating revenues and operating expenses.
Verizon Business Group
Our Business segment provides wireless and wireline communications services and products, video and data services, corporate networking solutions, security and managed
network services, local and long distance voice services and network access to deliver various IoT services and products. We provide these products and services to businesses,
government customers and wireless and wireline carriers across the U.S. and select products and services to customers around the world. The Business segment is organized in
four customer groups: Global Enterprise, Small and Medium Business, Public Sector and Other, and Wholesale.
Operating Revenues and Selected Operating Statistics
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Global Enterprise
Small and Medium Business
Public Sector and Other
Wholesale
Total Operating Revenues
Connections (‘000):
(2)
Wireless retail postpaid connections
Fios Internet connections
Fios video connections
Broadband connections
Voice connections
Net Additions in Period ('000):
(3)
Wireless retail postpaid
Wireless retail postpaid phones
Churn Rate:
Wireless retail postpaid
Wireless retail postpaid phones
(1)
(1)
2019
$
10,818
11,464
5,922
3,239
$
31,443
$
$
2018
11,201
10,752
5,833
3,748
31,534
$
$
2019 vs. 2018
(383)
712
89
(509)
(91)
(3.4)%
6.6
1.5
(13.6)
(0.3)
25,217
326
77
489
4,959
23,492
307
74
501
5,400
1,725
19
3
(12)
(441)
7.3
6.2
4.1
(2.4)
(8.2)
1,391
698
1,397
625
(6)
73
(0.4)
11.7
1.24%
0.99%
1.19%
0.98%
(2)
(3)
Service and other revenues included in our Business segment amounted to approximately $27.9 billion and $28.1 billion for the years ended December 31, 2019 and 2018,
respectively. Wireless equipment revenues included in our Business segment amounted to approximately $3.5 billion and $3.4 billion for the years ended December 31, 2019
and 2018, respectively.
As of end of period
Includes certain adjustments
Business revenues decreased $91 million, or 0.3%, during 2019 compared to 2018, primarily due to decreases in Global Enterprise and Wholesale revenues, partially offset by
increases in Small and Medium Business and Public Sector and Other revenues.
Global Enterprise
Global Enterprise offers services to large businesses, which are identified based on their size and volume of business with Verizon, as well as non-U.S. public sector customers.
Global Enterprise revenues decreased $383 million, or 3.4%, during 2019 compared to 2018, primarily due to declines in traditional data and voice communication services as a
result of competitive price pressures. These revenue decreases were partially offset by increases in wireless service revenue.
Small and Medium Business
Small and Medium Business offers wireless services and equipment, tailored voice and networking products, Fios services, IP networking, advanced voice solutions, security and
managed information technology services to our U.S.-based customers that do not meet the requirements to be categorized as Global Enterprise.
Small and Medium Business revenues increased $712 million, or 6.6%, during 2019 compared to 2018, primarily due to an increase in wireless postpaid service revenue of
11.7% as a result of increases in the amount of wireless retail postpaid connections. These increases were further driven by increased wireless equipment revenue resulting from
a shift to higher priced units in the mix of wireless devices sold and increases in
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the number of wireless devices sold, increased revenue related to our wireless device protection package, as well as increased revenue related to Fios services. These revenue
increases were partially offset by revenue declines related to the loss of voice and DSL service connections.
Small and Medium Business Fios revenues totaled $915 million and increased $110 million, or 13.7%, during 2019 compared to 2018, reflecting the increase in total
connections, as well as increased demand for higher broadband speeds.
Public Sector and Other
Public Sector and Other offers wireless products and services as well as wireline connectivity and managed solutions to U.S. federal, state and local governments and educational
institutions. These services include the business services and connectivity similar to the products and services offered by Global Enterprise, in each case, with features and
pricing designed to address the needs of governments and educational institutions.
Public Sector and Other revenues increased $89 million, or 1.5%, during 2019 compared to 2018, driven by increases in networking and wireless postpaid service revenue as a
result of an increase in wireless retail postpaid connections.
Wholesale
Wholesale offers wireline communications services including data, voice, local dial tone and broadband services primarily to local, long distance, and wireless carriers that use
our facilities to provide services to their customers.
Wholesale revenues decreased $509 million, or 13.6%, during 2019 compared to 2018, primarily due to declines in core data and traditional voice services resulting from the
effect of technology substitution and continuing contraction of market rates due to competition.
Operating Expenses
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Cost of services
Cost of wireless equipment
Selling, general and administrative expense
Depreciation and amortization expense
Total Operating Expenses
Cost of Services
Cost of services decreased $204 million, or 1.9%, during 2019 compared to 2018, primarily due to lower access costs resulting from a decline in voice connections, as well as
lower employee-related costs associated with the lower headcount resulting from the Voluntary Separation Program, offset by an increase in regulatory fees.
Cost of Wireless Equipment
Cost of wireless equipment increased $173 million, or 3.8%, during 2019 compared to 2018, primarily driven by a shift to higher priced units in the mix of wireless devices sold
and an increase in the number of wireless devices sold.
Selling, General and Administrative Expense
Selling, general and administrative expense increased $499 million, or 6.5%, during 2019 compared to 2018, due to increases in advertising expenses and sales commission
expense, which were partially offset by decreases in employee-related costs resulting from the Voluntary Separation Program. The increase in sales commission expense was
primarily due to a lower net deferral of commission costs in 2019 as compared to 2018 as a result of the adoption of Topic 606 on January 1, 2018 using a modified retrospective
approach.
Depreciation and Amortization Expense
Depreciation and amortization expense decreased $153 million, or 3.6%, during 2019 compared to 2018, driven by the change in the mix of total Verizon depreciable assets and
Business's usage of those assets.
$
$
2019
10,655
4,733
8,188
4,105
27,681
$
$
2018
10,859
4,560
7,689
4,258
27,366
$
$
2019 vs. 2018
(204)
173
499
(153)
315
(1.9)%
3.8
6.5
(3.6)
1.2
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Segment Operating Income and EBITDA
(dollars in millions)
Increase/(Decrease)
Years Ended December 31,
Segment Operating Income
Add Depreciation and amortization expense
Segment EBITDA
Segment operating income margin
Segment EBITDA margin
$
$
2019
3,762
4,105
7,867
12.0%
25.0%
$
$
2018
4,168
4,258
8,426
13.2%
26.7%
$
$
2019 vs. 2018
(406)
(153)
(559)
(9.7)%
(3.6)
(6.6)
The changes in the table above during the periods presented were primarily a result of the factors described in connection with operating revenues and operating expenses.
Special Items
Special items included in Income Before (Provision) Benefit For Income Taxes were as follows:
(dollars in millions)
Years Ended December 31,
Severance, pension and benefits charges (credits)
Selling, general and administrative expense
Other income (expense), net
Acquisition and integration related charges
Selling, general and administrative expense
Depreciation and amortization expense
Product realignment charges
Cost of services
Selling, general and administrative expense
Equity in losses of unconsolidated businesses
Depreciation and amortization expense
Impairment charges
Media goodwill impairment
Equity in losses of unconsolidated businesses
Early debt redemption costs
Other income (expense), net
Net gain from dispositions of assets and businesses
Selling, general and administrative expense
Total
$
(261)
3,909
$
—
6,577
3,604
725
186
50
4,591
—
—
—
—
—
303
147
207
1
—
—
531
22
$
204
126
$
2,157
(2,107)
2019
2018
The Consolidated Adjusted EBITDA non-GAAP measure presented in the Consolidated Net Income, Consolidated EBITDA and Consolidated Adjusted EBITDA discussion
(see "Consolidated Results of Operations") excludes all of the amounts included above, as described below.
The income and expenses related to special items included in our consolidated results of operations were as follows:
(dollars in millions)
Years Ended December 31,
Within Total Operating Expenses
Within Equity in losses of unconsolidated businesses
Within Other income (expense), net
Total
$
$
2019
129
50
3,730
3,909
$
$
2018
7,752
207
(1,382)
6,577
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Severance, Pension and Benefits Charges (Credits)
During 2019, in accordance with our accounting policy to recognize actuarial gains and losses in the period in which they occur, we recorded net pre-tax pension and benefits
charges of $126 million in our pension and postretirement benefit plans. The charges were recorded in Other income (expense), net in our consolidated statements of income and
were primarily driven by a decrease in our discount rate assumption used to determine the current year liabilities of our pension plans and postretirement benefit plans from a
weighted-average of 4.4% at December 31, 2018 to a weighted-average of 3.3% at December 31, 2019 ($4.3 billion), partially offset by the difference between our estimated
return on assets and our actual return on assets ($2.3 billion) and other assumption adjustments of $1.9 billion, of which $1.6 billion related to healthcare claims experience.
During 2019, we also recorded net pre-tax severance charges of $204 million in Selling, general and administrative expense in our consolidated statements of income.
During 2018, we recorded net pre-tax pension and benefits credits of $2.1 billion in accordance with our accounting policy to recognize actuarial gains and losses in the period in
which they occur. The pension and benefits remeasurement credits of $2.3 billion, which were recorded in Other income (expense), net in our consolidated statements of income,
were primarily driven by an increase in our discount rate assumption used to determine the current year liabilities of our pension plans and postretirement benefit plans from a
weighted-average of 3.7% at December 31, 2017 to a weighted-average of 4.4% at December 31, 2018 ($2.6 billion), and mortality and other assumption adjustments of $1.7
billion, $1.6 billion of which related to healthcare claims and trend adjustments, offset by the difference between our estimated return on assets of 7.0% and our actual return on
assets of (2.7)% ($1.9 billion). The credits were partially offset by $177 million due to the effects of participants retiring under the Voluntary Separation Program. During 2018,
we also recorded net pre-tax severance charges of $2.2 billion in Selling, general and administrative expense, primarily driven by the Voluntary Separation Program for select
U.S.-based management employees and other headcount reduction initiatives, which resulted in a severance charge of $1.8 billion ($1.4 billion after-tax), and $339 million in
severance costs recorded under other existing separation plans.
Due to the presentation of the other components of net periodic benefit cost, we recognize a portion of the pension and benefits charges (credits) in Other income (expense), net
in our consolidated statements of income.
See Note 11 to the consolidated financial statements for additional information related to severance, pension and benefits charges (credits).
Acquisition and Integration Related Charges
Acquisition and integration related charges of $553 million recorded during the year ended December 31, 2018 primarily related to the acquisition of Yahoo’s operating business
in June 2017.
Product Realignment Charges
Product realignment charges of $658 million recorded during the year ended December 31, 2018 primarily related to the discontinuation of the go90 platform and associated
content during the second quarter of 2018.
Impairment Charges
The impairment charges consist of write-downs of goodwill and other investments or assets. The goodwill impairment charges of $186 million and $4.6 billion recorded during
the years ended December 31, 2019 and 2018, respectively, for Verizon Media were a result of the Company's annual impairment test performed in the fourth quarter (see
"Critical Accounting Estimates"). In addition, we recorded an impairment charge of $50 million in Equity in losses of unconsolidated businesses related to a media joint venture
investment.
Early Debt Redemption Costs
During 2019 and 2018, we recorded early debt redemptions costs of $3.6 billion and $725 million, respectively.
We recognize early debt redemptions costs in Other income (expense), net in our consolidated statements of income. See Note 7 to the consolidated financial statements for
additional information related to our early debt redemptions.
Net Gain from Dispositions of Assets and Businesses
During 2019, we recorded a pre-tax net gain from dispositions of assets and businesses of $261 million in connection with the sale of various real estate properties and
businesses.
Operating Environment and Trends
The telecommunications industry is highly competitive. We expect competition to remain intense as traditional and non-traditional participants seek increased market share. Our
high-quality customer base and networks differentiate us from our competitors and give us the ability to plan and manage through changing economic and competitive
conditions. We remain focused on executing on the fundamentals of the business: maintaining a high-quality customer base, delivering strong financial and operating results and
strengthening our balance sheet. We will continue to invest for growth, which we believe is the key to creating value for our shareholders. We continue to lead in 4G LTE
performance while building momentum for our 5G network. Our strategy lays the foundation for the future through investments in our Intelligent Edge Network that enable
efficiencies throughout our core infrastructure and deliver flexibility to meet customer requirements.
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The U.S. wireless market has achieved a high penetration of smartphones, which reduces the opportunity for new phone connection growth for the industry. We expect future
revenue growth in the industry to be driven by expanding existing customer relationships, increasing the number of ways customers can connect with wireless networks and
services and increasing the penetration of other connected devices including wearables, tablets and IoT devices. We expect 5G technology will provide a significant opportunity
for growth in the industry in 2021 and beyond. With respect to our wireless connectivity products and services, we compete against other national wireless service providers,
including AT&T Inc., Sprint Corporation and T-Mobile USA, Inc., as well as various regional wireless service providers. We also compete for retail activations with resellers
that buy bulk wholesale service from wireless service providers, including Verizon, and resell it to their customers. Resellers may include cable companies. We face competition
from other communications and technology companies seeking to increase their brand recognition and capture customer revenue with respect to the provision of wireless
products and services, in addition to non-traditional offerings in mobile data. For example, Microsoft Corporation, Alphabet Inc., Apple Inc. and others are offering alternative
means for making wireless voice calls that, in certain cases, can be used in lieu of the wireless provider’s voice service, as well as alternative means of accessing video content.
With respect to wireless services and equipment, pricing plays an important role in the wireless competitive landscape. We compete in this area by offering our customers
services and devices that we believe they will regard as the best available value for the price. As the demand for wireless services continues to grow, wireless service providers
are offering a range of service plans at competitive prices. These service offerings will vary from time to time based on customer needs, technology changes and market
conditions and may be provided as standard plans or as part of limited time promotional offers.
We expect future service revenue growth opportunities to arise from increased access revenue as customers shift to higher access plans, as well as from increased connections per
account. Future service revenue growth opportunities will be dependent on expanding the penetration of our services, increasing the number of ways that our customers can
connect with our networks and services and the development of new ecosystems.We and other wireless service providers, as well as equipment manufacturers, offer device
payment options, which provide customers with the ability to pay for their device over a period of time, and some providers offer device leasing arrangements.
Current and potential competitors in the wireline service market include cable companies, wireless service providers, domestic and foreign telecommunications providers,
satellite television companies, Internet service providers, over-the-top providers and other companies that offer network services and managed enterprise solutions.
In addition, companies with a global presence are increasingly competing with us in our wireline services. A relatively small number of telecommunications and integrated
service providers with global operations serve customers in the global enterprise market and, to a lesser extent, the global wholesale market. We compete with these providers for
large contracts to provide integrated solutions to global enterprises. Many of these companies have strong market presence, brand recognition and existing customer
relationships, all of which contribute to intensifying competition that may affect our future revenue growth.
Despite this challenging environment, we expect that we will be able to grow key aspects of our wireline services. We continue to provide network reliability and offer products,
which include fiber-optic Internet access, several video services, and voice services. Further, we will continue to offer our business and government customers more robust IP
products and services, and advance our IoT strategies by leveraging business models that monetize usage on our networks at the connectivity, platform and solution layers.
The online advertising market continues to evolve as online users are migrating from traditional desktop to mobile and multiple-device usage. Also, there is a continued shift
towards programmatic advertising which presents opportunities to connect online advertisers with the appropriate online users in a rapid environment. Our Media business
competes with other online search engines, advertising platforms, digital video services and social networks. We are experiencing pressure from search and desktop usage and
believe the pressure in these sectors will continue. We are implementing initiatives to realize synergies across all of our media assets and build services around our core content
pillars to diversify revenue and return to growth.
We will also continue to focus on cost efficiencies to ensure we have the maximum flexibility to adjust to changes in the competitive and economic environments and maximize
returns to shareholders.
2020 Connection Trends
In our Consumer segment, we expect to continue to attract new customers and maintain high-quality retail postpaid customers, capitalizing on demand for data services and
providing our customers new ways of using wireless services in their daily lives. We expect that future connection growth will be driven by smartphones, tablets and other
connected devices such as wearables. We believe the combination of our wireless network performance and Mix & Match unlimited plans provides a superior customer
experience, supporting increased penetration of data services and the continued attraction and retention of higher valued retail postpaid connections. We expect to manage churn
by providing a consistent, reliable experience on our wireless service and focusing on improving the customer experience through simplified pricing and continued focus in our
distribution channels. We expect to continue to grow our Fios Internet connections as we seek to increase our penetration rates within our Fios service areas, further supported by
the demand for higher speed internet connections. In Fios video, the business continues to face ongoing pressure as observed throughout the linear television market. We expect
to manage market pressure by offering customers a choice of video service, including options such as Mix & Match on Fios and other offerings. We have experienced continuing
access line and DSL losses as customers have disconnected both primary and secondary lines and switched to alternative technologies such as wireless, VoIP and cable for voice
and data services.
In our Business segment, we offer wireless products and services to business and government customers across the U.S. We continue to grow our retail connections while facing
a competitive environment. We expect to maintain connection growth in part by adding capacity and density
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to our 4G LTE network, in addition to leading the build-out of 5G technology. We expect this connection growth, combined with our industry-leading network assets, will
provide additional opportunities to sell solutions, such as those around security, advanced communications and professional services. We expect to expand our existing services
offered to business customers through our Intelligent Edge Network, our multi-use platform.
2020 Operating Revenue Trends
In our Consumer segment, we expect to see a continuation of the service revenue trends from 2019 as customers shift to higher access plans with additional services and increase
the number of devices they connect with our networks and services. Equipment revenues are largely dependent on wireless device sales volumes, the mix of devices, promotions
and upgrades, which are subject to device lifecycles, iconic device launches and competition within the wireless industry. We anticipate an increase in wireless device upgrades
in the second half of the year as we expand the availability and reach of our 5G network.
In our Business segment, we expect overall revenue growth in 2020 as wireless services and our high-quality fiber-based products will offset secular declines from legacy
technologies and pressure from competition. We expect wireless revenue to expand, driven by connection growth led by Small and Medium Business. We expect our Fios
products, through increased penetration, will also contribute to revenue growth. Legacy traditional wireline services continue to face secular pressures.
Our Media Business, Verizon Media, is primarily made up of digital advertising products. We are experiencing revenue pressure from search and desktop usage, which started to
improve throughout 2019 and believe the pressure in those sectors will continue. We are focused on returning to revenue growth by implementing initiatives to realize synergies
across all of our media assets and building services around our core content pillars. We expect positive growth in mobile services and products.
2020 Operating Expense and Cash Flow from Operations Trends
We expect our consolidated operating income margin and adjusted consolidated EBITDA margin to remain strong as we continue to undertake initiatives to reduce our overall
cost structure by improving productivity and gaining efficiencies in our operations throughout the business in 2020 and beyond. Business Excellence initiatives include the
adoption of the zero-based budgeting methodology, driving capital efficiencies from the architecture of the networks, evolving our Information Technology strategy and the
continuing benefit from the Voluntary Separation Program. We believe our additional investments in our Business segment in both product simplification and continued focus on
process improvements and new work tools will drive cost savings and create incremental growth opportunities in areas such as 5G and One Fiber. The goal of the Business
Excellence initiative is to take $10 billion of cumulative cash outflows out of the business over four years, beginning with 2018. As part of this initiative, we are focusing on both
operating expenses and capital expenditures. Our Business Excellence initiatives produced cumulative cash savings of $5.7 billion through the end of 2019 from a mix of capital
and operational expenditure activities. The program remains on track to achieve our goal. Expenses related to programs funded through the reinvestment of program savings are
expected to apply offsetting pressures to our margins.
The implementation of Topic 606 resulted in the deferral of commission expense in both our Consumer and Business segments. In 2020, we expect a smaller year-over-year
benefit from the adoption of the standard due to the deferral of commission costs as compared to 2018 and 2019. The reduction in benefit creates a year-over-year headwind to
operating income.
We create value for our shareholders by investing the cash flows generated by our business in opportunities and transactions that support continued profitable growth, thereby
increasing customer satisfaction and usage of our products and services. In addition, we have used our cash flows to maintain and grow our dividend payout to shareholders.
Verizon’s Board of Directors increased the Company’s quarterly dividend by 2.1% during 2019, making this the thirteenth consecutive year in which we have raised our
dividend.
Our goal is to use our cash to create long-term value for our shareholders. We will continue to look for investment opportunities that will help us to grow the business, strengthen
our balance sheet, acquire spectrum licenses (see "Cash Flows from Investing Activities"), pay dividends to our shareholders and, when appropriate, buy back shares of our
outstanding common stock (see "Cash Flows from Financing Activities").
Capital Expenditures
Our 2020 capital program includes capital to fund advanced networks and services, including expanding our core networks, adding capacity and density to our 4G LTE network
in order to stay ahead of our customers’ increasing data demands and deploying our 5G network, transforming our structure to deploy the Intelligent Edge Network while
reducing the cost to deliver services to our customers, and pursuing other opportunities to drive operating efficiencies. We expect that the new network architecture will simplify
operations by eliminating legacy network elements, improve our 4G LTE coverage, speed the deployment of 5G technology, and create new enterprise opportunities in the
business market. The level and the timing of the Company’s capital expenditures within these broad categories can vary significantly as a result of a variety of factors outside of
our control, such as material weather events, equipment availability from vendors and permits from local governments. Capital expenditures for 2020 are expected to be in the
range of $17.0 billion to $18.0 billion, including the continued investment in our 5G network. Capital expenditures were $17.9 billion in 2019 and $16.7 billion in 2018. We
believe that we have significant discretion over the amount and timing of our capital expenditures on a Company-wide basis as we are not subject to any agreement that would
require significant capital expenditures on a designated schedule or upon the occurrence of designated events.
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Consolidated Financial Condition
(dollars in millions)
Years Ended December 31,
Cash flows provided by (used in)
Operating activities
Investing activities
Financing activities
Increase in cash, cash equivalents and restricted cash
$
$
35,746
(17,581)
(18,164)
1
$
$
34,339
(17,934)
(15,377)
1,028
2019
2018
We use the net cash generated from our operations to fund expansion and modernization of our networks, service and repay external financing, pay dividends, invest in new
businesses and spectrum and, when appropriate, buy back shares of our outstanding common stock. Our sources of funds, primarily from operations and, to the extent necessary,
from external financing arrangements, are sufficient to meet ongoing operating and investing requirements. We expect that our capital spending requirements will continue to be
financed primarily through internally generated funds. Debt or equity financing may be needed to fund additional investments or development activities or to maintain an
appropriate capital structure to ensure our financial flexibility. Our cash and cash equivalents are held both domestically and internationally, and are invested to maintain
principal and provide liquidity. See "Market Risk" for additional information regarding our foreign currency risk management strategies.
Our available external financing arrangements include an active commercial paper program, credit available under credit facilities and other bank lines of credit, vendor
financing arrangements, issuances of registered debt or equity securities, U.S. retail medium-term notes and other capital market securities that are privately-placed or offered
overseas. In addition, we monetize our device payment plan agreement receivables through asset-backed debt transactions.
Cash Flows Provided By Operating Activities
Our primary source of funds continues to be cash generated from operations. Net cash provided by operating activities increased by $1.4 billion during 2019, compared to the
similar period in 2018, primarily due to an increase in earnings and a decrease in discretionary contributions to qualified employee benefit plans, offset by changes in working
capital, which includes an increase in cash income taxes as well as severance payments as a result of the Voluntary Separation Program. We made $300 million and $1.7 billion
in discretionary employee benefits contributions to our defined benefit pension plan during 2019 and 2018, respectively. As a result of the discretionary pension contributions,
we expect that there will be no required pension funding until 2026, which will continue to benefit future cash flows. These contributions also improved the funded status of our
qualified pension plan.
Cash Flows Used In Investing Activities
Capital Expenditures
Capital expenditures continue to relate primarily to the use of capital resources to facilitate the introduction of new products and services, enhance responsiveness to competitive
challenges, maintain our existing infrastructure and increase the operating efficiency and productivity of our networks.
Capital expenditures, including capitalized software, were as follows:
(dollars in millions)
Years Ended December 31,
Capital expenditures (including capitalized software)
Total as a percentage of revenue
$
2019
17,939
13.6%
$
2018
16,658
12.7%
Capital expenditures increased in 2019 primarily due to an increase in investments to support multi-use fiber assets, which support the densification of our 4G LTE network and
our 5G technology deployment. Our investments are primarily related to network infrastructure to support the business.
Acquisitions
During 2019 and 2018, we invested $898 million and $1.4 billion, respectively, in acquisitions of wireless licenses. During 2019 and 2018, we also invested an insignificant
amount and $230 million, respectively, in acquisitions of businesses, net of cash acquired.
In 2019, the FCC completed two millimeter wave spectrum license auctions. We paid approximately $521 million for spectrum licenses in connection with these auctions. See
Note 3 to the consolidated financial statements for additional information.
In January 2018, Verizon acquired NextLink Wireless LLC (NextLink) from a wholly-owned subsidiary of XO Holdings for approximately $493 million, subject to certain
adjustments, of which $320 million (an option exercise price to acquire NextLink) was prepaid in the first quarter of 2017. The option exercise price represented the fair value of
the option. The remaining cash consideration was paid at the closing of the transaction. The spectrum acquired as part of the transaction is being used for our 5G technology
deployment.
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In February 2018, Verizon acquired Straight Path Communications Inc. (Straight Path), a holder of millimeter wave spectrum configured for 5G wireless services for total
consideration reflecting an enterprise value of approximately $3.1 billion, which was primarily settled with Verizon shares but also included transaction costs payable in cash of
approximately $736 million, consisting primarily of a fee paid to the FCC. The spectrum acquired as part of the transaction is being used for our 5G technology deployment.
During 2019 and 2018, we completed various other acquisitions for an insignificant amount of cash consideration.
See "Acquisitions and Divestitures" for information on our acquisitions.
Dispositions
During 2019, we received gross proceeds of approximately $1.0 billion for a sale-leaseback transaction for buildings and real estate. See Note 6 to the consolidated financial
statements for additional information.
Cash Flows Used In Financing Activities
We seek to maintain a mix of fixed and variable rate debt to lower borrowing costs within reasonable risk parameters and to protect against earnings and cash flow volatility
resulting from changes in market conditions. During 2019 and 2018, net cash used in financing activities was $18.2 billion and $15.4 billion, respectively.
2019
During 2019, our net cash used in financing activities of $18.2 billion was primarily driven by:
•
•
•
$23.9 billion used for repayments, redemptions and repurchases of long-term borrowings and finance lease obligations, which included $6.3 billion used for prepayments
and repayments of asset-backed long-term borrowings;
$10.0 billion used for dividend payments; and
$1.8 billion used for net debt related costs.
These uses of cash were partially offset by proceeds from long-term borrowings of $18.7 billion, which included $8.6 billion of proceeds from our asset-backed debt
transactions.
Proceeds from and Repayments, Redemptions, and Repurchases of Long-Term Borrowings
At December 31, 2019, our total debt decreased to $111.5 billion as compared to $113.1 billion at December 31, 2018. During both the years ended December 31, 2019 and
2018, our effective interest rate was 4.8%. The substantial majority of our total debt portfolio consists of fixed rate indebtedness, therefore, changes in interest rates do not have a
material effect on our interest payments. See also "Market Risk" and Note 7 to the consolidated financial statements for additional information.
At December 31, 2019, approximately $23.5 billion, or 21.1%, of the aggregate principal amount of our total debt portfolio consisted of foreign denominated debt, primarily the
Euro and British Pound Sterling. We have entered into cross currency swaps on substantially all of our foreign denominated debt in order to fix our future interest and principal
payments in U.S. dollars and mitigate the impact of foreign currency transaction gains or losses. See "Market Risk" for additional information.
Verizon may continue to repurchase debt securities issued by Verizon and its affiliates in the future through open market purchases, privately negotiated transactions, tender
offers, exchange offers, or otherwise, upon such terms and at such prices as Verizon may from time to time determine for cash or other consideration.
Other, net
Other, net financing activities during 2019 includes early redemption costs, see "Special Items" for additional information, as well as cash paid on debt exchanges and derivative-
related transactions. See Note 15 to the consolidated financial statements for additional information.
Dividends
The Verizon Board of Directors assesses the level of our dividend payments on a periodic basis taking into account such factors as long-term growth opportunities, internal cash
requirements and the expectations of our shareholders. During the third quarter of 2019, the Board increased our quarterly dividend payment by 2.1% to $0.6150 from $0.6025
per share from the previous quarter. This is the thirteenth consecutive year that Verizon’s Board of Directors has approved a quarterly dividend increase.
As in prior periods, dividend payments were a significant use of capital resources. During 2019, we paid $10.0 billion in dividends.
2018
During 2018, our net cash used in financing activities of $15.4 billion was primarily driven by:
•
•
$14.6 billion used for repayments, redemptions and repurchases of long-term borrowings and finance lease obligations, which included $3.6 billion used for prepayments
of asset-backed long-term borrowings; and
$9.8 billion used for dividend payments.
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These uses of cash were partially offset by proceeds from long-term borrowings of $10.8 billion, which included $4.8 billion of proceeds from our asset-backed debt
transactions.
Proceeds from and Repayments, Redemptions, and Repurchases of Long-Term Borrowings
At December 31, 2018, our total debt was $113.1 billion, and during the year ended December 31, 2018, our effective interest rate was 4.8%. The substantial majority of our total
debt portfolio consisted of fixed rate indebtedness, therefore, changes in interest rates did not have a material effect on our interest payments. See "Market Risk" and Note 7 to
the consolidated financial statements for additional information.
At December 31, 2018, approximately $17.1 billion, or 15.1%, of the aggregate principal amount of our total debt portfolio consisted of foreign denominated debt, primarily the
Euro and British Pound Sterling. We have entered into cross currency swaps on a majority of our foreign denominated debt in order to fix our future interest and principal
payments in U.S. dollars and mitigate the impact of foreign currency transaction gains or losses. See "Market Risk" for additional information.
Other, net
Other, net financing activities during 2018, included early debt redemption costs. See "Special Items" for additional information, as well as cash paid on debt exchanges and
derivative-related transactions.
Dividends
During the third quarter of 2018, the Board increased our quarterly dividend payment by 2.1% to $0.6025 per share.
As in prior periods, dividend payments were a significant use of capital resources. During 2018, we paid $9.8 billion in dividends.
Asset-Backed Debt
As of December 31, 2019, the carrying value of our asset-backed debt was $12.4 billion. Our asset-backed debt includes Asset-Backed Notes (ABS Notes) issued to third-party
investors (Investors) and loans (ABS Financing Facilities) received from banks and their conduit facilities (collectively, the Banks). Our consolidated asset-backed debt
bankruptcy remote legal entities (each, an ABS Entity or collectively, the ABS Entities) issue the debt or are otherwise party to the transaction documentation in connection with
our asset-backed debt transactions. Under the terms of our asset-backed debt, Cellco Partnership (Cellco) and certain other affiliates of Verizon (collectively, the Originators)
transfer device payment plan agreement receivables to one of the ABS Entities, which in turn transfers such receivables to another ABS Entity that issues the debt. Verizon
entities retain the equity interests in the ABS Entities, which represent the rights to all funds not needed to make required payments on the asset-backed debt and other related
payments and expenses.
Our asset-backed debt is secured by the transferred device payment plan agreement receivables and future collections on such receivables. The device payment plan agreement
receivables transferred to the ABS Entities and related assets, consisting primarily of restricted cash, will only be available for payment of asset-backed debt and expenses related
thereto, payments to the Originators in respect of additional transfers of device payment plan agreement receivables, and other obligations arising from our asset-backed debt
transactions, and will not be available to pay other obligations or claims of Verizon’s creditors until the associated asset-backed debt and other obligations are satisfied. The
Investors or Banks, as applicable, which hold our asset-backed debt have legal recourse to the assets securing the debt, but do not have any recourse to Verizon with respect to
the payment of principal and interest on the debt. Under a parent support agreement, Verizon has agreed to guarantee certain of the payment obligations of Cellco and the
Originators to the ABS Entities.
Cash collections on the device payment plan agreement receivables collateralizing our asset-backed debt securities are required at certain specified times to be placed into
segregated accounts. Deposits to the segregated accounts are considered restricted cash and are included in Prepaid expenses and other, and Other assets in our consolidated
balance sheets.
Proceeds from our asset-backed debt transactions are reflected in Cash flows from financing activities in our consolidated statements of cash flows. The asset-backed debt issued
and the assets securing this debt are included in our consolidated balance sheets. See Note 7 to the consolidated financial statements for additional information.
In May 2018, we entered into an ABS financing facility with a number of financial institutions (2018 ABS Financing Facility). One loan agreement was entered into in
connection with the 2018 ABS Financing Facility. In May 2019, the $540 million outstanding under the loan agreement was prepaid, and the loan agreement was terminated.
In September 2016, we entered into an ABS financing facility with a number of financial institutions (2016 ABS Financing Facility). Two loan agreements were entered into in
connection with the 2016 ABS Financing Facility in September 2016 and May 2017. In April and May 2019, we paid off both the 2016 and 2017 loans for an aggregate of $671
million, and the loan agreements were terminated.
In May 2019, the 2016 ABS Financing Facility was amended and restated (2019 ABS Financing Facility). One loan agreement was entered into in connection with the 2019
ABS Financing Facility. Under the 2019 loan agreement, we have the right to prepay all or a portion of the advances at any time without penalty, but in certain cases, with
breakage costs. During 2019, we received $4.8 billion of borrowings and prepaid $1.5 billion under the 2019 loan agreement.
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Long-Term Credit Facilities
At December 31, 2019
(dollars in millions)
Verizon revolving credit facility
(1)
Various export credit facilities
(2)
Total
(1)
Maturities
2022
2022-2027
$
$
Facility Capacity
9,500
5,500
15,000
$
$
Unused Capacity
9,390
—
9,390
$
Principal Amount
Outstanding
N/A
4,471
4,471
The revolving credit facility does not require us to comply with financial covenants or maintain specified credit ratings, and it permits us to borrow even if our business has
incurred a material adverse change. The revolving credit facility provides for the issuance of letters of credit.
(2)
During 2019 and 2018, we drew down $1.5 billion and $3.0 billion from these facilities, respectively. We use these credit facilities to finance equipment-related purchases.
Common Stock
Common stock has been used from time to time to satisfy some of the funding requirements of employee and shareholder plans. During the years ended December 31, 2019 and
2018, we issued 3.8 million and 3.5 million common shares from Treasury stock, respectively, which had an insignificant aggregate value.
In February 2020, the Verizon Board of Directors authorized a share buyback program to repurchase up to 100 million shares of the Company's common stock. The program will
terminate when the aggregate number of shares purchased reaches 100 million, or a new share repurchase plan superseding the current plan is authorized, whichever is sooner.
The program permits Verizon to repurchase shares over time, with the amount and timing of repurchases depending on market conditions and corporate needs. There were no
repurchases of common stock during 2019 or 2018 under our previously authorized share buyback program.
Credit Ratings
Verizon’s credit ratings did not change in 2019 or 2018.
Securities ratings assigned by rating organizations are expressions of opinion and are not recommendations to buy, sell or hold securities. A securities rating is subject to revision
or withdrawal at any time by the assigning rating organization. Each rating should be evaluated independently of any other rating.
Covenants
Our credit agreements contain covenants that are typical for large, investment grade companies. These covenants include requirements to pay interest and principal in a timely
fashion, pay taxes, maintain insurance with responsible and reputable insurance companies, preserve our corporate existence, keep appropriate books and records of financial
transactions, maintain our properties, provide financial and other reports to our lenders, limit pledging and disposition of assets and mergers and consolidations, and other similar
covenants.
We and our consolidated subsidiaries are in compliance with all of our restrictive covenants in our debt agreements.
Change In Cash, Cash Equivalents and Restricted Cash
Our Cash and cash equivalents at December 31, 2019 totaled $2.6 billion, a $151 million decrease compared to Cash and cash equivalents at December 31, 2018, primarily as a
result of the factors discussed above.
Restricted cash at December 31, 2019 totaled $1.3 billion, a $152 million increase compared to restricted cash at December 31, 2018, primarily due to cash collections on the
device payment plan agreement receivables that are required at certain specified times to be placed into segregated accounts.
Free Cash Flow
Free cash flow is a non-GAAP financial measure that reflects an additional way of viewing our liquidity that, when viewed with our GAAP results, provides a more complete
understanding of factors and trends affecting our cash flows. Free cash flow is calculated by subtracting capital expenditures from net cash provided by operating activities. We
believe it is a more conservative measure of cash flow since purchases of fixed assets are necessary for ongoing operations. Free cash flow has limitations due to the fact that it
does not represent the residual cash flow available for discretionary expenditures. For example, free cash flow does not incorporate payments made on finance lease obligations
or cash payments for business acquisitions or wireless licenses. Therefore, we believe it is important to view free cash flow as a complement to our entire consolidated statements
of cash flows.
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The following table reconciles net cash provided by operating activities to Free cash flow:
(dollars in millions)
Years Ended December 31,
Net cash provided by operating activities
Less Capital expenditures (including capitalized software)
Free cash flow
$
$
2019
35,746
17,939
17,807
$
$
2018
34,339
16,658
17,681
The increase in free cash flow during 2019 is a reflection of the increase in operating cash flows, partially offset by the increase in capital expenditures discussed above.
Employee Benefit Plans Funded Status and Contributions
Employer Contributions
We operate numerous qualified and nonqualified pension plans and other postretirement benefit plans. These plans primarily relate to our domestic business units. During 2019
and 2018, contributions to our qualified pension plans were $300 million and $1.0 billion, respectively. We made contributions of $71 million in 2019 to our nonqualified
pension plans.
The Company’s overall investment strategy is to achieve a mix of assets that allows us to meet projected benefit payments while taking into consideration risk and return. In an
effort to reduce the risk of our portfolio strategy and better align assets with liabilities, we have adopted a liability driven pension strategy that seeks to better match cash flows
from investments with projected benefit payments. We expect that the strategy will reduce the likelihood that assets will decline at a time when liabilities increase (referred to as
liability hedging), with the goal to reduce the risk of underfunding to the plan and its participants and beneficiaries; however, we also expect the strategy to result in lower asset
returns. Nonqualified pension contributions are estimated to be approximately $70 million in 2020.
Contributions to our other postretirement benefit plans generally relate to payments for benefits on an as-incurred basis since these other postretirement benefit plans do not have
funding requirements similar to the pension plans. We contributed $449 million to our other postretirement benefit plans in 2019 and $1.2 billion, including $679 million
discretionary contributions, in 2018. Contributions to our other postretirement benefit plans are estimated to be approximately $700 million in 2020.
Leasing Arrangements
See Note 6 to the consolidated financial statements for a discussion of leasing arrangements.
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Contractual Obligations
The following table provides a summary of our contractual obligations and commercial commitments at December 31, 2019. Additional detail about these items is included in
the notes to the consolidated financial statements.
(dollars in millions)
Payments Due By Period
Contractual Obligations
Long-term debt
(1)
Finance lease obligations
(2)
Total long-term debt, including current maturities
Interest on long-term
Operating leases
(2)
Purchase obligations
Finance obligations
(3)
Total
$
110,865
1,213
112,078
62,450
25,968
18,769
4,135
1,539
$
224,939
$
$
Less than
1 year
10,470
366
10,836
4,578
4,099
8,384
694
281
28,872
$
$
1 to 3 years
16,431
479
16,910
8,383
7,127
7,448
1,692
579
42,139
$
$
3 to 5 years
9,803
244
10,047
7,426
5,485
1,441
1,749
603
26,751
$
$
More than
5 years
74,161
124
74,285
42,063
9,257
1,496
—
76
127,177
debt
(1)
Other long-term liabilities
(4)
(5)
Total contractual obligations
(1)
(2)
(3)
(4)
Items included in long-term debt with variable coupon rates exclude unamortized debt issuance costs, and are described in Note 7 to the consolidated financial statements.
See Note 6 to the consolidated financial statements for additional information.
Items included in purchase obligations are primarily commitments to purchase content and network services, equipment, software and marketing services, which will be used
or sold in the ordinary course of business. These amounts do not represent our entire anticipated purchases in the future, but represent only those items that are the subject of
contractual obligations. We also purchase products and services as needed with no firm commitment. For this reason, the amounts presented in this table alone do not provide
a reliable indicator of our expected future cash outflows or changes in our expected cash position. See Note 16 to the consolidated financial statements for additional
information.
Other long-term liabilities represent estimated postretirement benefit and qualified pension plan contributions. Estimated qualified pension plan contributions include expected
minimum funding contributions, which commence in 2026 based on the plan's current funded status. Estimated postretirement benefit payments include expected future
postretirement benefit payments. These estimated amounts: (1) are subject to change based on changes to assumptions and future plan performance, which could impact the
timing or amounts of these payments; and (2) exclude expectations beyond 5 years due to uncertainty of the timing and amounts. See Note 11 to the consolidated financial
statements for additional information.
Represents future minimum payments under the sublease arrangement for our tower transaction. See Note 6 to the consolidated financial statements for additional information.
(5)
We are not able to make a reasonable estimate of when the unrecognized tax benefits balance of $2.9 billion and related interest and penalties will be settled with the respective
taxing authorities until issues or examinations are further developed. See Note 12 to the consolidated financial statements for additional information.
Guarantees
We guarantee the debentures of our operating telephone company subsidiaries as well as the debt obligations of GTE LLC, as successor in interest to GTE Corporation, that were
issued and outstanding prior to July 1, 2003. See Note 7 to the consolidated financial statements for additional information.
In connection with the execution of agreements for the sale of businesses and investments, Verizon ordinarily provides representations and warranties to the purchasers
pertaining to a variety of nonfinancial matters, such as ownership of the securities being sold, as well as financial losses. See Note 16 to the consolidated financial statements for
additional information.
As of December 31, 2019, letters of credit totaling approximately $632 million, which were executed in the normal course of business and support several financing
arrangements and payment obligations to third parties, were outstanding. See Note 16 to the consolidated financial statements for additional information.
Market Risk
We are exposed to various types of market risk in the normal course of business, including the impact of interest rate changes, foreign currency exchange rate fluctuations,
changes in investment, equity and commodity prices and changes in corporate tax rates. We employ risk management strategies, which may include the use of a variety of
derivatives including cross currency swaps, forward starting interest rate swaps, interest rate swaps, interest rate caps and foreign exchange forwards. We do not hold derivatives
for trading purposes.
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It is our general policy to enter into interest rate, foreign currency and other derivative transactions only to the extent necessary to achieve our desired objectives in optimizing
exposure to various market risks. Our objectives include maintaining a mix of fixed and variable rate debt to lower borrowing costs within reasonable risk parameters and to
protect against earnings and cash flow volatility resulting from changes in market conditions. We do not hedge our market risk exposure in a manner that would completely
eliminate the effect of changes in interest rates and foreign exchange rates on our earnings.
Counterparties to our derivative contracts are major financial institutions with whom we have negotiated derivatives agreements (ISDA master agreements) and credit support
annex (CSA) agreements which provide rules for collateral exchange. Negotiations and executions of new ISDA master agreements and CSA agreements with our counterparties
continued during 2018. The CSA agreements contain rating based thresholds such that we or our counterparties may be required to hold or post collateral based upon changes in
outstanding positions as compared to established thresholds and changes in credit ratings. At December 31, 2019, we held an insignificant amount and at December 31, 2018, we
posted approximately $0.1 billion of collateral related to derivative contracts under collateral exchange arrangements, which were recorded as Other current liabilities and
Prepaid expenses and other, respectively, in our consolidated balance sheets. While we may be exposed to credit losses due to the nonperformance of our counterparties, we
consider the risk remote and do not expect that any such nonperformance would result in a significant effect on our results of operations or financial condition due to our
diversified pool of counterparties. See Note 9 to the consolidated financial statements for additional information regarding the derivative portfolio.
Interest Rate Risk
We are exposed to changes in interest rates, primarily on our short-term debt and the portion of long-term debt that carries floating interest rates. As of December 31, 2019,
approximately 79% of the aggregate principal amount of our total debt portfolio consisted of fixed rate indebtedness, including the effect of interest rate swap agreements
designated as hedges. The impact of a 100-basis-point change in interest rates affecting our floating rate debt would result in a change in annual interest expense, including our
interest rate swap agreements that are designated as hedges, of approximately $248 million. The interest rates on our existing long-term debt obligations are unaffected by
changes to our credit ratings.
Certain of our floating rate debt and our interest rate derivative transactions utilize interest rates that are linked to the London Inter-Bank Offered Rate (LIBOR) as the
benchmark rate. LIBOR is the subject of recent U.S. and international regulatory guidance and proposals for reform. These reforms and other pressures may cause LIBOR to
become unavailable or to perform or be reported differently than in the past. The consequences of these developments cannot be entirely predicted but could include an increase
in the cost of our floating rate debt or exposure under our interest rate derivative transactions. We do not anticipate a significant impact to our financial position given our current
mix of variable and fixed-rate debt, taking into account the impact of our interest rate hedging.
The table that follows summarizes the fair values of our long-term debt, including current maturities, and interest rate swap derivatives as of December 31, 2019 and 2018. The
table also provides a sensitivity analysis of the estimated fair values of these financial instruments assuming 100-basis-point upward and downward shifts in the yield curve. Our
sensitivity analysis does not include the fair values of our commercial paper and bank loans, if any, because they are not significantly affected by changes in market interest rates.
(dollars in millions)
Long-term debt and related derivatives
At December 31, 2019
At December 31, 2018
Interest Rate Swaps
We enter into interest rate swaps to achieve a targeted mix of fixed and variable rate debt. We principally receive fixed rates and pay variable rates that are currently based on
LIBOR, resulting in a net increase or decrease to Interest expense. These swaps are designated as fair value hedges and hedge against interest rate risk exposure of designated
debt issuances. At December 31, 2019, the fair value of the asset and liability of these contracts were $568 million and $173 million, respectively. At December 31, 2018, the fair
value of the asset and liability of these contracts were insignificant and $813 million, respectively. At December 31, 2019 and 2018, the total notional amount of the interest rate
swaps was $17.0 billion and $19.8 billion, respectively.
Forward Starting Interest Rate Swaps
We have entered into forward starting interest rate swaps designated as cash flow hedges in order to manage our exposure to interest rate changes on future forecasted
transactions. At December 31, 2019 and 2018, the fair value of the liability of these contracts was $604 million and $60 million, respectively. At December 31, 2019 and 2018,
the total notional amount of the forward starting interest rate swaps was $3.0 billion and $4.0 billion, respectively.
Interest Rate Caps
We also have interest rate caps which we use as an economic hedge but for which we have elected not to apply hedge accounting. We enter into interest rate caps to mitigate our
interest exposure to interest rate increases on our ABS Financing Facility and ABS Notes. The fair value of the asset and liability of these contracts was insignificant at both
December 31, 2019 and 2018. At December 31, 2019 and 2018, the total notional value of these contracts was $679 million and $2.2 billion, respectively.
$
Fair Value
128,633
119,195
$
Fair Value assuming
+ 100 basis point shift
119,288
111,250
$
Fair Value assuming
- 100 basis point shift
139,980
128,957
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Foreign Currency Translation
The functional currency for our foreign operations is primarily the local currency. The translation of income statement and balance sheet amounts of our foreign operations into
U.S. dollars is recorded as cumulative translation adjustments, which are included in Accumulated other comprehensive income in our consolidated balance sheets. Gains and
losses on foreign currency transactions are recorded in the consolidated statements of income in Other income (expense), net. At December 31, 2019, our primary translation
exposure was to the British Pound Sterling, Euro, Australian Dollar and Japanese Yen.
Cross Currency Swaps
We have entered into cross currency swaps designated as cash flow hedges to exchange our British Pound Sterling, Euro, Swiss Franc and Australian Dollar-denominated cash
flows into U.S. dollars and to fix our cash payments in U.S. dollars, as well as to mitigate the impact of foreign currency transaction gains or losses. The fair value of the asset of
these contracts was $211 million and $220 million at December 31, 2019 and 2018, respectively. At December 31, 2019 and 2018, the fair value of the liability of these contracts
was $912 million and $536 million, respectively. At December 31, 2019 and 2018, the total notional amount of the cross currency swaps was $23.1 billion and $16.6 billion,
respectively.
Foreign Exchange Forwards
We also have foreign exchange forwards which we use as an economic hedge but for which we have elected not to apply hedge accounting. We enter into British Pound Sterling
and Euro foreign exchange forwards to mitigate our foreign exchange rate risk related to non-functional currency denominated monetary assets and liabilities of international
subsidiaries. At December 31, 2019, the fair value of the asset of these contracts was insignificant. At December 31, 2019 and 2018, the total notional amount of the foreign
exchange forwards was $1.1 billion and $600 million, respectively.
Critical Accounting Estimates and Recently Issued Accounting Standards
Critical Accounting Estimates
A summary of the critical accounting estimates used in preparing our financial statements is as follows:
Wireless Licenses and Goodwill
Wireless licenses and Goodwill are a significant component of our consolidated assets. Both our wireless licenses and goodwill are treated as indefinite-lived intangible assets
and, therefore are not amortized, but rather are tested for impairment annually in the fourth fiscal quarter, unless there are events requiring an earlier assessment or changes in
circumstances during an interim period providing impairment indicators are present. We believe our estimates and assumptions are reasonable and represent appropriate
marketplace considerations as of the valuation date. Although we use consistent methodologies in developing the assumptions and estimates underlying the fair value
calculations used in our impairment tests, these estimates and assumptions are uncertain by nature, may change over time and can vary from actual results. It is possible that in
the future there may be changes in our estimates and assumptions, including the timing and amount of future cash flows, margins, growth rates, market participant assumptions,
comparable benchmark companies and related multiples and discount rates, which could result in different fair value estimates. Significant and adverse changes to any one or
more of the above-noted estimates and assumptions could result in a goodwill impairment for one or more of our reporting units.
Wireless Licenses
The carrying value of our wireless licenses was approximately $95.1 billion as of December 31, 2019. We aggregate our wireless licenses into one single unit of accounting, as
we utilize our wireless licenses on an integrated basis as part of our nationwide wireless network. Our wireless licenses provide us with the exclusive right to utilize certain radio
frequency spectrum to provide wireless communication services. There are currently no legal, regulatory, contractual, competitive, economic or other factors that limit the useful
life of our wireless licenses.
In 2019, we performed a qualitative impairment assessment to determine whether it is more likely than not that the fair value of our wireless licenses was less than the carrying
amount. As part of our assessment we considered several qualitative factors including the historical business enterprise value of our wireless business, macroeconomic conditions
(including changes in interest rates and discount rates), industry and market considerations (including industry revenue and EBITDA margin projections), the recent and
projected financial performance of our wireless business as a whole, as well as other factors.
In 2018, our quantitative impairment test consisted of comparing the estimated fair value of our aggregate wireless licenses to the aggregated carrying amount as of the test date.
Our impairment test in 2019 indicated that it is more likely than not that the fair value of our wireless licenses remained above their carrying value and, therefore, did not result
in an impairment. Our impairment test in 2018 indicated that the fair value of our wireless licenses significantly exceeded their carrying value and, therefore, did not result in an
impairment.
Under our quantitative assessment, we estimated the fair value of our wireless licenses using the Greenfield approach. The Greenfield approach is an income-based valuation
approach that values the wireless licenses by calculating the cash flow generating potential of a hypothetical start-up company that goes into business with no assets except the
wireless licenses to be valued. A discounted cash flow analysis is used to estimate what a marketplace participant would be willing to pay to purchase the aggregated wireless
licenses as of the valuation date. As a result, we
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were required to make significant estimates about future cash flows specifically associated with our wireless licenses, an appropriate discount rate based on the risk associated
with those estimated cash flows and assumed terminal value and growth rates. We considered current and expected future economic conditions, current and expected availability
of wireless network technology and infrastructure and related equipment and the costs thereof as well as other relevant factors in estimating future cash flows. The discount rate
represented our estimate of the weighted-average cost of capital (WACC), or expected return, that a marketplace participant would have required as of the valuation date. We
developed the discount rate based on our consideration of the cost of debt and equity of a group of guideline companies as of the valuation date. Accordingly, our discount rate
incorporated our estimate of the expected return a marketplace participant would have required as of the valuation date, including the risk premium associated with the current
and expected economic conditions as of the valuation date. The terminal value growth rate represented our estimate of the marketplace’s long-term growth rate.
Goodwill
In November 2018, we announced a strategic reorganization of our business. The Company began reporting externally under the new structure as of April 1, 2019 which resulted
in certain changes to our operating segments and reporting units. Upon the date of reorganization, the goodwill of our historical Wireless reporting unit, historical Wireline
reporting unit and historical Verizon Connect reporting unit were reallocated to our new Consumer and Business reporting units using a relative fair value approach. At
December 31, 2019, the balance of our goodwill was approximately $24.4 billion, of which $17.1 billion was in our Consumer reporting unit and $7.3 billion was in our
Business reporting unit. To determine if goodwill is potentially impaired, we have the option to perform a qualitative assessment to determine whether it is more likely than not
that the fair value of a reporting unit is less than its carrying value. If we elect not to conduct the qualitative assessment or if indications of a potential impairment exist, the
determination of whether an impairment has occurred requires the determination of the fair value of each the reporting unit being assessed.
Under the qualitative assessment, we consider several qualitative factors, including the business enterprise value of the reporting unit from the last quantitative test and the excess
of fair value over carrying value from this test, macroeconomic conditions (including changes in interest rates and discount rates), industry and market considerations (including
industry revenue and EBITDA margin projections), the recent and projected financial performance of the reporting unit, as well as other factors.
Under our quantitative assessment, the fair value of the reporting unit is calculated using a market approach and a discounted cash flow method. The market approach includes
the use of comparative multiples to corroborate discounted cash flow results. The discounted cash flow method is based on the present value of two components-projected cash
flows and a terminal value. The terminal value represents the expected normalized future cash flows of the reporting unit beyond the cash flows from the discrete projection
period. The fair value of the reporting unit is calculated based on the sum of the present value of the cash flows from the discrete period and the present value of the terminal
value. The discount rate represented our estimate of the WACC, or expected return, that a marketplace participant would have required as of the valuation date. The application
of our goodwill impairment test required key assumptions underlying our valuation model. The discounted cash flow analysis factored in assumptions on discount rates and
terminal growth rates to reflect risk profiles of key strategic revenue and cost initiatives, as well as revenue and EBITDA growth relative to history and market trends and
expectations. The market multiples approach incorporated significant judgment involved in the selection comparable public company multiples and benchmarks. The selection of
companies was influenced by differences in growth and profitability, and volatility in market prices of peer companies. These valuation inputs are inherently uncertain, and an
adverse change in one or a combination of these inputs could trigger a goodwill impairment loss in the future.
A projected sustained decline in a reporting unit's revenues and earnings could have a significant negative impact on its fair value and may result in impairment charges. Such a
decline could be driven by, among other things: (1) further anticipated decreases in service pricing, sales volumes and long-term growth rate as a result of competitive pressures
or other factors; or (2) the inability to achieve or delays in achieving the goals in strategic initiatives. Also, adverse changes to macroeconomic factors, such as increases to long-
term interest rates, would also negatively impact the fair value of the reporting unit.
We performed impairment assessments of the impacted reporting units, specifically our historical Wireless, historical Wireline and historical Connect reporting units on
March 31, 2019, immediately before our strategic reorganization became effective. Our impairment assessments indicated that the fair value for each of our historical Wireless,
historical Wireline and historical Connect reporting units exceeded their respective carrying values, and therefore did not result in a goodwill impairment. We then performed
quantitative assessments of our Consumer and Business reporting units on April 1, 2019, immediately following our strategic reorganization. Our impairment assessments
indicated that the fair value for each of our Consumer and Business reporting units exceeded their respective carrying values and therefore, did not result in a goodwill
impairment. Our Media reporting unit was not impacted by the strategic reorganization and there was no indicator of impairment as of the reorganization date.
We performed qualitative impairment assessments for our Consumer and Business reporting units during the fourth quarter of 2019. Our qualitative assessments indicated that it
was more likely than not that the fair values for our Consumer and Business reporting units exceeded their respective carrying values and, therefore, did not result in an
impairment. We performed quantitative impairment assessments for our Media reporting unit in 2019 and 2018. For details on our Media reporting unit, refer to the discussion
below.
Our Media business, Verizon Media, experienced increased competitive and market pressures throughout 2018 that resulted in lower than expected revenues and earnings. These
pressures were expected to continue and have resulted in a loss of market positioning to our competitors in the digital advertising business. Our Media business also achieved
lower than expected benefits from the integration of the Yahoo Inc. and AOL Inc. (AOL) businesses.
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As of August 2018, Hans Vestberg became Chief Executive Officer of Verizon, and as of October 2018, K. Guru Gowrappan was appointed Chief Executive Officer of our
Media business. In connection with Verizon’s annual budget process during the fourth quarter of 2019 and 2018, the leadership at both Verizon Media and Verizon completed a
comprehensive five-year strategic planning review of Verizon Media's business prospects resulting in unfavorable adjustments to Verizon Media's financial projections. These
revised projections were used as a key input into Verizon Media's annual goodwill impairment tests performed in the fourth quarter of 2019 and 2018.
During the fourth quarter of 2019 and 2018, consistent with our accounting policy, we applied a combination of a market approach and a discounted cash flow method reflecting
current assumptions and inputs, including our revised projections, discount rate and expected growth rates, which resulted in the determination that the fair value of the Media
reporting unit was less than its carrying amount. As a result, we recorded a non-cash goodwill impairment charge of approximately $186 million ($176 million after-tax) in the
fourth quarter of 2019 and a charge of $4.6 billion ($4.5 billion after-tax) in the fourth quarter of 2018 in our consolidated statements of income. The goodwill balance of the
Media reporting unit has been fully written off as a result of these impairment charges.
We performed a quantitative impairment assessment for all of the other reporting units in 2018. Our impairment tests indicated that the fair value for each of our historical
Wireless, historical Wireline and historical Connect reporting units exceeded their respective carrying value and, therefore, did not result in an impairment.
Pension and Other Postretirement Benefit Plans
We maintain benefit plans for most of our employees, including, for certain employees, pension and other postretirement benefit plans. At December 31, 2019, in the aggregate,
pension plan benefit obligations exceeded the fair value of pension plan assets, which will result in future pension plan expense. Other postretirement benefit plans have larger
benefit obligations than plan assets, resulting in expense. Significant benefit plan assumptions, including the discount rate used, the long-term rate of return on plan assets, the
determination of the substantive plan and health care trend rates are periodically updated and impact the amount of benefit plan income, expense, assets and obligations.
Changes to one or more of these assumptions could significantly impact our accounting for pension and other postretirement benefits. A sensitivity analysis of the impact of
changes in these assumptions on the benefit obligations and expense (income) recorded, as well as on the funded status due to an increase or a decrease in the actual versus
expected return on plan assets as of December 31, 2019 and for the year then ended pertaining to Verizon’s pension and postretirement benefit plans, is provided in the table
below.
(dollars in millions)
Pension plans discount rate
Rate of return on pension plan assets
Postretirement plans discount rate
Rate of return on postretirement plan assets
Health care trend rates
Percentage point
change
+0.50 $
-0.50
+1.00
-1.00
+0.50
-0.50
+1.00
-1.00
+1.00
-1.00
Increase/(decrease) at
December 31, 2019*
(1,137)
1,266
(167)
167
(858)
948
(9)
9
626
(696)
* In determining its pension and other postretirement obligation, the Company used a weighted-average discount rate of 3.3%. The rate was selected to approximate the
composite interest rates available on a selection of high-quality bonds available in the market at December 31, 2019. The bonds selected had maturities that coincided with the
time periods during which benefits payments are expected to occur, were non-callable and available in sufficient quantities to ensure marketability (at least $300 million par
outstanding).
The annual measurement date for both our pension and other postretirement benefits is December 31. We use the full yield curve approach to estimate the interest cost
component of net periodic benefit cost for pension and other postretirement benefits. The full yield curve approach refines our estimate of interest cost by applying the individual
spot rates from a yield curve composed of the rates of return on several hundred high-quality fixed income corporate bonds available at the measurement date. These individual
spot rates align with the timing of each future cash outflow for benefit payments and therefore provide a more precise estimate of interest cost.
Income Taxes
Our current and deferred income taxes and associated valuation allowances are impacted by events and transactions arising in the normal course of business as well as in
connection with the adoption of new accounting standards, changes in tax laws and rates, acquisitions and dispositions of businesses and non-recurring items. As a global
commercial enterprise, our income tax rate and the classification of income taxes can be affected by many factors, including estimates of the timing and realization of deferred
income tax assets and the timing and amount of income tax payments. We account for tax benefits taken or expected to be taken in our tax returns in accordance with the
accounting standard relating to the uncertainty in income taxes, which requires the use of a two-step approach for recognizing and measuring tax benefits taken or expected to be
taken in a tax return. We review and adjust our liability for unrecognized tax benefits based on our best judgment given the facts, circumstances and information available at each
reporting date. To the extent that the final outcome of these tax positions is different than the amounts recorded, such differences may impact income tax expense and actual tax
payments. We recognize any interest and penalties accrued related to unrecognized tax benefits in income tax expense. Actual tax payments may materially differ from estimated
liabilities as a result of changes in tax laws as well
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as unanticipated transactions impacting related income tax balances. See Note 12 to the consolidated financial statements for additional information.
Property, Plant and Equipment
Our Property, plant and equipment balance represents a significant component of our consolidated assets. We record Property, plant and equipment at cost. We depreciate
Property, plant and equipment on a straight-line basis over the estimated useful life of the assets. We expect that a one year increase in estimated useful lives of our Property,
plant and equipment would result in a decrease to our 2019 depreciation expense of $2.7 billion and that a one year decrease would result in an increase of approximately $4.7
billion in our 2019 depreciation expense.
Accounts Receivable
We maintain allowances for uncollectible accounts receivable, including our direct-channel device payment plan agreement receivables, for estimated losses resulting from the
failure or inability of our customers to make required payments. Indirect-channel device payment loans are considered financial instruments and are initially recorded at fair
value net of imputed interest, and credit losses are recorded as incurred. However, loan balances are assessed quarterly for impairment and an allowance is recorded if the loan is
considered impaired. Our allowance for uncollectible accounts receivable is based on management’s assessment of the collectability of specific customer accounts and includes
consideration of the credit worthiness and financial condition of those customers. We record an allowance to reduce the receivables to the amount that is reasonably believed to
be collectible. We also record an allowance for all other receivables based on multiple factors including historical experience with bad debts, the general economic environment
and the aging of such receivables. Similar to traditional service revenue, we record direct device payment plan agreement bad debt expense based on an estimate of the
percentage of equipment revenue that will not be collected. This estimate is based on a number of factors including historical write-off experience, credit quality of the customer
base and other factors such as macroeconomic conditions. If there is a deterioration of our customers’ financial condition or if future actual default rates on receivables in general
differ from those currently anticipated, we may have to adjust our allowance for doubtful accounts, which would affect earnings in the period the adjustments are made.
Recently Issued Accounting Standards
See Note 1 to the consolidated financial statements for a discussion of recently issued accounting standard updates not yet adopted as of December 31, 2019.
Acquisitions and Divestitures
Acquisition of AOL Inc.
In May 2015, we entered into an Agreement and Plan of Merger with AOL Inc. pursuant to which we commenced a tender offer to acquire all of the outstanding shares of
common stock of AOL at a price of $50.00 per share, net to the seller in cash, without interest and less any applicable withholding taxes.
On June 23, 2015, we completed the tender offer and merger, and AOL became a wholly-owned subsidiary of Verizon. The aggregate cash consideration paid by Verizon at the
closing of these transactions was approximately $3.8 billion. Holders of approximately 6.6 million shares exercised appraisal rights under Delaware law. In September 2018, we
obtained court approval to settle this matter for total cash consideration of $219 million, of which an insignificant amount relates to interest, resulting in an insignificant gain. We
paid the cash consideration in October 2018.
XO Holdings
In February 2016, we entered into a purchase agreement to acquire XO Holdings' wireline business (XO), which owned and operated one of the largest fiber-based IP and
Ethernet networks in the U.S. Concurrently, we entered into a separate agreement to utilize certain wireless spectrum from a wholly-owned subsidiary of XO Holdings,
NextLink, that held XO's millimeter-wave wireless spectrum. The agreement included an option, subject to certain conditions, to acquire NextLink. In February 2017, we
completed our acquisition of XO for total cash consideration of approximately $1.5 billion, of which $100 million was paid in 2015, and we prepaid $320 million in connection
with the NextLink option which represented the fair value of the option.
In April 2017, we exercised our option to buy NextLink for approximately $493 million, subject to certain adjustments, of which $320 million was prepaid in the first quarter of
2017. The transaction closed in January 2018. The acquisition of NextLink was accounted for as an asset acquisition, as substantially all of the value related to the acquired
spectrum. Upon closing, we recorded approximately $657 million of wireless licenses, $110 million of a deferred tax liability and $58 million of other liabilities. See Note 3 to
the consolidated financial statements for additional information.
Straight Path
In May 2017, we entered into a purchase agreement to acquire Straight Path, a holder of millimeter wave spectrum configured for 5G wireless services, for total consideration
reflecting an enterprise value of approximately $3.1 billion. Under the terms of the purchase agreement, we agreed to pay: (1) Straight Path shareholders $184.00 per share,
payable in Verizon shares; and (2) certain transaction costs payable in cash of approximately $736 million, consisting primarily of a fee to be paid to the FCC. The transaction
closed in February 2018 at which time we issued
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approximately 49 million shares of Verizon common stock, valued at approximately $2.4 billion, and paid the associated cash consideration. See Note 3 to the consolidated
financial statements for additional information.
Spectrum License Transactions
From time to time, we enter into agreements to buy, sell or exchange spectrum licenses. We believe these spectrum license transactions have allowed us to continue to enhance
the reliability of our wireless network while also resulting in a more efficient use of spectrum. See Note 3 to the consolidated financial statements for additional information
regarding our spectrum license transactions.
Other
From time to time, we enter into strategic agreements to acquire various other businesses and investments. See Note 3 to the consolidated financial statements for additional
information.
Cautionary Statement Concerning Forward-Looking Statements
In this report we have made forward-looking statements. These statements are based on our estimates and assumptions and are subject to risks and uncertainties. Forward-
looking statements include the information concerning our possible or assumed future results of operations. Forward-looking statements also include those preceded or followed
by the words "anticipates," "believes," "estimates," "expects," "hopes" or similar expressions. For those statements, we claim the protection of the safe harbor for forward-
looking statements contained in the Private Securities Litigation Reform Act of 1995. We undertake no obligation to revise or publicly release the results of any revision to these
forward-looking statements, except as required by law. Given these risks and uncertainties, readers are cautioned not to place undue reliance on such forward-looking statements.
The following important factors, along with those discussed elsewhere in this report and in other filings with the SEC, could affect future results and could cause those results to
differ materially from those expressed in the forward-looking statements:
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
cyber attacks impacting our networks or systems and any resulting financial or reputational impact;
natural disasters, terrorist attacks or acts of war or significant litigation and any resulting financial or reputational impact;
disruption of our key suppliers’ or vendors' provisioning of products or services;
material adverse changes in labor matters and any resulting financial or operational impact;
the effects of competition in the markets in which we operate;
failure to take advantage of developments in technology and address changes in consumer demand;
performance issues or delays in the deployment of our 5G network resulting in significant costs or a reduction in the anticipated benefits of the enhancement to our
networks;
the inability to implement our business strategy;
adverse conditions in the U.S. and international economies;
changes in the regulatory environment in which we operate, including any increase in restrictions on our ability to operate our networks;
our high level of indebtedness;
an adverse change in the ratings afforded our debt securities by nationally accredited ratings organizations or adverse conditions in the credit markets affecting the cost,
including interest rates, and/or availability of further financing;
significant increases in benefit plan costs or lower investment returns on plan assets;
changes in tax laws or treaties, or in their interpretation; and
changes in accounting assumptions that regulatory agencies, including the SEC, may require or that result from changes in the accounting rules or their application,
which could result in an impact on earnings.
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Report of Management on Internal Control Over Financial Reporting
We, the management of Verizon Communications Inc., are responsible for establishing and maintaining adequate internal control over financial reporting of the company.
Management has evaluated internal control over financial reporting of the company using the criteria for effective internal control established in Internal Control–Integrated
Framework issued by the Committee of Sponsoring Organizations of the Treadway Commission in 2013.
Management has assessed the effectiveness of the company’s internal control over financial reporting as of December 31, 2019. Based on this assessment, we believe that the
internal control over financial reporting of the company is effective as of December 31, 2019. In connection with this assessment, there were no material weaknesses in the
company’s internal control over financial reporting identified by management.
The company’s financial statements included in this Annual Report have been audited by Ernst & Young LLP, independent registered public accounting firm. Ernst & Young
LLP has also provided an attestation report on the company’s internal control over financial reporting.
/s/
Hans E. Vestberg
Hans E. Vestberg
Chairman and Chief Executive Officer
/s/
Matthew D. Ellis
Matthew D. Ellis
Executive Vice President and Chief Financial Officer
/s/
Anthony T. Skiadas
Anthony T. Skiadas
Senior Vice President and Controller
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Report of Independent Registered Public Accounting Firm
To the Shareholders and the Board of Directors of Verizon Communications Inc.:
Opinion on Internal Control Over Financial Reporting
We have audited Verizon Communications Inc. and subsidiaries’ (Verizon) internal control over financial reporting as of December 31, 2019, based on criteria established in
Internal Control-Integrated Framework issued by the Committee of Sponsoring Organizations of the Treadway Commission (2013 framework) (the COSO criteria). In our
opinion, Verizon maintained, in all material respects, effective internal control over financial reporting as of December 31, 2019, based on the COSO criteria.
We also have audited, in accordance with the standards of the Public Company Accounting Oversight Board (United States) (PCAOB), the consolidated balance sheets of
Verizon as of December 31, 2019 and 2018, the related consolidated statements of income, comprehensive income, cash flows, and changes in equity for each of the three years
in the period ended December 31, 2019, and the related notes and our report dated February 21, 2020 expressed an unqualified opinion thereon.
Basis for Opinion
Verizon’s management is responsible for maintaining effective internal control over financial reporting and for its assessment of the effectiveness of internal control over
financial reporting included in the accompanying Report of Management on Internal Control Over Financial Reporting. Our responsibility is to express an opinion on Verizon's
internal control over financial reporting based on our audit. We are a public accounting firm registered with the PCAOB and are required to be independent with respect to
Verizon in accordance with the U.S. federal securities laws and the applicable rules and regulations of the Securities and Exchange Commission and the PCAOB.
We conducted our audit in accordance with the standards of the PCAOB. Those standards require that we plan and perform the audit to obtain reasonable assurance about
whether effective internal control over financial reporting was maintained in all material respects.
Our audit included obtaining an understanding of internal control over financial reporting, assessing the risk that a material weakness exists, testing and evaluating the design and
operating effectiveness of internal control based on the assessed risk, and performing such other procedures as we considered necessary in the circumstances. We believe that our
audit provides a reasonable basis for our opinion.
Definition and Limitations of Internal Control Over Financial Reporting
A company’s internal control over financial reporting is a process designed to provide reasonable assurance regarding the reliability of financial reporting and the preparation of
financial statements for external purposes in accordance with generally accepted accounting principles. A company’s internal control over financial reporting includes those
policies and procedures that (1) pertain to the maintenance of records that, in reasonable detail, accurately and fairly reflect the transactions and dispositions of the assets of the
company; (2) provide reasonable assurance that transactions are recorded as necessary to permit preparation of financial statements in accordance with generally accepted
accounting principles, and that receipts and expenditures of the company are being made only in accordance with authorizations of management and directors of the company;
and (3) provide reasonable assurance regarding prevention or timely detection of unauthorized acquisition, use, or disposition of the company’s assets that could have a material
effect on the financial statements.
Because of its inherent limitations, internal control over financial reporting may not prevent or detect misstatements. Also, projections of any evaluation of effectiveness to future
periods are subject to the risk that controls may become inadequate because of changes in conditions, or that the degree of compliance with the policies or procedures may
deteriorate.
/s/
Ernst & Young LLP
Ernst & Young LLP
New York, New York
February 21, 2020
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Report of Independent Registered Public Accounting Firm
To the Shareholders and the Board of Directors of Verizon Communications Inc.:
Opinion on the Financial Statements
We have audited the accompanying consolidated balance sheets of Verizon Communications Inc. and subsidiaries (Verizon) as of December 31, 2019 and 2018, the related
consolidated statements of income, comprehensive income, cash flows, and changes in equity for each of the three years in the period ended December 31, 2019, and the related
notes (collectively referred to as the "consolidated financial statements"). In our opinion, the consolidated financial statements present fairly, in all material respects, the financial
position of Verizon at December 31, 2019 and 2018, and the results of its operations and its cash flows for each of the three years in the period ended December 31, 2019, in
conformity with U.S. generally accepted accounting principles.
We also have audited, in accordance with the standards of the Public Company Accounting Oversight Board (United States) (PCAOB), Verizon’s internal control over financial
reporting as of December 31, 2019, based on criteria established in Internal Control–Integrated Framework issued by the Committee of Sponsoring Organizations of the
Treadway Commission (2013 framework) and our report dated February 21, 2020 expressed an unqualified opinion thereon.
Adoption of New Accounting Standards
ASU No. 2016-02
As discussed in Note 1 to the consolidated financial statements, effective January 1, 2019, Verizon changed its method of accounting for leases due to the adoption of
Accounting Standards Update (ASU) No. 2016-02, Leases (Topic 842), and the related amendments, using the modified retrospective method.
ASU No. 2014-09
As discussed in Note 1 to the consolidated financial statements, effective January 1, 2018 Verizon changed its method for recognizing revenue as a result of the adoption of ASU
No. 2014-09, Revenue from Contracts with Customers (Topic 606), and the amendments in ASUs 2015-14, 2016-08, 2016-10 and 2016-12 using the modified retrospective
method.
Basis for Opinion
These financial statements are the responsibility of Verizon’s management. Our responsibility is to express an opinion on Verizon’s financial statements based on our audits. We
are a public accounting firm registered with the PCAOB and are required to be independent with respect to Verizon in accordance with the U.S. federal securities laws and the
applicable rules and regulations of the Securities and Exchange Commission and the PCAOB.
We conducted our audits in accordance with the standards of the PCAOB. Those standards require that we plan and perform the audit to obtain reasonable assurance about
whether the financial statements are free of material misstatement, whether due to error or fraud. Our audits included performing procedures to assess the risks of material
misstatement of the financial statements, whether due to error or fraud, and performing procedures that respond to those risks. Such procedures included examining, on a test
basis, evidence regarding the amounts and disclosures in the financial statements. Our audits also included evaluating the accounting principles used and significant estimates
made by management, as well as evaluating the overall presentation of the financial statements. We believe that our audits provide a reasonable basis for our opinion.
Critical Audit Matters
The critical audit matters communicated below are matters arising from the current period audit of the financial statements that were communicated or required to be
communicated to the audit committee and that: (1) relate to accounts or disclosures that are material to the financial statements and (2) involved our especially challenging,
subjective or complex judgments. The communication of critical audit matters does not alter in any way our opinion on the consolidated financial statements, taken as a whole,
and we are not, by communicating the critical audit matters below, providing separate opinions on the critical audit matters or on the accounts or disclosures to which they relate.
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Impairment Evaluation for Wireline Goodwill
Description of the Matter
At March 31, 2019, the Company’s goodwill related to its historical Wireline reporting unit was $3.9 billion and represented 1.4% of total
assets. As discussed in Notes 1 and 4 of the consolidated financial statements, goodwill is not amortized but rather is tested for impairment at
the reporting unit level at least annually, or more frequently if impairment indicators are present. The impairment test compares the fair value
of the reporting unit (calculated using a combination of a market approach and a discounted cash flow method) to its carrying amount.
Effective April 1, 2019, the Company transitioned to its new segment reporting structure, which resulted in certain changes to its operating
segments and reporting units. On March 31, 2019 the Company performed an impairment assessment of the impacted reporting units,
including the Wireline reporting unit, immediately before the segment reorganization became effective.
Auditing management’s goodwill impairment test was complex and highly judgmental due to the inherent subjectivity of developing an
estimate of the fair value of the reporting unit, which is based on assumptions about future conditions, transactions, or events whose outcome
is uncertain and will therefore be subject to change over time. In particular, the fair value estimate was sensitive to significant assumptions
such as the weighted average cost of capital, revenue growth rate and operating margin, which are affected by expected future market or
economic conditions.
How We Addressed the Matter in
We obtained an understanding, evaluated the design and tested the operating effectiveness of controls over the Company’s goodwill
Our Audit
impairment review process. For example, we tested controls over the Company’s development of prospective financial information and
management’s review of other key assumptions.
To test the estimated fair value of the Company’s Wireline reporting unit prior to segment reorganization, our audit procedures included,
among others, assessing the suitability and application of the valuation methodologies selected and evaluating the significant assumptions
discussed above and underlying data used by the Company in its analysis. We compared the significant assumptions used by management to
current industry and economic trends, changes in the Company’s business model, customer base or product mix and other relevant factors.
We performed sensitivity analyses of significant assumptions to determine what changes in assumptions are particularly sensitive when
assessing the likelihood of impairment, or when calculating the amount of an impairment. In addition, we involved a valuation specialist to
assist in the evaluation of the assumptions and other relevant information that are most significant to the fair value estimate. We also
assessed the historical accuracy of management’s forecasts of financial results used in developing prior fair value estimates to assist in
evaluating the reliability of the current forecasts.
Valuation of Employee Benefit Obligations
Description of the Matter
The Company sponsors several pension plans and other post-employment benefit plans. At December 31, 2019, the Company’s aggregate
defined benefit pension obligation was $21.2 billion and exceeded the fair value of pension plan assets of $19.4 billion, resulting in an
unfunded defined benefit pension obligation of $1.8 billion. Also, at December 31, 2019, the other postretirement benefits obligation was
approximately $15.7 billion. As explained in Note 11 of the consolidated financial statements, the Company updates the estimates used to
measure employee benefit obligations and plan assets in the fourth quarter and upon a remeasurement event to reflect the actual return on
plan assets and updated actuarial assumptions.
Auditing the employee benefit obligations was complex due to the highly judgmental nature of the actuarial assumptions (e.g., discount rate,
health care cost trends, per capita claims cost trends and mortality rates) used in the measurement process. These assumptions had a
significant effect on the projected benefit obligation.
How We Addressed the Matter in
We obtained an understanding, evaluated the design and tested the operating effectiveness of controls over the employee benefits obligation
Our Audit
valuation process. For example, we tested controls over management’s review of the employee benefit obligation calculations, the significant
actuarial assumptions and the data inputs provided to the actuary.
To test the employee benefit obligations, our audit procedures included, among others, evaluating the methodologies used, the significant
actuarial assumptions discussed above and the underlying data used by the Company. We compared the actuarial assumptions used by
management to historical trends, current economic factors and evaluated the change in the employee benefit obligations from prior year due
to the change in service cost, interest cost, actuarial gains and losses, benefit payments, contributions and other activities. In addition, we
involved an actuarial specialist to assist in evaluating management’s methodology for determining the discount rate that reflects the maturity
and duration of the benefit payments and is used to measure the employee benefit obligations. As part of this assessment, we compared the
projected cash flows to prior year projections and compared the current year benefits paid to the prior year projected cash flows. To evaluate
the health care cost trends, per capita claims cost trends and the mortality rates, we involved an actuarial specialist to assist in evaluating the
assumptions and assessed whether the information is consistent with publicly available information, and whether any market data adjusted
for entity-specific adjustments were applied. We also tested the completeness and accuracy of the underlying data, including the participant
data provided to management’s actuarial specialists.
Income Taxes - Benefit from the disposition of stock of a foreign affiliate
Description of the Matter
As described in Note 12 to the consolidated financial statements, during the fourth quarter of 2019 the Company sold a minority interest in a
foreign affiliate to unrelated parties resulting in the recognition of a tax benefit of approximately $2.2 billion.
Auditing the recognition and measurement of this income tax benefit required significant auditor judgment because the determination of
whether the tax positions’ technical merits are more likely than not to be sustained in an audit by a taxing authority is based on the
application and interpretation of the relevant tax laws to the facts of the specific transaction.
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How We Addressed the Matter in
We obtained an understanding, evaluated the design and tested the operating effectiveness of controls over the Company’s income tax
Our Audit
processes. For example, we tested controls over management’s review of the income tax technical merits of the transaction and the related
recognition and measurement of the income tax benefit.
To test the income tax benefit related to this transaction, our audit procedures included, among others, assessing the suitability and
application of tax laws and legal rulings and evaluating the related conclusions. In addition, we involved our tax professionals to assist in the
review and evaluation of management’s third-party tax opinions and memoranda and other relevant agreements. We tested the completeness
and accuracy of the data and calculations used to determine the amount of the income tax benefit recognized.
/s/
Ernst & Young LLP
Ernst & Young LLP
We have served as Verizon's auditor since 2000.
New York, New York
February 21, 2020
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Consolidated Statements of Income Verizon Communications Inc. and Subsidiaries
(dollars in millions, except per share amounts)
Years Ended December 31,
Operating Revenues
Service revenues and other
Wireless equipment revenues
Total Operating Revenues
Operating Expenses
Cost of services (exclusive of items shown below)
Cost of wireless equipment
Selling, general and administrative expense (including net gain/(loss) on sale of divested businesses of
$(94), $0 and $1,774, respectively)
Depreciation and amortization expense
Media goodwill impairment
Total Operating Expenses
Operating Income
Equity in losses of unconsolidated businesses
Other income (expense), net
Interest expense
Income Before (Provision) Benefit For Income Taxes
(Provision) benefit for income taxes
Net Income
Net income attributable to noncontrolling interests
Net income attributable to Verizon
Net Income
Basic Earnings Per Common Share
Net income attributable to Verizon
Weighted-average shares outstanding (in millions)
Diluted Earnings Per Common Share
Net income attributable to Verizon
Weighted-average shares outstanding (in millions)
See Notes to Consolidated Financial Statements
$
4.65
4,140
$
3.76
4,132
$
7.36
4,089
$
4.66
4,138
$
3.76
4,128
$
7.37
4,084
$
$
$
31,772
22,954
29,896
16,682
186
101,490
30,378
(15)
(2,900)
(4,730)
22,733
(2,945)
19,788
523
19,265
19,788
$
$
$
32,185
23,323
31,083
17,403
4,591
108,585
22,278
(186)
2,364
(4,833)
19,623
(3,584)
16,039
511
15,528
16,039
$
$
$
30,916
22,147
28,592
16,954
—
98,609
27,425
(77)
(2,021)
(4,733)
20,594
9,956
30,550
449
30,101
30,550
$
110,305
21,563
131,868
$
108,605
22,258
130,863
$
107,145
18,889
126,034
2019
2018
2017
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Consolidated Statements of Comprehensive Income Verizon Communications Inc. and Subsidiaries
(dollars in millions)
Years Ended December 31,
Net Income
Other Comprehensive Loss, Net of Tax (Expense) Benefit
Foreign currency translation adjustments, net of tax of $(21), $(11) and $30
Unrealized gain (loss) on cash flow hedges, net of tax of $265, $(19) and $20
Unrealized gain (loss) on marketable securities, net of tax of $(2), $0 and $10
Defined benefit pension and postretirement plans, net of tax of $219, $284 and $144
Other comprehensive loss attributable to Verizon
Total Comprehensive Income
Comprehensive income attributable to noncontrolling interests
Comprehensive income attributable to Verizon
Total Comprehensive Income
See Notes to Consolidated Financial Statements
$
$
$
16
(736)
7
(659)
(1,372)
18,416
523
17,893
18,416
$
$
$
(117)
55
1
(858)
(919)
15,120
511
14,609
15,120
$
$
$
245
(31)
(14)
(214)
(14)
30,536
449
30,087
30,536
$
2019
19,788
$
2018
16,039
$
2017
30,550
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Consolidated Balance Sheets Verizon Communications Inc. and Subsidiaries
(dollars in millions, except per share amounts)
At December 31,
Assets
Current assets
Cash and cash equivalents
Accounts receivable, net of allowances of $733 and $765
Inventories
Prepaid expenses and other
Total current assets
Property, plant and equipment
Less accumulated depreciation
Property, plant and equipment, net
Investments in unconsolidated businesses
Wireless licenses
Goodwill
Other intangible assets, net
Operating lease right-of-use assets
Other assets
Total assets
Liabilities and Equity
Current liabilities
Debt maturing within one year
Accounts payable and accrued liabilities
Current operating lease liabilities
Other current liabilities
Total current liabilities
Long-term debt
Employee benefit obligations
Deferred income taxes
Non-current operating lease liabilities
Other liabilities
Total long-term liabilities
Commitments and Contingencies (Note 16)
Equity
Series preferred stock ($0.10 par value; 250,000,000 shares authorized; none issued)
Common stock ($0.10 par value; 6,250,000,000 shares authorized in each period; 4,291,433,646 issued in each period)
Additional paid in capital
Retained earnings
Accumulated other comprehensive income
Common stock in treasury, at cost (155,605,527 and 159,400,267 shares outstanding)
Deferred compensation – employee stock ownership plans and other
Noncontrolling interests
Total equity
Total liabilities and equity
$
—
429
13,419
53,147
998
(6,820)
222
1,440
62,835
291,727
$
—
429
13,437
43,542
2,370
(6,986)
353
1,565
54,710
264,829
$
10,777
21,806
3,261
9,024
44,868
100,712
17,952
34,703
18,393
12,264
184,024
$
7,190
22,501
—
8,239
37,930
105,873
18,599
33,795
—
13,922
172,189
$
$
2,594
25,429
1,422
8,028
37,473
265,734
173,819
91,915
558
95,059
24,389
9,498
22,694
10,141
291,727
$
$
2,745
25,102
1,336
5,453
34,636
252,835
163,549
89,286
671
94,130
24,614
9,775
—
11,717
264,829
2019
2018
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See Notes to Consolidated Financial Statements
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Consolidated Statements of Cash Flows Verizon Communications Inc. and Subsidiaries
(dollars in millions)
Years Ended December 31,
Cash Flows from Operating Activities
Net Income
Adjustments to reconcile net income to net cash provided by operating activities:
Depreciation and amortization expense
Employee retirement benefits
Deferred income taxes
Provision for uncollectible accounts
Equity in losses of unconsolidated businesses, net of dividends received
Net loss (gain) on sale of divested businesses
Media goodwill impairment
Changes in current assets and liabilities, net of effects from acquisition/disposition of businesses:
Accounts receivable
Inventories
Prepaid expenses and other
Accounts payable and accrued liabilities and Other current liabilities
Discretionary employee benefits contributions
Other, net
Net cash provided by operating activities
Cash Flows from Investing Activities
Capital expenditures (including capitalized software)
Acquisitions of businesses, net of cash acquired
Acquisitions of wireless licenses
Proceeds from dispositions of businesses
Other, net
Net cash used in investing activities
Cash Flows from Financing Activities
Proceeds from long-term borrowings
Proceeds from asset-backed long-term borrowings
Repayments of long-term borrowings and finance lease obligations
Repayments of asset-backed long-term borrowings
Dividends paid
Other, net
Net cash used in financing activities
Increase (decrease) in cash, cash equivalents and restricted cash
Cash, cash equivalents and restricted cash, beginning of period
Cash, cash equivalents and restricted cash, end of period (Note 1)
$
10,079
8,576
(17,584)
(6,302)
(10,016)
(2,917)
(18,164)
1
3,916
3,917
$
5,967
4,810
(10,923)
(3,635)
(9,772)
(1,824)
(15,377)
1,028
2,888
3,916
$
27,707
4,290
(23,837)
(400)
(9,472)
(4,439)
(6,151)
(289)
3,177
2,888
(17,939)
(29)
(898)
28
1,257
(17,581)
(16,658)
(230)
(1,429)
—
383
(17,934)
(17,247)
(5,880)
(583)
3,614
1,640
(18,456)
(1,471)
(76)
(2,807)
(2,359)
(300)
3,399
35,746
(2,667)
(324)
37
1,777
(1,679)
219
34,339
(5,674)
168
27
(459)
(3,411)
676
24,318
16,682
(284)
1,232
1,588
74
94
186
17,403
(2,657)
389
980
231
—
4,591
16,954
440
(14,463)
1,167
117
(1,774)
—
$
19,788
$
16,039
$
30,550
2019
2018
2017
See Notes to Consolidated Financial Statements
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Consolidated Statements of Changes in Equity Verizon Communications Inc. and Subsidiaries
(dollars in millions, except per share amounts, and shares in thousands)
Years Ended December 31,
Shares
Common Stock
Balance at beginning of year
Common shares issued
Balance at end of year
Additional Paid In Capital
Balance at beginning of year
Other
Balance at end of year
Retained Earnings
Balance at beginning of year
Opening balance sheet adjustment (Note 1)
Adjusted opening balance
Net income attributable to Verizon
Dividends declared ($2.435, $2.385, $2.335 per share)
Balance at end of year
Accumulated Other Comprehensive Income
Balance at beginning of year attributable to Verizon
Opening balance sheet adjustment (Note 1)
Adjusted opening balance
Foreign currency translation adjustments
Unrealized gain (loss) on cash flow hedges
Unrealized gain (loss) on marketable securities
Defined benefit pension and postretirement plans
Other comprehensive loss
Balance at end of year attributable to Verizon
Treasury Stock
Balance at beginning of year
Employee plans (Note 14)
Shareholder plans (Note 14)
Balance at end of year
Deferred Compensation-ESOPs and Other
Balance at beginning of year
Restricted stock equity grant
Amortization
Balance at end of year
Noncontrolling Interests
Balance at beginning of year
Opening balance sheet adjustment (Note 1)
Adjusted opening balance
Total comprehensive income
Distributions and other
1,565
1
1,566
523
(649)
1,591
44
1,635
511
(581)
1,508
—
1,508
449
(366)
353
140
(271)
222
416
162
(225)
353
449
157
(190)
416
(159,400)
3,790
4
(155,606)
(6,986)
166
—
(6,820)
(162,898)
3,494
4
(159,400)
(7,139)
153
—
(6,986)
(165,690)
2,787
5
(162,898)
(7,263)
124
—
(7,139)
2,370
—
2,370
16
(736)
7
(659)
(1,372)
998
2,659
630
3,289
(117)
55
1
(858)
(919)
2,370
2,673
—
2,673
245
(31)
(14)
(214)
(14)
2,659
43,542
410
43,952
19,265
(10,070)
53,147
35,635
2,232
37,867
15,528
(9,853)
43,542
15,059
—
15,059
30,101
(9,525)
35,635
13,437
(18)
13,419
11,101
2,336
13,437
11,182
(81)
11,101
4,291,434
—
4,291,434
$
429
—
429
4,242,374
49,060
4,291,434
$
424
5
429
4,242,374
—
4,242,374
$
424
—
424
2019
Amount
Shares
2018
Amount
Shares
2017
Amount
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Balance at end of year
Total Equity
$
1,440
62,835
$
1,565
54,710
$
1,591
44,687
See Notes to Consolidated Financial Statements
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Notes to Consolidated Financial Statements Verizon Communications Inc. and Subsidiaries
Note 1. Description of Business and Summary of Significant Accounting Policies
Description of Business
Verizon Communications Inc. (Verizon or the Company) is a holding company that, acting through its subsidiaries, is one of the world’s leading providers of communications,
information and entertainment products and services to consumers, businesses and government entities. With a presence around the world, we offer voice, data and video
services and solutions on our networks that are designed to meet customers’ demand for mobility, reliable network connectivity, security and control.
In November 2018, we announced a strategic reorganization of our business. Under the new structure, effective April 1, 2019, there are two reportable segments that we operate
and manage as strategic business units - Verizon Consumer Group (Consumer) and Verizon Business Group (Business).
Our Consumer segment provides consumer-focused wireless and wireline communications services and products. Our wireless services are provided across one of the most
extensive wireless networks in the United States (U.S.) under the Verizon brand and through wholesale and other arrangements. Our wireline services are provided in nine states
in the Mid-Atlantic and Northeastern U.S., as well as Washington D.C., over our 100% fiber-optic network under the Fios brand and over a traditional copper-based network to
customers who are not served by Fios. Our Consumer segment's wireless and wireline products and services are available to our retail customers, as well as resellers that
purchase wireless network access from us on a wholesale basis.
Our Business segment provides wireless and wireline communications services and products, video and data services, corporate networking solutions, security and managed
network services, local and long distance voice services and network access to deliver various Internet of Things (IoT) services and products. We provide these products and
services to businesses, government customers and wireless and wireline carriers across the U.S. and select products and services to customers around the world.
Consolidation
The method of accounting applied to investments, whether consolidated or equity, involves an evaluation of all significant terms of the investments that explicitly grant or
suggest evidence of control or influence over the operations of the investee. The consolidated financial statements include our controlled subsidiaries, as well as variable interest
entities (VIE) where we are deemed to be the primary beneficiary. For controlled subsidiaries that are not wholly-owned, the noncontrolling interests are included in Net income
and Total equity. Investments in businesses that we do not control, but have the ability to exercise significant influence over operating and financial policies, are accounted for
using the equity method. Equity method investments are included in Investments in unconsolidated businesses in our consolidated balance sheets. All significant intercompany
accounts and transactions have been eliminated.
Use of Estimates
We prepare our financial statements using U.S. generally accepted accounting principles (GAAP), which requires management to make estimates and assumptions that affect
reported amounts and disclosures. Actual results could differ from those estimates.
Examples of significant estimates include the allowance for doubtful accounts, the recoverability of property, plant and equipment, the incremental borrowing rate for the lease
liability, the recoverability of intangible assets and other long-lived assets, fair value measurements, including those related to financial instruments, goodwill, spectrum licenses
and intangible assets, unrecognized tax benefits, valuation allowances on tax assets, pension and postretirement benefit obligations, contingencies and the identification and
valuation of assets acquired and liabilities assumed in connection with business combinations.
Revenue Recognition
We earn revenue from contracts with customers, primarily through the provision of telecommunications and other services and through the sale of wireless equipment. These
services include a variety of communication and connectivity services for our Consumer and Business customers including other carriers that use our facilities to provide
services to their customers, as well as professional and integrated managed services for our large enterprises and government customers. We account for these revenues under
Accounting Standards Update (ASU) 2014-09, "Revenue from Contracts with Customers" (Topic 606), which we adopted on January 1, 2018, using the modified retrospective
approach. This standard update, along with related subsequently issued updates, clarifies the principles for recognizing revenue and develops a common revenue standard for
GAAP. The standard update also amends current guidance for the recognition of costs to obtain and fulfill contracts with customers such that incremental costs of obtaining and
direct costs of fulfilling contracts with customers are deferred and amortized consistent with the transfer of the related good or service.
We also earn revenues that are not accounted for under Topic 606 from leasing arrangements (such as those for towers and equipment), captive reinsurance arrangements
primarily related to wireless device insurance and the interest on equipment financed under a device payment plan agreement when sold to the customer by an authorized agent.
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Nature of Products and Services
Telecommunications
Service
We offer wireless services through a variety of plans on a postpaid or prepaid basis. For wireless service, we recognize revenue using an output method, either as the service
allowance units are used or as time elapses, because it reflects the pattern by which we satisfy our performance obligation through the transfer of service to the customer.
Monthly service is generally billed in advance, which results in a contract liability. See Note 2 for additional information. For postpaid plans, where monthly usage exceeds the
allowance, the overage usage represents options held by the customer for incremental services and the usage-based fee is recognized when the customer exercises the option
(typically on a month-to-month basis).
For our contracts related to wireline communication and connectivity services, in general, fixed monthly fees for service are billed one month in advance, which results in a
contract liability, and service revenue is recognized over the enforceable contract term as the service is rendered, as the customer simultaneously receives and consumes the
benefits of the services through network access and usage. While substantially all of our wireline service revenue contracts are the result of providing access to our networks,
revenue from services that are not fixed in amount and, instead, are based on usage are generally billed in arrears and recognized as the usage occurs.
Equipment
We sell wireless devices and accessories under the Verizon brand. Equipment revenue is generally recognized when the products are delivered to and accepted by the customer,
as this is when control passes to the customer. In addition to offering the sale of equipment on a standalone basis, we have two primary offerings through which customers pay
for a wireless device, in connection with a service contract: fixed-term plans and device payment plans.
Under a fixed-term plan, the customer is sold the wireless device without any upfront charge or at a discounted price in exchange for entering into a fixed-term service contract
(typically for a term of 24 months or less).
Under a device payment plan, the customer is sold the wireless device in exchange for a non-interest-bearing installment note, which is repaid by the customer, typically over a
24-month term, and concurrently enters into a month-to-month contract for wireless service. We may offer certain promotions that provide billing credits applied over a specified
term, contingent upon the customer maintaining service. The credits are included in the transaction price, which are allocated to the performance obligations based on their
relative selling price and are recognized when earned.
A financing component exists in both our fixed-term plans and device payment plans because the timing of the payment for the device, which occurs over the contract term,
differs from the satisfaction of the performance obligation, which occurs at contract inception upon transfer of the device to the customer. We periodically assess, at the contract
level, the significance of the financing component inherent in our fixed-term and device payment plan receivable based on qualitative and quantitative considerations related to
our customer classes. These considerations include assessing the commercial objective of our plans, the term and duration of financing provided, interest rates prevailing in the
marketplace, and credit risks of our customer classes, all of which impact our selection of appropriate discount rates. Based on current facts and circumstances, we determined
that the financing component in our existing wireless device payments and fixed-term contracts sold through the direct channel is not significant and therefore is not accounted
for separately. See Note 8 for additional information on the interest on equipment financed on a device payment plan agreement when sold to the customer by an authorized
agent in our indirect channel.
Wireless Contracts
For our wireless contracts, total contract revenue, which represents the transaction price for wireless service and wireless equipment, is allocated between service and equipment
revenue based on their estimated standalone selling prices. We estimate the standalone selling price of the device or accessory to be its retail price excluding subsidies or
conditional purchase discounts. We estimate the standalone selling price of wireless service to be the price that we offer to customers on month-to-month contracts that can be
cancelled at any time without penalty (i.e., when there is no fixed-term for service) or when service is procured without the concurrent purchase of a wireless device. In addition,
we also assess whether the service term is impacted by certain legally enforceable rights and obligations in our contract with customers, such as penalties that a customer would
have to pay to early terminate a fixed-term contract or billing credits that would cease if the month-to-month wireless service is canceled. The assessment of these legally
enforceable rights and obligations involves judgment and impacts our determination of the transaction price and related disclosures.
From time to time, we may offer certain promotions that provide our customers on device payment plans with the right to upgrade to a new device after paying a specified
portion of their device payment plan agreement amount and trading in their device in good working order. We account for this trade-in right as a guarantee obligation. The full
amount of the trade-in right's fair value is recognized as a guarantee liability and results in a reduction to the revenue recognized upon the sale of the device. The guarantee
liability was insignificant at December 31, 2019 and 2018. The total transaction price is reduced by the guarantee, which is accounted for outside the scope of Topic 606, and the
remaining transaction price is allocated between the performance obligations within the contract.
Our fixed-term plans generally include the sale of a wireless device at subsidized prices. This results in the creation of a contract asset at the time of sale, which represents the
recognition of equipment revenue in excess of amounts billed.
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For our device payment plans, billing credits are accounted for as consideration payable to a customer and are included in the determination of total transaction price, resulting in
a contract liability.
We may provide a right of return on our products and services for a short time period after a sale. These rights are accounted for as variable consideration when determining the
transaction price, and accordingly we recognize revenue based on the estimated amount to which we expect to be entitled after considering expected returns. Returns and credits
are estimated at contract inception and updated at the end of each reporting period as additional information becomes available. We also may provide credits or incentives on our
products and services for contracts with resellers, which are accounted for as variable consideration when estimating the amount of revenue to recognize.
Wireline Contracts
Total consideration for wireline services that are bundled in a single contract is allocated to each performance obligation based on our standalone selling price for each service.
While many contracts include one or more service performance obligations, the revenue recognition pattern is generally not impacted by the allocation since the services are
generally satisfied over the same period of time. We estimate the standalone selling price to be the price of the services when sold on a standalone basis without any promotional
discount. In addition, we also assess whether the service term is impacted by certain legally enforceable rights and obligations in our contract with customers such as penalties
that a customer would have to pay to early terminate a fixed-term contract. The assessment of these legally enforceable rights and obligations involves judgment and impacts our
determination of transaction price and related disclosures.
We may provide performance-based credits or incentives on our products and services for contracts with our Business customers, which are accounted for as variable
consideration when estimating the transaction price. Credits are estimated at contract inception and are updated at the end of each reporting period as additional information
becomes available.
Wireless and Wireline Contracts
For offers that include third-party providers, we evaluate whether we are acting as the principal or as the agent with respect to the goods or services provided to the customer.
This principal-versus-agent assessment involves judgment and focuses on whether the facts and circumstances of the arrangement indicate that the goods or services were
controlled by us prior to transferring them to the customer. To evaluate if we have control, we consider various factors including whether we are primarily responsible for
fulfillment, bear risk of loss and have discretion over pricing.
Other
Advertising revenues are generated through display advertising and search advertising. Display advertising revenue is generated by the display of graphical advertisements and
other performance-based advertising. Search advertising revenue is generated when a consumer clicks on a text-based advertisement on the search results page. Our Media
business, Verizon Media, primarily earns revenue through display advertising on Verizon Media properties, as well as on third-party properties through our advertising
platforms, search advertising and subscription arrangements. Revenue for display and search advertising contracts is recognized as ads are delivered, while subscription contracts
are recognized over time. We are generally the principal in transactions carried out through our advertising platforms, and therefore report gross revenue based on the amount
billed to our customers. The control and transfer of digital advertising inventory occurs in a rapid, real-time environment, where our proprietary technology enables us to
identify, enhance, verify and solely control digital advertising inventory that we then sell to our customers. Our control is further supported by us being primarily responsible to
our customers for fulfillment and the fact that we can exercise a level of discretion over pricing.
We offer telematics services including smart fleet management and optimization software. Telematics service revenue is generated primarily through subscription contracts. We
recognize revenue over time for our subscription contracts.
We report taxes collected from customers on behalf of governmental authorities on revenue-producing transactions on a net basis.
Maintenance and Repairs
We charge the cost of maintenance and repairs, including the cost of replacing minor items not constituting substantial betterments, principally to Cost of services as these costs
are incurred.
Advertising Costs
Costs for advertising products and services, as well as other promotional and sponsorship costs, are charged to Selling, general and administrative expense in the periods in
which they are incurred. See Note 15 for additional information.
Earnings Per Common Share
Basic earnings per common share are based on the weighted-average number of shares outstanding during the period. Where appropriate, diluted earnings per common share
include the dilutive effect of shares issuable under our stock-based compensation plans.
There were a total of approximately 2 million, 4 million and 5 million outstanding dilutive securities, primarily consisting of restricted stock units, included in the computation of
diluted earnings per common share for the years ended December 31, 2019, 2018 and 2017, respectively.
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Cash, Cash Equivalents and Restricted Cash
We consider all highly liquid investments with an original maturity of 90 days or less when purchased to be cash equivalents. Cash equivalents are stated at cost, which
approximates quoted market value and includes amounts held in money market funds.
Cash collections on the device payment plan agreement receivables collateralizing asset-backed debt securities are required at certain specified times to be placed into segregated
accounts. Deposits to the segregated accounts are considered restricted cash and are included in Prepaid expenses and other and Other assets in our consolidated balance sheets.
Cash, cash equivalents and restricted cash are included in the following line items in the consolidated balance sheets:
(dollars in millions)
At December 31,
Cash and cash equivalents
Restricted cash:
Prepaid expenses and other
Other assets
Cash, cash equivalents and restricted cash
$
1,221
102
3,917
$
1,047
124
3,916
$
174
(22)
1
$
2019
2,594
$
2018
2,745
Increase / (Decrease)
$
(151)
Investments in Debt and Equity Securities
Investments in equity securities that are not accounted for under equity method accounting or result in consolidation are to be measured at fair value. For investments in equity
securities without readily determinable fair values, Verizon elects the measurement alternative permitted under GAAP to measure these investments at cost, less any impairment,
plus or minus changes resulting from observable price changes in orderly transactions for an identical or similar investment of the same issuer. For investments in debt securities
without quoted prices, Verizon uses an alternative matrix pricing method. Investments in equity securities that do not result in consolidation of the investee are included in
Investments in unconsolidated businesses and debt securities are included in Other assets in our consolidated balance sheets.
Allowance for Doubtful Accounts
Accounts receivable are recorded in the consolidated financial statements at cost net of an allowance for credit losses, with the exception of indirect-channel device payment plan
loans. We maintain allowances for uncollectible accounts receivable, including our direct-channel device payment plan agreement receivables, for estimated losses resulting
from the failure or inability of our customers to make required payments. Indirect-channel device payment loans are considered financial instruments and are initially recorded at
fair value net of imputed interest, and credit losses are recorded as incurred. However, loan balances are assessed quarterly for impairment and an allowance is recorded if the
loan is considered impaired. Our allowance for uncollectible accounts receivable is based on management’s assessment of the collectability of specific customer accounts and
includes consideration of the credit worthiness and financial condition of those customers. We record an allowance to reduce the receivables to the amount that is reasonably
believed to be collectible. We also record an allowance for all other receivables based on multiple factors including historical experience with bad debts, the general economic
environment and the aging of such receivables. Similar to traditional service revenue, we record direct device payment plan agreement bad debt expense based on an estimate of
the percentage of equipment revenue that will not be collected. This estimate is based on a number of factors including historical write-off experience, credit quality of the
customer base and other factors such as macroeconomic conditions. We monitor the aging of our accounts with device payment plan agreement receivables and write-off account
balances if collection efforts are unsuccessful and future collection is unlikely.
Inventories
Inventory consists of wireless and wireline equipment held for sale, which is carried at the lower of cost (determined principally on either an average cost or first-in, first-out
basis) or net realizable value.
Plant and Depreciation
We record property, plant and equipment at cost. Property, plant and equipment are generally depreciated on a straight-line basis.
Leasehold improvements are amortized over the shorter of the estimated life of the improvement or the remaining term of the related lease, calculated from the time the asset was
placed in service.
When depreciable assets are retired or otherwise disposed of, the related cost and accumulated depreciation are deducted from the property, plant and equipment accounts and
any gains or losses on disposition are recognized in income.
We capitalize and depreciate network software purchased or developed within property, plant and equipment assets. We also capitalize interest associated with the acquisition or
construction of network-related assets. Capitalized interest is reported as a reduction in interest expense and depreciated as part of the cost of the network-related assets.
In connection with our ongoing review of the estimated useful lives of property, plant and equipment during 2018, we determined that the average useful lives of certain assets
would be increased. These changes in estimates were applied prospectively in 2018 and resulted in a decrease to
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depreciation expense of $271 million for the year ended December 31, 2018. While the timing and extent of current deployment plans are subject to ongoing analysis and
modification, we believe that the current estimates of useful lives are reasonable.
Computer Software Costs
We capitalize the cost of internal-use network and non-network software that has a useful life in excess of one year. Subsequent additions, modifications or upgrades to internal-
use network and non-network software are capitalized only to the extent that they allow the software to perform a task it previously did not perform. Planning, software
maintenance and training costs are expensed in the period in which they are incurred. Also, we capitalize interest associated with the development of internal-use network and
non-network software. Capitalized non-network internal-use software costs are amortized using the straight-line method over a period of 3 to 7 years and are included in Other
intangible assets, net in our consolidated balance sheets. For a discussion of our impairment policy for capitalized software costs, see "Goodwill and Other Intangible Assets"
below. Also, see Note 4 for additional information of internal-use non-network software reflected in our consolidated balance sheets.
Goodwill and Other Intangible Assets
Goodwill
Goodwill is the excess of the acquisition cost of businesses over the fair value of the identifiable net assets acquired. Impairment testing for goodwill is performed annually in the
fourth quarter or more frequently if impairment indicators are present.
To determine if goodwill is potentially impaired, we have the option to perform a qualitative assessment. However, we may elect to bypass the qualitative assessment and
perform a quantitative impairment test even if no indications of a potential impairment exist. The quantitative impairment test for goodwill is performed at the reporting unit
level and compares the fair value of the reporting unit (calculated using a combination of a market approach and a discounted cash flow method) to its carrying value. Estimated
fair values of reporting units are Level 3 measures in the fair value hierarchy, see Fair Value Measurements discussion below for additional information.
Under the qualitative assessment, we consider several qualitative factors, including the business enterprise value of the reporting unit from the last quantitative test and the excess
of fair value over carrying value from this test, macroeconomic conditions (including changes in interest rates and discount rates), industry and market considerations (including
industry revenue and Earnings before interest, taxes, depreciation and amortization ( EBITDA) margin projections), the recent and projected financial performance of the
reporting unit, as well as other factors.
The market approach includes the use of comparative multiples of guideline companies to corroborate discounted cash flow results. The discounted cash flow method is based on
the present value of two components, a projected cash flows and a terminal value. The terminal value represents the expected normalized future cash flows of the reporting unit
beyond the cash flows from the discrete projection period. The fair value of the reporting unit is calculated based on the sum of the present value of the cash flows from the
discrete period and the present value of the terminal value. The discount rate represents our estimate of the weighted-average cost of capital, or expected return, that a
marketplace participant would have required as of the valuation date. If the carrying value exceeds the fair value, an impairment charge is booked for the excess carrying value
over fair value, limited to the total amount of goodwill of that reporting unit. During the fourth quarter each year, we update our five-year strategic planning review for each of
our reporting units. Those plans consider current economic conditions and trends, estimated future operating results, our view of growth-rates and-anticipated future economic
and regulatory conditions.
See Note 4 for additional information regarding our goodwill impairment testing.
Intangible Assets Not Subject to Amortization
A significant portion of our intangible assets are wireless licenses that provide our wireless operations with the exclusive right to utilize designated radio frequency spectrum to
provide wireless communication services. While licenses are issued for only a fixed time, generally ten years, such licenses are subject to renewal by the Federal
Communications Commission (FCC). License renewals have occurred routinely and at nominal cost. Moreover, we have determined that there are currently no legal, regulatory,
contractual, competitive, economic or other factors that limit the useful life of our wireless licenses. As a result, we treat the wireless licenses as an indefinite-lived intangible
asset. We re-evaluate the useful life determination for wireless licenses each year to determine whether events and circumstances continue to support an indefinite useful life. We
aggregate our wireless licenses into one single unit of accounting, as we utilize our wireless licenses on an integrated basis as part of our nationwide wireless network.
We test our wireless licenses for potential impairment annually or more frequently if impairment indicators are present. We have the option to first perform a qualitative
assessment to determine whether it is necessary to perform a quantitative impairment test. However, we may elect to bypass the qualitative assessment in any period and proceed
directly to performing the quantitative impairment test. Our quantitative assessment consists of comparing the estimated fair value of our aggregate wireless licenses to the
aggregated carrying amount as of the test date. Using a quantitative assessment, we estimate the fair value of our aggregate wireless licenses using the Greenfield approach. The
Greenfield approach is an income based valuation approach that values the wireless licenses by calculating the cash flow generating potential of a hypothetical start-up company
that goes into business with no assets except the wireless licenses to be valued. A discounted cash flow analysis is used to estimate what a marketplace participant would be
willing to pay to purchase the aggregated wireless licenses as of the valuation date. If the estimated fair value of the aggregated wireless licenses is less than the aggregated
carrying amount of the wireless licenses, then an impairment charge is recognized. As part of our qualitative assessment, we consider several qualitative factors including the
business enterprise value of our historical Wireless segment, macroeconomic conditions (including changes in interest rates and discount rates), industry and market
considerations
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(including industry revenue and EBITDA margin projections), the recent and projected financial performance of our historical Wireless segment, as well as other factors. See
Note 4 for additional information regarding our impairment tests.
Interest expense incurred while qualifying activities are performed to ready wireless licenses for their intended use is capitalized as part of wireless licenses. The capitalization
period ends when the development is discontinued or substantially completed and the license is ready for its intended use.
Wireless licenses can be purchased through public auctions conducted by the FCC. Deposits required to participate in these auctions and purchase licenses are recorded as other
non-current assets until the corresponding licenses are received and within Net cash used in investing activities in our consolidated statements of cash flows.
Intangible Assets Subject to Amortization and Long-Lived Assets
Our intangible assets that do not have indefinite lives (primarily customer lists and non-network internal-use software) are amortized over their estimated useful lives. All of our
intangible assets subject to amortization and other long-lived assets are reviewed for impairment whenever events or changes in circumstances indicate that the carrying amount
of the asset may not be recoverable. If any indications of impairment are present, we would test for recoverability by comparing the carrying amount of the asset group to the net
undiscounted cash flows expected to be generated from the asset group. If those net undiscounted cash flows do not exceed the carrying amount, we would perform the next step,
which is to determine the fair value of the asset and record an impairment, if any. We re-evaluate the useful life determinations for these intangible assets each year to determine
whether events and circumstances warrant a revision to their remaining useful lives.
For information related to the carrying amount of goodwill, wireless licenses and other intangible assets, as well as the major components and average useful lives of our other
acquired intangible assets, see Note 4.
Fair Value Measurements
Fair value of financial and non-financial assets and liabilities is defined as an exit price, representing the amount that would be received to sell an asset or paid to transfer a
liability in an orderly transaction between market participants. The three-tier hierarchy for inputs used in measuring fair value, which prioritizes the inputs used in the
methodologies of measuring fair value for assets and liabilities, is as follows:
Level 1—Quoted prices in active markets for identical assets or liabilities
Level 2—Observable inputs other than quoted prices in active markets for identical assets and liabilities
Level 3—Unobservable pricing inputs in the market
Financial assets and financial liabilities are classified in their entirety based on the lowest level of input that is significant to the fair value measurements. Our assessment of the
significance of a particular input to the fair value measurements requires judgment and may affect the valuation of the assets and liabilities being measured and their
categorization within the fair value hierarchy.
Income Taxes
Our effective tax rate is based on pre-tax income, statutory tax rates, tax laws and regulations and tax planning strategies available to us in the various jurisdictions in which we
operate.
Deferred income taxes are provided for temporary differences in the basis between financial statement and income tax assets and liabilities. Deferred income taxes are
recalculated annually at tax rates in effect for the years in which those tax assets and liabilities are expected to be realized or settled. We record valuation allowances to reduce
our deferred tax assets to the amount that is more likely than not to be realized.
We use a two-step approach for recognizing and measuring tax benefits taken or expected to be taken in a tax return. The first step is recognition: we determine whether it is
more likely than not that a tax position will be sustained upon examination, including resolution of any related appeals or litigation processes, based on the technical merits of the
position. In evaluating whether a tax position has met the more-likely-than-not recognition threshold, we presume that the position will be examined by the appropriate taxing
authority that has full knowledge of all relevant information. The second step is measurement: a tax position that meets the more-likely-than-not recognition threshold is
measured to determine the amount of benefit to recognize in the financial statements. The tax position is measured at the largest amount of benefit that is greater than 50 percent
likely of being realized upon ultimate settlement. Differences between tax positions taken in a tax return and amounts recognized in the financial statements will generally result
in one or more of the following: an increase in a liability for income taxes payable, a reduction of an income tax refund receivable, a reduction in a deferred tax asset or an
increase in a deferred tax liability.
Significant management judgment is required in evaluating our tax positions and in determining our effective tax rate.
Stock-Based Compensation
We measure and recognize compensation expense for all stock-based compensation awards made to employees and directors based on estimated fair values. See Note 10 for
additional information.
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Foreign Currency Translation and Transactions
The functional currency of our foreign operations is generally the local currency. For these foreign entities, we translate their financial statements into U.S. dollars using average
exchange rates for the period for income statement amounts and using end-of-period exchange rates for assets and liabilities. We record these translation adjustments in
Accumulated other comprehensive income, a separate component of Equity, in our consolidated balance sheets. We record exchange gains and losses resulting from the
conversion of transaction currency to functional currency as a component of Other income (expense), net.
Employee Benefit Plans
Pension and postretirement health care and life insurance benefits earned during the year, as well as interest on projected benefit obligations, are accrued. Prior service costs and
credits resulting from changes in plan benefits are generally amortized over the average remaining service period of the employees expected to receive benefits. Expected return
on plan assets is determined by applying the return on assets assumption to the actual fair value of plan assets. Actuarial gains and losses are recognized in Other income
(expense), net in the year in which they occur. These gains and losses are measured annually as of December 31 or upon a remeasurement event. Verizon management
employees no longer earn pension benefits or earn service towards the Company retiree medical subsidy. See Note 11 for additional information.
We recognize a pension or a postretirement plan’s funded status as either an asset or liability in the consolidated balance sheets. Also, we measure any unrecognized prior service
costs and credits that arise during the period as a component of Accumulated other comprehensive income, net of applicable income tax.
Derivative Instruments
We enter into derivative transactions primarily to manage our exposure to fluctuations in foreign currency exchange rates and interest rates. We employ risk management
strategies, which may include the use of a variety of derivatives including cross currency swaps, forward starting interest rate swaps, interest rate swaps, interest rate caps and
foreign exchange forwards. We do not hold derivatives for trading purposes.
We measure all derivatives at fair value and recognize them as either assets or liabilities in our consolidated balance sheets. Our derivative instruments are valued primarily using
models based on readily observable market parameters for all substantial terms of our derivative contracts and thus are classified as Level 2. Changes in the fair values of
derivative instruments not qualifying for hedge accounting are recognized in earnings in the current period. For fair value hedges, the change in the fair value of the derivative
instruments is recognized in earnings, along with the change in the fair value of the hedged item. For cash flow hedges, the change in the fair value of the derivative instruments
is reported in Other comprehensive income (loss) and recognized in earnings when the hedged item is recognized in earnings. For net investment hedges of certain of our foreign
operations, the change in the fair value of the derivative instruments is reported in Other comprehensive income (loss) as part of the cumulative translation adjustment and
partially offset the impact of foreign currency changes on the value of our net investment. See Note 9 for additional information.
Variable Interest Entities
VIEs are entities that lack sufficient equity to permit the entity to finance its activities without additional subordinated financial support from other parties, have equity investors
that do not have the ability to make significant decisions relating to the entity’s operations through voting rights, do not have the obligation to absorb the expected losses, or do
not have the right to receive the residual returns of the entity. We consolidate the assets and liabilities of VIEs when we are deemed to be the primary beneficiary. The primary
beneficiary is the party that has the power to make the decisions that most significantly affect the economic performance of the VIE and has the obligation to absorb losses or the
right to receive benefits that could potentially be significant to the VIE.
Recently Adopted Accounting Standards
The following ASUs were issued by Financial Accounting Standards Board (FASB), and have been recently adopted by Verizon.
Description
Date of
Adoption
Effect on Financial Statements
ASU 2016-02, ASU 2018-01, ASU 2018-10, ASU 2018-11, ASU 2018-20 and ASU 2019-01, Leases (Topic 842)
The FASB issued Topic 842 requiring entities to recognize assets and liabilities on
the balance sheet for all leases, with certain exceptions. In addition, Topic 842
enables users of financial statements to further understand the amount, timing and
uncertainty of cash flows arising from leases. Topic 842 allowed for a modified
retrospective application and was effective as of the first quarter of 2019. Entities
were allowed to apply the modified retrospective approach: (1) retrospectively to
each prior reporting period presented in the financial statements with the cumulative-
effect adjustment recognized at the beginning of the earliest comparative period
presented; or (2) retrospectively at the beginning of the period of adoption (January
1, 2019) through a cumulative-effect adjustment. The modified retrospective
approach includes a number of optional practical expedients that entities may elect
to apply.
1/1/2019
We adopted Topic 842 beginning on January 1, 2019, using the modified
retrospective approach with a cumulative-effect adjustment to opening
retained earnings recorded at the beginning of the period of adoption.
Therefore, upon adoption, we have recognized and measured leases
without revising comparative period information or disclosure. We
recorded an increase of $410 million (net of tax) to retained earnings on
January 1, 2019 which related to deferred sale leaseback gains
recognized from prior transactions. Additionally, the adoption of the
standard had a significant impact in our consolidated balance sheet due
to the recognition of $22.1 billion of operating lease liabilities, along
with $23.2 billion of operating lease right-of-use-assets.
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The cumulative after-tax effect of the changes made to our consolidated balance sheet for the adoption of Topic 842 were as follows:
(dollars in millions)
Prepaid expenses and other
Operating lease right-of-use assets
Other assets
Accounts payable and accrued liabilities
Other current liabilities
Current operating lease liabilities
Deferred income taxes
Non-current operating lease liabilities
Other liabilities
Retained earnings
Noncontrolling interests
$
At December 31, 2018
5,453
—
11,717
22,501
8,239
—
33,795
—
13,922
43,542
1,565
$
Adjustments due to
Topic 842
(329)
23,241
(2,048)
(3)
(2)
2,931
139
19,203
(1,815)
410
1
$
At January 1, 2019
5,124
23,241
9,669
22,498
8,237
2,931
33,934
19,203
12,107
43,952
1,566
In addition to the increase to the operating lease liabilities and right-of-use assets and the derecognition of deferred sale leaseback gains through opening retained earnings, Topic
842 also resulted in reclassifying the presentation of prepaid and deferred rent to operating lease right-of-use assets. The operating lease right-of-use assets amount also includes
the balance of any prepaid lease payments, unamortized initial direct costs and lease incentives.
We elected the package of practical expedients permitted under the transition guidance within the new standard. Accordingly, we have adopted these practical expedients and did
not reassess: (1) whether an expired or existing contract is a lease or contains an embedded lease; (2) lease classification of an expired or existing lease; or (3) capitalization of
initial direct costs for an expired or existing lease. In addition, we have elected the land easement transition practical expedient, and did not reassess whether an existing or
expired land easement is a lease or contains a lease if it has not historically been accounted for as a lease.
We lease network equipment including towers, distributed antenna systems, small cells, real estate, connectivity mediums which include dark fiber, equipment, and other various
types of assets for use in our operations under both operating and finance leases. We assess whether an arrangement is a lease or contains a lease at inception. For arrangements
considered leases or that contain a lease that is accounted for separately, we determine the classification and initial measurement of the right-of-use asset and lease liability at the
lease commencement date, which is the date that the underlying asset becomes available for use.
For both operating and finance leases, we recognize a right-of-use asset, which represents our right to use the underlying asset for the lease term, and a lease liability, which
represents the present value of our obligation to make payments arising over the lease term. The present value of the lease payments is calculated using the incremental
borrowing rate for operating and finance leases. The incremental borrowing rate is determined using a portfolio approach based on the rate of interest that the Company would
have to pay to borrow an amount equal to the lease payments on a collateralized basis over a similar term. Management uses the unsecured borrowing rate and risk-adjusts that
rate to approximate a collateralized rate, which is updated on a quarterly basis.
In those circumstances where the Company is the lessee, we have elected to account for non-lease components associated with our leases (e.g., common area maintenance costs)
and lease components as a single lease component for substantially all of our asset classes. Additionally, in arrangements where we are the lessor, we have customer premise
equipment for which we apply the lease and non-lease component practical expedient and account for non-lease components (e.g., service revenue) and lease components as
combined components under the revenue recognition guidance in Topic 606 as the service revenues are the predominant components in the arrangements.
Rent expense for operating leases is recognized on a straight-line basis over the term of the lease and is included in either Cost of services or Selling, general and administrative
expense in our consolidated statements of income, based on the use of the facility or equipment on which rent is being paid. Variable rent payments related to both operating and
finance leases are expensed in the period incurred. Our variable lease payments consist of payments dependent on various external indicators, including real estate taxes,
common area maintenance charges and utility usage.
Operating leases with a term of 12 months or less are not recorded on the balance sheet; we recognize rent expense for these leases on a straight-line basis over the lease term.
We recognize the amortization of the right-of-use asset for our finance leases on a straight-line basis over the shorter of the lease term or the useful life of the right-of-use asset in
Depreciation and amortization expense in our consolidated statements of income. The interest expense related to finance leases is recognized using the effective interest method
based on the discount rate determined at lease commencement and is included within Interest expense in our consolidated statements of income.
See Note 6 for additional information related to leases, including disclosure required under Topic 842.
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Opening Equity Balance Sheet Adjustments from Accounting Standards Adopted in 2018
On January 1, 2018, we adopted Topic 606, ASU 2018-02, Income Statement-Reporting Comprehensive Income and other ASUs. We adopted Topic 606 using the modified
retrospective method. We early adopted ASU 2018-02, which allows a reclassification from accumulated other comprehensive income to retained earnings for stranded tax
effects resulting from Tax Cuts and Jobs Act (TCJA). The cumulative after-tax effect of the changes made to our consolidated balance sheet for the adoption of Topic 606, ASU
2018-02 and other ASUs was as follows:
Adjustments due to
(dollars in millions)
Retained earnings
Accumulated other comprehensive income
Noncontrolling interests
At December 31, 2017
35,635
2,659
1,591
Topic 606
2,890
—
44
ASU 2018-02
(652)
652
—
Other ASUs
(6)
(22)
—
At January 1,
2018
37,867
3,289
1,635
Recently Issued Accounting Standards
The following ASUs have been recently issued by the FASB.
Description
In June 2016, the FASB issued this standard update which requires certain
financial assets be measured at amortized cost net of an allowance for
estimated credit losses such that the net receivable represents the present
value of expected cash collection. In addition, this standard update requires
that certain financial assets be measured at amortized cost reflecting an
allowance for estimated credit losses expected to occur over the life of the
assets. The estimate of credit losses must be based on all relevant information
including historical information, current conditions and reasonable and
supportable forecasts that affect the collectability of the amounts. An entity
will apply the update through a cumulative effect adjustment to retained
earnings as of the beginning of the first reporting period in which the
guidance is effective (January 1, 2020). A prospective transition approach is
required for debt securities for which an other-than-temporary impairment
has been recognized before the effective date. Early adoption of this standard
is permitted.
Date of Adoption
Effect on Financial Statements
We established a cross-functional coordinated team to implement the
standard update. We have completed our assessment of the expected
impacts and updated our processes to meet the standards reporting and
disclosure requirements. Upon adoption of this standard on January 1,
2020, we expect the cumulative effect of initially applying the new
standard to result in a decrease to the opening balance of retained earnings
ranging from approximately $200 million to $300 million on a pre-tax
basis ($150 million to $225 million net of tax), primarily related to the
expected impact on certain device payment plan agreement receivables.
We do not expect our operating results to be significantly impacted by this
standard update.
ASU 2016-13, ASU 2018-19, ASU 2019-04, ASU 2019-05, Financial Instruments - Credit Losses (Topic 326)
1/1/2020
Note 2. Revenue and Contract Costs
We earn revenue from contracts with customers, primarily through the provision of telecommunications and other services and through the sale of wireless equipment. These
services include a variety of communication and connectivity services for our Consumer and Business customers including other carriers that use our facilities to provide
services to their customers, as well as professional and integrated managed services for our large enterprises and government customers. We account for these revenues under
Topic 606, which we adopted on January 1, 2018, using the modified retrospective approach. We also earn revenues that are not accounted for under Topic 606 from leasing
arrangements (such as those for towers and equipment), captive reinsurance arrangements primarily related to wireless device insurance and the interest on equipment financed
under a device payment plan agreement when sold to the customer by an authorized agent.
We applied the new revenue recognition standard to customer contracts not completed at the date of initial adoption. For incomplete contracts that were modified before the date
of adoption, the Company elected to use the practical expedient available under the modified retrospective method, which allows us to aggregate the effect of all modifications
when identifying satisfied and unsatisfied performance obligations, determining the transaction price and allocating transaction price to the satisfied and unsatisfied performance
obligations for the modified contract at transition. Results for reporting periods beginning after January 1, 2018 are presented under Topic 606, while amounts reported for prior
periods have not been adjusted and continue to be reported under accounting standards in effect for those periods.
Prior to the adoption of Topic 606, we were required to limit the revenue recognized when a wireless device was sold to the amount of consideration that was not contingent on
the provision of future services, which was typically limited to the amount of consideration received from the customer at the time of sale. Under Topic 606, the total
consideration in the contract is allocated between wireless equipment and service based on their relative standalone selling prices. This change primarily impacts our
arrangements that include sales of wireless devices at subsidized prices in conjunction with a fixed-term plan, also known as the subsidy model, for service. Accordingly, under
Topic 606, generally more equipment revenue is recognized upon sale of the equipment to the customer and less service revenue is recognized over the contract term than was
previously recognized under the prior "Revenue Recognition" (Topic 605) standard. At the time the equipment is sold, this allocation results in the recognition
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of a contract asset equal to the difference between the amount of revenue recognized and the amount of consideration received from the customer. As of January 2017, we no
longer offer Consumer customers new fixed-term plans with subsidized equipment pricing; however, we continue to offer fixed-term plans to our Business customers. At
December 31, 2019 and December 31, 2018, approximately 12% and 14% of retail postpaid connections were under fixed-term plans, respectively.
Topic 606 also requires the deferral of incremental costs incurred to obtain a customer contract, which are then amortized to expense, as a component of Selling, general and
administrative expense, over the respective periods of expected benefit. As a result, a significant amount of our sales commission costs, which were historically expensed as
incurred under our previous accounting, relating to our contracts to provide wireless and wireline services, are now deferred and amortized under Topic 606.
Finally, under Topic 605, at the time of the sale of a device, we imputed risk adjusted interest on the device payment plan agreement receivables. We recorded the imputed
interest as a reduction to the related accounts receivable and interest income was recognized over the financed device payment term. Under Topic 606, while there continues to
be a financing component in both the fixed-term plans and device payment plans, also known as the installment model, we have determined that this financing component for our
customer classes in the direct channels for wireless devices are not significant and therefore we no longer impute interest for these contracts. This change results in additional
revenue recognized upon the sale of wireless devices and no interest income recognized over the device payment term.
A reconciliation of the adjustments from the adoption of Topic 606 relative to Topic 605 on certain impacted financial statement line items in our consolidated statements of
income is as follows:
Year Ended December 31, 2018
Balances without
adoption of
Topic 606
$
109,964
20,474
130,438
32,240
23,189
32,588
(187)
17,771
(3,104)
$
$
$
14,667
481
14,186
14,667
$
$
$
$
(dollars in millions)
Operating Revenues
Service revenues and other
Wireless equipment revenues
Total Operating Revenues
Cost of services (exclusive of items shown below)
Cost of wireless equipment
Selling, general and administrative expense
Equity in losses of unconsolidated businesses
Income Before Provision For Income Taxes
Provision for income taxes
Net Income
Net income attributable to noncontrolling interests
Net income attributable to Verizon
Net Income
$
$
$
$
As reported
108,605
22,258
130,863
32,185
23,323
31,083
(186)
19,623
(3,584)
16,039
511
15,528
16,039
Adjustments
(1,359)
1,784
425
(55)
134
(1,505)
1
1,852
(480)
1,372
30
1,342
1,372
Revenue by Category
We have two reportable segments that we operate and manage as strategic business units, Consumer and Business. Revenue is disaggregated by products and services within
Consumer, and customer groups (Global Enterprise, Small and Medium Business, Public Sector and Other, and Wholesale) within Business. See Note 13 for additional
information on revenue by segment.
Corporate and other includes the results of our media business, Verizon Media, and other businesses. Verizon Media generated revenues from contracts with customers under
Topic 606 of approximately $7.5 billion and $7.7 billion for the years ended December 31, 2019 and 2018, respectively.
We also earn revenues that are not accounted for under Topic 606 from leasing arrangements (such as those for towers and equipment), captive reinsurance arrangements
primarily related to wireless device insurance and the interest on equipment financed under a device payment plan agreement when sold to the customer by an authorized agent.
As allowed by the practical expedient within Topic 842, we have elected to combine the lease and non-lease components for those arrangements of customer premise equipment
where we are the lessor as components accounted for under Topic 606. Revenues from arrangements that were not accounted for under Topic 606 were approximately
$3.1 billion and $4.5 billion for the years ended December 31, 2019 and 2018, respectively.
Remaining Performance Obligations
When allocating the total contract transaction price to identified performance obligations, a portion of the total transaction price may relate to service performance obligations
which were not satisfied or are partially satisfied as of the end of the reporting period. Below we disclose
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information relating to these unsatisfied performance obligations. Upon adoption, we elected to apply the practical expedient available under Topic 606 that provides the option
to exclude the expected revenues arising from unsatisfied performance obligations related to contracts that have an original expected duration of one year or less. This situation
primarily arises with respect to certain month-to-month service contracts. At December 31, 2019, month-to-month service contracts represented approximately 88% of our
wireless postpaid contracts and 61% of our wireline Consumer and Small and Medium Business contracts, compared to December 31, 2018, for which month-to-month service
contracts represented approximately 86% of our wireless postpaid contracts and 56% of our wireline Consumer and Small and Medium Business contracts
.
Additionally, certain contracts provide customers the option to purchase additional services. The fees related to these additional services are recognized when the customer
exercises the option (typically on a month-to-month basis).
Contracts for wireless services are generally either month-to-month and cancellable at any time (typically under a device payment plan) or contain terms ranging from greater
than one month to up to two years (typically under a fixed-term plan). Additionally, customers may incur charges based on usage or additional optional services purchased in
conjunction with entering into a contract that can be cancelled at any time and therefore are not included in the transaction price. The transaction price allocated to service
performance obligations, which are not satisfied or are partially satisfied as of the end of the reporting period, are generally related to our fixed-term plans.
Our Consumer group customers also include traditional wholesale resellers that purchase and resell wireless service under their own brands to their respective customers.
Reseller arrangements generally include a stated contract term, which typically extends longer than two years and, in some cases, include a periodic minimum revenue
commitment over the contract term for which revenues will be recognized in future periods.
Consumer customer contracts for wireline services generally have a service term of two years; however, this term may be shorter than twelve months or may be month-to-month.
Certain contracts with Business customers for wireline services extend into future periods, contain fixed monthly fees and usage-based fees, and can include annual commitments
in each year of the contract or commitments over the entire specified contract term; however, a significant number of contracts for wireline services with our Business customers
have a contract term that is twelve months or less.
Additionally, there are certain contracts with Business customers for wireline and telematics services and certain Media contracts with customers that have a contractual
minimum fee over the total contract term. We cannot predict the time period when revenue will be recognized related to those contracts; thus, they are excluded from the time
bands below. These contracts have varying terms spanning over approximately five years ending in November 2024 and have aggregate contract minimum payments totaling
$3.4 billion.
At December 31, 2019, the transaction price related to unsatisfied performance obligations for total Verizon that is expected to be recognized for 2020, 2021 and thereafter was
$20.2 billion, $9.4 billion and $1.6 billion, respectively. Remaining performance obligation estimates are subject to change and are affected by several factors, including
terminations and changes in the timing and scope of contracts, arising from contract modifications.
Accounts Receivable and Contract Balances
The timing of revenue recognition may differ from the time of billing to our customers. Receivables presented in our consolidated balance sheet represent an unconditional right
to consideration. Contract balances represent amounts from an arrangement when either Verizon has performed, by transferring goods or services to the customer in advance of
receiving all or partial consideration for such goods and services from the customer, or the customer has made payment to Verizon in advance of obtaining control of the goods
and/or services promised to the customer in the contract.
The following table presents information about receivables from contracts with customers:
At December 31,
(dollars in millions)
Receivables
(1)
Device payment plan agreement receivables
(2)
(1)
At December 31,
2018
$
12,104
8,940
$
At January 1,
2018
12,073
1,461
2019
$
12,078
11,741
(2)
Balances do not include receivables related to the following contracts: leasing arrangements (such as those for towers and equipment), captive reinsurance arrangements
primarily related to wireless device insurance and the interest on equipment financed under a device payment plan agreement when sold to the customer by an authorized
agent.
Included in device payment plan agreement receivables presented in Note 8. Balances do not include receivables related to contracts completed prior to January 1, 2018 and
receivables derived from the sale of equipment on a device payment plan through an authorized agent.
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The following table presents information about contract balances:
At December 31,
(dollars in millions)
Contract asset
Contract liability
$
2019
1,150
5,307
$
At December 31,
2018
1,003
4,943
$
At January 1,
2018
1,170
4,452
Contract assets primarily relate to our rights to consideration for goods or services provided to customers but for which we do not have an unconditional right at the reporting
date. Under a fixed-term plan, total contract revenue is allocated between wireless service and equipment revenues, as discussed above. In conjunction with these arrangements, a
contract asset is created, which represents the difference between the amount of equipment revenue recognized upon sale and the amount of consideration received from the
customer when the performance obligation related to the transfer of control of the equipment is satisfied. The contract asset is reclassified to accounts receivable as wireless
services are provided and billed. We have the right to bill the customer as service is provided over time, which results in our right to the payment being unconditional. The
contract asset balances are presented in our consolidated balance sheet as Prepaid expenses and other and Other assets. We assess our contract assets for impairment on a
quarterly basis and will recognize an impairment charge to the extent their carrying amount is not recoverable.
Contract assets increased $147 million during the year ended December 31, 2019. The change in the contract asset balance was primarily due to new contracts and increases in
sales promotions recognized upfront, driven by customer activity related to wireless and Fios services, partially offset by reclassifications to accounts receivable due to billings
on existing contracts and impairment charges of $113 million. Contract assets decreased $167 million during the year ended December 31, 2018. The change in the contract asset
balance was primarily due to reclassifications to accounts receivable due to billings on existing contracts and impairment charges of $116 million, offset by new contracts related
to wireless and Fios services.
Contract liabilities arise when we bill our customers and receive consideration in advance of providing the goods or services promised in the contract. We typically bill service
one month in advance, which is the primary component of the contract liability balance. Contract liabilities are recognized as revenue when services are provided to the
customer. The contract liability balances are presented in our consolidated balance sheet as Other current liabilities and Other liabilities.
Contract liabilities increased $364 million during the year ended December 31, 2019. The change in contract liabilities was primarily due to increases in sales promotions
recognized over time and upfront fees, as well as increases in deferred revenue related to advanced billings, partially offset by the satisfaction of performance obligations related
to wireless and Fios services. Contract liabilities increased $491 million during the year ended December 31, 2018. The change in contract liabilities was primarily due to
increases in sales promotions, as well as increases in deferred revenue related to advanced billings, partially offset by the satisfaction of performance obligations related to
wireless and Fios services.
Revenue recognized during the years ended December 31, 2019 and 2018 related to contract liabilities existing at January 1, 2019 and 2018 were $4.2 billion and $3.9 billion,
respectively, as performance obligations related to services were satisfied.
The balance of contract assets and contract liabilities recorded in our consolidated balance sheets were as follows:
At December 31,
(dollars in millions)
Assets
Prepaid expenses and other
Other assets
Total
Liabilities
Other current liabilities
Other liabilities
Total
$
$
4,651
656
5,307
$
$
$
$
848
302
1,150
$
$
2019
At December 31,
2018
757
246
1,003
4,207
736
4,943
Contract Costs
As discussed in Note 1, Topic 606 requires the recognition of an asset for incremental costs to obtain a customer contract, which is then amortized to expense over the respective
period of expected benefit. We recognize an asset for incremental commission costs paid to internal and external sales personnel and agents in conjunction with obtaining
customer contracts. We only defer these costs when we have determined the commissions are incremental costs that would not have been incurred absent the customer contract
and are expected to be recoverable. Costs to obtain a contract are amortized and recorded ratably as commission expense over the period representing the transfer of goods or
services to which the assets relate. Costs to obtain wireless contracts are amortized over both of our Consumer and Business customers' estimated device upgrade cycles, as such
costs are typically incurred each time a customer upgrades. Costs to obtain wireline contracts are amortized as expense over the estimated customer relationship period for our
Consumer customers. Incremental costs to obtain wireline contracts for our Business customers are insignificant. Costs to obtain contracts are recorded in Selling, general and
administrative expense.
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We also defer costs incurred to fulfill contracts that: (1) relate directly to the contract; (2) are expected to generate resources that will be used to satisfy our performance
obligation under the contract; and (3) are expected to be recovered through revenue generated under the contract. Contract fulfillment costs are expensed as we satisfy our
performance obligations and recorded to Cost of services. These costs principally relate to direct costs that enhance our wireline business resources, such as costs incurred to
install circuits.
We determine the amortization periods for our costs incurred to obtain or fulfill a customer contract at a portfolio level due to the similarities within these customer contract
portfolios.
Other costs, such as general costs or costs related to past performance obligations, are expensed as incurred.
Collectively, costs to obtain a contract and costs to fulfill a contract are referred to as deferred contract costs, and amortized over a 2 to 5-year period. Deferred contract costs are
classified as current or non-current within Prepaid expenses and other and Other assets, respectively.
The balances of deferred contract costs included in our consolidated balance sheets were as follows:
At December 31,
(dollars in millions)
Assets
Prepaid expenses and other
Other assets
Total
$
$
2,578
1,911
4,489
$
$
2019
At December 31,
2018
2,083
1,812
3,895
For the years ended December 31, 2019 and 2018, we recognized expense of $2.7 billion and $2.0 billion, respectively, associated with the amortization of deferred contract
costs, primarily within Selling, general and administrative expense in our consolidated statements of income.
We assess our deferred contract costs for impairment on a quarterly basis. We recognize an impairment charge to the extent the carrying amount of a deferred cost exceeds the
remaining amount of consideration we expect to receive in exchange for the goods and services related to the cost, less the expected costs related directly to providing those
goods and services that have not yet been recognized as expenses. There have been no impairment charges recognized for the years ended December 31, 2019 and 2018.
Note 3. Acquisitions and Divestitures
Spectrum License Transactions
Since 2017, we have entered into or completed several strategic spectrum transactions including:
•
During the fourth quarter of 2016, we entered into a license exchange agreement with affiliates of AT&T Inc. (AT&T) to exchange certain Advanced Wireless Services
(AWS) and Personal Communication Services (PCS) spectrum licenses. This non-cash exchange was completed in February 2017. As a result, we received $1.0 billion
of AWS and PCS spectrum licenses at fair value and recorded a pre-tax gain of $126 million in Selling, general and administrative expense in our consolidated statement
of income for the year ended December 31, 2017.
During the first quarter of 2017, we entered into a license exchange agreement with affiliates of Sprint Corporation to exchange certain PCS spectrum licenses. This non-
cash exchange was completed in May 2017. As a result, we received $132 million of PCS spectrum licenses at fair value and recorded an insignificant gain in Selling,
general and administrative expense in our consolidated statement of income for the year ended December 31, 2017.
During the third quarter of 2017, we entered into a license exchange agreement with affiliates of T-Mobile USA Inc. to exchange certain AWS and PCS spectrum
licenses. This non-cash exchange was completed in December 2017. As a result, we received $414 million of AWS and PCS spectrum licenses at fair value and recorded
a pre-tax gain of $143 million in Selling, general and administrative expense in our consolidated statement of income for the year ended December 31, 2017.
During 2018, we entered into and completed various wireless license transactions, including the purchase of Straight Path Communications Inc. (Straight Path) and
NextLink Wireless LLC (NextLink).
During 2019, the FCC completed two millimeter wave spectrum license auctions. Verizon participated in these auctions and was the high bidder on 9 and 1,066 licenses,
respectively, in the 24 Gigahertz (GHz) and 28 GHz bands. We submitted an application to the FCC and paid cash of approximately $521 million for the licenses. We
received the licenses during the fourth quarter of 2019.
During 2019, we entered into and completed various other wireless license acquisitions for an insignificant amount of cash consideration.
•
•
•
•
•
In December 2019, the FCC incentive auction for spectrum licenses in the upper 37 GHz, 39 GHz, and 47 GHz bands commenced. As an incumbent licensee, Verizon received
vouchers related to our existing 39 GHz licenses. These vouchers can be converted into cash, the amount of which will not be known until the conclusion of the auction, or
applied toward the purchase price of spectrum in the auction. At the conclusion
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of the auction, all existing licenses will be cancelled and new reconfigured licenses or cash will be distributed depending on the results of the auction. Due to the FCC's rules
restricting communications regarding the auction, we will not disclose our financial plans for the auction during the quiet period for this auction unless legally required. In
addition, as of this time, until the completion of the auction process, we cannot determine the resulting financial outcome, including a potential gain or loss. Such gain or loss, if
any, may be material.
Acquisition of AOL Inc.
In May 2015, we entered into an Agreement and Plan of Merger with AOL Inc. (AOL) pursuant to which we commenced a tender offer to acquire all of the outstanding shares of
common stock of AOL at a price of $50.00 per share, net to the seller in cash, without interest and less any applicable withholding taxes.
On June 23, 2015, we completed the tender offer and merger, and AOL became a wholly-owned subsidiary of Verizon. The aggregate cash consideration paid by Verizon at the
closing of these transactions was approximately $3.8 billion. Holders of approximately 6.6 million shares exercised appraisal rights under Delaware law. In September 2018, we
obtained court approval to settle this matter for total cash consideration of $219 million of which an insignificant amount relates to interest, resulting in an insignificant gain. We
paid the cash consideration in October 2018.
XO Holdings
In February 2016, we entered into a purchase agreement to acquire XO Holdings' wireline business (XO), which owned and operated one of the largest fiber-based Internet
Protocol and Ethernet networks in the U.S. Concurrently, we entered into a separate agreement to utilize certain wireless spectrum from a wholly-owned subsidiary of XO
Holdings, NextLink, that held XO's millimeter-wave wireless spectrum. The agreement included an option, subject to certain conditions, to acquire NextLink. In February 2017,
we completed our acquisition of XO for total cash consideration of approximately $1.5 billion, of which $100 million was paid in 2015, and we prepaid $320 million in
connection with the NextLink option which represented the fair value of the option.
In April 2017, we exercised our option to buy NextLink for approximately $493 million, subject to certain adjustments, of which $320 million was prepaid in the first quarter of
2017. The transaction closed in January 2018. The acquisition of NextLink was accounted for as an asset acquisition, as substantially all of the value related to the acquired
spectrum. Upon closing, we recorded approximately $657 million of wireless licenses, $110 million of a deferred tax liability and $58 million of other liabilities.
The consolidated financial statements include the results of XO's operations from the date the acquisition closed. If the acquisition of XO had been completed as of January 1,
2016, the results of operations of Verizon would not have been significantly different than our previously reported results of operations.
The acquisition of XO was accounted for as a business combination. The consideration was allocated to the assets acquired and liabilities assumed based on their fair values as of
the close of the acquisition. We recorded approximately $1.2 billion of property, plant and equipment, $120 million of goodwill and $194 million of other intangible assets.
Goodwill is calculated as the difference between the acquisition date fair value of the consideration transferred and the fair value of the net assets acquired. The goodwill
represents future economic benefits that we expect to achieve as a result of the acquisition.
Acquisition of Yahoo! Inc.’s Operating Business
In July 2016, Verizon entered into a stock purchase agreement (the Purchase Agreement) with Yahoo! Inc. (Yahoo). Pursuant to the Purchase Agreement, upon the terms and
subject to the conditions thereof, we agreed to acquire the stock of one or more subsidiaries of Yahoo holding all of Yahoo’s operating business for approximately $4.83 billion
in cash, subject to certain adjustments (the Transaction).
In February 2017, Verizon and Yahoo entered into an amendment to the Purchase Agreement, pursuant to which the Transaction purchase price was reduced by $350 million to
approximately $4.48 billion in cash, subject to certain adjustments. Subject to certain exceptions, the parties also agreed that certain user security and data breaches incurred by
Yahoo (and the losses arising therefrom) were to be disregarded: (1) for purposes of specified conditions to Verizon’s obligations to close the Transaction; and (2) in determining
whether a "Business Material Adverse Effect" under the Purchase Agreement had occurred.
Concurrently with the amendment of the Purchase Agreement, Yahoo and Yahoo Holdings, Inc., a wholly-owned subsidiary of Yahoo that Verizon agreed to purchase pursuant
to the Transaction, also entered into an amendment to the related reorganization agreement, pursuant to which Yahoo (which changed its name to Altaba Inc. following the
closing of the Transaction) retains 50% of certain post-closing liabilities arising out of governmental or third-party investigations, litigations or other claims related to certain
user security and data breaches incurred by Yahoo prior to its acquisition by Verizon, including an August 2013 data breach disclosed by Yahoo on December 14, 2016. At that
time, Yahoo disclosed that more than one billion of the approximately three billion accounts existing in 2013 had likely been affected. In accordance with the original
Transaction agreements, Yahoo will continue to retain 100% of any liabilities arising out of any shareholder lawsuits (including derivative claims) and investigations and actions
by the SEC.
In June 2017, we completed the Transaction. The aggregate purchase consideration at the closing of the Transaction was approximately $4.7 billion, including cash acquired of
$230 million.
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Prior to the closing of the Transaction, pursuant to a related reorganization agreement, Yahoo transferred all of the assets and liabilities constituting Yahoo’s operating business
to the subsidiaries that we acquired in the Transaction. The assets that we acquired did not include Yahoo’s ownership interests in Alibaba, Yahoo! Japan and certain other
investments, certain undeveloped land recently divested by Yahoo, certain non-core intellectual property or its cash, other than the cash from its operating business we
acquired. We received for our benefit and that of our current and certain future affiliates a non-exclusive, worldwide, perpetual, royalty-free license to all of Yahoo’s intellectual
property that was not conveyed with the business.
In October 2017, based upon information that we received in connection with our integration of Yahoo's operating business, we disclosed that we believe that the August 2013
data breach previously disclosed by Yahoo affected all of its accounts.
The acquisition of Yahoo’s operating business has been accounted for as a business combination. The fair values of the assets acquired and liabilities assumed were determined
using the income, cost, market and multiple period excess earnings approaches. The fair value measurements were primarily based on significant inputs that are not observable in
the market and thus represent a Level 3 measurement as defined in Accounting Standards Codification 820, Fair Value Measurements and Disclosures, other than long-term debt
assumed in the acquisition. The income approach was primarily used to value the intangible assets, consisting primarily of acquired technology and customer relationships. The
income approach indicates value for an asset based on the present value of cash flow projected to be generated by the asset. Projected cash flow is discounted at a required rate of
return that reflects the relative risk of achieving the cash flow and the time value of money. The cost approach, which estimates value by determining the current cost of
replacing an asset with another of equivalent economic utility, was used, as appropriate, for property, plant and equipment. The cost to replace a given asset reflects the estimated
reproduction or replacement cost for the property, less an allowance for loss in value due to depreciation.
In June 2018, we finalized the accounting for the Yahoo acquisition. The following table summarizes the final accounting for the assets acquired, including cash acquired of
$230 million, and liabilities assumed as of the close of the acquisition, as well as the fair value at the acquisition date of Yahoo’s noncontrolling interests:
(dollars in millions)
Cash payment to Yahoo’s equity holders
Estimated liabilities to be paid
Total consideration
Assets acquired:
Goodwill
Intangible assets subject to amortization
Property, plant, and equipment
Other
Total assets acquired
Liabilities assumed:
Total liabilities assumed
Net assets acquired:
Noncontrolling interest
Total consideration
(1)
As of December 31, 2017
$
$
4,673 $
38
4,711 $
Measurement-period
adjustments
(1)
— $
—
— $
Adjusted Fair Value
4,673
38
4,711
$
1,929 $
1,873
1,805
1,332
6,939
215 $
1
(6)
128
338
2,144
1,874
1,799
1,460
7,277
2,178
4,761
(50)
$
4,711 $
338
—
—
— $
2,516
4,761
(50)
4,711
Adjustments to the fair value measurements to reflect new information obtained about facts and circumstances that existed as of the acquisition date that, if known, would have
affected the measurement of the amounts recognized as of that date. The most significant adjustments related to an increase in goodwill and the recognition of liabilities per
certain pre-acquisition contingencies.
On the closing date of the Transaction, each unvested and outstanding Yahoo restricted stock unit award that was held by an employee who became an employee of Verizon was
replaced with a Verizon restricted stock unit award, which is generally payable in cash upon the applicable vesting date. The value of those outstanding restricted stock units on
the acquisition date was approximately $1.0 billion.
Goodwill is calculated as the difference between the acquisition date fair value of the consideration transferred and the fair value of the net assets acquired. The goodwill was
primarily attributable to increased synergies that were expected to be achieved from the integration of Yahoo’s operating business into our Media business. The goodwill related
to this acquisition is included within Corporate and other.
The consolidated financial statements include the results of Yahoo’s operating business from the date the acquisition closed. If the acquisition of Yahoo’s operating business had
been completed as of January 1, 2016, the results of operations of Verizon would not have been significantly different than our previously reported results of operations.
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Acquisition and Integration Related Charges
Related to the Yahoo Transaction, we recorded $473 million of acquisition and integration related charges during the year ended December 31, 2018, of which $273 million,
$195 million and an insignificant amount are related to Severance, Integration costs and Transaction costs, respectively. In connection with the Yahoo Transaction, we recorded
acquisition and integration related charges of approximately $762 million during the year ended December 31, 2017, of which $526 million, $166 million and $70 million related
to Severance, Integration costs and Transaction costs, respectively. These charges were recorded in Selling, general and administrative expense in our consolidated statements of
income.
Data Center Sale
In December 2016, we entered into a definitive agreement, which was subsequently amended in March 2017, with Equinix, Inc. (Equinix) pursuant to which we agreed to sell 23
customer-facing data center sites in the U.S. and Latin America for approximately $3.6 billion, subject to certain adjustments (Data Center Sale) . The transaction closed in May
2017.
For the year ended December 31, 2017, these sites generated an insignificant amount of revenues and earnings.
In connection with the Data Center Sale and other insignificant divestitures, we recorded a net gain on sale of divested businesses of approximately $1.8 billion in Selling,
general and administrative expense in our consolidated statement of income for the year ended December 31, 2017.
Straight Path
In May 2017, we entered into a purchase agreement to acquire Straight Path, a holder of millimeter wave spectrum configured for fifth-generation (5G) wireless services, for
total consideration reflecting an enterprise value of approximately $3.1 billion. Under the terms of the purchase agreement, we agreed to pay: (1) Straight Path shareholders
$184.00 per share, payable in Verizon shares; and (2) certain transaction costs payable in cash of approximately $736 million, consisting primarily of a fee to be paid to the FCC.
The transaction closed in February 2018 at which time we issued approximately 49 million shares of Verizon common stock, valued at approximately $2.4 billion, and paid the
associated cash consideration.
The acquisition of Straight Path was accounted for as an asset acquisition, as substantially all of the value related to the acquired spectrum. Upon closing, we recorded
approximately $4.5 billion of wireless licenses and $1.4 billion of a deferred tax liability. The spectrum acquired as part of the transaction is being used for our 5G technology
deployment. See Note 4 for additional information.
WideOpenWest, Inc.
In August 2017, we entered into a definitive agreement to purchase certain fiber-optic network assets in the Chicago market from WideOpenWest, Inc. (WOW!), a leading
provider of communications services. The transaction closed in December 2017. In addition, the parties entered into a separate agreement pursuant to which WOW! was to
complete the build-out of the network assets in 2019. This build-out was completed in 2019. The total cash consideration for the transactions was approximately $275 million, of
which $226 million was paid in December 2017. During 2019 and 2018, the remaining cash consideration was paid.
Other
In July 2019, Verizon completed a sale-leaseback transaction for buildings and real estate. See Note 6 for additional information related to the transaction. In connection with this
transaction and other insignificant transactions, we recorded a pre-tax net gain from dispositions of assets and businesses of $261 million in Selling, general and administrative
expense in our consolidated statement of income for the year ended December 31, 2019.
During 2019, 2018 and 2017, we completed various other acquisitions for an insignificant amount of cash consideration.
Note 4. Wireless Licenses, Goodwill and Other Intangible Assets
Wireless Licenses
The carrying amounts of Wireless licenses are as follows:
(dollars in millions)
At December 31,
Wireless licenses
$
2019
95,059
$
2018
94,130
At December 31, 2019 and 2018, approximately $6.2 billion and $8.6 billion, respectively, of wireless licenses were under development for commercial service for which we
were capitalizing interest costs. We recorded approximately $321 million and $515 million of capitalized interest on wireless licenses for each of the years ended
December 31, 2019 and 2018, respectively.
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For the year ended December 31, 2018, we recorded approximately $4.5 billion of wireless licenses in connection with the Straight Path acquisition and $657 million in
connection with the NextLink acquisition. See Note 3 for additional information regarding spectrum license transactions in 2019 and 2018.
The average remaining renewal period of our wireless license portfolio was 4.6 years as of December 31, 2019. See Note 1 for additional information.
As discussed in Note 1, we test our wireless licenses for potential impairment annually or more frequently if impairment indicators are present. In 2019, we performed a
qualitative assessment to determine whether it was more likely than not that the fair value of our wireless licenses was less than the carrying amount. In 2018, our quantitative
impairment test consisted of comparing the estimated fair value of our aggregate wireless licenses estimated using the Greenfield approach to the aggregated carrying amount of
the licenses as of the test date. In 2017, we performed a qualitative assessment to determine whether it was more likely than not that the fair value of our wireless licenses was
less than the carrying amount. Our assessments in 2019, 2018 and 2017 indicated that the fair value of our wireless licenses exceeded the carrying value and, therefore, did not
result in impairment.
Goodwill
The Company transitioned into our new reporting structure as of April 1, 2019, which resulted in certain changes to our operating segments and reporting units. Upon the date of
reorganization, the goodwill of our historical Wireless reporting unit, historical Wireline reporting unit and historical Verizon Connect reporting unit were reallocated to our new
Consumer and Business reporting units using a relative fair value approach.
Changes in the carrying amount of Goodwill are as follows:
(dollars in millions)
Consumer
Balance at January 1, 2018
Acquisitions (Note 3)
Reclassifications, adjustments and other
Media goodwill impairment
Balance at December 31, 2018
Acquisitions
Reclassifications, adjustments and other
Balance at March 31, 2019
Reporting Unit reallocation
(1)
Balance at April 1, 2019
Acquisitions
Media goodwill impairment
Reclassifications, adjustments and other
Balance at December 31, 2019
$
$
—
—
—
—
—
—
—
—
17,104
17,104
—
—
—
17,104
$
$
Business
—
—
—
—
—
—
—
—
7,269
7,269
2
—
(2)
7,269
$
$
Wireless
18,397
—
—
—
18,397
—
—
18,397
(18,397)
—
—
$
Wireline
3,955
(77)
(7)
—
3,871
20
1
3,892
(3,892)
—
—
—
—
$
—
$
$
Other
(2)
6,820
225
(108)
(4,591)
2,346
—
—
2,346
(2,084)
262
—
(186)
(60)
16
$
$
Total
29,172
148
(115)
(4,591)
24,614
20
1
24,635
—
24,635
2
(186)
(62)
24,389
—
—
—
(1)
(2)
Represents the reallocation of goodwill as a result of the Company reorganizing its segments as described in Note 1.
Goodwill is net of accumulated impairment charges of $4.6 billion as of December 31, 2018 and $4.8 billion as of December 31, 2019, related to our Media reporting unit.
We performed impairment assessments of the impacted reporting units, specifically our historical Wireless, historical Wireline and historical Connect reporting units on
March 31, 2019, immediately before our strategic reorganization became effective. Our impairment assessments indicated that the fair value for each of our historical Wireless,
historical Wireline and historical Connect reporting units exceeded their respective carrying values, and therefore did not result in a goodwill impairment. We then performed
quantitative assessments of our Consumer and Business reporting units on April 1, 2019, immediately following our strategic reorganization. Our impairment assessments
indicated that the fair value for each of our Consumer and Business reporting units exceeded their respective carrying values and therefore, did not result in a goodwill
impairment. Our Media reporting unit was not impacted by the strategic reorganization and there was no indicator of impairment as of the reorganization date.
We performed qualitative impairment assessments for our Consumer and Business reporting units during the fourth quarter of 2019. Our qualitative assessments indicated that it
was more likely than not that the fair values for our Consumer and Business reporting units exceeded their respective carrying values and, therefore, did not result in an
impairment. We performed quantitative impairment assessments for our Media reporting unit in 2019 and 2018. For details on our Media reporting unit, refer to the discussion
below.
Our Media business, Verizon Media, experienced increased competitive and market pressures throughout 2018 that resulted in lower than expected revenues and earnings. These
pressures were expected to continue and have resulted in a loss of market positioning to our competitors in the digital advertising business. Our Media business also achieved
lower than expected benefits from the integration of the Yahoo and AOL businesses.
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In connection with Verizon’s annual budget process during the fourth quarter of 2019 and 2018, the leadership at both Verizon Media and Verizon completed a comprehensive
five-year strategic planning review of Verizon Media's business prospects resulting in unfavorable adjustments to Verizon Media's financial projections. These revised
projections were used as a key input into Verizon Media's annual goodwill impairment tests performed in the fourth quarter of 2019 and 2018.
During the fourth quarter of 2019 and 2018, consistent with our accounting policy, we applied a combination of a market approach and a discounted cash flow method reflecting
current assumptions and inputs, including our revised projections, discount rate and expected growth rates, which resulted in the determination that the fair value of the Media
reporting unit was less than its carrying amount. As a result, we recorded a non-cash goodwill impairment charge of approximately $186 million ($176 million after-tax) in the
fourth quarter of 2019 and a charge of $4.6 billion ($4.5 billion after-tax) in the fourth quarter of 2018 in our consolidated statements of income. The goodwill balance of the
Media reporting unit has been fully written off as a result of these impairment charges.
We performed a quantitative impairment assessment for all of the other reporting units in 2018. Our impairment tests indicated that the fair value for each of our historical
Wireless, historical Wireline and historical Connect reporting units exceeded their respective carrying value and, therefore, did not result in an impairment.
For 2017, we performed a quantitative impairment assessment for all of our reporting units, except for our historical Wireless reporting unit, for which a qualitative assessment
was completed. For 2017, our impairment tests indicated that the fair value for each of our reporting units exceeded their respective carrying value and therefore, did not result in
goodwill impairment.
Other Intangible Assets
The following table displays the composition of Other intangible assets, net as well as the respective amortization period:
(dollars in millions)
2019
At December 31,
Customer lists (8 to 13 years)
Non-network internal-use software (3
to 7 years)
Other (2 to 25 years)
Total
$
$
Gross
Amount
3,896
20,530
1,967
26,393
$
$
Accumulated
Amortization
(1,511)
(14,418)
(966)
(16,895)
$
$
Net
Amount
2,385
6,112
1,001
9,498
$
$
Gross
Amount
3,951
18,603
1,988
24,542
$
$
Accumulated
Amortization
(1,121)
(12,785)
(861)
(14,767)
$
$
2018
Net
Amount
2,830
5,818
1,127
9,775
The amortization expense for Other intangible assets was as follows:
Years
2019
2018
2017
Estimated annual amortization expense for Other intangible assets is as follows:
Years
2020
2021
2022
2023
2024
$
(dollars in millions)
2,235
1,931
1,651
1,317
968
$
(dollars in millions)
2,311
2,217
2,213
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Note 5. Property, Plant and Equipment
The following table displays the details of Property, plant and equipment, which is stated at cost:
(dollars in millions)
At December 31,
Land
Buildings and equipment
Central office and other network equipment
Cable, poles and conduit
Leasehold improvements
Work in progress
Furniture, vehicles and other
Less accumulated depreciation
Property, plant and equipment, net
$
Lives (years)
-
7 to 45
3 to 50
7 to 50
5 to 20
-
3 to 20
$
2019
594
31,216
152,733
52,658
9,072
9,234
10,227
265,734
173,819
91,915
$
$
2018
807
30,468
147,250
49,859
8,580
6,362
9,509
252,835
163,549
89,286
Note 6. Leasing Arrangements
We enter into various lease arrangements for network equipment including towers, distributed antenna systems, small cells, real estate and connectivity mediums including dark
fiber, equipment, and other various types of assets for use in our operations. Our leases have remaining lease terms ranging from 1 year to 28 years, some of which include
options that we can elect to extend the leases term for up to 25 years, and some of which include options to terminate the leases. For the majority of leases entered into during the
current period, we have concluded it is not reasonably certain that we would exercise the options to extend the lease or terminate the lease. Therefore, as of the lease
commencement date, our lease terms generally do not include these options. We include options to extend the lease when it is reasonably certain that we will exercise that option.
During March 2015, we completed a transaction with American Tower Corporation (American Tower) pursuant to which American Tower acquired the exclusive rights to lease
and operate approximately 11,300 of our wireless towers for an upfront payment of $5.0 billion. We have subleased capacity on the towers from American Tower for a minimum
of 10 years at current market rates in 2015, with options to renew. We continue to include the towers in Property, plant and equipment, net in our consolidated balance sheets and
depreciate them accordingly. In addition to the rights to lease and operate the towers, American Tower assumed the interest in the underlying ground leases related to these
towers. While American Tower can renegotiate the terms of and is responsible for paying the ground leases, we are still the primary obligor for these leases and accordingly, the
present value of these ground leases are included in our operating lease right-of-use assets and operating lease liabilities. We do not expect to be required to make ground lease
payments unless American Tower defaults, which we determined to be remote.
The components of net lease cost were as follows:
(dollars in millions)
Year Ended December 31,
Operating lease cost
(1)
Finance lease cost:
Amortization of right-of-use assets
Interest on lease liabilities
Short-term lease cost
Variable lease cost
(1)
Sublease income
Total net lease cost
(1)
Classification
Cost of services
Selling, general and administrative expense
Depreciation and amortization expense
Interest expense
Cost of services
Selling, general and administrative expense
Cost of services
Selling, general and administrative expense
Service revenues and other
$
$
2019
4,746
330
38
40
218
(275)
5,097
(1)
Gain on sale and leaseback transaction, net
Selling, general and administrative expense
$
(391)
All operating lease costs, including short-term and variable lease costs, are split between Cost of services and Selling, general and administrative expense in the consolidated
statements of income based on the use of the facility or equipment that the rent is being paid on. See Note 1 for additional information. Variable lease costs represent payments
that are dependent on a rate or index, or on usage of the asset.
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Supplemental disclosure for the statement of cash flows related to operating and finance leases were as follows:
(dollars in millions)
Year Ended December 31,
Cash Flows from Operating Activities
Cash paid for amounts included in the measurement of lease liabilities
Operating cash flows for operating leases
Operating cash flows for finance leases
Cash Flows from Financing Activities
Financing cash flows for finance leases
Supplemental lease cash flow disclosures
Operating lease right-of-use assets obtained in exchange for new operating lease liabilities
Right-of-use assets obtained in exchange for new finance lease liabilities
Supplemental disclosures for the balance sheet related to finance leases were as follows:
(dollars in millions)
At December 31,
Assets
Property, plant and equipment, net
Liabilities
Debt maturing within one year
Long-term debt
Total Finance lease liabilities
$
$
336
780
1,116
$
939
2019
3,510
564
(352)
$
(4,392)
(38)
2019
The weighted-average remaining lease term and the weighted-average discount rate of our leases were as follows:
At December 31,
Weighted-average remaining lease term (years)
Operating Leases
Finance Leases
Weighted-average discount rate
Operating Leases
Finance Leases
The Company's maturity analysis of operating and finance lease liabilities as of December 31, 2019 were as follows:
(dollars in millions)
Years
2020
2021
2022
2023
2024
Thereafter
Total lease payments
Less interest
Present value of lease liabilities
Less current obligation
Long-term obligation at December 31, 2019
$
$
Operating Leases
4,099
3,764
3,363
3,001
2,484
9,257
25,968
4,314
21,654
3,261
18,393
$
$
Finance Leases
366
271
208
152
92
124
1,213
97
1,116
336
780
4.0%
3.2%
9
5
2019
As of December 31, 2019, we have contractually obligated lease payments amounting to $1.9 billion for office facility operating leases and small cell colocation and fiber
operating leases that have not yet commenced. We have legally obligated lease payments for various other operating leases that have not yet commenced for which the total
obligation was not significant. We have certain rights and obligations for these leases, but have not recognized an operating lease right-of-use asset or an operating lease liability
since they have not yet commenced.
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Real Estate Transaction
On July 23, 2019, Verizon completed a sale-leaseback transaction for buildings and real estate. We received total gross proceeds of approximately $1.0 billion. We leased back a
portion of the buildings and real estate sold and accounted for it as an operating lease. The term of the leaseback is for two years with four options to renew for an additional
three months each. The proceeds received as a result of this transaction have been classified in Other, net within Cash Flows from Investing Activities in our consolidated
statement of cash flows for the year ended December 31, 2019. The net gain as a result of this transaction is included in the components of net lease cost table above.
Disclosures Related to Periods Prior to Adoption of Topic 842
Total rent expense under operating leases amounted to $4.1 billion in 2018 and $3.8 billion in 2017.
Amortization of capital leases was included in Depreciation and amortization expense in the consolidated statements of income. Capital lease amounts included in Property, plant
and equipment were as follows:
(dollars in millions)
At December 31,
Capital leases
Less accumulated amortization
Total
$
$
2018
1,756
998
758
Note 7. Debt
Outstanding long-term debt obligations as of December 31, 2019 and 2018 are as follows:
(dollars in millions)
At December 31,
Verizon Communications
Maturities
2019-2024
2025-2029
2030-2055
2019-2024
2025-2029
Alltel Corporation
Operating telephone company subsidiaries—debentures
2025-2029
2030-2055
2019-2024
2025-2029
2030-2055
GTE LLC
Other subsidiaries—asset-backed debt
Finance lease obligations (average rate of 3.2% and 4.1% in 2019 and 2018,
respectively)
Unamortized discount, net of premium
Unamortized debt issuance costs
Total long-term debt, including current maturities
Less long-term debt maturing within one year
Total long-term debt
Total long-term debt, including current maturities
Plus short-term notes payable
Total debt
(1)
The
Interest
Rates %
1.38 – 5.51
1.38 – 6.80
2.65 – 8.95
Floating
Floating
6.80
7.88
7.88 – 8.00
6.00 – 8.38
5.13 – 8.75
8.75
6.94
1.42 – 3.56
Floating
(1)
(1)
(1)
2019
$
19,885
30,038
47,777
2,210
1,789
38
58
141
286
339
141
250
8,116
4,277
1,116
(4,480)
(492)
111,489
10,777
$
$
$
100,712
111,489
—
111,489
$
$
$
$
2018
24,242
23,711
54,662
2,868
1,789
116
118
147
288
361
178
266
7,962
2,139
905
(6,298)
(541)
112,913
7,040
105,873
112,913
150
113,063
2019-2024
2025-2029
2019-2024
2019-2024
debt obligations bore interest at a floating rate based on the London Interbank Offered Rate (LIBOR) plus an applicable interest margin per annum.
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Maturities of long-term debt (secured and unsecured) outstanding, including current maturities, excluding unamortized debt issuance costs, at December 31, 2019 are as follows:
Years
2020
2021
2022
2023
2024
Thereafter
$
(dollars in millions)
10,470
7,269
9,162
5,591
4,212
74,161
During 2019, we received $18.7 billion of proceeds from long-term borrowings, which included $8.6 billion of proceeds from asset-backed debt transactions. The net proceeds
were used for general corporate purposes including the repayment of debt. We used $23.9 billion of cash to repay, redeem and repurchase long-term borrowings and finance
lease obligations, including $6.3 billion to prepay and repay asset-backed, long-term borrowings.
During 2018, we received $10.8 billion of proceeds from long-term borrowings, which included $4.8 billion of proceeds from asset-backed debt transactions. The net proceeds
were used for general corporate purposes including the repayment of debt. We used $14.6 billion of cash to repay, redeem and repurchase long-term borrowings and finance
lease obligations, including $3.6 billion to prepay and repay asset-backed, long-term borrowings.
2019 Significant Debt Transactions
The following tables show the significant transactions involving the senior unsecured debt securities of Verizon and its subsidiaries that occurred during the year ended
December 31, 2019.
Exchange Offers
(dollars in millions)
Verizon 1.750% - 5.150% notes and floating rate notes, due 2021 - 2025
GTE LLC 8.750% debentures, due 2021
Verizon 4.016% notes due 2029
(1)
Total
(1)
Principal Amount
Exchanged
$
3,892
21
—
$
3,913
$
$
Principal Amount Issued
—
—
4,000
4,000
The principal amount issued in exchange does not include either an insignificant amount of cash paid in lieu of the issuance of fractional new notes or accrued and unpaid
interest paid on the old notes accepted for exchange to the date of exchange.
Tender Offers
(dollars in millions)
Verizon 4.672% - 5.012% notes due 2054 - 2055
Verizon 3.850% - 6.550% notes due 2039 - 2055
Verizon and other subsidiaries 5.050% - 8.950% notes and debentures due 2021 - 2041
Total
(1)
Principal Amount
Purchased
$
4,500
3,816
593
$
8,909
$
$
Cash Consideration
(1)
5,030
4,828
837
10,695
The total cash consideration includes the tender offer consideration, plus any accrued and unpaid interest to the date of purchase.
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Redemptions, Repurchases and Repayments
(dollars in millions)
Verizon 5.900% notes due 2054
Verizon 1.375% notes due 2019
Verizon 1.750% notes due 2021
Verizon 3.000% notes due 2021
Verizon 3.500% notes due 2021
Verizon 2.625% notes due 2020
Verizon 3.500% notes due 2021
Verizon floating rate (LIBOR + 0.770%) notes due 2019
Verizon 4.200% notes due 2046
Verizon floating rate (LIBOR + 0.370%) notes due 2019
Verizon 2.600% - 4.300% Internotes due 2022 - 2029
Open market repurchases of various Verizon notes
Total
(1)
Percentages
Principal Redeemed/
Repurchased/ Repaid
$
500
206
621
930
315
831
736
229
2,059
306
201
543
$
7,477
Amount Paid as % of
Principal
(1)
100.000%
100.000%
100.000%
101.061%
102.180%
100.037%
102.238%
100.000%
100.000%
100.000%
100.000%
Various
represent price paid to redeem, repurchase and repay.
In February 2020, we redeemed, in whole, approximately $1.5 billion aggregate principal amount of 4.95% Notes due 2047.
Issuances
(dollars in millions)
Verizon 3.875% notes due 2029
(2)
Verizon 5.000% notes due 2051
Verizon 0.875% notes due 2027
Verizon 1.250% notes due 2030
Verizon 2.500% notes due 2031
Verizon 0.875% notes due 2032
Verizon 1.500% notes due 2039
Verizon 1.875% notes due 2030
Verizon 2.100% notes due 2026
Verizon 2.650% notes due 2030
Verizon 3.500% notes due 2039
Total
(1)
(2)
Principal Amount Issued
$
$
€
€
£
€
€
£
A$
A$
A$
1,000
510
1,250
1,250
500
800
500
550
450
300
500
$
$
Net Proceeds
(1)
994
506
1,391
1,385
647
882
545
672
307
205
341
7,875
Net proceeds were net of discount and issuance costs.
An amount equal to the net proceeds from this green bond will be used to fund, in whole or in part, "Eligible Green Investments." "Eligible Green Investments" include new
and existing investments made by us during the period from two years prior to the issuance of the green bond through the maturity date of the green bond, in the following
categories: (1) renewable energy; (2) energy efficiency; (3) green buildings; (4) sustainable water management; and (5) biodiversity and conservation.
Short-Term Borrowing and Commercial Paper Program
In July 2018, we entered into a short-term uncommitted credit facility with the ability to borrow up to $700 million. As of December 31, 2019 and 2018, there was no
outstanding balance.
As of December 31, 2019 and 2018, we had no commercial paper outstanding.
Asset-Backed Debt
As of December 31, 2019, the carrying value of our asset-backed debt was $12.4 billion. Our asset-backed debt includes Asset-Backed Notes (ABS Notes) issued to third-party
investors (Investors) and loans (ABS Financing Facilities) received from banks and their conduit facilities (collectively, the Banks). Our consolidated asset-backed debt
bankruptcy remote legal entities (each, an ABS Entity or collectively, the ABS Entities) issue the debt or are otherwise party to the transaction documentation in connection with
our asset-backed debt transactions. Under the terms of our asset-backed debt, Cellco Partnership (Cellco) and certain other affiliates of Verizon (collectively, the Originators)
transfer device payment plan agreement receivables to one of the ABS Entities, which in turn transfers such receivables to another ABS Entity that issues the debt. Verizon
entities retain the equity interests in the ABS Entities, which represent the rights to all funds not needed to make required payments on the asset-backed debt and other related
payments and expenses.
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Our asset-backed debt is secured by the transferred device payment plan agreement receivables and future collections on such receivables. The device payment plan agreement
receivables transferred to the ABS Entities and related assets, consisting primarily of restricted cash, will only be available for payment of asset-backed debt and expenses related
thereto, payments to the Originators in respect of additional transfers of device payment plan agreement receivables, and other obligations arising from our asset-backed debt
transactions, and will not be available to pay other obligations or claims of Verizon’s creditors until the associated asset-backed debt and other obligations are satisfied. The
Investors or Banks, as applicable, which hold our asset-backed debt have legal recourse to the assets securing the debt, but do not have any recourse to Verizon with respect to
the payment of principal and interest on the debt. Under a parent support agreement, Verizon has agreed to guarantee certain of the payment obligations of Cellco and the
Originators to the ABS Entities.
Cash collections on the device payment plan agreement receivables collateralizing our asset-backed debt securities are required at certain specified times to be placed into
segregated accounts. Deposits to the segregated accounts are considered restricted cash and are included in Prepaid expenses and other, and Other assets in our consolidated
balance sheets.
Proceeds from our asset-backed debt transactions are reflected in Cash flows from financing activities in our consolidated statements of cash flows. The asset-backed debt issued
and the assets securing this debt are included in our consolidated balance sheets.
ABS Notes
During the year ended December 31, 2019, we completed the following ABS Notes transactions:
Expected Weighted-
average Life to
Maturity (in years)
2.50
(1)
(dollars in millions)
March 2019
A-1a Senior class notes
A-1b Senior floating rate class notes
B Junior class notes
C Junior class notes
March 2019 total
June 2019
A-1a Senior class notes
A-1b Senior floating rate class notes
B Junior class notes
C Junior class notes
June 2019 total
October 2019
A-1a Senior class notes
A-1b Senior floating rate class notes
B Junior class notes
C Junior class notes
October 2019 total
Total
(1)
Interest Rates %
2.930
LIBOR + 0.330
3.020
3.220
Principal Amount
Issued
$
900
100
69
53
1,122
2.50
3.22
3.40
2.330
LIBOR + 0.450
2.400
2.600
(1)
2.52
2.52
3.28
3.47
855
145
69
53
1,122
1.940
LIBOR + 0.420
2.060
2.160
(1)
2.51
2.51
3.23
3.41
$
1,276
150
98
76
1,600
3,844
The one-month LIBOR at December 31, 2019 was 1.763%.
Under the terms of each series of ABS Notes, there is a two year revolving period during which we may transfer additional receivables to the ABS Entity. In April, July and
November 2019, the two year revolving period of the ABS Notes we issued in March, June and October 2017, respectively, ended, and we began to repay principal on the 2017-
1, 2017-2 and 2017-3 Class A senior ABS Notes. In October 2019, in connection with an optional acquisition of receivables and redemption of 2016-1 Notes, we made a
principal payment, in whole, for an insignificant amount. During the year ended December 31, 2019, we made aggregate principal repayments of $3.3 billion, for all ABS Notes.
In January 2020, we issued $1.6 billion aggregate principal amount of senior and junior Asset-Backed Notes through an ABS Entity.
ABS Financing Facility
In May 2018, we entered into an ABS financing facility with a number of financial institutions (2018 ABS Financing Facility). One loan agreement was entered into in
connection with the 2018 ABS Financing Facility. In May 2019, the $540 million outstanding under the loan agreement was prepaid, and the loan agreement was terminated.
In September 2016, we entered into an ABS financing facility with a number of financial institutions (2016 ABS Financing Facility). Two loan agreements were entered into in
connection with the 2016 ABS Financing Facility in September 2016 and May 2017. In April and May 2019, we paid off both the 2016 and 2017 loans for an aggregate of $671
million, and the loan agreements were terminated.
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In May 2019, the 2016 ABS Financing Facility was amended and restated (2019 ABS Financing Facility). Under the terms of the 2019 ABS Financing Facility, which is an
uncommitted facility, the financial institutions make advances under asset-backed loans backed by device payment plan agreement receivables of both consumer and business
customers. One loan agreement was entered into in connection with the 2019 ABS Financing Facility. The 2019 loan agreement has a final maturity date in May 2023 and bears
interest at floating rates. There is a one year revolving period until May 2020, which may be extended with the approval of the financial institutions. Under the 2019 loan
agreement, we have the right to prepay all or a portion of the advances at any time without penalty, but in certain cases, with breakage costs. Subject to certain conditions, we
may also remove receivables from the ABS Entity. In May 2019, we borrowed $1.8 billion under the 2019 loan agreement. In August 2019, we prepaid $1.5 billion of the loan
made in May 2019 under the 2019 loan agreement. In November 2019, we borrowed an additional $1.5 billion under the 2019 loan agreement. In December 2019, the 2019 loan
agreement was amended to increase the facility by an additional $1.5 billion, and an additional $1.5 billion was borrowed under the 2019 loan agreement. The aggregate
outstanding balance under the 2019 ABS Financing Facility was $3.3 billion as of December 31, 2019. In January 2020, we prepaid $1.3 billion of the loan under the 2019 loan
agreement.
Variable Interest Entities
The ABS Entities meet the definition of a VIE for which we have determined that we are the primary beneficiary as we have both the power to direct the activities of the entity
that most significantly impact the entity’s performance and the obligation to absorb losses or the right to receive benefits of the entity. Therefore, the assets, liabilities and
activities of the ABS Entities are consolidated in our financial results and are included in amounts presented on the face of our consolidated balance sheets.
The assets and liabilities related to our asset-backed debt arrangements included in our consolidated balance sheets were as follows:
At December 31,
(dollars in millions)
Assets
Accounts receivable, net
Prepaid expenses and other
Other assets
Liabilities
Accounts payable and accrued liabilities
Debt maturing within one year
Long-term debt
11
5,578
6,791
7
5,352
4,724
$
10,525
1,180
3,856
$
8,861
989
2,725
2019
At December 31,
2018
See Note 8 for additional information on device payment plan agreement receivables used to secure asset-backed debt.
Long-Term Credit Facilities
At December 31, 2019
(dollars in millions)
Verizon revolving credit facility
(1)
Various export credit facilities
(2)
Total
(1)
Maturities
2022
2022-2027
$
$
Facility Capacity
9,500
5,500
15,000
$
$
Unused Capacity
9,390
—
9,390
$
Principal Amount
Outstanding
N/A
4,471
4,471
The revolving credit facility does not require us to comply with financial covenants or maintain specified credit ratings, and it permits us to borrow even if our business has
incurred a material adverse change. The revolving credit facility provides for the issuance of letters of credit.
(2)
During 2019 and 2018, we drew down $1.5 billion and $3.0 billion from these facilities, respectively. We use these credit facilities to finance equipment-related purchases.
Non-Cash Transaction
During the years ended December 31, 2019, 2018 and 2017, we financed, primarily through vendor financing arrangements, the purchase of approximately $563 million, $1.1
billion, and $501 million, respectively, of long-lived assets consisting primarily of network equipment. At both December 31, 2019 and 2018, $1.1 billion relating to these
financing arrangements, including those entered into in prior years and liabilities assumed through acquisitions, remained outstanding. These purchases are non-cash financing
activities and therefore are not reflected within Capital expenditures in our consolidated statements of cash flows.
Early Debt Redemptions
During 2019, 2018 and 2017, we recorded losses on early debt redemptions of $3.7 billion, $681 million, and $2.0 billion, respectively.
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We recognize losses on early debt redemptions in Other income (expense), net, in our consolidated statements of income. The total losses are reflected as an adjustment to
reconcile net income to Net cash used in operating activities and the portion of the losses representing cash payments are reflected within Net cash used in financing activities in
our consolidated statements of cash flows.
Guarantees
We guarantee the debentures of our operating telephone company subsidiaries. As of December 31, 2019, $765 million aggregate principal amount of these obligations remained
outstanding. Each guarantee will remain in place for the life of the obligation unless terminated pursuant to its terms, including the operating telephone company no longer being
a wholly-owned subsidiary of Verizon.
We also guarantee the debt obligations of GTE LLC as successor in interest to GTE Corporation that were issued and outstanding prior to July 1, 2003. As of
December 31, 2019, $391 million aggregate principal amount of these obligations remain outstanding.
Debt Covenants
We and our consolidated subsidiaries are in compliance with all of our restrictive covenants in our debt agreements.
Note 8. Wireless Device Payment Plans
Under the Verizon device payment program, our eligible wireless customers purchase wireless devices under a device payment plan agreement. Customers that activate service
on devices purchased under the device payment program pay lower service fees as compared to those under our fixed-term service plans, and their device payment plan charge is
included on their wireless monthly bill. As of January 2017, we no longer offer Consumer customers new fixed-term, subsidized service plans for phones; however, we continue
to offer subsidized plans to our Business customers. We also continue to service existing plans for customers who have not yet purchased and activated devices under the
Verizon device payment program.
Wireless Device Payment Plan Agreement Receivables
The following table displays device payment plan agreement receivables, net, that are recognized in our consolidated balance sheets:
(dollars in millions)
At December 31,
Device payment plan agreement receivables, gross
Unamortized imputed interest
Device payment plan agreement receivables, net of unamortized imputed interest
Allowance for credit losses
Device payment plan agreement receivables, net
Classified in our consolidated balance sheets:
Accounts receivable, net
Other assets
Device payment plan agreement receivables, net
$
$
13,045
5,522
18,567
$
$
12,624
5,546
18,170
$
$
2019
19,493
(454)
19,039
(472)
18,567
$
$
2018
19,313
(546)
18,767
(597)
18,170
Included in our device payment plan agreement receivables, net at December 31, 2019 and December 31, 2018, are net device payment plan agreement receivables of $14.3
billion and $11.5 billion, respectively, which have been transferred to ABS Entities and continue to be reported in our consolidated balance sheets. See Note 7 for additional
information. We believe the carrying value of our installment loans receivables approximate their fair value using a Level 3 expected cash flow model.
We may offer certain promotions that allow a customer to trade in their owned device in connection with the purchase of a new device. Under these types of promotions, the
customer receives a credit for the value of the trade-in device. In addition, we may provide the customer with additional future credits that will be applied against the customer’s
monthly bill as long as service is maintained. We recognize a liability for the customer's right to trade-in the device measured at fair value, which is determined by considering
several factors, including the weighted-average selling prices obtained in recent resales of similar devices eligible for trade-in. Future credits are recognized when earned by the
customer. Device payment plan agreement receivables, net does not reflect the trade-in device liability. At December 31, 2019 and December 31, 2018, the amount of trade-in
liability was $103 million and $64 million, respectively.
From time to time, we offer certain marketing promotions that allow our customers to upgrade to a new device after paying down a certain specified portion of the required
device payment plan agreement amount, as well as trading in their device in good working order. When a customer enters into a device payment plan agreement with the right to
upgrade to a new device, we account for this trade-in right as a guarantee obligation.
For indirect channel wireless contracts with customers, we impute risk adjusted interest on the device payment plan agreement receivables. We record the imputed interest as a
reduction to the related accounts receivable. Interest income, which is included within Service revenues and
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other in our consolidated statements of income, is recognized over the financed device payment term. See Note 2 for additional information on financing considerations with
respect to wireless direct channel contracts with customers.
When originating device payment plan agreements for Consumer customers, we use internal and external data sources to create a credit risk score to measure the credit quality of
a customer and to determine eligibility for the device payment program. If a customer is either new to Verizon or has 45 days or less of customer tenure with Verizon, the credit
decision process relies more heavily on external data sources. If the customer has more than 45 days of customer tenure with Verizon (an existing customer), the credit decision
process relies on a combination of internal and external data sources. External data sources include obtaining a credit report from a national consumer credit reporting agency, if
available. Verizon uses its internal data and/or credit data obtained from the credit reporting agencies to create a custom credit risk score. The custom credit risk score is
generated automatically (except with respect to a small number of applications where the information needs manual intervention) from the applicant’s credit data using Verizon’s
proprietary custom credit models, which are empirically derived and demonstrably and statistically sound. The credit risk score measures the likelihood that the potential
customer will become severely delinquent and be disconnected for non-payment. For a small portion of new customer applications, a traditional credit report is not available
from one of the national credit reporting agencies because the potential customer does not have sufficient credit history. In those instances, alternate credit data is used for the
risk assessment.
Based on the custom credit risk score, we assign each customer to a credit class, each of which has specified offers of credit including an account level spending limit and either
a maximum amount of credit allowed per device or a required down payment percentage. During the fourth quarter of 2018, Verizon moved all Consumer customers, new and
existing, from a required down payment percentage, between zero and 100%, to a maximum amount of credit per device.
Subsequent to origination, Verizon monitors delinquency and write-off experience as key credit quality indicators for its portfolio of device payment plan agreements and fixed-
term service plans. The extent of our collection efforts with respect to a particular customer are based on the results of proprietary custom empirically derived internal behavioral
scoring models that analyze the customer’s past performance to predict the likelihood of the customer falling further delinquent. These customer scoring models assess a number
of variables, including origination characteristics, customer account history and payment patterns. Based on the score derived from these models, accounts are grouped by risk
category to determine the collection strategy to be applied to such accounts. We continuously monitor collection performance results and the credit quality of our device payment
plan agreement receivables based on a variety of metrics, including aging. Verizon considers an account to be delinquent and in default status if there are unpaid charges
remaining on the account on the day after the bill’s due date.
The balance and aging of the device payment plan agreement receivables on a gross basis were as follows:
(dollars in millions)
At December 31,
Unbilled
Billed:
Current
Past due
Device payment plan agreement receivables, gross
$
1,002
288
19,493
$
986
284
19,313
$
2019
18,203
$
2018
18,043
Activity in the allowance for credit losses for the device payment plan agreement receivables was as follows:
(dollars in millions)
2019
Balance at January 1,
Bad debt expense
Write-offs
Balance at December 31,
$
$
597
915
(1,040)
472
$
$
2018
848
459
(710)
597
Sales of Wireless Device Payment Plan Agreement Receivables
In 2015 and 2016, we established programs pursuant to a Receivables Purchase Agreement (RPA) to sell from time to time, on an uncommitted basis, eligible device payment
plan agreement receivables to a group of primarily relationship banks (Purchasers) on both a revolving and non-revolving basis, collectively the Programs. Under the Programs,
eligible device payment plan agreement receivables were transferred to the Purchasers for upfront cash proceeds and additional consideration upon settlement of the receivables,
referred to as the deferred purchase price. In December 2017, the RPA and all other related transaction documents were terminated and as of December 31, 2017 we had no
further continuing involvement with any of the receivables sold under the RPA program.
There were no sales of device payment plan agreement receivables under the Programs during 2017.
Deferred Purchase Price
Collections of deferred purchase price were $1.4 billion during 2017. During 2017, we repurchased all outstanding receivables previously sold to the Purchasers in exchange for
the obligation to pay the associated deferred purchase price to the wholly-owned subsidiaries that were bankruptcy remote special purpose entities (Sellers). At
December 31, 2017, our deferred purchase price receivable was fully satisfied. Collections
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following the repurchase of receivables were insignificant, $195 million and $238 million during 2019, 2018 and 2017, respectively. Collections of both deferred purchase price
and repurchased receivables were recorded in Cash flows used in investing activities in our consolidated statement of cash flows.
Note 9. Fair Value Measurements and Financial Instruments
Recurring Fair Value Measurements
The following table presents the balances of assets and liabilities measured at fair value on a recurring basis as of December 31, 2019:
(dollars in millions)
Level 1
(1)
Assets:
Other assets:
Fixed income securities
Interest rate swaps
Cross currency swaps
Foreign exchange forwards
Total
Liabilities:
Other liabilities:
Interest rate swaps
Cross currency swaps
Forward starting interest rate swaps
Total
$
$
—
—
—
—
$
$
173
912
604
1,689
$
$
—
—
—
—
$
$
173
912
604
1,689
$
$
—
—
—
—
—
$
$
442
568
211
5
1,226
$
$
—
—
—
—
—
$
$
442
568
211
5
1,226
Level 2
(2)
Level 3
(3)
Total
The following table presents the balances of assets and liabilities measured at fair value on a recurring basis as of December 31, 2018:
(dollars in millions)
Level 1
Assets:
Other assets:
Fixed income securities
Interest rate swaps
Cross currency swaps
Interest rate caps
Total
Liabilities:
Other liabilities:
Interest rate swaps
Cross currency swaps
Forward starting interest rate swaps
Interest rate caps
Total
(1)
(2)
(1)
Level 2
(2)
Level 3
(3)
Total
$
—
—
—
—
$
405
3
220
14
$
—
—
—
—
$
405
3
220
14
$
—
$
642
$
—
$
642
$
—
—
—
—
$
813
536
60
4
$
—
—
—
—
$
813
536
60
4
$
—
$
1,413
$
—
$
1,413
Quoted prices in active markets for identical assets or liabilities
Observable inputs other than quoted prices in active markets for identical assets and liabilities
(3)
Unobservable pricing inputs in the market
Certain of our equity investments do not have readily determinable fair values and are excluded from the tables above. Such investments are measured at cost, less any
impairment, plus or minus changes resulting from observable price changes in orderly transactions for an identical or similar investment of the same issuer and are included in
Investments in unconsolidated businesses in our consolidated balance sheets. As of December 31, 2019 and December 31, 2018, the carrying amount of our investments without
readily determinable fair values was $284 million and $248 million, respectively. During 2019, there were insignificant adjustments due to observable price changes and we
recognized an insignificant impairment charge. Cumulative adjustments due to observable price changes and impairment charges were insignificant.
Fixed income securities consist primarily of investments in municipal bonds. For fixed income securities that do not have quoted prices in active markets, we use alternative
matrix pricing resulting in these debt securities being classified as Level 2.
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Derivative contracts are valued using models based on readily observable market parameters for all substantial terms of our derivative contracts and thus are classified within
Level 2. We use mid-market pricing for fair value measurements of our derivative instruments. Our derivative instruments are recorded on a gross basis.
We recognize transfers between levels of the fair value hierarchy as of the end of the reporting period. There were no transfers between Level 1 and Level 2 during 2019 and
2018.
Fair Value of Short-term and Long-term Debt
The fair value of our debt is determined using various methods, including quoted prices for identical terms and maturities, which is a Level 1 measurement, as well as quoted
prices for similar terms and maturities in inactive markets and future cash flows discounted at current rates, which are Level 2 measurements. The fair value of our short-term
and long-term debt, excluding finance leases, was as follows:
(dollars in millions)
At December 31,
Carrying
Amount
Short- and long-term debt, excluding finance leases
$
110,373
$
2019
Fair
Value
129,200
$
Carrying
Amount
112,159
$
2018
Fair
Value
118,535
Derivative Instruments
The following table sets forth the notional amounts of our outstanding derivative instruments:
(dollars in millions)
At December 31,
Interest rate swaps
Cross currency swaps
Forward starting interest rate swaps
Interest rate caps
Foreign exchange forwards
$
2019
17,004
23,070
3,000
679
1,130
$
2018
19,813
16,638
4,000
2,218
600
Interest Rate Swaps
We enter into interest rate swaps to achieve a targeted mix of fixed and variable rate debt. We principally receive fixed rates and pay variable rates that are currently based on
LIBOR, resulting in a net increase or decrease to Interest expense. These swaps are designated as fair value hedges and hedge against interest rate risk exposure of designated
debt issuances. We record the interest rate swaps at fair value in our consolidated balance sheets as assets and liabilities. Changes in the fair value of the interest rate swaps are
recorded to Interest expense, which are offset by changes in the fair value of the hedged debt due to changes in interest rates.
During 2019, we entered into interest rate swaps with a total notional value of $510 million and settled interest rate swaps with a total notional value of $3.3 billion. During
2018, we entered into interest rate swaps with a total notional value of $730 million and settled interest rate swaps with a total notional value of $1.1 billion.
The ineffective portion of these interest rate swaps was $54 million and insignificant for the years ended December 31, 2019 and 2018, respectively.
The following amounts were recorded in Long-term debt in our consolidated balance sheets related to cumulative basis adjustments for fair value hedges:
(dollars in millions)
At December 31,
Carrying amount of hedged liabilities
Cumulative amount of fair value hedging adjustment included in the carrying amount of the hedged liabilities
Cross Currency Swaps
We have entered into cross currency swaps designated as cash flow hedges to exchange our British Pound Sterling, Euro, Swiss Franc and Australian Dollar-denominated cash
flows into U.S. dollars and to fix our cash payments in U.S. dollars, as well as to mitigate the impact of foreign currency transaction gains or losses.
During 2019, we entered into cross currency swaps with a total notional value of $6.4 billion and did not settle any cross currency swaps. A pre-tax loss of $385 million was
recognized in Other comprehensive loss with respect to these swaps.
During 2018, we did not enter into or settle any cross currency swaps. A pre-tax loss of $720 million was recognized in Other comprehensive loss with respect to these swaps.
$
2019
17,337
433
$
2018
18,903
(785)
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A portion of the losses recognized in Other comprehensive loss was reclassified to Other income (expense), net to offset the related pre-tax foreign currency transaction gain or
loss on the underlying hedged item.
Forward Starting Interest Rate Swaps
We have entered into forward starting interest rate swaps designated as cash flow hedges in order to manage our exposure to interest rate changes on future forecasted
transactions.
During 2019, we did not enter into any forward starting interest rate swaps and we settled forward starting interest rate swaps with a total notional value of $1.0 billion. A pre-tax
loss of $565 million, resulting from interest rate movements was recognized in Other comprehensive loss with respect to these swaps.
During 2018, we entered into forward starting interest rate swaps with a total notional value of $4.0 billion. A pre-tax loss of $60 million was recognized in Other comprehensive
loss with respect to these swaps.
We hedge our exposure to the variability in future cash flows of based on the expected maturities of the related forecasted debt issuance.
Net Investment Hedges
We have designated certain foreign currency instruments as net investment hedges to mitigate foreign exchange exposure related to non-U.S. dollar net investments in certain
foreign subsidiaries against changes in foreign exchange rates. The notional amount of the Euro-denominated debt as a net investment hedge was €750 million as of both
December 31, 2019 and 2018, respectively.
Undesignated Derivatives
We also have the following derivative contracts which we use as economic hedges but for which we have elected not to apply hedge accounting.
Interest Rate Caps
We enter into interest rate caps to mitigate our interest exposure to interest rate increases on our ABS Financing Facility and ABS Notes. During both 2019 and 2018, we
recognized an insignificant amount in Interest expense related to interest rate caps.
Foreign Exchange Forwards
We enter into British Pound Sterling and Euro foreign exchange forwards to mitigate our foreign exchange rate risk related to non-functional currency denominated monetary
assets and liabilities of international subsidiaries. During 2019, we entered into foreign exchange forwards with a total notional value of $12.0 billion and settled foreign
exchange forwards with a total notional value of $11.5 billion. During 2018, we entered into foreign exchange forwards with a total notional value of $2.8 billion and settled
foreign exchange forwards with a total notional value of $2.2 billion. During 2019 and 2018, a pre-tax loss of insignificant amount was recognized in Other income (expense),
net.
Treasury Rate Locks
During 2019, we entered into treasury rate locks with a total notional value of $1.5 billion to hedge the tender offers conducted in May 2019 for fifteen series of notes issued by
Verizon with coupon rates ranging from 4.672% to 5.012% and maturity dates ranging from 2054 to 2055 (May Tender offers). In addition, we entered into treasury rate locks
with a total notional value of $1.5 billion to hedge the tender offers conducted in November and December 2019 for eleven and twenty series of notes and debentures,
respectively, issued by Verizon and other subsidiaries with coupon rates ranging from 3.850% to 8.950% and maturity dates ranging from 2021 to 2055 (November and
December Tender offers). Upon the early settlement of the May, November and December Tender Offers, we settled these hedges and recognized an insignificant gain in Other
income (expense), net.
During 2018, we entered into treasury rate locks with a total notional value of $2.0 billion to hedge the tender offers conducted in September 2018 for eight series of notes issued
by Verizon with coupon rates ranging from 3.850% to 5.012% and maturity dates ranging from 2039 to 2055 (September Tender Offers). Upon the early settlement of the
September Tender Offers, we settled these hedges and recognized an insignificant loss in Other income (expense), net.
Concentrations of Credit Risk
Financial instruments that subject us to concentrations of credit risk consist primarily of temporary cash investments, short-term and long-term investments, trade receivables,
including device payment plan agreement receivables, certain notes receivable, including lease receivables, and derivative contracts.
Counterparties to our derivative contracts are major financial institutions with whom we have negotiated derivatives agreements (ISDA master agreements) and credit support
annex (CSA) agreements which provide rules for collateral exchange. Negotiations and executions of new ISDA master agreements and CSA agreements with our counterparties
continued during 2018. The CSA agreements contain rating based thresholds such that we or our counterparties may be required to hold or post collateral based upon changes in
outstanding positions as compared to established thresholds and changes in credit ratings. At December 31, 2019, we held an insignificant amount and at December 31, 2018, we
posted approximately $0.1 billion of collateral related to derivative contracts under collateral exchange arrangements, which were recorded as Other current liabilities and
Prepaid expenses and other, respectively, in our consolidated balance sheets. While we may be exposed to credit
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losses due to the nonperformance of our counterparties, we consider the risk remote and do not expect that any such nonperformance would result in a significant effect on our
results of operations or financial condition due to our diversified pool of counterparties.
Note 10. Stock-Based Compensation
Verizon Long-Term Incentive Plan
In May 2017, Verizon’s shareholders approved the 2017 Long-Term Incentive Plan (the 2017 Plan) and terminated Verizon's authority to grant new awards under the Verizon
2009 Long-Term Incentive Plan (the 2009 Plan). The 2017 Plan provides for broad-based equity grants to employees, including executive officers, and permits the granting of
stock options, stock appreciation rights, restricted stock, restricted stock units, performance shares, performance stock units and other awards. Upon approval of the 2017 Plan,
Verizon reserved for issuance under the 2017 Plan the number of shares that were remaining but not issued under the 2009 Plan. Shares subject to outstanding awards under the
2009 Plan that expire, are canceled or otherwise terminated will also be available for awards under the 2017 Plan. As of December 31, 2019, 89 million shares are reserved for
future issuance under the 2017 Plan.
Restricted Stock Units
Restricted Stock Units (RSUs) granted under the 2017 Plan generally vest in three equal installments on each anniversary of the grant date. The RSUs that are paid in stock upon
vesting and are thus classified as equity awards are measured using the grant date fair value of Verizon common stock and are not remeasured at the end of each reporting period.
The RSUs that are settled in cash are classified as liability awards and the liability is measured at its fair value at the end of each reporting period. All RSUs granted under the
2017 Plan have dividend equivalent units, which will be paid to participants at the time the RSU award is paid, and in the same proportion as the RSU award.
In February 2018, Verizon announced a broad-based employee special award of RSUs under the 2017 Plan to eligible full-time and part-time employees. These RSUs are vested
in two equal installments on each anniversary of the grant date and paid in cash. The first installment of the restricted stock units was vested and paid in February 2019 and the
remaining restricted stock units will be vested and paid in February 2020.
In connection with our acquisition of Yahoo’s operating business, on the closing date of the Transaction each unvested and outstanding Yahoo RSU award that was held by an
employee who became an employee of Verizon was replaced with a Verizon RSU award, which is generally payable in cash upon the applicable vesting date. These awards are
classified as liability awards and are measured at fair value at the end of each reporting period.
We estimate forfeitures at the time of grant and revise those estimates in subsequent periods if actual forfeitures differ from those estimates. We use historical data to estimate
forfeitures and recognize that estimated compensation cost of restricted stock units, net of estimated forfeitures, on a straight-line basis over the vesting period.
Performance Stock Units
The 2017 Plan also provides for grants of Performance Stock Units (PSUs) that generally vest at the end of the third year after the grant. As defined by the 2017 Plan, the Human
Resources Committee of the Board of Directors determines the number of PSUs a participant earns based on the extent to which the corresponding performance goals have been
achieved over the three-year performance cycle. The PSUs are classified as liability awards because the PSU awards are paid in cash upon vesting. The PSU award liability is
measured at its fair value at the end of each reporting period and, therefore, will fluctuate based on the price of Verizon common stock as well as performance relative to the
targets. All PSUs granted under the 2017 Plan have dividend equivalent units, which will be paid to participants at the time that PSU award is determined and paid, and in the
same proportion as the PSU award. The granted and cancelled activity for the PSU award includes adjustments for the performance goals achieved.
The following table summarizes Verizon’s Restricted Stock Unit and Performance Stock Unit activity:
Restricted Stock Units
(shares in thousands)
Outstanding January 1, 2017
Granted
Payments
Cancelled/Forfeited
Outstanding December 31, 2017
Granted
Payments
Cancelled/Forfeited
Outstanding December 31, 2018
Granted
Payments
Cancelled/Forfeited
Outstanding December 31, 2019
Equity Awards
13,308
4,216
(4,825)
(66)
12,633
4,134
(5,977)
(213)
10,577
3,169
(6,397)
(90)
7,259
Liability Awards
—
25,168
(8,487)
(2,690)
13,991
15,157
(6,860)
(2,362)
19,926
5,814
(9,429)
(1,598)
14,713
Performance
Stock Units
17,919
6,564
(6,031)
(217)
18,235
5,779
(4,526)
(2,583)
16,905
4,593
(3,255)
(2,692)
15,551
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As of December 31, 2019, unrecognized compensation expense related to the unvested portion of Verizon’s RSUs and PSUs was approximately $765 million and is expected to
be recognized over approximately two years.
The equity RSUs granted in 2019 and 2018 have weighted-average grant date fair values of $56.66 and $49.19 per unit, respectively. During 2019, 2018 and 2017, we paid $737
million, $773 million and $750 million, respectively, to settle RSUs and PSUs classified as liability awards.
Stock-Based Compensation Expense
After-tax compensation expense for stock-based compensation related to RSUs and PSUs described above included in Net income attributable to Verizon was $872 million,
$720 million and $384 million for 2019, 2018 and 2017, respectively.
Note 11. Employee Benefits
We maintain non-contributory defined benefit pension plans for certain employees. In addition, we maintain postretirement health care and life insurance plans for certain
retirees and their dependents, which are both contributory and non-contributory, and include a limit on our share of the cost for certain current and future retirees. In accordance
with our accounting policy for pension and other postretirement benefits, operating expenses include service costs associated with pension and other postretirement benefits
while other credits and/or charges based on actuarial assumptions, including projected discount rates, an estimated return on plan assets, and impact from health care trend rates
are reported in Other income (expense), net. These estimates are updated in the fourth quarter to reflect actual return on plan assets and updated actuarial assumptions or upon a
remeasurement. The adjustment is recognized in the income statement during the fourth quarter or upon a remeasurement event pursuant to our accounting policy for the
recognition of actuarial gains and losses.
Pension and Other Postretirement Benefits
Pension and other postretirement benefits for certain employees are subject to collective bargaining agreements. Modifications in benefits have been bargained from time to time,
and we may also periodically amend the benefits in the management plans. The following tables summarize benefit costs, as well as the benefit obligations, plan assets, funded
status and rate assumptions associated with pension and postretirement health care and life insurance benefit plans.
Obligations and Funded Status
(dollars in millions)
Pension
At December 31,
Change in Benefit Obligations
Beginning of year
Service cost
Interest cost
Plan amendments
Actuarial (gain) loss, net
Benefits paid
Curtailment and termination benefits
Settlements paid
End of year
Change in Plan Assets
Beginning of year
Actual return on plan assets
Company contributions
Benefits paid
Settlements paid
End of year
Funded Status
End of year
$
(1,797)
$
(1,751)
$
(14,926)
$
(15,189)
17,816
3,385
371
(1,248)
(873)
19,451
19,175
(494)
1,066
(1,475)
(456)
17,816
1,175
103
449
(984)
—
743
1,119
(26)
1,183
(1,101)
—
1,175
$
19,567
247
695
—
2,860
(1,248)
—
(873)
21,248
$
21,531
284
690
230
(1,418)
(1,475)
181
(456)
19,567
$
16,364
96
629
(22)
(414)
(984)
—
—
15,669
$
19,460
127
615
(8)
(2,729)
(1,101)
—
—
16,364
2019
2018
2019
Health Care and Life
2018
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(dollars in millions)
Pension
At December 31,
Amounts recognized on the balance sheet
Noncurrent assets
Current liabilities
Noncurrent liabilities
Total
Amounts recognized in Accumulated Other Comprehensive Income (Pre-tax)
Prior service cost (benefit)
Total
$
$
524
524
$
$
585
585
$
$
(3,749)
(3,749)
$
$
(4,698)
(4,698)
$
$
5
(67)
(1,735)
(1,797)
$
$
3
(71)
(1,683)
(1,751)
$
$
—
(603)
(14,323)
(14,926)
$
$
—
(292)
(14,897)
(15,189)
2019
2018
2019
Health Care and Life
2018
The accumulated benefit obligation for all defined benefit pension plans was $21.2 billion and $19.5 billion at December 31, 2019 and 2018, respectively.
2018 Collective Bargaining Negotiations
The extension agreement ratified in August 2018 extended our collective bargaining agreements with the Communications Workers of America and the International
Brotherhood of Electrical Workers that were due to expire on August 3, 2019 for four years until August 5, 2023. Amendments triggered by the collective bargaining
negotiations were made to certain pension plans for certain union-represented employees and retirees. The impact of the plan amendments was an increase in our defined benefit
pension plans plan obligations and a net decrease to Accumulated other comprehensive income of $230 million (net of taxes of $170 million). The annual impact of the amount
recorded in Accumulated other comprehensive income that will be reclassified to net periodic benefit cost is insignificant.
2017 Postretirement Plan Amendments
During 2017, amendments were made to certain postretirement plans related to retiree medical benefits for management and certain union-represented employees and retirees.
The impact of the plan amendments was a reduction in our postretirement benefit plan obligations of approximately $527 million, which has been recorded as a net increase to
Accumulated other comprehensive income of $317 million (net of taxes of $210 million). The impact of the amount recorded in Accumulated other comprehensive income that
will be reclassified to net periodic benefit cost is insignificant.
2016 Collective Bargaining Negotiations
During 2016, we adopted changes to our defined benefit pension plans and other postretirement benefit plans to reflect the agreed upon terms and conditions of the collective
bargaining agreements ratified in June 2016. The impact includes a net increase to Accumulated other comprehensive income of $2.9 billion (net of taxes of $1.8 billion). The
amount recorded in Accumulated other comprehensive income will be reclassified to net periodic benefit cost on a straight-line basis over the average remaining service period
of the respective plans’ participants, which, on a weighted-average basis, is 12.2 years for defined benefit pension plans and 7.8 years for other postretirement benefit plans. The
above-noted reclassification resulted in a decrease to net periodic benefit cost and increase to pre-tax income of approximately $658 million during 2019, 2018 and 2017,
respectively.
Information for pension plans with an accumulated benefit obligation in excess of plan assets follows:
(dollars in millions)
At December 31,
Projected benefit obligation
Accumulated benefit obligation
Fair value of plan assets
$
2019
21,190
21,134
19,388
$
2018
19,510
19,461
17,757
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Net Periodic Benefit Cost (Income)
The following table summarizes the components of net periodic benefit cost (income) related to our pension and postretirement health care and life insurance plans:
(dollars in millions)
Pension
Years Ended December 31,
Service cost - Cost of services
Service cost - Selling, general and administrative expense
Service cost
Amortization of prior service cost (credit)
Expected return on plan assets
Interest cost
Remeasurement loss (gain), net
Curtailment and termination benefits
Other components
Total
$
$
2019
202
45
247
61
(1,130)
695
606
—
232
479
$
$
2018
230
54
284
48
(1,293)
690
369
181
(5)
279
$
$
2017
215
65
280
39
(1,262)
683
337
11
(192)
88
$
$
2019
78
18
96
(971)
(37)
629
(480)
—
(859)
(763)
$
$
Health Care and Life
2018
104
23
127
(976)
(44)
615
(2,658)
—
(3,063)
(2,936)
$
$
2017
116
33
149
(949)
(53)
659
546
—
203
352
The service cost component of net periodic benefit cost (income) is recorded in Cost of services and Selling, general and administrative expense in the consolidated statements of
income while the other components, including mark-to-market adjustments, if any, are recorded in Other income (expense), net.
Other pre-tax changes in plan assets and benefit obligations recognized in other comprehensive (income) loss are as follows:
(dollars in millions)
Pension
At December 31,
Prior service cost (benefit)
Reversal of amortization items
Prior service cost (benefit)
Total recognized in other comprehensive loss (income) (pre-tax)
$
(61)
(61)
$
(48)
182
$
(39)
(39)
$
971
949
$
976
968
$
949
405
$
2019
—
$
2018
230
$
2017
—
$
2019
(22)
$
Health Care and Life
2018
(8)
$
2017
(544)
The estimated prior service cost for the defined benefit pension plans that will be amortized from Accumulated other comprehensive income into net periodic benefit cost over
the next fiscal year is $61 million. The estimated prior service cost for the defined benefit postretirement plans that will be amortized from Accumulated other comprehensive
income into net periodic benefit income over the next fiscal year is $1.0 billion.
Assumptions
The weighted-average assumptions used in determining benefit obligations follow:
Pension
At December 31,
Discount Rate
Rate of compensation increases
The weighted-average assumptions used in determining net periodic cost follow:
Pension
At December 31,
Discount rate in effect for determining service cost
Discount rate in effect for determining interest cost
Expected return on plan assets
Rate of compensation increases
2019
4.60%
3.80
6.80
3.00
2018
4.10%
3.40
7.00
3.00
2017
4.70%
3.40
7.70
3.00
2019
4.60%
4.00
4.30
N/A
Health Care and Life
2018
3.90%
3.20
4.80
N/A
2017
4.60%
3.50
4.50
N/A
2019
3.30%
3.00
2018
4.40%
3.00
2019
3.20%
N/A
Health Care and Life
2018
4.30%
N/A
In determining our pension and other postretirement benefit obligations, we used a weighted-average discount rate of 3.3% in 2019. The rates were selected to approximate the
composite interest rates available on a selection of high-quality bonds available in the market at December 31, 2019. The bonds selected had maturities that coincided with the
time periods during which benefits payments are expected to occur, were non-callable and available in sufficient quantities to ensure marketability (at least $300 million par
outstanding).
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In order to project the long-term target investment return for the total portfolio, estimates are prepared for the total return of each major asset class over the subsequent 10-year
period. Those estimates are based on a combination of factors including the current market interest rates and valuation levels, consensus earnings expectations and historical
long-term risk premiums. To determine the aggregate return for the pension trust, the projected return of each individual asset class is then weighted according to the allocation
to that investment area in the trust’s long-term asset allocation policy.
The assumed health care cost trend rates are as follows:
Health Care and Life
At December 31,
Healthcare cost trend rate assumed for next year
Rate to which cost trend rate gradually declines
Year the rate reaches the level it is assumed to remain thereafter
2019
6.10%
4.50
2027
2018
6.30%
4.50
2027
2017
7.00%
4.50
2026
A one-percentage point change in the assumed health care cost trend rate would have the following effects:
(dollars in millions)
One-Percentage Point
Effect on 2019 service and interest cost
Effect on postretirement benefit obligation as of December 31, 2019
$
Increase
20
626
$
Decrease
(21)
(696)
Plan Assets
The Company’s overall investment strategy is to achieve a mix of assets that allows us to meet projected benefit payments while taking into consideration risk and return. While
target allocation percentages will vary over time, the current target allocation for plan assets is designed so that 48% to 68% of the assets have the objective of achieving a return
in excess of the growth in liabilities (comprised of public equities, private equities, real estate, hedge funds and emerging debt) and 35% to 55% of the assets are invested as
liability hedging assets (where cash flows from investments better match projected benefit payments, typically longer duration fixed income) and a maximum of 15% is in
cash. This allocation will shift as funded status improves to a higher allocation of liability hedging assets. Target policies will be revisited periodically to ensure they are in line
with fund objectives. Both active and passive management approaches are used depending on perceived market efficiencies and various other factors. Due to our diversification
and risk control processes, there are no significant concentrations of risk, in terms of sector, industry, geography or company names.
Pension and healthcare and life plans assets do not include significant amounts of Verizon common stock.
Pension Plans
The fair values for the pension plans by asset category at December 31, 2019 are as follows:
(dollars in millions)
Asset Category
Cash and cash equivalents
Equity securities
Fixed income securities
U.S. Treasuries and agencies
Corporate bonds
International bonds
Other
Real estate
Other
Private equity
Hedge funds
Total investments at fair value
Investments measured at NAV
Total
$
737
293
14,284
5,167
19,451
$
6,674
$
5,760
$
1,850
—
—
6,674
—
164
5,760
737
129
1,850
1,986
3,818
1,355
768
810
1,768
524
25
—
—
218
3,149
1,304
768
—
—
145
26
—
810
$
Total
1,529
2,988
$
Level 1
1,507
2,850
$
Level 2
22
135
$
Level 3
—
3
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The fair values for the pension plans by asset category at December 31, 2018 are as follows:
(dollars in millions)
Asset Category
Cash and cash equivalents
Equity securities
Fixed income securities
U.S. Treasuries and agencies
Corporate bonds
International bonds
Other
Real estate
Other
Private equity
Hedge funds
Total investments at fair value
Investments measured at NAV
Total
$
664
459
12,246
5,570
17,816
$
5,614
$
4,847
$
1,785
—
—
5,614
—
373
4,847
664
86
1,785
1,684
3,645
1,113
—
727
1,557
124
19
—
—
127
3,244
1,076
—
—
—
277
18
—
727
$
Total
1,701
2,253
$
Level 1
1,694
2,220
$
Level 2
7
20
$
Level 3
—
13
The following is a reconciliation of the beginning and ending balance of pension plan assets that are measured at fair value using significant unobservable inputs:
(dollars in millions)
Equity
Securities
Balance at January 1, 2018
Actual gain (loss) on plan assets
Purchases (sales)
Transfers out
Balance at December 31, 2018
Actual gain (loss) on plan assets
Purchases (sales)
Transfers out
Balance at December 31, 2019
$
$
1
1
11
—
13
1
(11)
—
3
$
$
Corporate
Bonds
104
(7)
177
3
277
(1)
18
(149)
145
$
$
International
Bonds
20
3
(5)
—
18
(1)
9
—
26
$
$
Real
Estate
627
134
(34)
—
727
30
53
—
810
$
$
Private
Equity
580
25
59
—
664
32
41
—
737
$
$
Hedge
Funds
185
—
62
(161)
86
—
116
(73)
129
$
$
Total
1,517
156
270
(158)
1,785
61
226
(222)
1,850
Health Care and Life Plans
The fair values for the other postretirement benefit plans by asset category at December 31, 2019 are as follows:
(dollars in millions)
Asset Category
Cash and cash equivalents
Equity securities
Fixed income securities
U.S. Treasuries and agencies
Corporate bonds
International bonds
Total investments at fair value
Investments measured at NAV
Total
$
28
76
18
567
176
743
$
514
$
53
$
—
28
76
18
514
—
—
—
53
—
—
—
—
$
Total
220
225
$
Level 1
167
225
$
Level 2
53
—
$
Level 3
—
—
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The fair values for the other postretirement benefit plans by asset category at December 31, 2018 are as follows:
(dollars in millions)
Asset Category
Cash and cash equivalents
Equity securities
Fixed income securities
U.S. Treasuries and agencies
Corporate bonds
International bonds
Total investments at fair value
Investments measured at NAV
Total
$
24
96
18
848
327
1,175
$
808
$
40
$
—
24
96
18
808
—
—
—
40
—
—
—
—
$
Total
471
239
$
Level 1
431
239
$
Level 2
40
—
$
Level 3
—
—
The following are general descriptions of asset categories, as well as the valuation methodologies and inputs used to determine the fair value of each major category of assets.
Cash and cash equivalents include short-term investment funds (less than 90 days to maturity), primarily in diversified portfolios of investment grade money market instruments
and are valued using quoted market prices or other valuation methods. The carrying value of cash equivalents approximates fair value due to the short-term nature of these
investments.
Investments in securities traded on national and foreign securities exchanges are valued by the trustee at the last reported sale prices on the last business day of the year or, if no
sales were reported on that date, at the last reported bid prices. Government obligations, corporate bonds, international bonds and asset-backed debt are valued using matrix
prices with input from independent third-party valuation sources. Over-the-counter securities are valued at the bid prices or the average of the bid and ask prices on the last
business day of the year from published sources or, if not available, from other sources considered reliable such as multiple broker quotes.
Commingled funds not traded on national exchanges are priced by the custodian or fund's administrator at their net asset value (NAV). Commingled funds held by third-party
custodians appointed by the fund managers provide the fund managers with a NAV. The fund managers have the responsibility for providing this information to the custodian of
the respective plan.
The investment manager of the entity values venture capital, corporate finance and natural resource limited partnership investments. Real estate investments are valued at
amounts based upon appraisal reports prepared by either independent real estate appraisers or the investment manager using discounted cash flows or market comparable data.
Loans secured by mortgages are carried at the lesser of the unpaid balance or appraised value of the underlying properties. The values assigned to these investments are based
upon available and current market information and do not necessarily represent amounts that might ultimately be realized. Because of the inherent uncertainty of valuation,
estimated fair values might differ significantly from the values that would have been used had a ready market for the securities existed. These differences could be material.
Forward currency contracts, futures, and options are valued by the trustee at the exchange rates and market prices prevailing on the last business day of the year. Both exchange
rates and market prices are readily available from published sources. These securities are classified by the asset class of the underlying holdings.
Hedge funds are valued by the custodian at NAV based on statements received from the investment manager. These funds are valued in accordance with the terms of their
corresponding offering or private placement memoranda.
Commingled funds, hedge funds, venture capital, corporate finance, natural resource and real estate limited partnership investments for which fair value is measured using the
NAV per share as a practical expedient are not leveled within the fair value hierarchy and are included as a reconciling item to total investments.
Employer Contributions
In 2019, we made a $300 million discretionary contribution to our qualified pension plans, $71 million of contributions to our nonqualified pension plans and $449 million of
contributions to our other postretirement benefit plans. No qualified pension plans contributions are expected to be made in 2020. Nonqualified pension plans contributions are
estimated to be approximately $70 million and contributions to our other postretirement benefit plans are estimated to be approximately $700 million in 2020.
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Estimated Future Benefit Payments
The benefit payments to retirees are expected to be paid as follows:
(dollars in millions)
Year
2020
2021
2022
2023
2024
2025 to 2029
$
Pension Benefits
2,227
1,680
1,620
1,577
1,072
5,248
$
Health Care and Life
961
947
930
968
951
4,569
Savings Plan and Employee Stock Ownership Plans
We maintain four leveraged employee stock ownership plans (ESOP). We match a certain percentage of eligible employee contributions to certain savings plans with shares of
our common stock from this ESOP. At December 31, 2019, the number of allocated shares of common stock in this ESOP was 49 million. There were no unallocated shares of
common stock in this ESOP at December 31, 2019. All leveraged ESOP shares are included in earnings per share computations.
Total savings plan costs were $897 million in 2019, $1.1 billion in 2018 and $838 million in 2017.
Severance Benefits
The following table provides an analysis of our severance liability:
(dollars in millions)
Year
2017
2018
2019
Beginning of Year
$
656
627
2,156
$
Charged to
Expense
581
2,093
260
$
Payments
(564)
(560)
(1,847)
$
Other
(46)
(4)
(4)
$
End of Year
627
2,156
565
Severance, Pension and Benefits (Credits) Charges
During 2019, in accordance with our accounting policy to recognize actuarial gains and losses in the period in which they occur, we recorded net pre-tax pension and benefits
charges of $126 million in our pension and postretirement benefit plans. The charges were recorded in Other income (expense), net in our consolidated statement of income and
were primarily driven by a decrease in our discount rate assumption used to determine the current year liabilities of our pension plans and postretirement benefit plans from a
weighted-average of 4.4% at December 31, 2018 to a weighted-average of 3.3% at December 31, 2019 ($4.3 billion), partially offset by the difference between our estimated
return on assets and our actual return on assets ($2.3 billion) and other assumption adjustments of $1.9 billion, of which $1.6 billion related to healthcare claims experience.
During 2019, we also recorded net pre-tax severance charges of $260 million in Selling, general and administrative expense in our consolidated statements of income.
During 2018, we recorded net pre-tax pension and benefits credits of $2.1 billion in accordance with our accounting policy to recognize actuarial gains and losses in the period in
which they occur. The pension and benefits remeasurement credits of $2.3 billion, which were recorded in Other income (expense), net in our consolidated statements of income,
were primarily driven by an increase in our discount rate assumption used to determine the current year liabilities of our pension plans and postretirement benefit plans from a
weighted-average of 3.7% at December 31, 2017 to a weighted-average of 4.4% at December 31, 2018 ($2.6 billion), and mortality and other assumption adjustments of $1.7
billion, $1.6 billion of which related to healthcare claims and trend adjustments, offset by the difference between our estimated return on assets of 7.0% and our actual return on
assets of (2.7)% ($1.9 billion). The credits were partially offset by $177 million due to the effect of participants retiring under the Voluntary Separation Program.
In September 2018, Verizon announced a Voluntary Separation Program for select U.S.-based management employees. Approximately 10,400 eligible employees separated from
the Company under this program as of the end of June 2019. The severance benefit payments to these employees were substantially completed by the end of September 2019.
Principally as a result of this program but also as a result of other headcount reduction initiatives, the Company recorded a severance charge of $1.8 billion ($1.4 billion after-tax)
during the year ended December 31, 2018, which was recorded in Selling, general and administrative expense in our consolidated statement of income. During 2018, we also
recorded $339 million in severance costs under our other existing separation plans.
During 2017, we recorded net pre-tax severance, pension and benefits charges of $1.4 billion, exclusive of acquisition related severance charges, in accordance with our
accounting policy to recognize actuarial gains and losses in the period in which they occur. The pension and benefits remeasurement charges of approximately $911 million,
which were recorded in Other income (expense), net in our consolidated statements of income, were primarily driven by a decrease in our discount rate assumption used to
determine the current year liabilities of our pension and postretirement benefit plans from a weighted-average of 4.2% at December 31, 2016 to a weighted-average of 3.7% at
December 31, 2017 ($2.6 billion). The charges were partially offset by the difference between our estimated return on assets of 7.0% and our actual return on assets
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of 14.0% ($1.2 billion), a change in mortality assumptions primarily driven by the use of updated actuarial tables (MP-2017) issued by the Society of Actuaries ($227 million)
and other assumption adjustments ($320 million). As part of these charges, we also recorded severance costs of $497 million under our existing separation plans, which were
recorded in Selling, general and administrative expense in our consolidated statement of income.
Note 12. Taxes
The components of income before provision (benefit) for income taxes are as follows:
(dollars in millions)
Years Ended December 31,
Domestic
Foreign
Total
$
$
2019
21,655
1,078
22,733
$
$
2018
19,801
(178)
19,623
$
$
2017
19,645
949
20,594
The components of the provision (benefit) for income taxes are as follows:
(dollars in millions)
Years Ended December 31,
Current
Federal
Foreign
State and Local
Total
Deferred
Federal
Foreign
State and Local
Total
Total income tax provision (benefit)
$
1,150
(13)
95
1,232
2,945
$
175
30
184
389
3,584
$
(14,360)
(66)
(37)
(14,463)
(9,956)
$
518
221
974
1,713
$
2,187
267
741
3,195
$
3,630
200
677
4,507
2019
2018
2017
The following table shows the principal reasons for the difference between the effective income tax rate and the statutory federal income tax rate:
Years Ended December 31,
Statutory federal income tax rate
State and local income tax rate, net of federal tax benefits
Preferred stock disposition
Affordable housing credit
Employee benefits including ESOP dividend
Impact of tax reform re-measurement
Internal restructure
Noncontrolling interests
Non-deductible goodwill
Other, net
Effective income tax rate
2019
21.0 %
3.7
(9.9)
(0.4)
(0.3)
—
—
(0.5)
0.1
(0.7)
13.0 %
2018
21.0 %
3.7
—
(0.6)
(0.3)
—
(9.1)
(0.5)
4.7
(0.6)
18.3 %
2017
35.0 %
1.6
—
(0.6)
(0.5)
(81.6)
(0.6)
(0.6)
1.0
(2.0)
(48.3)%
The effective income tax rate for 2019 was 13.0% compared to 18.3% for 2018. The decrease in the effective income tax rate and the provision for income taxes was primarily
due to the recognition of approximately $2.2 billion of a non-recurring tax benefit in connection with the disposition of preferred stock, representing a minority interest in a
foreign affiliate in 2019 compared to the non-recurring deferred tax benefit of approximately $2.1 billion, as a result of an internal reorganization of legal entities within the
historical Wireless business, which was offset by a goodwill charge that is not deductible for tax purposes in 2018.
The effective income tax rate for 2018 was 18.3% compared to (48.3)% for 2017. The increase in the effective income tax rate and the provision for income taxes was primarily
due to the non-recurring, non-cash income tax benefit of $16.8 billion recorded in 2017 for the re-measurement of U.S. deferred tax liabilities at the lower 21% U.S. federal
corporate income tax rate, as a result of the enactment of the TCJA on December 22, 2017. In addition, the provision for income taxes for 2018 includes the tax impact of the
Media goodwill impairment charge not deductible for tax purposes, offset by the reduction in the statutory U.S federal corporate income tax rate from 35% to 21%, effective
January 1, 2018 under the TCJA and a non-recurring deferred tax benefit of approximately $2.1 billion as a result of an internal reorganization of legal entities within the
historical Wireless business.
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In December 2017, the Securities and Exchange Commission staff issued Staff Accounting Bulletin (SAB) 118 to provide guidance for companies that had not completed their
accounting for the income tax effects of the TCJA. Due to the complexities involved in accounting for the enactment of the TCJA, SAB 118 allowed for a provisional estimate of
the impacts of the TCJA in our earnings for the year ended December 31, 2017, as well as up to a one year measurement period that ended on December 22, 2018, for any
subsequent adjustments to such provisional estimate. In 2018, Verizon completed its analysis of the impacts of the TCJA, including analyzing the effects of any IRS and U.S.
Treasury guidance issued, and state tax law changes enacted, within the one year measurement period resulting in no significant adjustments to the $16.8 billion provisional
amount recorded in December 2017.
The amounts of cash taxes paid by Verizon are as follows:
(dollars in millions)
Years Ended December 31,
Income taxes, net of amounts refunded
Employment taxes
Property and other taxes
Total
$
$
2019
3,583
1,044
1,551
6,178
$
$
2018
2,213
1,066
1,598
4,877
$
$
2017
4,432
1,207
1,737
7,376
Deferred Tax Assets and Liabilities
Deferred taxes arise because of differences in the book and tax bases of certain assets and liabilities. Significant components of deferred tax assets and liabilities are as follows:
(dollars in millions)
At December 31,
Deferred Tax Assets
Employee benefits
Tax loss and credit carry forwards
Other - assets
Valuation allowances
Deferred tax assets
Deferred Tax Liabilities
Spectrum and other intangible amortization
Depreciation
Other - liabilities
Deferred tax liabilities
Net deferred tax liability
$
22,388
16,884
6,742
46,014
34,619
$
21,976
15,662
3,976
41,614
33,726
$
5,048
3,012
5,595
13,655
(2,260)
11,395
$
5,403
3,576
1,650
10,629
(2,741)
7,888
2019
2018
At December 31, 2019, undistributed earnings of our foreign subsidiaries indefinitely invested outside the U.S. amounted to approximately $3.8 billion. The majority of
Verizon's cash flow is generated from domestic operations and we are not dependent on foreign cash or earnings to meet our funding requirements, nor do we intend to repatriate
these undistributed foreign earnings to fund U.S. operations. Furthermore, a portion of these undistributed earnings represents amounts that legally must be kept in reserve in
accordance with certain foreign jurisdictional requirements and are unavailable for distribution or repatriation. As a result, we have not provided U.S. deferred taxes on these
undistributed earnings because we intend that they will remain indefinitely reinvested outside of the U.S. and therefore unavailable for use in funding U.S. operations.
Determination of the amount of unrecognized deferred taxes related to these undistributed earnings is not practicable.
At December 31, 2019, we had net after-tax loss and credit carry forwards for income tax purposes of approximately $3.0 billion that primarily relate to state and foreign taxes.
Of these net after-tax loss and credit carry forwards, approximately $2.0 billion will expire between 2020 and 2039 and approximately $1.0 billion may be carried forward
indefinitely.
During 2019, the valuation allowance decreased approximately $481 million. The balance of the valuation allowance at December 31, 2019 and the 2019 activity is primarily
related to state and foreign taxes.
Unrecognized Tax Benefits
A reconciliation of the beginning and ending balance of unrecognized tax benefits is as follows:
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(dollars in millions)
2019
Balance at January 1,
Additions based on tax positions related to the current year
Additions for tax positions of prior years
Reductions for tax positions of prior years
Settlements
Lapses of statutes of limitations
Balance at December 31,
$
$
2,871
149
297
(300)
(58)
(89)
2,870
$
$
2018
2,355
160
699
(248)
(40)
(55)
2,871
$
$
2017
1,902
219
756
(419)
(42)
(61)
2,355
Included in the total unrecognized tax benefits at December 31, 2019, 2018 and 2017 is $2.4 billion, $2.3 billion and $1.9 billion, respectively, that if recognized, would
favorably affect the effective income tax rate.
We recognized the following net after-tax expenses related to interest and penalties in the provision for income taxes:
Years Ended December 31,
2019
2018
2017
The after-tax accruals for the payment of interest and penalties in the consolidated balance sheets are as follows:
At December 31,
2019
2018
$
(dollars in millions)
385
348
$
(dollars in millions)
35
75
77
Verizon and/or its subsidiaries file income tax returns in the U.S. federal jurisdiction, and various state, local and foreign jurisdictions. As a large taxpayer, we are under audit by
the IRS and multiple state and foreign jurisdictions for various open tax years. The IRS is currently examining the Company’s U.S. income tax returns for tax years 2013-2014
and Cellco Partnership's U.S. income tax return for tax year 2013-2014. Tax controversies are ongoing for tax years as early as 2005. The amount of the liability for
unrecognized tax benefits will change in the next twelve months due to the expiration of the statute of limitations in various jurisdictions and it is reasonably possible that various
current tax examinations will conclude or require reevaluations of the Company’s tax positions during this period. An estimate of the range of the possible change cannot be
made until these tax matters are further developed or resolved.
Note 13. Segment Information
Reportable Segments
As discussed in Note 1, in November 2018, we announced a strategic reorganization of our business. Under the new structure, effective April 1, 2019, there are two reportable
segments that we operate and manage as strategic business units - Consumer and Business. We measure and evaluate our reportable segments based on segment operating
income, consistent with the chief operating decision maker’s assessment of segment performance.
Our segments and their principal activities consist of the following:
Segment
Verizon Consumer
Group
Description
Our Consumer segment provides consumer-focused wireless and wireline communications services and products. Our wireless services are
provided across one of the most extensive wireless networks in the United States under the Verizon brand and through wholesale and other
arrangements. Our wireline services are provided in nine states in the Mid-Atlantic and Northeastern U.S., as well as Washington D.C., over our
100% fiber-optic network under the Fios brand and over a traditional copper-based network to customers who are not served by Fios.
Our Business segment provides wireless and wireline communications services and products, video and data services, corporate networking
solutions, security and managed network services, local and long distance voice services and network access to deliver various IoT services and
products. We provide these products and services to businesses, government customers and wireless and wireline carriers across the U.S. and select
products and services to customers around the world.
Verizon
Business Group
Our Consumer segment's wireless and wireline products and services are available to our retail customers, as well as resellers that purchase wireless network access from us on a
wholesale basis. Our Business segment’s wireless and wireline products and services are organized by the primary customer groups targeted by these offerings: Global
Enterprise, Small and Medium Business, Public Sector and Other, and Wholesale.
Corporate and other includes the results of our media business,Verizon Media, and other businesses, investments in unconsolidated businesses, unallocated corporate expenses,
certain pension and other employee benefit related costs and interest and financing expenses. Corporate and
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other also includes the historical results of divested businesses and other adjustments and gains and losses that are not allocated in assessing segment performance due to their
nature. Although such transactions are excluded from the business segment results, they are included in reported consolidated earnings. Gains and losses from these transactions
that are not individually significant are included in segment results as these items are included in the chief operating decision maker’s assessment of segment performance.
We completed our acquisition of Yahoo's operating business on June 13, 2017 and as such results are included since the acquisition date.
In May 2017, we completed the Data Center Sale, where we sold 23 customer-facing data center sites in the U.S. and Latin America to Equinix. The results of operations for this
divestiture and other insignificant transactions are included within Corporate and other for all periods presented to reflect comparable segment operating results consistent with
the information regularly reviewed by our chief operating decision maker.
The reconciliation of segment operating revenues and expenses to consolidated operating revenues and expenses below includes the effects of special items that the chief
operating decision maker does not consider in assessing segment performance, primarily because of their nature.
The following tables provides operating financial information for our two reportable segments:
(dollars in millions)
Total
Reportable
Segments
$
65,384
18,048
7,384
10,815
11,447
5,922
3,198
301
122,499
26,539
22,952
24,827
15,458
89,776
$
32,723
2019
External Operating Revenues
Service
Wireless equipment
Other
Global Enterprise
Small and Medium Business
Public Sector and Other
Wholesale
Intersegment revenues
Total Operating Revenues
(1)
Cost of services
Cost of wireless equipment
Selling, general and administrative expense
Depreciation and amortization expense
Total Operating Expenses
Operating Income
(1)
Consumer
$
65,384
18,048
7,384
—
—
—
—
240
91,056
15,884
18,219
16,639
11,353
62,095
$
28,961
$
$
Business
—
—
—
10,815
11,447
5,922
3,198
61
31,443
10,655
4,733
8,188
4,105
27,681
3,762
Service and other revenues and Wireless equipment revenues included in our Business segment amounted to approximately $27.9 billion and $3.5 billion, respectively, for the
year ended December 31, 2019.
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(dollars in millions)
Total
Reportable
Segments
$
64,207
18,874
6,447
11,197
10,732
5,830
3,713
296
121,296
26,194
23,323
23,390
16,210
89,117
$
32,179
2018
External Operating Revenues
Service
Wireless equipment
Other
Global Enterprise
Small and Medium Business
Public Sector and Other
Wholesale
Intersegment revenues
Total Operating Revenues
(1)
Cost of services
Cost of wireless equipment
Selling, general and administrative expense
Depreciation and amortization expense
Total Operating Expenses
Operating Income
(1)
Consumer
$
64,207
18,874
6,447
—
—
—
—
234
89,762
15,335
18,763
15,701
11,952
61,751
$
28,011
$
$
Business
—
—
—
11,197
10,732
5,830
3,713
62
31,534
10,859
4,560
7,689
4,258
27,366
4,168
Service and other revenues and Wireless equipment revenues included in our Business segment amounted to approximately $28.1 billion and $3.4 billion, respectively, for the
year ended December 31, 2018.
(dollars in millions)
Total
Reportable
Segments
$
63,769
17,292
5,735
11,444
9,793
5,652
3,978
304
117,967
26,075
22,147
24,740
15,791
88,753
$
29,214
2017
External Operating Revenues
Service
Wireless equipment
Other
Global Enterprise
Small and Medium Business
Public Sector and Other
Wholesale
Intersegment revenues
Total Operating Revenues
(1)
Cost of services
Cost of wireless equipment
Selling, general and administrative expense
Depreciation and amortization expense
Total Operating Expenses
Operating Income
(1)
Consumer
$
63,769
17,292
5,735
—
—
—
—
258
87,054
14,981
17,713
17,292
11,308
61,294
$
25,760
$
$
Business
—
—
—
11,444
9,793
5,652
3,978
46
30,913
11,094
4,434
7,448
4,483
27,459
3,454
Service and other revenues and Wireless equipment revenues included in our Business segment amounted to approximately $29.3 billion and $1.6 billion, respectively, for the
year ended December 31, 2017.
The following table provides Fios revenues for our two reportable segments:
(dollars in millions)
Years Ended December 31,
Consumer
Business
Total Fios revenue
$
$
2019
11,175
967
12,142
$
$
2018
11,056
883
11,939
$
$
2017
10,903
788
11,691
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The following table provides Wireless service revenue for our reportable segments and includes intersegment activity:
(dollars in millions)
Years Ended December 31,
Consumer
Business
Total Wireless service revenue
$
$
2019
53,791
11,188
64,979
$
$
2018
52,459
10,484
62,943
$
$
2017
51,954
11,093
63,047
Reconciliation to Consolidated Financial Information
A reconciliation of the reportable segment operating revenues to consolidated operating revenues is as follows:
(dollars in millions)
Years Ended December 31,
Operating Revenues
Total reportable segments
Corporate and other
Reconciling items:
Operating results from divested businesses (Note 3)
Eliminations
Consolidated Operating Revenues
$
—
(443)
131,868
$
—
(369)
130,863
$
368
(399)
126,034
$
122,499
9,812
$
121,296
9,936
$
117,967
8,098
2019
2018
2017
A reconciliation of the total reportable segments’ operating income to consolidated income before provision for income taxes is as follows:
(dollars in millions)
Years Ended December 31,
Operating Income
Total reportable segments
Corporate and other
Reconciling items:
Severance charges
Other components of net periodic pension and benefit (charges) credits (Note 11)
Net gain on sale of divested businesses (Note 3)
Acquisition and integration related charges (Note 3)
Gain on spectrum license transactions (Note 3)
Operating results from divested businesses
Impairment charges
Product realignment charges
Net gain from dispositions of assets and businesses
Consolidated operating income
Equity in losses of unconsolidated businesses
Other income (expense), net
Interest expense
Income Before (Provision) Benefit For Income Taxes
$
(204)
(813)
—
—
—
—
(186)
—
261
30,378
(15)
(2,900)
(4,730)
22,733
$
(2,157)
(823)
—
(553)
—
—
(4,591)
(451)
—
22,278
(186)
2,364
(4,833)
19,623
$
(497)
(800)
1,774
(884)
270
149
—
(682)
—
27,425
(77)
(2,021)
(4,733)
20,594
$
32,723
(1,403)
$
32,179
(1,326)
$
29,214
(1,119)
2019
2018
2017
No single customer accounted for more than 10% of our total operating revenues during the years ended December 31, 2019, 2018 and 2017. International operating revenues are
not significant.
The chief operating decision maker does not review disaggregated assets on a segment basis; therefore, such information is not presented. Depreciation included in the measure
of segment profitability is primarily allocated based on proportional usage.
Note 14. Equity and Comprehensive Income
Equity
In December 2019, 46,100 preferred shares of a foreign affiliate of Verizon was sold for cash consideration of $51 million and is reflected in non-controlling interests. The
preferred shares pay cumulative dividends of 8.25% per annum.
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Common Stock
In February 2020, the Verizon Board of Directors authorized a share buyback program to repurchase up to 100 million shares of the Company's common stock. The program will
terminate when the aggregate number of shares purchased reaches 100 million, or a new share repurchase plan superseding the current plan is authorized, whichever is sooner.
During the years ended December 31, 2019, 2018, and 2017, Verizon did not repurchase any shares of Verizon’s common stock under our previously authorized share buyback
programs. At December 31, 2019, the maximum number of shares that could be purchased by or on behalf of Verizon under our share buyback program was 100 million.
Common stock has been used from time to time to satisfy some of the funding requirements of employee and shareholder plans. During the years ended December 31, 2019,
2018, and 2017, we issued 3.8 million, 3.5 million and 2.8 million common shares from Treasury stock, respectively, which had an insignificant aggregate value.
In connection with our acquisition of Straight Path in February 2018, we issued approximately 49 million shares of Verizon common stock, valued at approximately $2.4 billion.
Accumulated Other Comprehensive Income
Comprehensive income consists of net income and other gains and losses affecting equity that, under U.S. GAAP, are excluded from net income. Significant changes in the
components of Other comprehensive income, net of provision for income taxes are described below.
The changes in the balances of Accumulated other comprehensive income by component are as follows:
Foreign
currency
translation
adjustments
$
(713)
245
—
245
(468)
(15)
(483)
(117)
—
(117)
(600)
16
—
16
$
(584)
$
Defined benefit
pension and
postretirement
plans
$
3,420
327
(541)
(214)
3,206
682
3,888
(164)
(694)
(858)
3,030
—
(659)
(659)
$
2,371
$
$
(dollars in millions)
Balance at January 1, 2017
Other comprehensive income
Amounts reclassified to net income
Net other comprehensive income (loss)
Balance at December 31, 2017
Opening balance sheet adjustment (Note 1)
Adjusted opening balance
Other comprehensive income (loss)
Amounts reclassified to net income
Net other comprehensive income (loss)
Balance at December 31, 2018
Other comprehensive income (loss)
Amounts reclassified to net income
Net other comprehensive income (loss)
Balance at December 31, 2019
Unrealized gains
(losses) on cash flow
hedges
$
(80)
818
(849)
(31)
(111)
(24)
(135)
(574)
629
55
(80)
(699)
(37)
(736)
(816)
Unrealized gains
(losses) on
marketable securities
$
46
10
(24)
(14)
32
(13)
19
—
1
1
20
8
(1)
7
$
27
Total
2,673
1,400
(1,414)
(14)
2,659
630
3,289
(855)
(64)
(919)
2,370
(675)
(697)
(1,372)
998
The amounts presented above in net other comprehensive income (loss) are net of taxes. The amounts reclassified to net income related to unrealized gains (losses) on cash flow
hedges in the table above are included in Other income (expense), net and Interest expense in our consolidated statements of income. See Note 9 for additional information. The
amounts reclassified to net income related to unrealized gains (losses) on marketable securities in the table above are included in Other income (expense), net in our consolidated
statements of income. The amounts reclassified to net income related to defined benefit pension and postretirement plans in the table above are included in Cost of services and
Selling, general and administrative expense in our consolidated statements of income. See Note 11 for additional information.
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Note 15. Additional Financial Information
The following tables provide additional financial information related to our consolidated financial statements:
Income Statement Information
(dollars in millions)
Years Ended December 31,
Depreciation expense
Interest costs on debt balances
Net amortization of debt discount
Capitalized interest costs
Advertising expense
Other income (expense), net
Interest income
Other components of net periodic benefit (cost) income
Early debt extinguishment costs
Other, net
$
$
121
627
(3,604)
(44)
(2,900)
$
$
94
3,068
(725)
(73)
2,364
$
$
82
(11)
(1,983)
(109)
(2,021)
$
2019
14,371
5,221
165
(656)
3,071
$
2018
15,186
5,399
174
(740)
2,682
$
2017
14,741
5,256
155
(678)
2,643
Balance Sheet Information
(dollars in millions)
At December 31,
Prepaid expenses and other
Prepaid taxes
Deferred contract costs
Restricted cash
Other prepaid expense and other
$
Accounts payable and accrued liabilities
Accounts payable
Accrued expenses
Accrued vacation, salaries and wages
Interest payable
Taxes payable
$
Other current liabilities
Dividends payable
Contract liability
Other
$
$
2,566
4,651
1,807
9,024
$
$
2,512
4,207
1,520
8,239
$
7,725
5,984
4,885
1,441
1,771
21,806
$
$
7,232
5,948
6,268
1,570
1,483
22,501
$
2,438
2,578
1,221
1,791
8,028
$
$
348
2,083
1,047
1,975
5,453
2019
2018
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Cash Flow Information
(dollars in millions)
Years Ended December 31,
Cash Paid
Interest, net of amounts capitalized
Income taxes, net of amounts refunded
Other, net Cash Flows from Operating Activities
Changes in device payment plan agreement non-current receivables
Early debt extinguishment costs
Other, net
$
Other, net Cash Flows from Financing Activities
Net debt related costs
Change in short-term obligations, excluding current maturities
Other, net
$
$
(1,797)
—
(1,120)
(2,917)
$
$
(141)
(790)
(893)
(1,824)
$
$
(3,599)
(170)
(670)
(4,439)
$
23
3,604
(228)
3,399
$
$
(509)
725
3
219
$
$
(579)
1,983
(728)
676
$
4,714
3,583
$
4,408
2,213
$
4,369
4,432
2019
2018
2017
Note 16. Commitments and Contingencies
In the ordinary course of business, Verizon is involved in various commercial litigation and regulatory proceedings at the state and federal level. Where it is determined, in
consultation with counsel based on litigation and settlement risks, that a loss is probable and estimable in a given matter, the Company establishes an accrual. In none of the
currently pending matters is the amount of accrual material. An estimate of the reasonably possible loss or range of loss in excess of the amounts already accrued cannot be made
at this time due to various factors typical in contested proceedings, including: (1) uncertain damage theories and demands; (2) a less than complete factual record; (3) uncertainty
concerning legal theories and their resolution by courts or regulators; and (4) the unpredictable nature of the opposing party and its demands. We continuously monitor these
proceedings as they develop and adjust any accrual or disclosure as needed. We do not expect that the ultimate resolution of any pending regulatory or legal matter in future
periods will have a material effect on our financial condition, but it could have a material effect on our results of operations for a given reporting period.
Verizon is currently involved in approximately 25 federal district court actions alleging that Verizon is infringing various patents. Most of these cases are brought by non-
practicing entities and effectively seek only monetary damages; a small number are brought by companies that have sold products and could seek injunctive relief as well. These
cases have progressed to various stages and a small number may go to trial in the coming 12 months if they are not otherwise resolved.
In connection with the execution of agreements for the sales of businesses and investments, Verizon ordinarily provides representations and warranties to the purchasers
pertaining to a variety of nonfinancial matters, such as ownership of the securities being sold, as well as indemnity from certain financial losses. From time to time,
counterparties may make claims under these provisions, and Verizon will seek to defend against those claims and resolve them in the ordinary course of business.
Subsequent to the sale of Verizon Information Services Canada in 2004, we continue to provide a guarantee to publish directories, which was issued when the directory business
was purchased in 2001 and had a 30-year term (before extensions). The preexisting guarantee continues, without modification, despite the subsequent sale of Verizon
Information Services Canada and the spin-off of our domestic print and Internet yellow pages directories business. The possible financial impact of the guarantee, which is not
expected to be adverse, cannot be reasonably estimated as a variety of the potential outcomes available under the guarantee result in costs and revenues or benefits that may
offset each other. We do not believe performance under the guarantee is likely.
As of December 31, 2019, letters of credit totaling approximately $632 million, which were executed in the normal course of business and support several financing
arrangements and payment obligations to third parties, were outstanding.
During 2019, Verizon entered into a renewable energy purchase agreement (REPA) with a third party. The REPA is based on the expected operation of a renewable energy-
generating facility and has a fixed price term of 12 years from the commencement of the facility's entry into commercial operation, which is expected to begin by the end of
2020. The REPA generally is expected to be financially settled based on the prevailing market price as energy is generated by the facility.
We have various commitments, totaling $18.8 billion, primarily to purchase programming and network services, equipment, software and marketing services, which will be used
or sold in the ordinary course of business, from a variety of suppliers. Of this total amount, $8.4 billion is attributable to 2020, $7.5 billion is attributable to 2021 through 2022,
$1.4 billion is attributable to 2023 through 2024 and $1.5 billion is attributable to years thereafter. These amounts do not represent our entire anticipated purchases in the future,
but represent only those items that are the subject of contractual obligations. Our commitments are generally determined based on the noncancelable quantities or termination
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amounts. Purchases against our commitments totaled approximately $10.9 billion for 2019, $9.0 billion for 2018 and $8.2 billion for 2017. Since the commitments to purchase
programming services from television networks and broadcast stations have no minimum volume requirement, we estimated our obligation based on number of subscribers at
December 31, 2019, and applicable rates stipulated in the contracts in effect at that time. We also purchase products and services as needed with no firm commitment.
Note 17. Quarterly Financial Information (Unaudited)
(dollars in millions, except per share amounts)
Quarter Ended
2019
Operating Revenues
Operating Income
Net Income
Net Income Attributable to Verizon
Basic Earnings Per Share Attributable to Verizon
(1)
Diluted Earnings Per Share Attributable to
2018
Operating Revenues
Operating Income
Net Income
Net Income Attributable to Verizon
Basic Earnings Per Share Attributable to Verizon
(1)
First Quarter
$
32,128
7,709
5,160
5,032
$
$
1.22
1.22
$
$
Verizon
(1)
$
Second Quarter
32,071
7,850
4,074
3,944
0.95
0.95
$
$
$
Third Quarter
32,894
8,180
5,337
5,194
1.26
1.25
$
$
$
Fourth Quarter
34,775
6,639
5,217
5,095
1.23
1.23
$
$
$
Full Year
131,868
30,378
19,788
19,265
4.66
4.65
$
31,772
7,349
4,666
4,545
$
32,203
6,617
4,246
4,120
$
32,607
7,675
5,062
4,924
$
34,281
637
2,065
1,939
$
130,863
22,278
16,039
15,528
$
$
1.11
1.11
$
$
1.00
1.00
$
$
1.19
1.19
$
$
0.47
0.47
$
$
3.76
3.76
Diluted Earnings Per Share Attributable to Verizon
(1)
(1)
Net income attributable to Verizon per common share is computed independently for each quarter and the sum of the quarters may not equal the annual amount.
Results of operations for 2019 and 2018 include the following after-tax charges (credits) attributable to Verizon:
(dollars in millions)
2019
First
Quarter
Severance, pension and benefits charges (credits)
Early debt redemption costs
Acquisition and integration related charges
Product realignment charges
Net gain from dispositions of assets and businesses
Disposition of preferred stock
Impairment charges
Historical Wireless legal entity restructuring
$
(71)
—
—
—
—
—
—
—
$
Second
Quarter
—
1,140
—
—
—
—
—
—
$
Third
Quarter
215
—
—
—
(224)
—
—
—
$
Fourth
Quarter
108
1,520
—
—
—
(2,247)
214
—
$
First
Quarter
—
184
82
—
—
—
—
—
$
2018
Second
Quarter
250
—
92
509
—
—
—
—
$
Third
Quarter
(335)
352
103
—
—
—
—
—
$
Fourth
Quarter
108
—
142
—
—
—
4,527
(2,065)
Disposition of Preferred Stock
During the fourth quarter of 2019, we completed the disposition of preferred stock, representing a minority interest in a foreign affiliate, which resulted in a non-recurring
income tax benefit of approximately $2.2 billion in our consolidated statement of income for the year ended December 31, 2019.
Historical Wireless Legal Entity Restructuring
During the fourth quarter of 2018, we completed an internal reorganization of legal entities within the historical Wireless business which resulted in a non-recurring income tax
benefit of approximately $2.1 billion in our consolidated statement of income for the year ended December 31, 2018, which reduced our deferred tax liability by the same
amount.
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Verizon Communications Inc. and Subsidiaries
Principal Subsidiaries of Registrant at December 31, 2019
Name
Verizon Delaware LLC
Verizon Maryland LLC
Verizon New England Inc.
Verizon New Jersey Inc.
Verizon New York Inc.
Verizon Pennsylvania LLC
Verizon Virginia LLC
Bell Atlantic Mobile Systems LLC
Cellco Partnership
(d/b/a Verizon Wireless)
GTE LLC
GTE Wireless LLC
MCI Communications Corporation
Verizon Americas Inc.
Verizon Business Global LLC
State of Incorporation /
Organization
Delaware
Delaware
New York
New Jersey
New York
Delaware
Virginia
Delaware
EXHIBIT 21
Delaware
Delaware
Delaware
Delaware
Delaware
Delaware
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Consent of Independent Registered Public Accounting Firm and Report on Schedule
Consent
We consent to the incorporation by reference in the following Registration Statements:
EXHIBIT 23
Form S-4, No. 333-11573; Form S-8, No. 333-41593; Form S-8, No. 333-50146; Form S-4, No. 333-76171; Form S-8, No. 333-76171; Form S-8, No. 333-53830; Form S-8,
No. 333-82690; Form S-4, No. 333-124008; Form S-8, No. 333-124008; Form S-4, No. 333-132651; Form S-8, No. 333-172501; Form S-8, No. 333-172999; Form S-8, No.
333-200398; Form S-8, No. 333-217717; Form S-8, No. 333-223523; and Form S-3, No. 333-233608;
of our reports dated February 21, 2020, with respect to the consolidated financial statements and the effectiveness of internal control over financial reporting of Verizon
Communications Inc. ("Verizon"), incorporated by reference in this Annual Report (Form 10-K) of Verizon for the year ended December 31, 2019, and the financial statement
schedule of Verizon, included herein.
Report on Schedule
To the Shareholders and the Board of Directors of Verizon Communications Inc.:
We have audited the consolidated financial statements of Verizon as of December 31, 2019 and 2018, and for each of the three years in the period ended December 31, 2019, and
have issued our report thereon dated February 21, 2020 incorporated by reference in this Annual Report (Form 10-K) of Verizon from the 2019 Annual Report to Shareholders of
Verizon. Our audits of the consolidated financial statements included the financial statement schedule listed in Item 15(a) of this Annual Report (Form 10-K) (the “schedule”).
This schedule is the responsibility of Verizon's management. Our responsibility is to express an opinion on Verizon’s schedule based on our audits.
In our opinion, the schedule presents fairly, in all material respects, the information set forth therein when considered in conjunction with the consolidated financial statements.
/s/ Ernst & Young LLP
Ernst & Young LLP
New York, New York
February 21, 2020
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EXHIBIT 24
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, her true and lawful attorneys-in-
fact and agents with full power of substitution, for her and in her name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as she might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Shellye L. Archambeau
Shellye L. Archambeau
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POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-
fact and agents with full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Mark T. Bertolini
Mark T. Bertolini
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POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-
fact and agents with full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Vittorio Colao
Vittorio Colao
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POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, her true and lawful attorneys-in-
fact and agents with full power of substitution, for her and in her name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as she might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Melanie L. Healey
Melanie L. Healey
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POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-
fact and agents with full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Clarence Otis, Jr.
Clarence Otis, Jr.
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
2259378_1668.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-
fact and agents with full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Daniel H. Schulman
Daniel H. Schulman
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2259378_1669.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-
fact and agents with full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Rodney E. Slater
Rodney E. Slater
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2259378_1670.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, her true and lawful attorneys-in-
fact and agents with full power of substitution, for her and in her name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as she might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Kathryn A. Tesija
Kathryn A. Tesija
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2259378_1671.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, her true and lawful attorneys-in-
fact and agents with full power of substitution, for her and in her name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as she might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Carol B. Tomé
Carol B. Tomé
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2259378_1672.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Matthew D. Ellis and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-fact and agents with
full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form 10-K, and to file the
same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems appropriate, with the
Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each and every act and thing
requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and confirming all that said
attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Hans E. Vestberg
Hans E. Vestberg
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2259378_1673.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg, Matthew D. Ellis and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-
fact and agents with full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form
10-K, and to file the same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems
appropriate, with the Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each
and every act and thing requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and
confirming all that said attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Gregory G. Weaver
Gregory G. Weaver
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2259378_1674.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg and Anthony T. Skiadas and each of them, his true and lawful attorneys-in-fact and agents with
full power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form 10-K, and to file the
same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems appropriate, with the
Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each and every act and thing
requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and confirming all that said
attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Matthew D. Ellis
Matthew D. Ellis
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2259378_1675.png
POWER OF ATTORNEY
WHEREAS, VERIZON COMMUNICATIONS INC., a Delaware corporation (hereinafter referred to as the “Company”), proposes to file with the Securities and
Exchange Commission under the provisions of the Securities Exchange Act of 1934, as amended, an annual report on Form 10-K (the “Form 10-K”) for the fiscal year ended
December 31, 2019.
NOW, THEREFORE, the undersigned hereby appoints Hans E. Vestberg and Matthew D. Ellis and each of them, his true and lawful attorneys-in-fact and agents with full
power of substitution, for him and in his name, place and stead, in any and all capacities, to sign the Form 10-K and any and all amendments to the Form 10-K, and to file the
same, with all exhibits thereto and all documents in connection therewith, making such changes in the Form 10-K as such person or persons so acting deems appropriate, with the
Securities and Exchange Commission, granting unto said attorneys-in-fact and agents, and each of them, full power and authority to do and perform each and every act and thing
requisite and necessary to be done in and about the premises, as fully to all intents and purposes as he might or could do in person, hereby ratifying and confirming all that said
attorneys-in-fact and agents or any of them, or his, her or their substitute or substitutes, may lawfully do or cause to be done by virtue hereof.
IN WITNESS WHEREOF, the undersigned has executed this Power of Attorney this 20
th
day of February, 2020.
/s/ Anthony T. Skiadas
Anthony T. Skiadas
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EXHIBIT 31.1
I, Hans E. Vestberg, certify that:
1.
2.
3.
4.
I have reviewed this annual report on Form 10-K of Verizon Communications Inc.;
Based on my knowledge, this report does not contain any untrue statement of a material fact or omit to state a material fact necessary to make the statements made, in
light of the circumstances under which such statements were made, not misleading with respect to the period covered by this report;
Based on my knowledge, the financial statements, and other financial information included in this report, fairly present in all material respects the financial condition,
results of operations and cash flows of the registrant as of, and for, the periods presented in this report;
The registrant’s other certifying officer and I are responsible for establishing and maintaining disclosure controls and procedures (as defined in Exchange Act Rules
13a-15(e) and 15d-15(e)) and internal control over financial reporting (as defined in Exchange Act Rules 13a-15(f) and 15d-15(f)) for the registrant and have:
(a)
Designed such disclosure controls and procedures, or caused such disclosure controls and procedures to be designed under our supervision, to ensure that
material information relating to the registrant, including its consolidated subsidiaries, is made known to us by others within those entities, particularly during
the period in which this report is being prepared;
Designed such internal control over financial reporting, or caused such internal control over financial reporting to be designed under our supervision, to
provide reasonable assurance regarding the reliability of financial reporting and the preparation of financial statements for external purposes in accordance
with generally accepted accounting principles;
Evaluated the effectiveness of the registrant’s disclosure controls and procedures and presented in this report our conclusions about the effectiveness of the
disclosure controls and procedures, as of the end of the period covered by this report based on such evaluation; and
Disclosed in this report any change in the registrant’s internal control over financial reporting that occurred during the registrant’s most recent fiscal quarter
that has materially affected, or is reasonably likely to materially affect, the registrant’s internal control over financial reporting; and
(b)
(c)
(d)
5.
The registrant’s other certifying officer and I have disclosed, based on our most recent evaluation of internal control over financial reporting, to the registrant’s auditors
and the audit committee of the registrant’s board of directors (or persons performing the equivalent functions):
(a)
(b)
All significant deficiencies and material weaknesses in the design or operation of internal control over financial reporting which are reasonably likely to
adversely affect the registrant’s ability to record, process, summarize and report financial information; and
Any fraud, whether or not material, that involves management or other employees who have a significant role in the registrant’s internal control over
financial reporting.
Date: February 21, 2020
/s/
Hans E. Vestberg
Hans E. Vestberg
Chairman and Chief Executive Officer
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EXHIBIT 31.2
I, Matthew D. Ellis, certify that:
1.
2.
3.
4.
I have reviewed this annual report on Form 10-K of Verizon Communications Inc.;
Based on my knowledge, this report does not contain any untrue statement of a material fact or omit to state a material fact necessary to make the statements made, in
light of the circumstances under which such statements were made, not misleading with respect to the period covered by this report;
Based on my knowledge, the financial statements, and other financial information included in this report, fairly present in all material respects the financial condition,
results of operations and cash flows of the registrant as of, and for, the periods presented in this report;
The registrant’s other certifying officer and I are responsible for establishing and maintaining disclosure controls and procedures (as defined in Exchange Act Rules
13a-15(e) and 15d-15(e)) and internal control over financial reporting (as defined in Exchange Act Rules 13a-15(f) and 15d-15(f)) for the registrant and have:
(a)
Designed such disclosure controls and procedures, or caused such disclosure controls and procedures to be designed under our supervision, to ensure that
material information relating to the registrant, including its consolidated subsidiaries, is made known to us by others within those entities, particularly during
the period in which this report is being prepared;
Designed such internal control over financial reporting, or caused such internal control over financial reporting to be designed under our supervision, to
provide reasonable assurance regarding the reliability of financial reporting and the preparation of financial statements for external purposes in accordance
with generally accepted accounting principles;
Evaluated the effectiveness of the registrant’s disclosure controls and procedures and presented in this report our conclusions about the effectiveness of the
disclosure controls and procedures, as of the end of the period covered by this report based on such evaluation; and
Disclosed in this report any change in the registrant’s internal control over financial reporting that occurred during the registrant’s most recent fiscal quarter
that has materially affected, or is reasonably likely to materially affect, the registrant’s internal control over financial reporting; and
(b)
(c)
(d)
5.
The registrant’s other certifying officer and I have disclosed, based on our most recent evaluation of internal control over financial reporting, to the registrant’s auditors
and the audit committee of the registrant’s board of directors (or persons performing the equivalent functions):
(a)
(b)
All significant deficiencies and material weaknesses in the design or operation of internal control over financial reporting which are reasonably likely to
adversely affect the registrant’s ability to record, process, summarize and report financial information; and
Any fraud, whether or not material, that involves management or other employees who have a significant role in the registrant’s internal control over
financial reporting.
Date: February 21, 2020
/s/
Matthew D. Ellis
Matthew D. Ellis
Executive Vice President and Chief Financial Officer
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2259378_1678.png
EXHIBIT 32.1
CERTIFICATION OF CHIEF EXECUTIVE OFFICER PURSUANT TO SECTION 906 OF THE SARBANES-OXLEY ACT OF 2002, PURSUANT TO SECTION 1350 OF
CHAPTER 63 OF TITLE 18 OF THE UNITED STATES CODE
I, Hans E. Vestberg, Chairman and Chief Executive Officer of Verizon Communications Inc. (the Company), certify that:
(1) the report of the Company on Form 10-K for the annual period ending December 31, 2019 (the Report) fully complies with the requirements of section 13(a) of the
Securities Exchange Act of 1934 (the Exchange Act); and
(2) the information contained in the Report fairly presents, in all material respects, the financial condition and results of operations of the Company as of the dates and for
the periods referred to in the Report.
Date: February 21, 2020
/s/
Hans E. Vestberg
Hans E. Vestberg
Chairman and Chief Executive Officer
A signed original of this written statement required by Section 906, or other document authenticating, acknowledging, or otherwise adopting the signature that appears in typed
form within the electronic version of this written statement required by Section 906, has been provided to Verizon Communications Inc. and will be retained by Verizon
Communications Inc. and furnished to the Securities and Exchange Commission or its staff upon request.
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EXHIBIT 32.2
CERTIFICATION OF CHIEF FINANCIAL OFFICER PURSUANT TO SECTION 906 OF THE SARBANES-OXLEY ACT OF 2002, PURSUANT TO SECTION 1350 OF
CHAPTER 63 OF TITLE 18 OF THE UNITED STATES CODE
I, Matthew D. Ellis, Executive Vice President and Chief Financial Officer of Verizon Communications Inc. (the Company), certify that:
(1) the report of the Company on Form 10-K for the annual period ending December 31, 2019 (the Report) fully complies with the requirements of section 13(a) of the
Securities Exchange Act of 1934 (the Exchange Act); and
(2) the information contained in the Report fairly presents, in all material respects, the financial condition and results of operations of the Company as of the dates and for
the periods referred to in the Report.
Date: February 21, 2020
/s/
Matthew D. Ellis
Matthew D. Ellis
Executive Vice President and Chief Financial Officer
A signed original of this written statement required by Section 906, or other document authenticating, acknowledging, or otherwise adopting the signature that appears in typed
form within the electronic version of this written statement required by Section 906, has been provided to Verizon Communications Inc. and will be retained by Verizon
Communications Inc. and furnished to the Securities and Exchange Commission or its staff upon request.
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Hvilken proces man normalt vil benytte ved godkendelse af miljøtoksin?
(MST, reference 1):
side 5:
Hovedparten af befolkningen skal fortsat beskyttes (dvs.
hensyntagen til særligt udsatte skal også inddrages).
��
Der skal tages specifikt hensyn til børn.
��
Det fastholdes, at der højst anvendes en samlet
usikkerhedsfaktor på 10.000, når resultater fra dyreforsøg
overføres til mennesker.
1
��
Der accepteres fortsat en livstidsrisiko på 10
-6
.
Denne vejledning indarbejder disse principper og gennemgår
de metoder, som skal anvendes ved fastsættelse kvalitetskriterier
for jord, luft og drikkevand med henblik på at
beskytte sundheden
2
.
1.1.2 Generelle principper for fastsættelse af kvalitetskriterier for kemikalier
Kvalitetskriterierne fastsættes på et niveau, hvor udsættelse
gennem et helt liv ikke fører til skadevirkninger i befolkningen.
De fastsættes på baggrund af den eksisterende viden og
under hensyntagen til de mangler, der ligger i datagrundlaget.
For at minimere risici for skadelig påvirkning af befolkningen
indgår beskyttelse af særligt følsomme grupper fx børn,
gravide, syge, ældre og svækkede ved fastsættelse af kvalitetskriterier.
Viden om et kemisk stofs sundhedsskadelige egenskaber og
om bestemte befolkningsgruppers særlige følsomhed er
sjældent så eksakt, at der kan fastsættes et kvalitetskriterium,
der præcist definerer skillelinien (hvis en sådan overhovedet
findes) mellem et ufarligt og farligt niveau. Kvalitetskriterierne
kan således ikke opfattes som en streg i sandet, hvor
enhver overskridelse er farlig. Ved fastsættelse af kvalitetskriterier
for kemikalier skal anvendes en forsigtighedstilgang,
da målet er at sikre et højt beskyttelsesniveau for alle
ved udsættelse over et helt liv.
1
: Her er NTP studiet og Ramazinistudiet særdeles relevant. NTP studiet bruger
eksponeringer omkring (over og under) nuværende grænseværdier. Dermed bør grænseværdierne
sænkes med en faktor 10.000. Rammazinistudiet viser effekter ved langt lavere værdier, altså burde
eksponeringen være endnu lavere
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Hvilke krav vil der normalt blive stillet til et miljøtoksin, førend det godkendes?
Hvilke tests vil man normalt udføre, forud for godkendelse?
Ref 1 (MST):
Det videnskabelige grundlag for fastsættelse af sundhedsmæssigt
baserede kvalitetskriterier for kemiske
stoffer i jord, luft og drikkevand består af en
farlighedsvurdering, en dosis- respons (effekt) vurdering
(farlighedskarakterisering), samt en eksponeringsvurdering
2
.
Farlighedsvurderingen og
farlighedskarakteriseringen tager udgangspunkt i undersøgelser af
det pågældende stofs toksikologiske
effekter i mennesker og i dyr.
På næste side gives en oversigt over det væsentligste indhold i de enkelte kapitler i miljøstyrelsens
vejledning
2
Der er ikke foretaget en sådan vurdering for RF-EMF i DK.
Fra EU foreligger:
1999/519/EC:
Council Recommendation of 12 July 1999 on the limitation of exposure of the general public to
electromagnetic fields (0 Hz to 300 GHz).
https://op.europa.eu/en/publication-detail/-/publication/9509b04f-1df0-4221-bfa2-
c7af77975556/language-en
(ICNIRPs standard stort set pakket ind i EU anbefaling til medlemslandende,
Ikke bindende - Ifølge denne recommendation er ICNIRPs grænseværdier et minimumskrav (for
beskyttelse af mennesker) og der er ingen recommendation for beskyttelse af miljøet. Ifølge
recomendationen er det op til det enkelte medlemdsland selv at følge med I forskningen på feltet og
vurdere om der skal skrappere grænseværdier for beskyttelse af menneskers sundhed (punkt 19). Dette er
IKKE sket i DK, jvf implementationsrapport og DK har ikke fastalgt gennemførselsforanstaltninger i
forbindelse med basisrestriktionerne. Jeg vil mene, at Dk ikke lever op til recommendation III, V, VI og
VII.
På side 17 i “First Implementation report 1999-2001”:
"Denmark follows the ICNIRP recomendations and
has not implementedany legally binding
measures
to protect the
public
against exposure to electromagnetic fields. Its Labour Inspectorate follows
ICNIRP recomendations when evaluating exposure.
"https://ec.europa.eu/health/ph_determinants/environment/EMF/implement_rep_en.pdf
Second Implementation report 2002-2007:
(2st version)
https://op.europa.eu/en/publication-
detail/-/publication/5dbcd92f-7849-4017-8cee-742f40ff8143
s 4-5 (og Skema 2) :
De fleste medlemsstater har gennemført henstillingen, og nogle har indført
bindende foran-staltninger for at begrænse offentlighedens eksponering for elektromagnetiske felter......
Imidlertid er der i Cypern, Danmark, Tyskland, Irland, Litauen, Slovenien og Slovakiet ikke fastlagt
gennemførselsforanstaltninger i forbindelse med basisrestriktioner.
Ifølge 1999/519/EC anbefales det at evaluere hvert 3. år (se side 3 stk VII.). Så der burde være en
rapport hvert 3. år fra 1999-2020 – men vi har kun kunnet finde de to.
Se desuden ref 4: Hollandsk regeringsrapport om EMF Grænseværdier i Europa:
Comparison of international policies on electromagnetic fields 2018.pdf
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I kapitel 2 omtales
Datagrundlaget
som anvendes som udgangspunkt for arbejdet. Data hentes
primært fra internationale og nationale dokumenter, via litteratursøgning i internationale databaser,
samt fra originalartikler.
3
Kapitel 3 behandler de faglige metoder, der anvendes i forbindelse med farlighedsvurderingen og
farlighedskarakteriseringen. Dosis-effekt og dosis-responssammenhænge og udpegning af NOAEL
(No Observed Adverse Effect Level) og LOAEL (Lowest Observed Adverse Effect Level)
beskrives.
I kapitel 4 beskrives hvordan farlighedskarakteriseringen udmunder i udpegning af en kritisk effekt,
4
som danner udgangspunkt for fastsættelse af en
tolerabel daglig indtagelse,TDI.
Her omtales,
hvordan anvendelsen af usikkerhedsfaktorer indgår i beregningerne.
I kapitel 5 omtales, hvordan TDI beregnes for kræftfremkaldende stoffer uden tærskelværdi.
5
Risikoniveauet for TDI-værdien defineres, og der gives retningslinier medhensyn til valg af metode
til, hvordan beregningen af dette risikoniveau foretages.
3
Kapitel 2: “kvalitetetskriterierne
vil som oftest være baseret på viden opnået fra dyreforsøg
med mere veldefineret udsættelse eller in vitro data”.
- For EMF igenoreres dyrestudierne, påstås
irrelevante for mennesker!
“Ved
fastsættelsen af kvalitetskriterier anvendes der internationalt anerkendte principper. I denne
forbindelse skal fremhæves de principper og metoder, der er beskrevet i to publikationer af WHO/ IPCS
6,7
om
udarbejdelsen af vejledende grænseværdier og risikovurdering af kemisk udsættelse “
“Det anbefales generelt, at data, der skal danne udgangspunkt for beregning af kvalitetskriteriet,
altid hjemskaffes som originallitteratur til vurdering af den konkrete undersøgelses kvalitet og relevans.”
Der er ikke fastsat nogen form for dosis-effekt sammenhænge for hverken mennesker eller miljø.
Der vil altid være huller I viden, men der er virkelig mange eksperimentelle dyrestudier (insekter og en
lang række hvirveldyr) af forskellig art som man kunne anvende til at undersøge dette aspekt for RF-
EMR. Ref 1, s20: En længerevarende dyreeksperimentel undersøgelse vil således kunne give viden om
forskellige typer effekter ved forskellige eksponeringsniveauer (dosis-effekt), og om hvor lang tid det
tager, før de optræder i forhold til eksponeringen.
Bemærk side 24 vedr. Artsspecifikke effekter. For
FR-EMR er der observeret effekter I så mange dyrearter, at man kan udelukke at effekterne af EMR kun
ses i én dyreart. Derfor må dyreforsøgene vurderes som repræsentative for mennesker.
Dette er relevant ift EMF, idet det også gælder agens i kategori 2B, jvf side 36 i dokumentet.
Bemærk iøvrigt hvad der skrives om genotoksiske agens. Da der er mindst 40 studier som viser DNA
skader er dette ikke uvæsentligt.
4
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Supplerende bemærkninger:
Det største problem er at de definerede normer går på kemiske miljøgifte. Men det er
relevant til sammenligning af fremdrage procedurerne for kemiske stoffer i både DK (MST)
og EU. De er meget velbeskrevne.
Desuden har EU kommissionens “
Scientific Committee on Health, Environmental and
Emerging Risks
“ =SCHEER defineret EMR som muligt miljøtoksin (fysisk hazard), som
foreløbigt vurderes af være af størst mulig betydning for ikke bare menneskers sundhed men
også for økosystemer og andre arter (Ref 2, punkt 4.4): Højeste ranking for “urgency”,
højeste ranking for “scale” (omfang), og højeste rank for interactions (interaktion med ikke
bare mennsker men også økosystemer og andre arter). Desuden tilføjes:
This concern is
more related to the change to 5G rather than a completely new concern. Preliminary
Estimation of importance: RF-EMR gives højest mulig rank
Endelig har EEA vurderet at forsigtighedsprincippet bør tages i anvendelse overfor RF EMR
(Ref 3, nederst side 38 til side 39):
It is therefore very important that large scale emerging
technologies, such as biotechnologies, nanotechnologies and information
and communication
technologies,
apply the precautionary principle based on the experiences and lessons learned from
these and other case studies.
Det afviger fra EUs normale procedurer at udpege en privat organisation til at fastsætte
grænseværdier. Da der er tale om et “large scale ermerging” miljøtoksin burde EU burde
rådgivning fra EEA højere.
Samtidig siger EU også at det er op til de enkelte lande at vurdere om det er nødvendigt med
strammere grænseværdier end dem ICNIRP fastsætter (- se fodnote 2 ovenfor) – men dette
vedrører kun eksponering af mennsker. Der er INGEN miljøvurdering overhovedet, af
effekter på selve miljøet.
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2259378_1684.png
Comparison
of
international
policies on
electromagnetic fields
(power frequency and radiofrequency fields)
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2259378_1686.png
Comparison of international policies on electromagnetic fields
(power frequency and radiofrequency fields)
This document is an update of an earlier overview from
May 2011 (RIVM 118/2011). It was prepared as part of a
research project commissioned by the Ministry of
Infrastructure and Water Management and the Ministry
of Social Affairs and Employment of the Netherlands.
The information that forms the basis for this summary
was obtained from searches of governmental and
scientific websites, scientific publications, policy
summaries by other organisations and personal contacts
with experts in the countries in question. The information
was last updated in the period from January to July 2017
1
.
recommendation are derived from the 1998 guidelines for
limiting exposure to EMF by the International Commission
on Non-Ionizing Radiation Protection (ICNIRP). ICNIRP has
issued new guidelines for EMF with frequencies between
1 hertz and 100 kilohertz in 2010, and for frequencies
between 0 and 1 hertz in 2014, but these have not yet led to
changes in the EU recommendation.
In 2013, the European Parliament and the Council of the EU
issued a directive (2013/35/EU, further called ‘EU directive’)
on the minimum health and safety requirements regarding
the exposure of workers to the risks arising from physical
agents (EMF). It contains exposure limit values for the
induced electric fields and the absorbed power in the body
and action levels for the strength of EMF outside the body
(for values at selected frequencies, see
Table 2).
The limits
for static and low frequency fields in the EU directive are
derived from the 2009 and 2010 ICNIRP guidelines for
limiting exposure to static and low frequency time-varying
EMF. The limits for radiofrequency fields are derived from
the 1998 ICNIRP guidelines. ICNIRP has reconfirmed the
validity of its 1998 guidelines for EMF with frequencies
between 100 kilohertz and 300 gigahertz in a 2009
statement. For the sake of consistency, the terminology of
the EU recommendation and EU directive is also used for
equivalent public and occupational exposure limits in
national legislation in the present summary, regardless of
whether these are derived directly from ICNIRP or from
other sources.
The European Parliament and Council of the EU have also
issued directives on the marketing of low voltage electrical
equipment (2014/35/EU) and radio equipment (2014/53/EU),
which require that such equipment does not endanger the
health or safety of persons. The European Committee for
Electrotechnical Standardisation (CENELEC), in liaison with
the European Telecommunications Standards Institute
(ETSI), has developed harmonised standards for
measurement and calculation of EMF exposure which can
be used to demonstrate that this requirement is met.
Introduction
Time-varying electric, magnetic and electromagnetic fields
(EMF) are generated by moving electric charges and by
variable electric fields such as those generated near a
conductor for alternating current. Power frequency EMF are
generated in the production, transport, distribution and use
of electricity. The frequency of alternating current and the
resulting EMF is 50 hertz in Africa, most of Asia, Australia,
Europe and part of South America and 60 hertz in the
remainder of America, the Philippines, Korea, Saudi-Arabia
and part of Japan. Radiofrequency EMF are generated,
among others, by mobile telecommunication systems,
broadcasting transmitters, radar installations, microwave
ovens and dryers, plastic welders, certain medical
applications and equipment for electronic article
surveillance and identification.
In 1999, the Council of the European Union (EU) published
a Recommendation (1999/519/EC, further called ‘EU
recommendation’) on the limitation of exposure of the
general public to EMF (0 hertz to 300 gigahertz). It contains
basic restrictions for the induced electric fields and currents
and the absorbed power in the body and reference levels
for the strength of EMF outside the body (for values at
selected frequencies, see
Table 1).
The limits in the EU
Disclaimer:
The author has taken care to obtain correct and up-to-date
information from relevant websites, policy documents and experts in the
countries in question. However, no rights can be deduced from any of the
information in this document. For further information and corrections,
please contact Dr. R. Stam, National Institute for Public Health and the
Environment, the Netherlands. E-mail:
[email protected]
power frequency and radiofrequency fields
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Apart from ICNIRP, influential guidelines on the protection
against risks of EMF have also been published by the
Institute of Electrical and Electronics Engineers (IEEE), for
both exposure of the general public and controlled
environments (occupational exposure). For power
frequency fields, the IEEE basic restrictions for induced
electric fields are similar to those of ICNIRP and EU for
exposure of the head (brain) but less strict than ICNIRP for
exposure of the rest of the body. For radiofrequency fields,
IEEE basic restrictions are the same as those of ICNIRP and
EU. The reference levels of IEEE are less strict than those
of ICNIRP and EU (for radiofrequency fields only at some
frequencies). Differences in the limits between different
guidelines are mainly caused by differences in the
dosimetric models of the human body and in the use of
safety factors. The limits advised by IEEE are used in
national EMF legislation of some countries outside the EU
and referred to in a safety standard of the North Atlantic
Treaty Organization (NATO).
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Comparison of international policies on electromagnetic fields
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Exposure of the general public, power frequency fields
European Union
Because the EU recommendation is not legally binding, EMF
policy in member states can be divided into three different
approaches. Details on limits at selected frequencies per
member state can be found in
Table 1
and a visual overview
in
Figure 1.
In the
first group
of member states the EU
recommendation has been transposed in binding national
legislation or national policy. This means that the basic
restrictions and reference levels must be applied. EU
member states in this group are the
Czech Republic, Estonia,
France, Greece, Hungary, Ireland, Luxemburg, Portugal
and
Romania.
In the
Czech Republic,
the reference levels differ
from the EU recommendation, but the basic restrictions are
the same. In
France
the limits only apply to new or modified
installations. In
Germany
and
Slovakia
the reference levels in
the EU recommendation are applied as
de facto
exposure
limits, without reference to basic restrictions.
In the
second group
of member states, the national limits
based on the EU recommendation or ICNIRP are not
binding, there are more lenient limits or there is no
regulation. However, it may be that the authorities or grid
companies apply the limits in the EU recommendation in
practice. EU member states in this group are
Austria, Cyprus,
Denmark, Finland, Latvia, Malta, the Netherlands, Spain, Sweden
and
the United Kingdom.
Whether or not they have legally binding limits on the
strength of power frequency fields, in some of the EU
member states in the first and second group a
precautionary policy has been advised by the government
or voluntarily agreed to by the electricity supply sector to
limit the exposure of members of the general population
to power frequency magnetic fields. Alternatively, the
legislation contains an obligation to minimise fields as far
as this can be done with reasonable cost and with
reasonable consequences. The motivation is either the
epidemiological evidence for a possibly increased risk of
childhood leukaemia in children who live near overhead
power lines, or a more general argument to keep fields as
low as reasonably possible in the light of scientific
uncertainty. These precautionary policies in addition to
formal legislation are as follows:
First group
France:
A ministerial recommendation advises the
Prefectures to avoid as far as possible the creation of new
hospitals, maternity wards and childcare facilities near
power lines, cables, transformers and bus bars where
children are exposed to a magnetic field stronger than
1 microtesla. For new or modified electricity infrastructure,
the grid operator usually tries to avoid as much as possible
the creation of new electricity infrastructure near such
locations when planning a new grid development. The grid
operator has the legal obligation to monitor the strength of
EMF near power lines in urbanised areas. Citizens can also
request information about the strength of EMF from local
power lines via their mayor.
Germany:
National legislation requires that all possibilities to
minimise EMF should be exhausted in accordance with the
technical state of the art when creating or substantially
modifying direct current and alternating current facilities
with voltages greater than 1 kilovolt. High-voltage power
lines for alternating current on a newly planned route may
not pass over buildings meant for the long-term stay of
people. The obligation to minimise EMF only applies to
locations with homes, hospitals, schools, childcare facilities,
playgrounds or any other location not exclusively meant for
the temporary stay of people. Minimisation measures need
to be proportional with regard to cost, functionality, or
negative effects on the environment, well-being and
occupational safety.
Luxemburg:
There is a ministerial recommendation not to
create any new living spaces in the immediate vicinity of
overhead power lines (within 20 metres for 65 kilovolt lines
and 30 metres for 100 to 220 kilovolt lines).
Second group
Austria:
Although precautionary limits are not formally
advised, the panel of experts appointed by the relevant
authority for new electricity lines requiring environmental
impact assessment usually require compliance with a
maximum magnetic flux density of 1 microtesla (1% of the
reference level in the EU recommendation), derived from
Swiss legislation.
power frequency and radiofrequency fields
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Denmark:
The Danish Health Authority (Sundhetsstyrelsen)
recommended in 1993 not to build new homes or children’s
institutions close to power lines or new power lines close to
homes or children’s institutions. The exact distance was left
to pragmatic considerations. The Danish electricity sector
has published guidelines for situations where measures at
reasonable cost to reduce the magnetic field must be
investigated. Like the Danish Health Authority’s advice,
the guidelines apply only to new developments.
Finland:
The Radiation safety authority (STUK) recommends
avoiding the construction of permanent residences in areas
where the magnetic flux density continuously exceeds the
level of approximately 0.4 microtesla.
Netherlands:
A ministerial recommendation advises local
authorities and grid companies to avoid as far as reasonably
possible creating new situations with long-term stay of
children in areas around overhead high-voltage power lines
with an annually averaged magnetic flux density greater
than 0.4 microtesla. The advice applies when making
spatial plans and determining the trajectory of overhead
high-voltage power lines, or when changing existing plans
or existing overhead high-voltage power lines. For existing
situations, the reference level in the EU recommendation
should apply.
United Kingdom:
In response to the conclusions of a national
stakeholders’ dialogue, the government noted that ICNIRP
exposure guidelines in place in the United Kingdom remain
appropriate. It also supports the implementation of
low-cost options such as optimal phasing to reduce the
magnetic field of overhead power lines, but considers
additional exposure reduction by creating exclusion zones
between homes and power lines to be disproportionate in
the light of the evidence on the potential health risks. The
government also supported exploring the reinforcement of
best practice for wiring of distribution circuits and providing
consistent, helpful and proportionate public health
messages to raise awareness.
In the
third group
of member states, there are stricter
basic restrictions and/or reference levels, based on the
precautionary principle or due to public pressure. These
stricter reference levels are often applied as a
de facto
exposure limit that may not be exceeded. Since there is a
great diversity in particular rules and limits, a summary is
given per member state:
Belgium:
In Belgium, the limitation of EMF exposure of the
general population is a matter for the three devolved
regions. In Flanders, a ministerial recommendation for the
planning of new power lines states that passing over
schools and childcare centres should be avoided and
passing over homes kept to a minimum. New schools and
childcare centres should not be placed in the magnetic
field zone with year-averaged exposure greater than
0.4 microtesla (0.4% of the reference level in de EU
recommendation). In addition, an indoor environment
decree requires those responsible for building or managing
homes and public buildings to keep exposure to power
frequency magnetic fields below 10 microtesla (10% of the
reference level in de EU recommendation) and advises
them to strive for a ‘quality aim’ of 0.2 microtesla (0.2% of
the reference level in de EU recommendation). In the
Brussels region, a ministerial instruction for environmental
permits requires that the magnetic field in places near
newly installed transformers where children under 15 may
stay is kept below a 24-hour average of 0.4 microtesla.
Wallonia does not have a precautionary policy for power
frequency magnetic fields, but applies the limits in the EU
recommendation to transformers.
Bulgaria:
Minimal distances between homes and power lines
or substations are in force depending on voltage. There are
no other limits for exposure of the general public to power
frequency EMF except for limits on emission by video
screens. At a distance of 50 centimetres from video screens,
the limit is 0.5% of the reference level in the EU
recommendation for electric field strength and 0.25% for
magnetic flux density.
Croatia:
For public spaces in general, limits for the electric
and magnetic field identical to the reference levels in the EU
recommendation may not be exceeded. For ‘sensitive
areas’ (homes, offices, schools, playgrounds, kindergartens,
maternity wards, hospitals, homes for the elderly and
disabled and tourist accommodations), the limits for the
electric and magnetic field are 40% of the reference levels
in the EU recommendation.
Italy:
For all low frequency sources other than power lines,
the reference levels and basic restrictions in the EU
recommendation apply. For 50-hertz electric and magnetic
fields from power lines and associated installations, the
reference level in the EU recommendation may not be
exceeded. In addition, a precautionary ‘attention value’ and
‘quality goal’ apply to 24-hour median exposure in homes,
playgrounds, schools and places where people can stay for
more than four hours. The ‘attention value’ of 10% of the
EU reference level for magnetic flux density applies to
existing situations. The ‘quality goal’ of 3% of the EU
reference level for magnetic flux density applies to new
situations. An even stricter limit for magnetic flux density
(0.2% of the reference level) was adopted in three regions
before the federal law came into force. This too applies to
power lines near homes, schools and other places where
people may stay for more than 4 hours per day.
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Comparison of international policies on electromagnetic fields
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2259378_1690.png
Lithuania:
A limit of 10% (electric field) or 20% (magnetic
field) of the reference level in the EU recommendation
applies inside residential and public buildings. A limit of
20% (electric field) or 40% (magnetic field) of the reference
level in the EU recommendation applies to the living
environment outside buildings.
Poland:
A limit of 20% (electric field) or 75% (magnetic field)
of the reference level in the EU recommendation applies to
residential areas.
Slovenia:
A limit of 10% of the reference level in the EU
recommendation applies to electric and magnetic fields
from new or modified sources near homes, schools,
kindergartens, hospitals, sanatoria, playgrounds, parks,
recreational areas, public buildings and buildings with a
tourist destination. For other locations, limits equal to the
reference levels in the EU recommendation apply.
Figure
Overview of limits for exposure of the general population to power frequency EMF in the EU.
Group
1
(purple): legal limits derived from EU recommendation, precautionary policy in some countries;
Group
2
(pink): no legal limits or limits less strict than in EU recommendation, precautionary policy in some countries;
Group
3
(yellow): stricter limits than in EU recommendation.
group 1
group 2
group 3
non EU countries
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Other countries
Different approaches to limiting exposure to power
frequency EMF also exist in industrialised countries outside
Europe. Seven examples are given below and further details
on exposure limits can be found in
Table 1.
Australia:
No official government regulation or guidelines for
exposure of the general population to EMF with frequencies
lower than 3 kilohertz are currently in place. The Australian
Radiation Protection and Nuclear Safety Agency (ARPANSA)
has stated that the ICNIRP low frequency guidelines are
consistent with its interpretation of the scientific basis for
the protection of the general public from exposure to low
frequency EMF. The grid operators have a ‘prudent
avoidance’ policy to take reasonable steps to limit field
exposures from new facilities (overhead power lines,
underground cables and substations) at no cost or very low
cost while not unduly compromising other issues such as
worker safety, site availability, reliability and environmental
impact.
China:
A national standard for protection of the general
population under the Environmental Protection Law sets
limits for environmental exposure to EMF, but does not
apply to household appliances. The limits for power
frequency magnetic fields equal the reference levels in the
EU recommendation up to 800 hertz, but are lower for
frequencies greater than 800 hertz. For electric fields the
limits are lower than the reference levels in the EU
recommendation for all frequencies. The standard also cites
the precautionary principle and encourages facility and
equipment owners to take effective measures to reduce
public exposure.
India:
There is no national regulation of the strength of
power frequency EMF. Technical standards for the electricity
supply sector give minimal distances to buildings, but these
measures are related to electrical safety.
Japan:
Ministerial regulations for technical standards of
electrical equipment and railways limit power frequency
magnetic fields to the reference level in the 2010 ICNIRP
guidelines (200 microtesla at 50 hertz). The limit for power
frequency electric fields (3000 volt per metre at 50 hertz) is
lower than that in the ICNIRP guidelines and EU
recommendation and meant to prevent electric shocks.
Russia:
General rules for the protection are set in a 1999
framework law. Exposure limits for specific frequency
ranges are set in so-called ‘Hygienic-epidemiological
standards’. The public exposure limit for power frequency
magnetic fields is 5% of the reference level in the EU
recommendation for living quarters, preschool, children’s,
general and medical institutions; 10% of the reference level
in the EU recommendation for non-residential parts of
residential buildings and in public and administrative
buildings; 20% of the reference level in the EU
recommendation in inhabited areas outside residential
built-up areas; equal to the reference level in the EU
recommendation in non-populated areas with occasional
stay of people.
Switzerland:
An Ordinance relating to Protection from
Non-Ionising Radiation has been in force since 2000.
Exposure limits identical to the reference levels in the EU
recommendation apply to all areas accessible to the public.
A stricter, precautionary limit on magnetic flux density of
1% of the reference level in the EU recommendation applies
at so called places of sensitive use (for example apartments,
schools, children’s playgrounds) to the following classes of
installations, unless the owner can prove that all technically
possible and economically acceptable measures to reduce
exposure have been taken: new high voltage power lines
(overhead and cables); significant modification of existing
high voltage power lines; existing and new transformers
and substations. For existing high voltage power lines, the
phase order has to be optimised when the precautionary
limit on magnetic flux density is exceeded.
United States:
No federal legislation is in force. In some states
(Colorado, Connecticut, Hawaii, Maryland, Ohio), variations
on the ‘prudent avoidance’ principle have been adopted.
This means that exposure of the public to EMF of 60 hertz
must be limited at reasonable cost. In other states, fixed
limits for the electric or magnetic field of power lines are
set, varying from 20% to 240% of the reference level in the
EU recommendation (Florida, Minnesota, Montana, New
Jersey, New York, Oregon).
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Comparison of international policies on electromagnetic fields
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Exposure of the general public, radiofrequency fields
European Union
Because the EU recommendation is not legally binding, EMF
policy in member states can be divided into three different
approaches. Details on exposure limits per member state
can be found in
Table 1
and a visual overview in
Figure 2.
In the
first group
of member states the EU recommendation
has been transposed in binding national legislation or
national policy. This means that the basic restrictions and
reference levels must be applied. Member states in this
group are
Cyprus, Czech Republic, Estonia, Finland, France,
Hungary, Ireland, Malta, Portugal, Romania
and
Spain.
In
Germany
and
Slovakia
the reference levels have become
de facto
exposure limits. In
France
there is an additional legal
obligation to provide information on options for exposure
reduction when selling or promoting a mobile phone and to
provide citizens with measurement results for the strength
of radiofrequency EMF in their homes or in public buildings.
In the
second group
of member states, the national limits
based on the EU recommendation or ICNIRP are not
binding, there are more lenient limits or there is no
regulation. Member states in this group are
Austria,
Denmark, Latvia, the Netherlands, Sweden
and
the United
Kingdom.
In some countries, for example the Netherlands
and the United Kingdom, telecommunication companies
have signed up to a voluntary code to respect the limits in
the EU recommendation in places accessible to the public.
In the United Kingdom the national planning policy
framework for local government also requires that
applications for expansion of base stations certify that
these limits will not be exceeded.
In the
third group
of member states, there are stricter
reference levels and/or basic restrictions based on the
precautionary principle and/or due to public pressure.
The limits chosen are sometimes based on the principle ‘as
low as reasonably achievable without endangering service’.
One practical choice for stricter limits can be to adopt the
lower limit for interference in the European standards for
electromagnetic compatibility (for example in Belgium). In
other countries the reasons for particular limits are unclear
or arbitrary (for example in Greece and Italy). In some
member states the stricter reference levels are applied as
exposure limits that may not be exceeded. Since there is a
great diversity in particular rules and limits, a summary is
given per member state:
Belgium:
The advertising and sale of mobile phones specially
designed for children younger than 7 years is prohibited.
For all other phones, information must be provided on
specific absorption rate and possibilities to lower exposure.
power frequency and radiofrequency fields
Regulation of exposure limits in Belgium is a matter for the
three devolved regions. In Flanders, the limit for electrical
field strength per antenna for telecommunication is 7% of
the reference level in the EU recommendation in places of
stay like homes, schools, rest homes and nurseries. The
maximum exposure in all publicly accessible places is 50%
of the reference level for frequencies between 10 megahertz
and 10 gigahertz. The Brussels Region limits total exposure
in residences for frequencies between 100 kilohertz and 300
gigahertz to a power density of 2% of the reference level in
the EU recommendation (corresponding with 15% for the
electric field strength). For the same frequency range,
Wallonia sets a fixed limit for the electrical field strength
per antenna in residences which is 7% of the reference level
at 900 megahertz.
Bulgaria:
Fixed limits for electrical field strength and power
density are set. Their percentage of the reference levels in
the EU recommendation decreases with frequency. For
power density it is 2% at 900 megahertz and less than 2%
for higher frequencies.
Croatia:
For public spaces in general, fixed limits for the
electric and magnetic fields are applied which are 95% of
the reference levels in the EU recommendation (90% for
power density). For ‘sensitive areas’ (homes, offices,
schools, playgrounds, kindergartens, maternity wards,
hospitals, homes for the elderly and disabled and tourist
accommodations), the limits for the electric and magnetic
field are 40% of the reference levels in the EU
recommendation (16% for power density).
Greece:
The law on electronic communications sets basic
restrictions of 70% of those in the EU recommendation
and 60% when antenna stations are located closer than
300 metres from the property boundaries of schools,
kindergartens, hospitals or eldercare facilities. Installation
of mobile phone antenna stations is not allowed within the
property boundaries of aforementioned facilities. Reference
levels calculated from these two basic restrictions are 84%
and 77% of the reference levels in the EU recommendation
(70% and 60% for power density).
Italy:
For EMF from high frequency sources other than fixed
systems for telecommunication and radio or TV broadcasting,
the reference levels and basic restrictions in the EU
recommendation apply. For EMF from fixed systems for
telecommunication and radio or TV broadcasting, there are
exposure limits in terms of the strength of environmental
EMF that may not be exceeded. In contrast with the limits
in the EU recommendation, these are constant (not
frequency dependent) between 3 megahertz and 3 gigahertz.
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2259378_1693.png
The exposure limit for electric field strength at
900 megahertz is 49% of the reference level in the EU
recommendation (22% for power density). In homes,
schools, playgrounds and places where people may stay
for longer than four hours, the ‘attention value’ for electric
field strength is 15% of the reference level in the EU
recommendation at 900 megahertz (2% for power density).
The ‘quality goal’ for highly frequented outdoor areas is
identical to the attention value.
Lithuania:
There are limits for EMF with frequencies between
10 megahertz and 300 gigahertz inside and surrounding
residential and public buildings which may not be exceeded
and are lower than the reference levels in the EU
recommendation. The percentage varies with frequency,
but for power density the limit is 10% of the EU reference
level at 900 megahertz.
Luxemburg:
Precautionary policy is applied to mobile
telephony through a law on classified locations and
technical standards. These set a fixed exposure limit for the
electrical field strength per radiating element for antennas
with a power of 100 watt and higher which is 7% of the
reference level in the EU recommendation at 900
megahertz. The limit for other antennas and for the total
number of antenna elements in one location equals the
reference level in the EU recommendation.
Poland:
In locations that are accessible to the public,
frequency-dependent exposure limits lower than the
reference levels in the EU recommendation are set for
electrical field strength and power density. At 900 megahertz
the limit for electrical field strength is 17% of the reference
level in the EU recommendation (2% for power density).
Figure
2
Overview of limits for exposure of the general population to radiofrequency EMF in the EU.
Group
1
(purple): legal limits derived from EU recommendation; Group
2
(pink): no legal limits or limits less strict than in
EU recommendation; Group
3
(yellow): stricter limits than in EU recommendation.
group 1
group 2
group 3
non EU countries
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Slovenia:
For frequencies higher than 10 kilohertz, exposure
limits for electric and magnetic field strength of 31% of the
reference levels in the EU recommendation (10% for power
density) apply in ‘sensitive areas’ such as homes, schools
and hospitals. In all other locations the reference levels in
the EU recommendation are applied as
de facto
exposure
limits that may not be exceeded.
Other countries
Industrialised countries outside the EU also have different
ways of limiting exposure of the public to radiofrequency
EMF. Seven examples are given below and further details on
exposure limits can be found in
Table 1.
Australia:
The mandatory basic restrictions and reference
levels in the national radiation protection and
radiocommunication standards are identical to those in the
EU recommendation.
China:
A national standard for protection of the general
population under the Environmental Protection Law sets
limits for environmental exposure to EMF, but does not
apply to wireless communication terminal equipment.
The limits are lower than the reference levels in the EU
recommendation, but the percentage varies with frequency.
At 900 megahertz the limit for electric field strength is 29%
of the reference level in the EU recommendation (9% for
power density). The standard also cites the precautionary
principle and encourages facility and equipment owners to
take effective measures to reduce public exposure. The
basic restrictions for mobile phones in a separate standard
are identical to those in the EU recommendation.
India:
A ministerial memorandum amending the Unified
Access Service License sets limits on exposure of the
general public to EMF from telecommunication base
stations. The limit is 33% of the reference levels in the EU
recommendation for electric and magnetic field strength
and 10 % for power density. Government-approved
interministerial committee recommendations set a limit on
the specific absorption rate for mobile handsets which is
80% of the basic restriction for local exposure of the head
in the EU recommendation.
Japan:
The ministerial radiofrequency radiation protection
guidelines for human exposure to EMF contain a mandatory
basic restriction for mobile phones which is identical to that
in the EU recommendation. The guidelines also contain
mandatory basic restrictions with reference levels for the
strength of EMF from mobile phone base stations, which
are almost identical to the reference levels in the EU
recommendation.
Russia:
General conditions for protection of the population
are set in a 1999 framework law. Limits for specific frequency
ranges are set in subsequent ‘Hygienic-epidemiological
requirements’. The exposure limit for power density for
EMF with frequencies between 300 megahertz and 300
gigahertz in and around residential buildings and inside
public and industrial premises is 2% of the reference level in
the EU recommendation. The reason is to prevent biological
effects that are not generally seen as a health risk in
Western countries. There is no basic restriction in terms of
specific absorption rate, but there is a limit on the plain
wave power density of mobile phones which is 22% of the
reference level in the EU recommendation.
Switzerland:
An Ordinance relating to Non-Ionising Radiation
is in force since 2000. Mandatory exposure limits identical
to the reference levels in the EU recommendation apply in
all areas accessible to the public. A stricter, precautionary
limit for the electric field strength of approximately 10 % of
the reference level in the EU Recommendation applies at so
called places of sensitive use (for example apartments,
schools, children’s playgrounds) near mobile phone
antennae, broadcasting and radar installations.
United States:
The basic restriction for whole body exposure
in federal legislation for radio transmitters is identical to
that in the EU recommendation. However, the reference
levels are higher because a different model is used to
calculate them. At 900 megahertz the difference is 15% and
14% for the electric and magnetic field strength respectively
(33% for power density). The reference levels are applied as
de facto
exposure limits for non-portable devices. For
portable devices close to the body, the mandatory basic
restriction for local exposure of all parts of the body except
the extremities is 80% of the basic restriction for head and
trunk in the EU recommendation. The basic restriction for
the extremities (hands, wrists, ankles, feet, outer ears) is
identical to the basic restriction for limbs in the EU
recommendation.
In addition to the above legal obligations, in Australia,
Austria, Belgium, Cyprus, Denmark, Finland, France,
Germany, Greece, Ireland, India, Italy, Luxemburg, the
Netherlands, Spain, Sweden, Russia, Switzerland, the
United Kingdom and the United States the government or
national scientific organisations have published advice on
how to reduce exposure to radiofrequency EMF from
mobile phones, such as limiting calling time, using
earpieces or speakers, not holding the phone close to the
body, avoiding calls in areas with poor reception and
texting instead of calling.
power frequency and radiofrequency fields
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Occupational exposure, Power frequency fields
European Union
In all member states of the EU, protection or workers
against the risks of EMF is regulated by national legislation
based on directive 2013/35/EU. The directive contains
general rules and appendices with exposure limits. The
directive distinguishes three layers of action levels for low
frequency magnetic fields: low action levels related to
sensory effects exposure limit values (equivalent to
ICNIRP’s 2010 basic restrictions for the central nervous
system) and high action levels and limb action levels related
to health effects exposure limit values (equivalent to
ICNIRP’s 2010 basic restrictions for the peripheral nervous
system). When the action levels are exceeded, this is an
indication that the related exposure limit values could be
exceeded.
The directive sets minimum requirements, but allows
member states to set stricter rules or limits, which are
detailed below and in
Table 2.
The directive also gives
member states the possibility to apply a conditional
exemption from the exposure limits (but not from the
general rules) for worker exposure related to magnetic
resonance imaging (MRI) for patients in the health sector, to
apply a different but equivalent or more specific protection
system for military personnel and to allow the exposure
limits to be temporarily exceeded under certain conditions
for specific sectors or activities in duly justified
circumstances. Details of whether and how individual
member states have applied these possibilities for
exemptions can be found in
Table 2.
Two member states
have action levels and/or exposure limit values that differ
from those in the EU directive:
Czech Republic:
For EMF with frequencies from 1 hertz to 10
megahertz, there is only one action level, which is equivalent
to the low action level in the EU directive. Nevertheless,
there are still two levels of exposure limit values for the
internal electric field, the higher for exposure of the head
and the lower for exposure of the rest of the body.
Poland:
For EMF with frequencies between 0 and 300
gigahertz, there are six sets of action levels delimiting a
‘danger zone’, ‘threat zone’ and ‘intermediate zone’, action
levels for local exposure of extremities and ancillary action
levels for peak levels for modulated fields. The two levels of
exposure limit values for the internal electric field are
identical to the sensory effects and health effects exposure
limit values in the EU directive, but have been extended to
frequencies between 0 and 1 hertz based on the 2014
ICNIRP guidelines for magnetic fields below 1 hertz.
Other countries
Australia:
There are radiation protection regulations which
are only applicable to Commonwealth employees and set
limits on occupational exposure to EMF from ‘controlled
apparatus’, that is, specified categories of devices that
could cause EMF which exceed these limits (for example
induction heaters). Its reference levels and basic restrictions
are identical to those in the 2009 and 2010 ICNIRP
guidelines on static and low frequency fields. They
therefore have the same basis as the limits in the EU
directive, but apply to a narrower range of devices. The
reference levels equal the low action levels in the EU
directive. For non-Commonwealth employees there is
no official government regulation but the ARPANSA advice
on the ICNIRP guidelines also applies to workers.
China:
The national standard with occupational exposure
limits for physical agents in the workplace has a limit of
5 kilovolt per metre for exposure to power frequency
electric fields. There are no occupational limits for power
frequency magnetic fields.
India:
There are no legally binding limits on occupational
exposure to power frequency EMF. Protection of workers
would therefore fall under general health and safety
legislation such as the Factories Act.
Japan:
There are no legally binding limits on occupational
exposure to power frequency EMF. The Japan Society for
Occupational Health has recommended occupational
exposure limits for EMF in terms of the strength of external
electric and magnetic field, which are identical to the low
action levels in the EU directive.
Russia:
A national standard sets limits for power frequency
magnetic fields, which depend on the exposure duration.
For exposures shorter than 1 hour, the limit for whole body
exposure is 33% of the high action level, but for 8 hours it is
2% of the high action level in the EU directive. The limit for
‘limbs only’ exposure is four to ten times higher than the
limit for whole body exposure.
Switzerland:
The federal law on accident insurance gives
general rules to prevent illness caused by physical agents.
The national accident insurer has specified that exposure
limits identical to the occupational reference levels in the
1998 ICNIRP guidelines may not be exceeded. For power
frequency, the limit is 50% of the low action level in the EU
directive for the magnetic field and 100% for the electric
field.
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United States:
There are no legal limits for occupational
exposure to power frequency EMF. The American
Conference of Governmental Industrial Hygienists has
recommended ‘threshold limit values’ which are 20% of the
high action level in EU directive for magnetic fields but
125% of the high action level for electric fields. These are to
be used by trained industrial hygienists as a supplement to
their occupational safety and health program.
NATO:
The standardisation treaty for protection of military
personnel of the North Atlantic Treaty Organization (NATO)
refers to a standard of the Institute of Electrical and
Electronics Engineers (IEEE). The level of the IEEE equivalent
of exposure limit values for the induced electric field in the
brain is similar to that of the sensory effects exposure limit
values in the EU directive. The IEEE equivalent of exposure
limit values for the rest of the body are less strict than the
health effects exposure limit values in the EU directive
(263% at 50 hertz for restricted working environments).
The corresponding IEEE equivalent of action levels are less
strict than the EU high action levels, due to different
dosimetric considerations and safety factors. The IEEE
limits for contact currents are also less strict than those in
the EU directive.
Occupational exposure, radiofrequency fields
European Union
In all member states of the EU, protection or workers
against the risks of EMF is regulated by national legislation
based on directive 2013/35/EU. The directive sets minimum
requirements, but allows member states to set stricter rules
or limits and conditional exemptions, which are detailed
below and in
Table 2.
For radiofrequency fields, the EU
directive has action levels in terms of the electric field
strength, magnetic flux density and power density outside
the body, which are related to the health effects exposure
limit values (equivalent to ICNIRP occupational basic
restrictions for specific absorption rate and power density).
One member state has action levels that differ from those
in the EU directive:
Poland:
For EMF with frequencies between 0 and 300
gigahertz, there are six sets of action levels delimiting a
‘danger zone’, ‘threat zone’ and ‘intermediate zone’, action
levels for local exposure of extremities and ancillary action
levels for peak levels for modulated fields. The exposure
limit values for specific absorption rate are identical to the
health effects exposure limit values in the EU directive.
Other countries
Australia:
The national radiation protection regulations,
which are only applicable to Commonwealth employees,
set limits on occupational exposure to EMF from ‘controlled
apparatus’, that is specified categories of devices that could
cause EMF exceeding these limits (for example diathermy
equipment). Its reference levels and basic restrictions are
set by the national radiation protection standard and are
identical to those in the 1998 ICNIRP guidelines. They
therefore have the same basis as the limits in the EU
directive, but apply to a narrower range of devices.
In addition, a national radiocommunications standard
limits the exposure of ‘aware users’ of mobile
radiofrequency devices to basic restrictions identical to
those in the EU directive.
China:
The national standard with occupational exposure
limits for physical agents in the workplace has limits for
radiofrequency EMF with frequencies from 100 kilohertz to
300 gigahertz. For frequencies from 100 kilohertz to
300 megahertz, exposure limits are 8% to 41% of the action
levels in the EU directive. For frequencies from 300
megahertz to 300 gigahertz, exposure limits do not vary
with frequency but depend on the duration of exposure.
At 900 megahertz the limit for whole body exposure varies
from 222% of the EU action level for short exposure to 1%
of the EU action level for 8-hour average exposure. Limits
for partial body exposure are ten times higher than those
for whole body exposure.
power frequency and radiofrequency fields
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India:
There are no legally binding limits on occupational
exposure to radiofrequency EMF. Protection of workers
would therefore fall under general health and safety
legislation such as the Factories Act.
Japan:
There are no legally binding limits on occupational
exposure to radiofrequency EMF. The Japan Society for
Occupational Health has recommended occupational
exposure limits for EMF in terms of the strength of external
electric and magnetic field and power density. These are
identical to the thermal effects action levels in the EU
directive.
Russia:
The relevant ‘Hygienic-epidemiological
requirements’ set a fixed limit per frequency band for
maximum exposure to radiofrequency EMF with
frequencies between 3 kilohertz and 300 gigahertz which is
44% of the action value for power density in the EU
directive at 900 megahertz for whole body exposure and
222% for peak exposure of limbs. There are also lower
time-dependent limits.
Switzerland:
The federal law on accident insurance gives
general rules to prevent illness caused by physical agents.
The national accident insurer has specified that exposure
limits identical to the action levels in the EU directive may
not be exceeded.
United States:
The equivalent of exposure limit values for
whole body and for local exposure of the extremities
(hands, wrists, ankles, feet, outer ears) in the federal
legislation for transmitters are identical to those for whole
body and for local exposure of limbs in the EU directive. The
equivalent of exposure limit values for local exposure of all
parts of the body except the extremities is 80% of that in
the EU directive. The equivalent of action levels for electric
and magnetic field strength are 18% higher than those in
the EU directive (33% for power density), because a
different model is used to calculate them. The equivalent of
exposure limit values in the United States must be used for
portable devices close to the body. The action levels are
applied as
de facto
exposure limits for non-portable devices.
NATO:
The standardisation treaty for protection of military
personnel of the North Atlantic Treaty Organization (NATO)
refers to a standard of the Institute of Electrical and
Electronics Engineers (IEEE) with the same level of the
equivalent of exposure limit values and action levels as
those in the federal legislation of the United States, with
the exception of the IEEE equivalent of exposure limit
values for local exposure of the head which is identical to
that in the EU directive. The limits for contact currents are
higher than those in the EU directive.
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2259378_1698.png
Table
Reference levels or exposure limits for the general public for electromagnetic fields in inhabited areas in member
states of the European Union and selected industrial nations outside the European Union (situation July
2017)
50
Hz
900
MHz
equivalent plain
wave power density
(W/m
2
)
800
MHz
equivalent plain
wave power density
(W/m
2
)
2 00
MHz
equivalent plain
wave power density
(W/m
2
)
0
[10]
—
0.
1.7
5)
10
10
—
10
10
10
0
6
10)
10
10
0.
3)
magnetic flux
density
(µT)
magnetic flux
density
(µT)
magnetic flux
density
(µT)
electric field
strength
(V/m)
Country:
999/5 9/EC
Austria
Belgium
Bulgaria
Croatia
Cyprus
Czech Republic
Denmark
Estonia
Finland
France
Germany
Greece
Hungary
Ireland
Italy
Latvia
Lithuania
Luxemburg
Malta
Netherlands
Poland
Portugal
Romania
Slovakia
Slovenia
Spain
Sweden
United Kingdom
5000
[5000]
—
—
(4
2000
5)
[5000]
2000
—
5000
[5000]
5000
8)
5000
9)
5000
5000
5000
11)
—
—
500
4)
00
[100]
1)
0
2)
—
(4
40
5)
[100]
200
—
6)
100
[100]
7)
100
8)
00
9)
100
100
100
11)
3
12)
—
20
4)
electric field
strength
(V/m)
4
[41]
2
3)
0. 4
[0.14]
—
—
0.055
5)
0.14
0.14
—
0.14
0.14
0.14
0. 4
0.11
10)
0.14
0.14
0.02
13)
—
—
0.14
0.14
—
—
0.14
0.14
0. 4
0.04
18)
0.14
[0.14]
[0.14]
0.
4.5
[4.5]
—
0.
0.72
5)
4.5
4.5
—
4.5
4.5
4.5
4.5
2.7
10)
4.5
4.5
13)
electric field
strength
(V/m)
58
[58]
29
3)
—
23
5)
58
58
—
58
58
58
58
45
10)
58
58
6
13)
—
—
58
16)
58
—
7
58
58
58
8
18)
58
[58]
[58]
0.20
[0.20]
—
—
0.078
5)
0.20
0.20
—
0.20
0.20
0.20
0.20
0.15
10)
0.20
0.20
0.02
13)
—
—
0.20
0.20
—
—
0.20
0.20
0.20
0.06
18)
0.20
[0.20]
[0.20]
0.
9
[9]
—
0.
1.4
5)
9
9
—
9
9
9
9
5.4
10)
9
9
13)
6
[61]
3
3)
—
17
5)
41
41
—
41
41
41
4
32
10)
41
41
6
13)
—
—
41
16)
41
—
7
41
41
4
3
18)
41
[41]
[41]
—
25
5)
61
61
—
61
61
61
6
47
10)
61
61
6
13)
—
—
61
16)
61
—
7
61
61
6
9
18)
61
[61]
[61]
—
0.45
4.5
4.5
—
0.
4.5
4.5
4.5
0.45
18)
4.5
[4.5]
[4.5]
—
0.9
9
9
—
0.
9
9
9
0.9
18)
9
[9]
[9]
magnetic flux
density
(µT)
0.20
[0.20]
—
—
0.084
5)
0.20
0.20
—
0.20
0.20
0.20
0.20
0.16
10)
0.20
0.20
0.02
13)
—
—
0.20
0.20
—
—
0.20
0.20
0.20
0.06
18)
0.20
[0.20]
[0.20]
electric field
strength
(V/m)
—
5000
15)
[5000]
[5000]
17)
000
5000
5000
5000
500
18)
[5000]
19)
[5000]
[9000]
100
15)
[100]
[100]
17)
75
100
100
00
0
18)
[100]
19)
[100]
[360]
10
10
—
0.
10
10
0
18)
10
[10]
[10]
Australia
China
India
Japan
Russia
Switzerland
U.S.A.
—
4000
—
3000
20)
500
—
—
24)
—
00
—
200
20)
5
21)
22)
41
2
13
48
—
4
23)
—
0.14
0.04
0.041
0.16
—
—
—
4.5
0.4
0.45
6
0.
—
6
58
2
18
61
—
6
23)
—
0.20
0.04
0.058
0.20
—
—
—
9
0.4
0.9
10
0.
—
0
61
2
20
61
—
6
23)
—
0.20
0.04
0.063
0.20
—
—
—
10
0.4
1.1
10
0.
—
0
—
24)
power frequency and radiofrequency fields
|
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2259378_1699.png
Legend to Table 1: All limits are given as root mean square (rms)
value. Where necessary magnetic flux density was calculated from
magnetic field strength using a magnetic permeability of 4π
×
10
-7
H/m. Normal typeface: reference level for the external field in the
meaning of Recommendation 1999/519/EC, derived from basic
restriction. Application is mandatory unless value is in square
brackets. Italic typeface: mandatory exposure limit in terms of the
external field outside the body. Radiofrequency limits are
standardised to approximate mobile telecommunication frequency
bands in Europe, but actual network frequencies may vary.
Notes:
1) For new power lines requiring environmental impact assessment,
authorities usually require compliance with Swiss limit of 1 µT
2) Flanders: indoor environment limit 10 µT, quality aim 0.2 µT,
government recommendation for new situations near power line
0.4 µT; Brussels: 0.4 µT near new transformers and 100 µT near
existing transformers; Wallonia: 5000 V/m and 100 µT near
transformers
3) Limit in table is for publicly accessible places in Flanders, limit
per antenna in places of stay 3.0 V/m at 900 MHz, 4.2 V/m at
1800 MHz, 4.5 V/m at 2100 MHz; Wallonia: limit per antenna
3 V/m; Brussels: limit per location 0.096 W/m
2
at 900 MHz,
0.19 W/m
2
at 1800 MHz, 0.22 W/m
2
at 2100 MHz
4) Minimal distances to power lines and to electrical distribution
systems, differentiated by voltage; separate regulation for video
display units
5) In homes, offices, schools, kindergartens, playgrounds, hospitals,
care homes, tourist facilities; for other public spaces reference
levels in 1999/519/EC apply
6) Danish Health Authority recommends that new homes and new
institutions where children stay should not be built close to
existing power lines and new power lines should not be built
close to existing homes and institutions where children stay
7) Radiation safety authority recommends avoiding construction of
permanent residences and premises meant for children in areas
where magnetic flux density exceeds 0.4 µT
8) For new or modified installations; there is also government
advice to local authorities not to create new establishments with
children in zones with magnetic flux density above 1 µT
9) For new or modified installations exhaust all possibilities to
minimise EMF; new power lines > 220 kV may not span
buildings for long-term stay of people
10) For antenna stations closer than 300 m to sensitive locations
(schools, kindergartens, hospitals, care homes); elsewhere 35
V/m, 0.11 µT, 3.1 W/m
2
at 900 MHz; 49 V/m, 0.16 µT, 6.3 W/m
2
at
1800 MHz; 51 V/m, 0.17 µT, 7 W/m
2
at 2100 MHz
11) For new energy infrastructure, State Companies and energy
developers must comply with ICNIRP limits and associated EU
Recommendations as an intrinsic part of the planning process
12) For new situations with power lines near homes, schools,
playgrounds, places with stay > 4 hours; 10 µT for existing
situations near homes, schools, playgrounds, places with stay
> 4 hours; 100 µT and 5000 kV/m for all other exposures from
power lines
13) EMF from fixed systems for telecommunication and radio or TV
broadcasting near homes and their outdoor annexes, in schools
and playgrounds, in places with stay greater than 4 hours;
elsewhere 20 V/m, 0.06 µT, 1 W/m
2
14) Inside residential and public buildings; limits for living
environment outside residential and public buildings 1000 V/m,
40 µT
15) Security conditions for electricity lines, there are also voluntary
minimal distances to power lines for new developments
16) Limit per antenna at places where people can stay 3.0 V/m,
applies to antennas with power of 100 W and higher
17) Ministerial recommendation: create no new situations of
long-term stay of children in magnetic flux density greater than
0.4 µT around overhead power lines, otherwise reference level in
1999/519/EC applies
18) Applies to homes, hospitals, health resorts, public buildings,
tourism buildings, schools, nurseries, playgrounds, parks,
recreational areas; otherwise limit for external electric and
magnetic field strength equal to reference level in 1999/519/EC;
for power frequency limits apply to new or reconstructed sources
only
19) No binding national limits for 50 Hz fields, but in practice
electricity companies and the authorities apply the limits in
1999/519/EC
20) Limit listed is for 50 Hz fields, power frequency is 50 Hz in East
Japan and 60 Hz in West Japan
21) Limit for living quarters, children’s, preschool, general and
medical institutions; non-residential premises 10 µT, inhabited
areas outdoors 20 µT, uninhabited areas 100 µT
22) Limit at places of sensitive use (buildings in which persons
regularly stay for longer periods, playgrounds) for all high
voltage installations except existing powerlines; otherwise
reference level in 1999/519/EC applies at all places accessible for
the public
23) Limit at places of sensitive use (buildings in which persons
regularly stay for longer periods, playgrounds) for individual
antenna installations; otherwise reference level in 1999/519/EC
applies at all places accessible for the public
24) Power frequency is 60 Hz; no federal regulation, limits in some
states, prudent avoidance policy in others (measures to reduce
exposure at reasonable cost)
16
|
Comparison of international policies on electromagnetic fields
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
2259378_1700.png
Table
2
Occupational reference levels or exposure limits for electromagnetic fields in member states of the European
Union and selected industrial nations outside the European Union (situation July
2017)
50
Hz
electric field
strength (high AL)
(V/m)
magnetic flux
density (high AL)
(µT)
900
MHz
alternative
protection system
for armed forces
temporary
exemption
from ELV for
specific sectors or
activities
yes
yes
2)
yes
no
yes
yes
no
no
no
yes
no
yes
4)
Yes
5)
yes
6)
no
yes
7)
no
no
yes
9)
yes
no
no
no
yes
yes
yes
12)
yes
no
yes
13)
conditional
exemption
from ELV for MRI
yes
yes
yes
yes
yes
yes
equivalent plain
wave power
density
(W/m
2
)
—
—
—
—
—
—
Country:
20 3/35/EU
Austria
Belgium
Bulgaria
Croatia
Cyprus
Czech Republic
Denmark
Estonia
Finland
France
Germany
Greece
Hungary
Ireland
Italy
Latvia
Lithuania
Luxemburg
Malta
Netherlands
Poland
Portugal
Romania
Slovakia
Slovenia
Spain
Sweden
United Kingdom
magnetic flux
density
(µT)
electric field
strength
(V/m)
20000
20000
1)
20000
20000
20000
20000
10000
20000
20000
20000
20000
3)
20000
20000
20000
20000
20000
20000
20000
20000
20000
20000
10000
10)
20000
11)
20000
20000
20000
20000
20000
20000
6000
6000
1)
6000
6000
6000
6000
1000
6000
6000
6000
6000
3)
6000
6000
6000
6000
6000
6000
6000
6000
6000
6000
2000
10)
6000
11)
6000
6000
6000
6000
6000
6000
90
90
1)
90
90
90
90
90
90
90
90
90
3)
90
90
90
90
90
90
90
90
90
90
60
10)
90
11)
90
90
90
90
90
90
0.30
0.30
1)
0.30
0.30
0.30
0.30
0.30
0.30
0.30
0.30
0.30
3)
0.30
0.30
0.30
0.30
0.30
0.30
0.30
0.30
0.30
0.30
0.20
10)
0.30
11)
0.30
0.30
0.30
0.30
0.30
0.30
yes
no
no
yes (NATO)
yes
yes
no
no
yes (NATO)
yes
no
no
Yes (NATO)
yes (NATO)
no
yes
yes
yes
8)
yes (NATO)
9)
yes
yes
yes
yes
yes
yes
yes
yes (NATO)
yes
yes
22.5
no
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
—
yes
yes
yes
yes
4)
yes
4)
yes
no
6)
yes
no
7)
yes
yes
yes
9)
yes
yes
no
yes
yes
yes
yes
yes
yes
yes
Australia
China
India
Japan
Russia
Switzerland
U.S.A.
0000
5000
—
—
15)
—
0000
17)
—
18)
000
—
—
—
15)
2000
16)
500
17)
—
18)
92
—
—
—
15)
—
90
17)
—
0.3
—
—
—
15)
—
0.30
17)
—
22.5
50
14)
—
—
15)
0
16)
22.5
17)
30
power frequency and radiofrequency fields
|
17
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Legend to Table 2: All limits are given as root mean square (rms)
value. Where necessary magnetic flux density was calculated from
magnetic field strength using a magnetic permeability of
4π × 10
7
 H/m.
Normal typeface: action level (AL)/reference level for
the external field in the meaning of Directive 2013/35/EU or ICNIRP
guidelines, derived from exposure limit value (ELV)/basic restriction.
Application is mandatory unless value is in square brackets. Italic
typeface: mandatory exposure limit in terms of the external field
outside the body.
Notes:
1) Limits in EU recommendation 1999/519/EC apply to pregnant
workers; AL may not be exceeded for workers younger than
18 years; sensory effects ELV may only be exceeded for resistance
welding and electricity supply sector
2) Sensory and health effects ELV may be temporarily exceeded for
workers in delimited areas in establishments for generation,
transport and distribution of electrical energy
3) Limits in EU recommendation 1999/519/EC apply to pregnant
workers; sensory effects ELV may not be exceeded for workers
younger than 18 years
4) Exemption with additional obligations to those in Directive
2013/35/EU
5) For any temporary exemption from ELV for a specific sector or
activity, the National Occupational Health & Safety Council shall
give its expert opinion beforehand
6) Regional radiation safety officer may allow exposure of workers
to exceed health effects ELV in specific circumstances where
state-of-the-art technical and organisational protection
measures have been implemented; annexes to national
legislation contain list of equipment requiring risk assessment
approval, including MRI
7) Ministers of Labour and Social Policy and of Health may grant a
conditional and temporary derogation at the request of the
employer, with additional requirements for MRI
8) Scope extended: military personnel or national security, public
security and customs officials as determined by Lithuanian
intelligence regulations
9) Employer is obliged to check the appropriateness of the
measures taken with an approved expert acting within the
competences and authority of the labour inspectorate
10) Values listed are for basic ‘threat’ AL, there are also higher
‘danger’ AL, lower ‘intermediate’ AL for indirect effects and
ancillary AL for modulated fields
11) Employer shall ensure that the exposure of workers to
electromagnetic fields is reduced to the lowest possible level, but
in any case it should not exceed ELV
12) Sensory and health effects ELV may be temporarily exceeded for
workers in police, other units and services for protection, rescue
and relief in specific circumstances
13) Temporary conditional exemption from ELV for electrolysis,
dielectric heating, induction heating, manual resistance welding,
MRI equipment other than that for patients
14) Limit for short exposures, for longer exposures limits decrease
down to 0.5 W/m
2
(continuous wave) or 0.25 W/m
2
(pulsed) for
8 hours with whole body exposure
15) No legal limits for workers, Japan Society for Occupational
Health has recommended occupational exposure limits in terms
of the strength of external electric and magnetic field and power
density identical to the low action levels and thermal effects
action levels in the EU directive
16) Limit for exposures shorter than 1 hour, for longer exposures
limits decrease down to 100 µT for 8 hours; for radiofrequency
fields there are also limits on exposure x time
17) For pregnant workers, exposure limits identical to the reference
levels in EU recommendation 1999/519/EC apply
18) No legal limits for workers, American Conference of
Governmental Industrial Hygienists has recommended
‘threshold limit values’ of 25000 V/m and 1000 µT at 60 Hz as
guidelines to assist in the control of potential workplace health
hazards
18
|
Comparison of international policies on electromagnetic fields
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
2259378_1703.png
Rianne Stam
Colophon
The author thanks the many scientific and policy experts
who contributed information and reviewed a draft
version of the document.
Author: Rianne Stam
© RIVM 2017
Parts of this publication may be reproduced, provided
acknowledgement is given to the ‘National Institute for
Public Health and the Environment, RIVM’, along with
the title and year of publication.
Published by:
National Institute for Public Health
and the Environment, RIVM
PO Box 1 | 3720 BA Bilthoven
The Netherlands
www.rivm.nl/en
January 2018
Committed to
health and sustainability
010344
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Metoder til fastsættelse af
kvalitetskriterier for kemiske stoffer i
jord, luft og drikkevand med henblik
på at beskytte sundheden
Vejl edn in g f r a Mil jøst yr el sen
Nr. 5
2006
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Indhold
FORORD
1
IN D LED N IN G
5
7
1.1 H
VAD ER KVALIT ET SKRIT ERIER
7
1.1.1 Formål med fastsættelse af kvalitetskriterier for
kemikalier
7
1.1.2 Generelle principper for fastsættelse af
kvalitetskriterier for kemikalier
9
1.2 V
EJLED N IN G EN S OPBYG N IN G OG IN D HOLD
10
1.3 Æ
N D RIN G ER I FORHOLD T IL T ID LIG ERE PRAKSIS
12
R
EFEREN C ER
13
2 D AT AG RUN D LAG FOR VURD ERIN G AF
FARLIG H ED
2.1 D
AT A FRA M EN N ESKER
2.2 D
YREEKSPERIM EN T ELLE UN D ERSØG ELSER
2.3 A
N D RE T YPER D AT A
2.4 I
N D HEN T N IN G AF D AT A
R
EFEREN C ER
3 FARLIG H ED SVURD ERIN G OG
FARLIG H ED SKARAKT ERISERIN G
3.1
D
OSIS
-
EFFEKT OG D OSIS
-
RESPON S
20
21
22
24
24
25
26
26
27
27
29
SAM M EN HÆ N G E
3.2 F
AST SÆ T T ELSE AF N UL
-
EFFEKT N IVEAU OG
LAVEST E EFFEKT N IVEAU
3.3 B
EN C HM ARK
-
M ET OD EN
3.4 U
D PEG N IN G AF KRIT ISK EFFEKT
3.5 R
ELEVAN S AF VISSE EFFEKT ER I FORSØG SD YR
R
EFEREN C ER
14
14
16
17
18
19
20
4 BEREG N IN G AF T D I FOR ST OFFER M ED
T Æ RSKELVÆ RD I
4.1 T D I-
BEG REBET
4.2 A
N VEN D ELSE AF USIKKERHED SFAKT ORER
4.2.1
Usikkerhedsfaktor I
4.2.2
Usikkerhedsfaktor II
3
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
4.2.3
4.2.4
Usikkerhedsfaktor III
Samlet usikkerhedsfaktor
R
EFEREN C ER
5 BEREG N IN G AF T D I FOR
KRÆ FT FREM KALD EN D E ST OFFER
5.1
29
32
33
34
K
RÆ FT FREM KALD EN D E ST OFFER M ED OG UD EN
T Æ RSKELVÆ RD I
34
5.2 V
URD ERIN G AF KRÆFT FREM KALD EN D E EFFEKT
35
5.3 B
EREG N IN G AF
T D I
FOR KRÆFT FREM KALD EN D E
ST OFFER UD EN T ÆRSKELVÆRD I
37
5.3.1
T olerabelt risikoniveau
37
5.3.2
M etode til beregning af T DI og livstidsrisiko 37
5.3.3
Anvendelse af risikoestimater angivet i litteraturen38
R
EFEREN C ER
39
6 BEREG N IN G AF KVALIT ET SKRIT ERIER FOR
KEM IKALIER
40
6.1 G
EN EREL M ET OD E FOR BEREG N IN G AF ET
40
6.1.2 Anvendelse af T DI
41
6.1.3 Eksponeringsbetragtninger
42
6.2 B
EREG N IN G AF LUFT KVALIT ET SKRIT ERIET
43
6.3 B
EREG N IN G AF JORD KVALIT ET SKRIT ERIET
45
6.4 B
EREG N IN G AF D RIKKEVAN D SKVALIT ET SKRIT ERIET
47
R
EFEREN C ER
49
KVALIT ET SKRIT ERIUM
BILAG 1
K
VAN T IT AT IV VURD ERIN G VED BEN YT T ELSE AF
T 25
EKST RAPOLAT ION SM ET OD EN
.
Anbefaling af T 25-metoden
Anvendelse af T 25-metoden
R
EFEREN C ER
BILAG 2
B
AG G RUN D FOR AN VEN D T E EKSPON ERIN G SVÆRD IER
VED BEREG N IN G AF KVALIT ET SKRIT ERIER
50
50
50
51
54
55
55
57
58
59
62
62
Luft, daglig standardeksponering
Jord, daglig standardeksponering
Drikkevand, daglig standardeksponering
BILAG 3
A
N VEN D T E FORKORT ELSER
4
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Forord
Principperne for vurdering og fastsættelse af kvalitetskriteri-
er for kemikalier med henblik på at beskytte sundheden er
1
beskrevet tidligere . M en i forbindelse med M iljøministerens
redegørelse om jordforureningsloven i 2003, besluttede re-
geringen at nedsætte en arbejdsgruppe, som fik til opgave at
”vurdere,
hvorvidt de sundhedsmæssige kvalitetskriterier ligger
på det rigtige niveau i relation til international praksis, samt
give forslag til ændringer.
Arbejdsgruppen udpegede en række politiske valg, der ind-
går i principperne for fastsættelse af kvalitetskriterier. På
den baggrund blev der i december 2005 indgået en aftale
mellem M iljøministeren og et bredt udsnit af Folketingets
partier, som bl.a. fastlægger følgende
generelle principper
for fastsættelsen
af forebyggende kriterier :
H ovedparten af befolkningen skal fortsat beskyttes (dvs.
hensyntagen til særligt udsatte skal også inddrages).
D er skal tages specifikt hensyn til børn.
Det fastholdes, at der højst anvendes en samlet
usikkerhedsfaktor på 10.000, når resultater fra dy-
reforsøg overføres til mennesker.
-6
D er accepteres fortsat en livstidsrisiko på 10 .
D enne vejledning indarbejder disse principper og gennem-
går de metoder, som skal anvendes ved fastsættelse kvali-
tetskriterier for jord, luft og drikkevand med henblik på at
2
beskytte sundheden .
1
M iljøstyrelsens Vejledning nr. 1 ”Sundhedsmæssig vurdering af
kemiske stoffer i drikkevand ”, 1992, og i bilag til M iljøstyrelsens
Vejledning nr. 6, 1990 ”Begrænsning af luftforurening fra virk-
somheder” samt i M iljøprojekt nr. 12, 1995 ”T oksikologiske kva-
litetskriterier for jord og drikkevand”.
2
Principper for fastsættelse af kvalitetskriterier med henblik på at
beskytte miljøet er tilsvarende beskrevet i M iljøstyrelsens vejled-
5
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Vejledningen henvender sig til centrale og lokale myndighe-
der, herunder embedslægeinstitutionerne, konsulenter, råd-
givere og virksomheder.
M iljøstyrelsen fastsætter løbende kvalitetskriterier for kon-
krete kemiske stoffer i jord, luft og drikkevand med henblik
på at beskytte sundheden, jf. M iljøbeskyttelsesloven § 14,
stk. 1,. Kvalitetskriterierne bliver fastsat på baggrund af
videnskabelige rapporter og efter drøftelse i en styregruppe
med deltagelse af bl.a. Fødevarestyrelsen, Arbejdstilsynet og
Sundhedsstyrelsen.
D enne vejledning og detaljeringsgraden, ikke mindst i den
3
tilhørende faglige rapport , skal give grundlag for større
forståelse for, hvordan kvalitetskriterier skal udarbejdes.
Kvalitetskriterierne anvendes dels til at vurdere alvoren af
en allerede given forurening, og dels når myndighederne
stiller krav i forbindelse med udledning af konkrete stoffer til
omgivelserne.
ning nr. 4 (2004): Principper for fastsættelse af vandkvalitetskrite-
rier for stoffer i overfladevand.
3
M iljøprojekt N r. 974, M iljøstyrelsen (2005). Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik på
fastsættelse af kvalitetskriterier for luft, jord og vand. Rapporten er
udarbejdet af Institut for Fødevaresikkerhed og Ernæring, Føde-
varedirektoratet (nu D anmarks Fødevareforskning) i samarbejde
med M iljøstyrelsen.
6
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
1 Indledning
1.1 Hvad er kval it et skr it er ier
1.1.1 Formål med fastsættelse af kvalitetskriterier for kemikali-
er
D enne vejledning beskriver den administrative praksis ved
fastsættelse af kvalitetskriterier for kemikalier med henblik
på at beskytte sundheden.
Kvalitetskriterier danner basis for en række vurderinger af
administrativ karakter, som vedrører både jord, luft og drik-
kevand.
M ålsætningen ved fastsættelsen af kvalitetskriterier for ke-
mikalier er, at de skal medvirke til
at forebygge forurening og
skader på sundheden.
Kvalitetskriterierne ses som et element
i lovens overordnede politiske målsætning om at oppebære
et højt beskyttelsesniveau for befolkningens sundhed og
sikre en bæredygtig udvikling, herunder fremme af renere
teknologi.
Kvalitetskriterierne angiver et højt beskyttelsesniveau, hvor
ingen effekt kan forventes, selv ved udsættelse gennem et
helt liv, eller hvis der er tale om et stof uden tærskelværdi,
en teoretisk forøget risiko for kræft hos én ud af en million
mennesker, som er udsat for stoffer gennem et helt liv på 70
år.
Kvalitetskriterierne bruges af myndighederne i forbindelse
med vurdering af alvoren af et givet forureningsniveau. D et
kan være relevant, hvis der er tale om en eksisterende foru-
rening (fortidens synder), eller hvis der skal fastsættes krav-
værdier for udledning af konkrete stoffer i miljøet (forebyg-
gende). For begge situationer kan andre forhold end de
sundhedsmæssige spille ind, såsom baggrundsniveauer og
tekniske/økonomiske overvejelser. Ved indsatsen i forhold til
eksisterende forureninger kan der også være behov for at
7
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vurdere, hvad der er sundhedsmæssigt forsvarligt, når der
tages hensyn til overordnede samfundsmæssige prioriterin-
ger. M ed udgangspunkt i de sundhedsmæssigt fastsatte kva-
litetskriterier udarbejdes således en række administrativt
fastsatte kriterier.
Eksempler på administrative kriterier som er baseret på kva-
litetskriterier er:
1. Luftkvalitetskriteriet anvendes som udgangspunkt til at
fastsætte bidrags værdier (B-værdier), der anvendes i
forbindelse med regulering af virksomheders udslip af
kemiske stoffer til udeluften.
2. Luftkvalitetskriteriet anvendes til at vurdere afdamp-
ning af kemiske stoffer fra jordforureninger. D et an-
vendes også ved kortlægning og offentlig oprydning af
forurenede grunde.
3. Jordkvalitetskriterier anvendes som udgangspunkt ved
fastsættelse af administrative kriterier, der anvendes ved
de lokale myndigheders kortlægning af forurenede
grunde og i forbindelse med vurderinger af arealanven-
delse, samt ved offentlig oprydning af forurenede
4
grunde
.
4. Jordkvalitetskriteriet anvendes endvidere som udgangs-
punktet for fastsættelse af afskæringskriteriet for visse
immobile stoffer. Afskæringskriteriet anvendes ved let-
tere forurenede områder som skillelinie mellem det ni-
veau, hvor det er nødvendigt at fjerne jorden og det ni-
veau, hvor det er tilstrækkeligt at iværksætte særlige
forholdsregler i forbindelse med følsom anvendelse af
områderne, som fx private haver eller børneinstitutio-
ner.
5. D rikkevandskvalitetskriteriet anvendes af de centrale og
decentrale myndigheder i forbindelse med håndtering
af konkrete sager med kemisk forurening af drikkevand,
som et supplement til de kravværdier, der er fastsat i
bekendtgørelsen om vandkvalitet.
6. D rikkevandskvalitetskriterierne anvendes som ud-
gangspunkt ved fastsættelse af grundvandskvalitetskri-
terier i tilknytning til nedsivning fra jordforureninger,
Kvalitetskriterierne omfatter normalt ikke en vurdering af om
arealer kan anvendes til dyrkning af nytteplanter eller til afgræs-
ning for husdyr.
4
8
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idet grundvandet skal være af en kvalitet, så de fastsatte
drikkevandskrav/ -kvalitetskriterier kan overholdes.
D er eksisterer en række vejledninger og lister, som nærmere
beskriver baggrunden for, hvordan et kvalitetskriterium kan
5
anvendes.
1.1.2 Generelle principper for fastsættelse af kvalitetskriterier
for kemikalier
Kvalitetskriterierne fastsættes på et niveau, hvor udsættelse
gennem et helt liv ikke fører til skadevirkninger i befolknin-
gen. D e fastsættes på baggrund af den eksisterende viden og
under hensyntagen til de mangler, der ligger i datagrundla-
get.
For at minimere risici for skadelig påvirkning af befolknin-
gen indgår beskyttelse af særligt følsomme grupper fx børn,
gravide, syge, ældre og svækkede ved fastsættelse af kvali-
tetskriterier.
Viden om et kemisk stofs sundhedsskadelige egenskaber og
om bestemte befolkningsgruppers særlige følsomhed er
sjældent så eksakt, at der kan fastsættes et kvalitetskriterium,
der præcist definerer skillelinien (hvis en sådan overhovedet
findes) mellem et ufarligt og farligt niveau. Kvalitetskriteri-
erne kan således ikke opfattes som en streg i sandet, hvor
enhver overskridelse er farlig. Ved fastsættelse af kvalitets-
kriterier for kemikalier skal anvendes en forsigtighedstil-
gang, da målet er at sikre et højt beskyttelsesniveau for alle
ved udsættelse over et helt liv.
Et kvalitetskriterium skal således opfattes som en sikker-
hedsgrænse og ikke en faregrænse. En overskridelse er ”det
gule lys”, som advarer om, at her er noget, som måske kan
blive et reelt problem.
Luftvejledningen, M iljøstyrelsens Vejledning nr. 2, 2001; Op-
rydning på forurenede lokaliteter
5
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1.2 Vejl edn in gen s opbygn in g og in dh ol d
Vejledningen udstikker retningslinier for den faglige risiko-
vurdering og for de metoder/ principper der anvendes.
D ernæst beskrives proceduren for beregning af kvalitetskri-
terierne (se figur 1).
D ata-og litteratursøgning
Farlighedsvurdering og
farlighedskarakterisering;
identifikation af kritisk
effekt
Stoffer med tærskel-
værdi: T D I ud fra
N OAEL for den
kritiske effekt; anven-
delse af usikkerheds-
Stoffer uden tærskel-
værdi: Beregning af
T D I svarende til en
tolerabel livstidsrisiko-
dosis.
Beregning af kvalitetskriterie
med udgangspunkt i T D I-
værdi og eksponeringsværdi
for de aktuelle medier.
Figur 1.
Fr emgan gsmåden ved ber egn in g af kval it et skr it er ium
(TDI=Tol er abel Dagl igt In dt ag)
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D et videnskabelige grundlag for fastsættelse af sundheds-
mæssigt baserede kvalitetskriterier for kemiske stoffer i jord,
luft og drikkevand består af en farlighedsvurdering, en do-
sis-respons (effekt) vurdering (farlighedskarakterisering),
samt en eksponeringsvurdering. Farlighedsvurderingen og
farlighedskarakteriseringen tager udgangspunkt i undersø-
gelser af det pågældende stofs toksikologiske effekter i men-
nesker og i dyr.
I kapitel 2 omtales
Datagrundlaget
som anvendes som ud-
gangspunkt for arbejdet. D ata hentes primært fra internati-
onale og nationale dokumenter, via litteratursøgning i inter-
nationale databaser, samt fra originalartikler.
Kapitel 3 behandler de faglige metoder, der anvendes i for-
bindelse med farlighedsvurderingen og farlighedskarakteri-
seringen. D osis-effekt og dosis-responssammenhænge og
udpegning af N OAEL (N o Observed Adverse Effect Level)
og LOAEL (Lowest Observed Adverse Effect Level) be-
skrives.
I kapitel 4 beskrives hvordan farlighedskarakteriseringen
udmunder i udpegning af en kritisk effekt, som danner ud-
gangspunkt for fastsættelse af en
tolerabel daglig indtagelse,
T DI.
H er omtales, hvordan anvendelsen af usikkerhedsfak-
torer indgår i beregningerne.
I kapitel 5 omtales, hvordan T D I beregnes for kræftfrem-
kaldende stoffer uden tærskelværdi. Risikoniveauet for
T D I-værdien defineres, og der gives retningslinier med
hensyn til valg af metode til, hvordan beregningen af dette
risikoniveau foretages.
Kapitel 6 beskriver, hvordan den videre beregning af kvali-
tetskriterier for kemiske stoffer i jord, luft og drikkevand
foretages ud fra de fastsatte T D I-værdier. I bilag 2 til vej-
ledningen omtales rationalet for at anvende konkrete stan-
dardbetragtninger m.h.t. personers udsættelse for forure-
ninger gennem jord, luft og drikkevand. Endvidere omtales
hvilke andre faktorer (fx hensyntagen til lugt eller smag)
end de rent sundhedsmæssige, der i visse tilfælde kan have
indflydelse på kvalitetskriteriet.
11
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2259378_1715.png
1.3 Æ dr in ger i f or h ol d t il t idl iger e pr aksis
n
Ved fastsættelsen af kvalitetskriterier anvendes der interna-
tionalt anerkendte principper. I denne forbindelse skal
fremhæves de principper og metoder, der er beskrevet i to
6,7
publikationer af WH O/ IPC S om udarbejdelsen af vejle-
dende grænseværdier og risikovurdering af kemisk udsættel-
8,9
se. WH O´s publikationer omhandlende risikovurdering og
fastsættelse af vejledende grænseværdier for en række kemi-
ske stoffer i drikkevand og luft har også indgået i arbejdet.
På tilsvarende vis er der en tæt sammenhæng med de prin-
cipper og metoder, der anvendes i forbindelse med EU´s
10
risikovurderingsprogram for kemiske stoffer .
På visse områder indebærer denne vejledning, at den hidti-
dige praksis for fastsættelse af kvalitetskriterier justeres. D et-
te gælder fx for beregning af kvalitetskriterier for kemikalier
i luft og drikkevand, idet der nu som udgangspunkt anven-
des standardværdier for børns udsættelse (se kapitel 6 og
bilag 2).
I forbindelse med ekstrapolering af tolerabelt risikoniveau
for genotoksiske kræftfremkaldende stoffer (dvs. kræftfrem-
kaldende stoffer hvor der ikke anses at være en tærskelværdi
for effekt), anvendes lineær ekstrapolation ud fra den så-
6
WH O/IPC S (1994). Assessing human health risks of chemicals:
D erivation of guidance values for health-based exposure limits.
Environmental H ealth C riteria no. 170. International Programme
on C hemical Safety.
7
WHO/IPC S (1999). Principals for the assessment of risks to
human health from exposure to chemicals. Environmental H ealth
C riteria no. 210. International Programme on C hemical Safety.
8
WHO (1996). G uidelines for drinking-water quality 2
nd
edition,
vol 2. H ealth C riteria and other supporting information. Interna-
tional Programme on C hemical Safety.
9
WHO (2000). Air Quality G uidelines for Europe, 2
nd
edition.
WH O Regional Publications, European Series, no. 91.
10
EEC (2003). T echnical G uidance D ocument in support of
C ommission D irective 93/67/EEC on risk assessment for new
notified substances and C ommission Regulation (EC ) N o.
1488/94 on risk assessment for existing substances and D irective
98/8/EC of the European Parliament and of the C ouncil concern-
ing the placing of biocidal products on the market.
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2259378_1716.png
kaldte T 25- metode udviklet i forbindelse med EU´s risiko-
vurderingsprogram (kapitel 5).
H vis datagrundlaget er til stede, anbefales det at anvende
benchmark-metoden ved fastsættelse af T D I (kapitel 3).
D et skal bemærkes, at denne vejledning anvender begrebet
usikkerhedsfaktorer, hvor man tidligere anvendte begrebet
sikkerhedsfaktorer. D els beskriver ordet
usikkerhed
i højere
grad faktorernes anvendelse, idet de netop tager højde for
usikkerheder. D els imødegås den misforståelse, at en stor
sikkerhedsfaktor for et stof medfører større sikkerhed for
dette stof i forhold til en lille anvendt sikkerhedsfaktor for et
andet stof. Faktorerne anvendes derimod for at opnå et ens-
artet beskyttelsesniveau, og størrelsen af faktorerne afspejler
usikkerheder som følge af usikker viden og manglende data-
grundlag.
D e angivne metoder i vejledningen anvendes fremover ved
fastsættelse af kvalitetskriterier.
D e ændringer der er sket i forhold til tidligere praksis bety-
der ikke, at de eksisterende kvalitetskriterier skal ”laves om”,
idet anvendelse af de nye metoder ikke vurderes at påvirke
beskyttesesniveauet væsentligt. N år et kvalitetskriterium
tages op til revurdering bør dette ske både m.h.t. til revur-
dering af de sundhedsmæssige data og af de eksponerings-
mæssige forhold. En revurdering foretages derfor fuldt ud
med alle de vurderingsmæssige og beregningsmæssige faser,
der er beskrevet i vejledningen.
Ref er en cer
Bekendtgørelse af Lov om miljøbeskyttelse (M iljøbeskyttel-
sesloven). Lovbekendtgørelse nr. 753 af 25. august 2001.
M iljøstyrelsen (1991). Orientering om ny miljøbeskyttelses-
lov. Orientering nr. 6, 1991.
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2 Datagrundlag for vurdering af far-
lighed
Fastsættelse af kvalitetskriterier for et kemisk stof sker på
baggrund af eksisterende viden om stoffets sundhedsskade-
lige egenskaber.
Kvalitetskriterierne fastsættes med henblik på beskyttelse af
menneskers sundhed, og det ideelle datagrundlag for fast-
sættelse af et kvalitetskriterium er derfor viden, hvor menne-
sker har været udsat for det konkrete stof. For langt de fleste
kemiske stoffer er der kun begrænset viden om veldefineret
udsættelse og effekter hos mennesker, og kvalitetetskrite-
rierne vil som oftest være baseret på viden opnået fra dyre-
11
forsøg med mere veldefineret udsættelse eller
in vitro
data .
For en mere detaljeret beskrivelse af nedenstående afsnit
henvises til kapitel 2, M iljøprojekt N r. 974 (2005).
2.1 Dat a f r a men n esker
Fordelen ved at anvende data, hvor mennesker har været
udsat for et kemisk stof, er, at man undgår at skulle overføre
data fra dyreforsøg, og estimere hvad en tilsvarende udsæt-
telse betyder hos mennesker. Erfaringer med menneskers
udsættelse kan stamme fra en række forskellige typer under-
søgelser og afrapporteringer, der groft kan deles op på føl-
gende måde:
-
-
-
case reports og kliniske undersøgelser
befolkningsundersøgelser (fx arbejdsmiljø eller udvalgte dele
af befolkningen)
undersøgelser af frivillige forsøgspersoner
11
D ata fra reagensglasforsøg.
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Ved
case reports og kliniske undersøgelser
opnås data fra for-
giftningstilfælde eller erfaringer fra undersøgelser i klinik-
ken, hvor personer fx i behandlingsøjemed udsættes for
stoffer for at vurdere eventuelle allergiske reaktioner. For-
delen ved disse typer data er, at man her umiddelbart kan se
en sammenhæng mellem udsættelse og (akutte) effekter.
I
befolkningsundersøgelser
vurderes en større gruppe af men-
nesker mere systematisk med hensyn til sammenhængen
mellem udsættelse og sundhedsskader. D isse undersøgelser
kan fx omfatte sundhedsovervågning af særlige grupper i
arbejdsmiljøet, hvor personerne er karakteriseret ved en
særlig udsættelse, eller man kan undersøge, om der hos per-
soner, der har udviklet nogle konkrete sygdomme, er nogle
fælles karakteristika med hensyn til kemiske påvirkninger.
Fordelen ved at anvende data fra denne type undersøgelser
er, at man er meget tæt på den målgruppe, man ønsker at
beskytte med kvalitetskriterierne. Samtidig ses effekterne i
sammenhæng med den dagligdag, som mennesker nu en-
gang fungerer i, hvor man udsættes for en kompleks blan-
ding af livsstilsfaktorer og miljøfaktorer. Ulempen er, at det
ofte er vanskeligt at vurdere omfanget af udsættelsen af en
given komponent, og at det pga. mange andre samvirkende
faktorer kan være svært at påvise sammenhænge, som kan
være sløret af al ”støjen” fra andre faktorer. Ligesom under-
søgelserne kun sjældent kan dokumentere en årsags-
virkningssammenhæng, vil de også kun uhyre sjældent kun-
ne anvendes til at dokumentere manglende sammenhæng,
dvs. frikende stoffer.
I
undersøgelser med frivillige forsøgspersoner
udsætter man i
reglen forsøgspersonerne i en kortere varighed for et kon-
kret stof for at vurdere effekterne. D isse undersøgelser er
meget sammenlignelige med dyreforsøg, hvor man tilsva-
rende har en meget veldefineret udsættelse. D e naturlige og
etiske begrænsninger ved disse undersøgelser betyder, at der
hos mennesker kun kan undersøges for lettere grader af
akutte effekter og i sammenhæng med kortere tids forsøgs-
udsættelse. Endvidere er forsøgspersonerne sjældent særligt
følsomme, som visse undergrupper i befolkningen kan være.
M an skal være meget opmærksom på det etiske aspekt
m.h.t. anvendelse af frivillige forsøgspersoner. I forbindelse
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med vurdering af konkrete humane undersøgelser i risiko-
vurderingssammenhæng, bør anvendelsen af disse data vur-
deres nøje såvel ud fra etiske som kvalitetsmæssige hensyn.
Især ældre undersøgelser kan være udført under stærkt kriti-
sable forhold og med store undersøgelsesmæssige mangler.
Kvalitetskriterier for kemikalier fastsættes ud fra eksisteren-
de data, og det frarådes generelt at igangsætte humanforsøg
for at opnå øget viden om konkrete stoffers skadelige effek-
ter.
2.2 Dyr eeksper imen t el l e un der søgel ser
For de fleste kemiske stoffer foreligger der ikke data fra
menneskers udsættelse, hvorfor kvalitetskriterier hyppigst
baseres på data fra dyreeksperimentelle undersøgelser.
Resultaterne fra dyreforsøgene anvendes således som model
og anvendes til at forudsige hvilke effekter, der kan forven-
tes hos mennesker. D yreeksperimentelle data kan også be-
nyttes som supplement til humane data, der ikke er entydi-
ge, eller til at udpege de aktive stoffer, når mennesker har
været udsat og reageret over for blandinger af stoffer.
Fordelene ved dyreforsøg er, at der er tale om standardise-
rede forsøgsbetingelser, og at der er mulighed for at afsløre
væsentlig flere effekter hos forsøgsdyr end hos mennesker,
da organer og væv kan undersøges efter forsøgets afslut-
ning. D er er også mulighed for at undersøge virkningsme-
kanismer og detaljerede dosis-effekt og dosis-
responssammenhænge for enkeltstoffer.
Ideelt set ønskes der ved fastsættelsen af kvalitetskriterier for
et kemikalie et fuldt datasæt bestående af dyreeksperimen-
telle undersøgelser til vurdering af en række toksikologiske
egenskaber: T oksikokinetik (optagelse og udskillelse), akut
toksicitet, irritation, sensibilisering (allergi), toksicitet ved
gentagen administration af stoffet, mutagenicitet og geno-
toksicitet (påvirkning af arvematerialet), kræftfremkaldende
effekter, samt effekter på reproduktion og fosterudvikling.
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2259378_1720.png
D yreforsøg har imidlertid også begrænsninger, da nogle
effekter kan være vanskelige at afsløre fx lettere grader af
slimhindeirritation i øjne og luftveje, lettere grader af på-
virkning af centralnervesystemet og visse typer nerveskader.
Endelig kan nogle dyrearter udvikle artspecifikke effekter
over for visse stoffer, hvor relevansen i forhold til udsættelse
af mennesker er meget omdiskuteret (se afsnit 3).
D et er endvidere vigtigt at vurdere kvaliteten af de dy-
reeksperimentelle undersøgelser, der anvendes som ud-
gangspunkt for fastsættelse af kvalitetskriterier. Undersøgel-
ser af høj kvalitet, som er udført efter eller på niveau med
OEC D ´s eller EU´s retningslinier for forsøgsdyrstestning,
bør foretrækkes. Ved risikovurderingen i forbindelse med
fastsættelse af kvalitetskriterier er der dog ikke nogle formel-
le kvalitetskrav til undersøgelserne, idet en lang række un-
dersøgelser i den videnskabelige litteratur ofte vil være ud-
ført i forskningsøjemed uden at undersøgelserne er udført
efter en officiel forsøgsguideline eller i overensstemmelse
12
med G LP-reglerne. Sådanne undersøgelser, der ofte er
kvalitetssikret i peer-reviewede tidsskrifter, kan indeholde
væsentlig information. Forsøgets kvalitet og validitet må i de
aktuelle tilfælde vurderes, og der tages stilling til om forsø-
get kan være af betydning ved fastsættelse af et kvalitetskri-
terium.
På baggrund af de etiske aspekter ved dyreforsøg arbejdes
der internationalt med at udvikle alternative
in vitro
meto-
der.
2.3 An dr e t yper dat a
Ud over forsøg på levende dyr foreligger der ofte undersø-
gelser der er udført på udtagne organer, væv eller isolerede
celler. D isse
in vitro
metoder finder især anvendelse til vur-
dering af stoffers toksiske effekt på organ-/celleniveau sær-
ligt m.h.t. mutagene og genotoksiske effekter.
12
G LP står for G ood Laboratory Practice, og er et regelsæt ud-
viklet af OEC D for at sikre kvaliteteten af undersøgelserne.
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2259378_1721.png
N ormalt kan
in vitro
forsøg ikke anvendes til at fastlægge
tærskel for effekt (N OAEL e.l.), men de vil indgå i bedøm-
melsen af stoffets farlighed. In vitro-data kan således styrke
mistanken om skadeeffekter og derved påvirke valget af
usikkerhedsfaktorer (se afsnit 4).
Ved mangel på data for et konkret stof kan data fra nært
beslægtede stoffer indgå i vurderingen ud fra betragtninger
om kemisk strukturlighed og sammenfaldende effekter. Så-
danne data kan have indflydelse på den rent kvalitative, men
også i visse tilfælde i den kvantitative vurdering, hvis det
konkret vurderes, at der er grundlag for meget snævert kob-
lede analogislutninger.
Endvidere kan der udføres en mere systematisk analyse ved-
rørende kvantitative struktur-aktivitets relationer (engelsk:
Quantitative Structure Activity Relationships – QSARs).
Anvendelse af denne form for computerbaserede modeller
har i en række tilfælde vist sig som et alternativ til dyrefor-
søg med henblik på forudsigelse af toksikologiske egenska-
13
ber (M ST 2001 ). Vurderingerne kan sjældent anvendes
som udgangspunkt for beregning af kvalitetskriteriet, men
vil i visse tilfælde kunne anvendes til styrkelse af mistanken
om konkrete effekter. QSAR vil således kunne påvirke val-
get af usikkerhedsfaktorer ved beregning af kvalitetskriteriet.
2.4 In dh en t n in g af dat a
Som udgangspunkt for udarbejdelse af kvalitetskriterier
anvendes i udstrakt grad internationalt anerkendte stofmo-
nografier og dokumenter, hvor det aktuelle stof er vurderet
og beskrevet m.h.t. dets sundhedsskadelige effekter. En
række af disse værker (kilder) er nævnt i afsnit 2.5.1 i M il-
jøprojekt N r. 974 (2005) . Sådanne dokumenter, der ofte er
baseret på en grundig faglig vurdering ved en særlig nedsat
ekspertgruppe, vil typisk kunne anvendes til at udpege de
relevante undersøgelser og data, der skal anvendes til den
videre beregning af kvalitetetskriteriet. D et anbefales gene-
13
M iljøstyrelsen (2001). Report on the advisory list for selfclassi-
fication of dangerous substances. Environmental Project N o. 636
2001. http://www.mst.dk/udgiv/publications/2001/87-7944-694-
9/html/
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relt, at data, der skal danne udgangspunkt for beregning af
kvalitetskriteriet, altid hjemskaffes som originallitteratur til
vurdering af den konkrete undersøgelses kvalitet og rele-
vans.
Endvidere søges i en række relevante databaser (se afsnit
2.5.2 i den faglige rapport). Sådanne søgninger er især rele-
vante, hvis en international stofmonografi for det konkrete
stof ikke foreligger, eller hvis vurderingen ligger nogle år
tilbage.
For visse stoffer kan man komme ud for at datasøgning
giver så ringe resultat, at der ikke er tilstrækkeligt data-
grundlag til at foretage en vurdering af stoffet. For eksempel
hvis der kun er akutte studier til rådighed, eller ingen studier
fastlægger N O(A)EL/LO(A)EL.
Ref er en cer
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier i jord, luft og drikkevand.
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3 Farlighedsvurdering og farligheds-
karakterisering
Farlighedsvurderingen og farlighedskarakteriseringen har til
formål at beskrive stoffets farlige egenskaber. D er opstilles i
videst muligt omfang dosis-effekt og dosis-respons sam-
menhænge, der danner baggrund for identifikation af den
kritiske effekt. D en kritiske effekt er den effekt, der anses for
at være den afgørende ved den sundhedsmæssige vurdering.
N uleffekt niveauet (evt. laveste effektniveau) for denne ef-
fekt anvendes til beregning af T D I (tolerabelt dagligt indtag/
tolerabelt daglig eksponering), som i den videre proces be-
nyttes til beregning af kvalitetskriteriet.
3.1 Dosis-ef f ekt og dosis-r espon s sammen h æ ge
n
Udsættelse for et kemisk stof kan medføre forskellige typer
effekter afhængig af eksponeringsvej, eksponeringens stør-
relse og varighed. Lettere grader af effekter kan være forbi-
gående genevirkninger i form af fx slimhindeirritation, mens
alvorlige effekter kan være dødeligt forløbende akutte for-
giftninger eller udvikling af kroniske sygdomme som kræft.
En længerevarende dyreeksperimentel undersøgelse vil såle-
des kunne give viden om forskellige typer effekter ved for-
skellige eksponeringsniveauer (dosis-effekt), og om hvor
lang tid det tager, før de optræder i forhold til eksponerin-
gen.
Yderligere vil man fra undersøgelsen kunne se, hvor stor en
andel af de doserede dyr der er ramt af effekten (dosis-
respons). Visse effekter kan være opdelt i forskellige svær-
hedsgrader eller stadier, hvor der så for hver af disse kan
foreligge dosis-responssammenhænge.
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2259378_1724.png
Figur 1 Eksempler på dosisrespons-sammenhænge
Ovenstående figur viser, hvordan dosisrepons-kurver for
forskellige effekter kan optegnes ud fra konkrete forsøgsdata
med forskellige eksponeringsniveauer og observerede effek-
ter ved disse (markeret med krydser). Kurve a angiver fx
dosis-respons forløbet for luftvejsirritation hos forsøgsdyre-
ne, og er her karakteriseret ved at være meget stejl (alle dyr
påvirkes inden for et forholdsvist lille dosisinterval, dvs. lille
spredning i følsomhed). Kurve b angiver forekomsten af
kræftsvulster og viser en dosisrespons sammenhæng ved
højere eksponeringsniveauer, og beskriver en noget fladere
dosis-respons sammenhæng (dvs. dyrenes følsomhed over
for udvikling af kræft er mere spredt). N OAEL-
markeringerne på figuren repræsenterer eksponeringsni-
veauer, hvor der ikke blev fundet statistisk signifikant flere
dyr i eksponeringsgruppen end i kontrolgruppen, der udvik-
ler den pågældende effekt, mens LOAEL-værdierne repræ-
senterer det laveste eksponeringsniveau, der har medført en
signifikant forøget forekomst af effekten.
D en faglige baggrundsrapport (M iljøprojekt N r. 974 (2005)
) angiver i afsnit 3.1 mere detaljerede beskrivelser og tolk-
ningen af forskellige dosis-respons forløb.
3.2 Fast sæ t el se af n ul -ef f ekt n iveau og l avest e ef -
t
f ekt n iveau
For langt de fleste typer effekter vurderes der at være en
tærskelværdi, der adskiller effektniveauer fra ikke-
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effektniveauer, dvs. eksponeringen skal overskride en vis
tærskelværdi før dosis er tilstrækkelig til at udløse effekt.
N iveauet umiddelbart under denne teoretiske tærskelværdi
betegnes nuleffektniveauet, der er den højeste dosis, der ikke
medfører effekt. D osisniveauet umiddelbart over tærskel-
værdien betegnes laveste effektniveau, da dette er det laveste
dosisniveau, der lige netop udløser effekten.
I praksis anvendes for nuleffektniveauet det såkaldte
no ob-
served adverse effect level, N OAEL,
der er den højeste af de i
forsøget anvendte doser, hvor der i et konkret forsøg ikke er
observeret
den givne effekt. For laveste effekt-niveau anven-
des det såkaldte
lowest observed adverse effect level, LOAEL,
der er den laveste dosis i forsøget hvor der er observeret den
givne effekt.
I litteraturen anvendes betegnelserne N OAEL og N OEL
(no
observed effect level)
samt LOAEL og LOEL (lowest
ob-
served effect level).
N år betegnelserne anvendes korrekt, er
det for at sondre mellem om de effektniveauer eller nul-
effektniveauer der beskrives, er i forhold til
skadelige (adver-
se)
effekter eller effekter generelt, hvor også lettere grader af
effekter som påvirkning af enzymniveauer og andre effekter
af ikke direkte skadelig karakter er omfattet.
M an må dog være opmærksom på, at denne skelnen mellem
skadelige og ikke-skadelige effekter i mange tilfælde ikke er
gjort konsekvent i litteraturen, og at betegnelserne ofte be-
nyttes i flæng. D et kan således i konkrete tilfælde være van-
skeligt at afgøre, hvor grænsen går for, om en effekt skal
tolkes som skadelig eller ej, og dermed om et LOEL snarere
skal tolkes som et LOAEL.
Se endvidere afsnit 3.2 i den faglige rapport (1).
3.3 Ben ch mar k-met oden
N O(A)EL/ LO(A)EL metoden til udpegning af et ekspone-
ringsniveau er afhængig af, hvilke eksponeringsniveauer
man har valgt ved udførelse af et forsøg, og i nogle tilfælde
har man måske ikke engang fundet et N O(A)EL. D ette har
medført, at en nyere metode, benchmark-metoden, visse
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steder har vundet indpas i forbindelse med risikovurderin-
ger, idet der ikke anvendes en N O(A)EL eller LO(A)EL
men en benchmark-dosis for den videre beregning af T D I.
Ved denne metode foretages en computerbaseret modelle-
ring af dosis-responskurven ud fra de tilgængelige data. På
dosis-respons kurven findes ED
5
– eller ED
10
-niveauet (dvs.
det eksponeringsniveau, der medfører respons hos 5% eller
10% af de eksponerede). D enne dosis vælges derpå som
udgangspunkt (benchmark-dosis, BM D
5
eller BM D
10
) for
den videre beregning på tilsvarende måde som man anven-
der en N O(A)EL- eller LO(A)EL-værdi.
M etoden anvendes af de canadiske miljømyndigheder og af
US EPA, og også af WH O i forbindelse med ”Air quality
G uidelines for Europe” (2). WH O angiver i denne forbin-
delse, at en BM D
5
ud fra en gennemsnitsbetragtning kan
sammenlignes med et N O(A)EL, mens en BM D
10
kan
sammenlignes med et LO(A)EL.
WH O omtaler også anvendelsen af benchmark-metoden
som en alternativ metode i forbindelse med publikation om
risikovurdering fra 1999 (3) og i forbindelse med publikati-
on om fastsættelse af vejledende grænseværdier fra 1994
(4).
På nuværende tidspunkt haves der kun sparsom erfaring
med anvendelsen af metoden herhjemme. Som det faglige
miljøprojekt anfører, kan benchmark-metoden ikke umid-
delbart anvendes for alle typer data, og metoden kræver for
de relevante effektområder, hvor den kan anvendes, ofte
flere dosis-niveauer end der sædvanligvis haves.
Benchmark-metoden er, når der foreligger tilstrækkelige
data, et supplement til den traditionelle N O(A)EL/
LO(A)EL metode i forbindelse med fastsættelse af kvali-
tetskriterier. Uanset hvilken metode man vælger, bør man
vurdere og begrunde den fra gang til gang, dvs. man bør
referere til og begrunde de anvendte beregningsmetoder
eller henvise til de originalreferencer, hvor den benyttede
benchmark-dosis er beregnet.
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3.4 Udpegn in g af kr it isk ef f ekt
Ved den samlede vurdering af dosis-effekt og dosis-respons
sammenhænge foretages udpegning af den kritiske effekt
samt udpegning af den N O(A)EL/ LO(A)EL værdi (evt.
benchmarkdosis), der vurderes som mest relevant ved fast-
sættelse af kvalitetskriteriet. Ofte, men ikke nødvendigvis, vil
dette være den laveste N O(A)EL/ LO(A)EL værdi, der er
rapporteret vedrørende en skadelig effekt eller potentielt
skadelig effekt.
Ved udpegning af den kritiske effekt vurderes relevansen af
eksponeringsmåden (eksponeringsvejen i en given undersø-
gelse) i forhold til eksponeringsvejen for det medie (jord,
luft eller vand) kvalitetskriteriet skal udarbejdes for. Alvor-
ligheden af forskellige effekter sammenholdes i forhold til,
hvor langt de ligger fra hinanden i eksponeringsniveau. D et
vurderes fx om en alvorlig effekt kan være en følge af min-
dre alvorlige effekter, som således kan ses som en forløber
og indikator for udvikling af en egentlig skadeeffekt. Endvi-
dere vurderes i det konkrete tilfælde, om der optræder visse
artsspecifikke effekter hos forsøgsdyrene, og om dokumen-
tationen er tilstrækkelig til, at disse fund kan vurderes at
være irrelevante i forhold til mennesker (se afsnit 3.5).
Ved tvivlstilfælde om udpegning af kritisk effekt og
N O(A)EL/LO(A)EL værdi kan det være nødvendigt at
udpege flere N O(A)ELs/LO(A)ELs for de potentielt kriti-
ske effekter og anvende disse sideløbende ved den efterføl-
gende beregning af T D I/ kvalitetskriterier. D ette er for at
vurdere, hvordan anvendelse af usikkerhedsfaktorer og
andre beregningsmæssige forhold får indflydelse på kvali-
tetskriteriet, når der anvendes forskellige udgangspunkter
m.h.t. kritisk effekt og N O(A)EL/LO(A)EL.
3.5 Rel evan s af visse ef f ekt er i f or søgsdyr
Som udgangspunkt anvendes dyremodeller som troværdige
modeller ved forudsigelse af stoffets egenskaber hos menne-
sker. Visse effekter, der optræder i forsøgsdyr, har vist sig at
være tæt knyttet til bestemte dyrearter. I tilfælde, hvor der
foreligger dokumentation for at effekterne alene er forårsa-
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get af en sådan artsspecifik virkningsmåde, anses disse for at
være af meget begrænset relevans ved den videre vurdering
af stoffet.
Især inden for kræftområdet har man fundet flere typer
svulster (tumorer), hvor relevansen i forhold til mennesker i
de enkelte tilfælde bør vurderes nøjere. I M iljøprojekt N r.
974 (2005) er en række af disse beskrevet i afsnit 3.7.
Ref er en cer
(1) M iljøprojekt N r. 974 (2005). Principper for sundheds-
mæssig vurdering af kemiske stoffer med henblik på fastsæt-
telse af kvalitetskriterier for luft, jord og vand.
(2) WH O (2000). Air Quality G uidelines for Europe.
WH O regional Publications, European Series, N o. 91.
(3) WH O (1999). Principles for the assessment of risks to
human health from exposure to chemicals. Environmental
H ealth C riteria 210. International Programme on C hemical
Safety.
(4) WH O (1994). Assessing human health risks of chemi-
cals: derivation of guidance values for health-based expo-
sure limits. Environmental H ealth C riteria 170. Interna-
tional Programme on C hemical Safety.
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4 Beregning af TDI for stoffer med
tærskelværdi
4.1 TDI-begr ebet
D et sidste trin i farlighedskarakteriseringen er beregning af
tolerabelt dagligt indtag,
T DI (eller
tolerabel koncentration,
T K ).
Ved beregning for stoffer, hvor der anses at være en
nedre tærskel for effekt anvendes usikkerhedsfaktorer:
N O(A)EL
T DI (T K ) =
a

UF
I
x UF
II
x UF
III
Alternativt kan et LO(A)EL eller en Benchmark-dosis BM D
x
anvendes, se afsnit 3.3.
D en tolerable daglige indtagelse (T D I) er et udtryk for den
daglige gennemsnitsdosis (fra alle kilder), som befolkningen
vurderes at kunne udsættes for (tolerere) gennem et helt
livsforløb, uden at der forventes at opstå sundhedsskadelige
effekter.
T D I angives sædvanligvis i enheden mg/kg legemsvægt per
dag.
Analogt til T D I kan betegnelsen tolerabel koncentration
(T K) defineres som den koncentration af et stof i jord, luft
eller drikkevand som befolkningen vurderes at kunne udsæt-
tes for (tolerere) gennem et helt livsforløb, uden at der for-
ventes at opstå sundhedsskadelige effekter. T K angives fx i
3
enheden mg/m (luft), mg/l (drikkevand), eller i mg/kg
(jord).
For nogle stoffer er det nødvendigt at fastsætte en PT WI –
værdi (Provisional T olerable Weekly Intake – PT WI), der
angiver det tolerable ugentlige indtag, i stedet for T D I.
PT WI benyttes sædvanligvis over for stoffer, hvor det er
a
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vigtigt at understrege, at det er den samlede eksponering
over længere tid, der er af betydning for forekomst af effek-
ter (fx bly og cadmium).
Begrundelse for anvendelse af usikkerhedsfaktorer omtales
kort nedenfor, idet en mere detaljeret beskrivelse er givet i
M iljøprojekt N r. 974 (2005) afsnit 4.4
4.2 An ven del se af usikker h edsf akt or er
I kommentarerne til M iljøbeskyttelsesloven angives at ”M il-
jøministeriet ved udstedelse af regler og vejledninger kan
operere med fx sikkerhedsfaktorer ved fastsættelse af græn-
seværdier eller retningslinier for forureningsmæssige bereg-
ninger på de områder, hvor der ikke foreligger et tilstrække-
ligt eksakt vidensgrundlag”
T idligere har man anvendt begrebet sikkerhedsfaktorer. D et
har imidlertid vist sig, at denne betegnelse kan misforstås,
således at man forventer større sikkerhed, jo større sikker-
hedsfaktor der anvendes. D ette er ikke i overensstemmelse
med, hvordan faktorerne anvendes, idet de benyttes for at
tage hensyn til usikkerheder og manglende viden i data-
grundlaget, dvs. jo større usikkerhed jo større faktor. Ved
brugen af disse faktorer tilstræbes det, at der opnås et ensar-
tet beskyttelsesniveau udtrykt ved T D I-værdien. På denne
baggrund er det derfor mere korrekt at anvende betegnelsen
usikkerhedsfaktorer.
Også i udenlandsk litteratur anvendes forskellige termer for
denne faktor fx: safety factor, uncertainty factor, Sicher-
heitsfaktor, assessment factor, bedömningsfaktor.
N edenfor angives hvilke elementer og hensyn, der indgår i
de tre usikkerhedsfaktorer.
4.2.1 Usikkerhedsfaktor I
Usikkerhedsfaktor I (UF
I
) anvendes for at tage højde for, at
mennesker kan være mere følsomme over for et givent stof
end forsøgsdyr. D enne faktor har historisk været sat til 10.
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Ekstrapolation af data fra dyr til mennesker kan opfattes
som omhandlende to forskellige aspekter:
1) korrektion af dosis for forskelle i kropsstørrelse mel-
lem forsøgsdyr og mennesker, såkaldt allometrisk
skalering, og
2) andre former for forskelle mellem forsøgsdyr og
mennesker, som ikke nødvendigvis afspejles i forskelle-
ne i kropsstørrelse.
M iljøprojekt N r. 974 (2005) har gennemgået den eksiste-
rende viden og understøtter, at der fortsat som udgangs-
punkt anvendes en standardværdi på 10 for UF
I
, hvilket
også er i overensstemmelse med international praksis, når
dosis hos dyr omsættes til human dosis med samme enhed.
H vis der foreligger veldokumenteret viden om toksikokine-
tiske og/eller toksikodynamiske forskelle mellem det givne
forsøgsdyr og mennesker, anbefales det at tage udgangs-
punkt i denne viden med henblik på fastsættelse af en data-
specifik faktor i stedet for anvendelse af en standardværdi
på 10. I den forbindelse kan 10-faktoren evt. opdeles i un-
derfaktorer, hvor størrelsen af disse ”delfaktorer” må vurde-
res konkret fra gang til gang.
Ved beregning af tolerabel koncentration (T K), hvor ud-
gangspunktet er dyreforsøg, hvor eksponeringen foregår via
inhalation, bør ekstrapolering til humaneksponering ved
inhalation foretages direkte ud fra eksponeringsniveauet
3
angivet i mg stof /m (omregnet til kontinuerlig gennem-
snitskoncentration per dag), frem for at foretage omregning
fra indåndet dosis til mg/kg lgv/d for forsøgsdyrene. Ved at
anvende indåndingskoncentrationen direkte svarer dette til
at doseringen foretages i forhold til stofskiftet, hvilket anses
for at være den mest relevante metode, når der skal korrige-
res for forskelle i kropsstørrelse. Anvendelse af en UF
I
skal
ses i lyset heraf og bør derfor i denne situation ligge lavere
0,5
end 10. En værdi på en halv tierpotens (10 ) kan som ud-
gangspunkt anvendes til resterende forskelle m.h.t. artsfor-
skelle i kinetik og dynamik, medmindre konkrete data tilsi-
ger højere eller lavere værdi.
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D er bør i videst muligt omfang tages hensyn til en række
mætningsfænomener (fx mætning af absorption, metabo-
lisme eller udskillelse), der kan forekomme i dyreforsøg ved
høj dosering, idet disse mætningsfænomener ofte ikke vil
være relevante ved lavere miljømæssigt relevante niveauer. I
sådanne tilfælde bør der om muligt omregnes til ”effektiv”
dosis/ koncentration som dyrene har været udsat for.
4.2.2 Usikkerhedsfaktor II
Usikkerhedsfaktor II (UF
II
) anvendes for at tage højde for,
at nogle individer i befolkningen kan være mere følsomme
over for et givent stof end den generelle befolkning (for
eksempel børn, gravide, ældre, svækkede, kronisk syge).
D enne faktor har oftest været sat til 10. Forskellene i føl-
somhed skyldes den biologiske variation, der findes mellem
mennesker. Faktorer som alder, køn, graviditet, genotype,
helbred, og livsstil kan være medvirkende til en øget biolo-
gisk følsomhed, som afspejler dels forskelle i toksikokinetik
og dels i toksikodynamik.
M iljøprojekt N r. 974 (2005) henviser til en række analyser,
der har vurderet variationen mellem mennesker og dermed
størrelsen af UF
II
. Sammenfattende understøtter disse ana-
lyser anvendelse af en standardværdi på 10 for denne varia-
tion.
D enne usikkerhedsfaktor skal derfor som udgangpunkt sæt-
tes til 10. En alternativ værdi kan anvendes, hvis udgangs-
punktet for N O(A)EL/LO/A)EL værdien specifikt er relate-
ret til data for særligt følsomme personer eller den kritiske
effekt er en effekt, hvor man har særligt kendskab til variati-
onsbredden i følsomhed.
4.2.3 Usikkerhedsfaktor III
Usikkerhedsfaktor III (UF
III
) anvendes for at tage højde for
manglende kvalitet og relevans af de tilgængelige data. I
relation til fastsættelse af kvalitetskriterier i jord, luft og
drikkevand har denne faktor typisk varieret fra 1 til 100
afhængigt af datagrundlaget for de pågældende stoffer.
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I UF
III
indgår bl.a. følgende elementer :
•
kvaliteten af datasættet (fx ekstrapolation fra subkronisk
nuleffektniveau til kronisk nuleffektniveau),,
•
ekstrapolation fra en eksponeringsvej til en anden (”rou-
te to route” ekstrapolation fx omregning fra oral dosis til
inhalationsdosis),
•
ekstrapolation fra LO(A)EL til N O(A)EL,
•
og alvorligheden af effekterne (fx kræftfremkaldende
effekter).
D et er ikke muligt at pege på en specifik størrelsesorden for
en standardværdi, hverken for de enkelte delelementer af
UF
III
eller for den samlede UF
III
.
D er henvises til M iljøprojekt N r. 974 (2005) for en nærme-
re beskrivelse af UF
III
i rapportens afsnit 4.4.3.
N edenfor anføres mere kortfattet retningslinierne for fast-
sættelse af UF
III
.
K valitet og relevans af data
UF
III
skal tage højde for, om der er kvalitetsmæssige eller
datamæssige mangler. Vurdering af kvalitet, omfatter vurde-
ring af om de enkelte undersøgelser (og især undersøgelser-
ne der refererer til de kritiske effekter og effektniveauer) er
udført og afrapporteret på en måde, så resultaterne anses
for relevante og pålidelige. Selve omfanget af datasættet
vurderes for data vedrørende alle relevante effektområder i
relation til kortvarig og langvarig eksponering, og det vurde-
res om der i datasættet er væsentlige mangler i forhold til
vurdering af kritisk effekt og estimering af T D I. En faktor
på 1 anvendes ved datasæt, som vurderes at være fuldt til-
strækkeligt for det givne stof, mens der ved mindre eller
større mangler har været anbefalet faktorer i størrelsesorde-
nen 3-10. I visse tilfælde med store mangler kan en faktor
på helt op til 100 komme på tale. Fastlæggelse af UF
III
må
ofte baseres på en ekspertvurdering og foretages under hen-
syntagen til det enkelte stofs toksikologiske profil.
Et særligt aspekt, er manglende viden om børn og ufødtes
følsomhed for konkrete kemiske påvirkninger. For at beskyt-
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te børn og ufødte er det vigtigt ved fastsættelse af UF
III
at
vurdere om der er tilstrækkelig viden om disse forhold ud
fra reproduktionsforsøg og flergenerationsforsøg. Er disse
forhold ikke tilstrækkeligt belyst bør mangel på data have
indflydelse på valget af UF
III
. Størrelsen af en sådan delfak-
tor må ses i sammenhæng med stoffets toksikologiske profil
og hvilke øvrige data, der haves.
Ekstrapolation fra en eksponeringsvej til en anden
Ved mangel på data for den relevante eksponeringsvej kan
det blive nødvendigt at foretage en “route-to-route” ekstra-
polation. D e analyser, der er foretaget med hensyn til eks-
trapolation fra oralt N O(A)EL til et N O(A)EC ved inhala-
tion, peger generelt på, at en ekstrapoleret værdi ofte vil
være væsentligt højere end en observeret værdi (dvs toksici-
teten undervurderes). D et modsatte gør sig generelt gæl-
dende når der ekstrapoleres fra oralt N O(A)EL til
N O(A)EL ved hudkontakt, hvor den ekstrapolerede værdi
ofte vil være lavere end en observeret værdi (dvs. toksicite-
ten overvurderes). D er kan imidlertid ikke peges på en kon-
kret størrelse for usikkerhedsfaktor III ved disse ekstrapola-
tioner, der hviler på et meget usikkert grundlag. Vurderin-
gen af om en ”route-to route” ekstrapolation skal foretages,
og i hvilken udstrækning der skal anvendes en usikkerheds-
faktor i tilknytning hertil, må bero på en ekspertvurdering i
det konkrete tilfælde.
For stoffer, hvor der kun findes subakutte eller subkroniske
undersøgelser, er det ikke muligt at fastsætte et N O(A)EL
for livstidseksponering, som generelt må forventes at ligge
lavere. D er har været foretaget flere analyser af forholdet
mellem N OAELs og LOAELs opnået i studier af forskellige
eksponeringsvarigheder. M ed baggrund i disse synes der at
være belæg for en usikkerhedsfaktor af størrelsesorden mi-
nimum 10. En af de nyere analyser har således vist, at en
faktor på 10 vil være tilstrækkelig i knap 90% af tilfældene,
når der var tale om ekstrapolation fra subkroniske data,
mens der ved ekstrapolation fra subakutte data skulle an-
vendes en væsentlig højere faktor (> 20).
Ved ekstrapolation fra LO(A)EL til N O(A)EL kan der ikke
peges på en generel faktorstørrelse, som afspejler en generel
31
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
usikkerhed. Praksis inden for området og de tilgængelige
analyser af problemstillingen peger på, at en værdi omkring
en faktor 10 i langt de fleste tilfælde er tilstrækkelig. Vurde-
ringen må imidlertid bero på en ekspertvurdering i hvert
enkelt tilfælde.
M ed baggrund i vægtning af ovenstående aspekter anvendes
en UF
III
på 10 som udgangspunkt. D enne værdi kan så kor-
rigeres, når der er grundlag for dette i konkrete tilfælde.
D enne problemstilling kan i visse situationer omgås, når det
ud fra data er muligt at beregne en benchmark-dosis, såle-
des at denne anvendes i stedet for LO(A)EL-værdien.
Alvorligheden af effekter
D et har været praksis ved fastsættelse af kvalitetskriterier, at
særligt alvorlige effekter (fx kræftfremkaldende effekt eller
fosterbeskadigende effekter) afspejles i usikkerhedsfaktor
III. D et gælder især i de tilfælde, hvor den alvorlige effekt
optræder ved lave dosisniveauer. H er kan anvendes
en ekstra
faktor
på op til 10 for at tage hensyn til dette. For at få den
endelige værdi for UF
III
ganger man de enkelte værdier
sammen.
Sammenfattende kan det konkluderes, at det ikke er muligt
at sætte en standardværdi for en samlet UF
III
. Usikkerheder-
ne inden for de forskellige områder må vægtes, når der tages
stilling til en samlet faktor for UF
III
, da en multiplikation af
mange delfaktorer i UF
III
kan give en meget høj værdi, og i
visse tilfælde give et skævt billede af det samlede vi-
dengrundlag og kvaliteten heraf. Fastsættelse af UF
III
bør
således i høj grad bero på en ekspertvurdering, hvor valget
af faktoren og elementerne heri tydeligt begrundes.
4.2.4 Samlet usikkerhedsfaktor
Ved beregning af T D I divideres N O(A)EL evt. LO(A)EL
med de tre usikkerhedsfaktorer, der således ganges sammen.
Ved multiplikation af UF
I
, UF
II
og UF
III
bør der imidlertid
tages stilling til størrelsen af den samlede usikkerhedsfaktor,
32
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og der bør foretages en overordnet vurdering i forhold til
det givne datasæt.
En meget stor usikkerhedsfaktor, der kan medføre en meget
lille T D I-værdi, betyder ikke nødvendigvis, at stoffet er lige
så potent eller farligt som andre, mere velkendte stoffer med
tilsvarende lave T D I-værdi. D en beregnede lave værdi må
snarere ses som en følge af store usikkerheder i datagrund-
laget. En samlet usikkerhedsfaktor på 10.000 og derover,
bør derfor ikke anvendes.
Ref er en cer
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier for luft, jord og vand.
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2259378_1737.png
5 Beregning af TDI for kræftfremkal-
dende stoffer
5.1 Kr æ t f r emkal den de st of f er med og uden t æ skel -
f
r
væ di
r
Kræftfremkaldende stoffer anses for at kunne deles op i to
grupper grundet deres virkningsmekanisme. D en ene grup-
pe består af stoffer, der virker kræftfremkaldende som følge
af evnen til at påvirke cellernes delings- og differentierings-
hastighed. D ette kan ske gennem direkte eller indirekte på-
virkning af cellernes receptorer. For sådanne stoffer antages
der at være en nedre tærskelværdi for denne effekt. D erfor
kan T D I beregnes ved hjælp af usikkerhedsfaktorer, som
omtalt i forrige afsnit.
D en anden gruppe af kræftfremkaldende stoffer virker gen-
nem kemisk interaktion med cellernes arvemasse, og den
kræftfremkaldende effekt vurderes at være en følge af stof-
fets beskadigelse af cellernes arveanlæg (muta-
gen/genotoksisk aktivitet). For disse stoffer anses der ikke at
være et nedre eksponeringsniveau uden øget risiko for ska-
devirkninger. For sådanne stoffer anvendes ikke usikker-
hedsfaktorer ved beregning af T D I. I stedet beregnes T D I
ved hjælp af en matematisk modelberegning, hvor man på
forhånd definerer et risikoniveau man vil acceptere, og be-
regner så hvilken udsættelse, som giver denne risiko.
Ved vurdering af kræftfremkaldende effekt er det således af
stor betydning, om det kræftfremkaldende stof falder ind
under den ene eller den anden kategori. D er findes stoffer,
som både er genotoksiske – dvs. kræftfremkaldende uden
tærskel for effekt, og kræftfremkaldende ved andre meka-
nismer, hvor der anses at være en tærskel. Ved vurdering af
denne type stoffer, kræver det en ekspertvurdering at afgø-
re, om de data der ligger til grund, bedst giver grundlag for
at vurdere stoffet som tilhørende den ene eller anden kate-
gori. D er har således i EU været arbejdet på at udvikle
34
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2259378_1738.png
nærmere vejledning i hvordan disse typer stoffer kan vurde-
14
res .
5.2 Vur der in g af kr æ t f r emkal den de ef f ekt
f
EU, WH O IARC (International Agency for Research on
C ancer) og US EPA anvender en række forholdsvis sam-
menlignelige procedurer/ kriterier ved vurdering af, om et
stof skal i kategorien ”kræftfremkaldende”. Stofferne ind-
placeres i forskellige underkategorier alt efter dokumentati-
onens omfang, og under hensyntagen til om dokumentatio-
nen stammer fra humandata eller dyredata.
Yderligere indgår der i vurderingerne også stillingtagen til
virkningsmekanismer, fx om stoffer virker gennem en mu-
tagen/ genotoksisk mekanisme. I EU´s klassificeringssystem
for kemiske stoffer er der også kriterier for, hvornår et stof
skal kategoriseres som ”mutagent”.
Principperne for inddeling af kræftfremkaldende stoffer i
kategorier er mere udførligt beskrevet i M iljøprojekt N r. 974
(2005) afsnit 3.6.
Ved vurdering af et stofs kræftfremkaldende effekt i forbin-
delse med risikokarakterisering og beregning af kvalitetskri-
terier tages der så vidt muligt udgangspunkt i de ovennævn-
te vurderinger, idet der suppleres med opdateret viden fra
litteraturen. D et vurderes om der er dokumentation for at
den kræftfremkaldende effekt er en følge af genotoksisk
virkning, og om stoffet derfor skal betragtes som værende
uden en nedre tærskel for effekt.
H vis data taler for, at stoffet virker gennem en ikke-
genotoksisk mekanisme, anses stoffet for at besidde en tær-
skelværdi for skadelig effekt. For en række stoffer vil data og
viden vedrørende virkningsmekanisme være meget mangel-
fuld, og det kan være vanskeligt at sondre, om stoffet skal
betragtes som værende enten med eller uden tærskelværdi.
Sådanne tvivlstilfælde kan bedst håndteres ved at betragte
14
European Food Safety Authority (2005). Opinion on a H armo-
nised Approach for Risk Assessment of Compounds Which are
both G enotoxic and C arcinogenic.
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stoffet som havende en tærskelværdi, og i den forbindelse
anvende en øget usikkerhedsfaktor (UF
III
) for at tage hensyn
til usikkerheden om eksistensen af en tærskelværdi.
D er bør således være et vist datagrundlag, der peger hen
mod en genotoksisk mekanisme, før stoffet vurderes efter en
model uden nedre grænse.
Ved vurderingen af kræftfremkaldende effekt tages stilling
til om den er knyttet til bestemte eksponeringsveje, og om
disse er relevante i forbindelse med et kvalitetskriterium for
stoffet i jord, luft eller drikkevand.
Visse kræftformer kan være forsøgsdyrsspecifikke, og når
sådanne kræftfund kan dokumenteres som ikke-relevante i
human sammenhæng, tillægges disse fund kun begrænset
vægt (se afsnit 3.5).
Ved vurderinger i relation til kvalitetskriterier tages der alene
stilling til om stoffet skal betragtes som kræftfremkaldende,
og om stoffet ud fra dets virkningsmekanisme skal anses for
at have en tærskelværdi eller ej. D er foretages således ikke
en mere detaljeret indplacering i forskellige kategorier i for-
hold til dokumentationens art og omfang, dvs. der inddeles
ikke i kategorier for humane og dyreeksperimentelle kræft-
fremkaldende stoffer.
Et stof, som på baggrund af dokumentationen indplaceres i
EU’s C arc1 eller C arc 2, i IARC ’s gruppe 1 eller gruppe
2A/2B, og/eller i US EPA’s gruppe A eller B1/B2, vil som
udgangspunkt medføre, at stoffet betragtes som kræftfrem-
kaldende, med mindre der er nyere undersøgelser eller vel-
underbyggede informationer og fortolkninger af data, der
taler imod en sådan vurdering.
T ilsvarende gælder stoffer, som er opført på Arbejdstilsy-
nets liste over stoffer, som anses for at være kræftfremkal-
dende. D et skal dog understreges, at stoffer, som hverken er
vurderet af EU, IARC og/eller US EPA eller er indplaceret i
en lavere kategori (EU C arc3, IARC gruppe 3 og/eller US
EPA gruppe C /D ), godt kan blive betragtet som kræftfrem-
kaldende i relation til fastsættelse af kvalitetskriterier for
kemikalier i jord, luft og drikkevand, hvis der er velunder-
byggede data, der taler for det. D et kan for eksempel være i
36
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
tilfælde af, at der er publiceret nye undersøgelser siden en
eventuel vurdering er foretaget af EU, IARC og/eller US
EPA, eller der kan være stor kemisk strukturlighed med
andre kendte kræftfremkaldende stoffer. I sidstnævnte til-
fælde kan QSAR-modellering indgå som supplerende støtte
for vurderingen.
5.3 Ber egn in g af TDI f or kr æ t f r emkal den de st of f er
f
uden t æ skel væ di
r
r
5.3.1 Tolerabelt risikoniveau
T D I-værdien for kræftfremkaldende stoffer uden tærskel-
værdi fastsættes til en værdi, der repræsenterer et accepteret
risikoniveau for udvikling af kræft. D enne værdi har traditi-
-6
onelt været fastsat til en 10 livstidsrisiko, og vil også med
udsendelse af denne vejledning være det ønskede risikoni-
veau.
Konkret betyder dette, at man med udgangspunkt i human-
data eller dyreforsøg, hvor den kræftfremkaldende effekt er
påvist, ved hjælp af matematisk modellering estimerer dosis-
respons kurvens forløb så langt ned i lav-
-6
eksponeringsområdet, at en eksponering svarende til en 10
livstidsrisiko kan beregnes. T D I er således den daglige gen-
nemsnitseksponering, der ud fra
teoretiske beregninger
svarer
til en forøget risiko for cancer på 1 ud af en million menne-
sker, som er udsat for stoffet gennem en hel livstid.
5.3.2 Metode til beregning af TDI og livstidsrisiko
D er er udviklet forskellige metoder til beregning af, hvor
stor en risiko for udvikling af svulster en given eksponering
for et genotoksisk kræftfremkaldende stof udgør. For alle
metoder gælder, at der anvendes en eller anden form for
matematisk ekstrapolation fra dosisniveauer med de kendte
eksperimentelle værdier for forekomsten af svulster til de
som regel meget lavere dosisniveauer, der svarer til en fore-
komst hos 1 ud af en million. M etoderne beskriver relatio-
nen mellem den daglige eksponering (udtrykt som dosis
37
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2259378_1741.png
eller koncentration) og den sammenhørende sandsynlighed
for udvikling af svulster.
Beskrivelse af forskellige metoder og sammenligning mellem
disse fremgår af M iljøprojekt N r. 974 (2005) afsnit 5.3 og
5.4.
D en foretrukne metode til fastsættelse af T D I er T 25-
metoden, som også anvendes i EU-regi. D en baserer sig
ligesom one-hit metoden på lineær ekstrapolation med ud-
gangspunkt i laveste dosisniveau, hvor der optræder signifi-
15
kant forøget antal svulster .
M etoden er en simplificeret lineær metode med udgangs-
punkt i en beregnet T 25-dosis. T 25-dosis defineres i denne
sammenhæng som den kroniske eksponering (enhed: mg/kg
3
legemsvægt per dag eller mg/m ), som vil give 25% af for-
søgsdyrene svulster i et specifikt væv, efter korrektion for
den spontane hyppighed, indenfor den standardiserede le-
vetid for den pågældende dyreart. M ed udgangspunkt i
denne T 25-dosis foretages lineær ekstrapolation ved simpel
forholdsregning ned til en dosis, der svarer til et tolerabelt
risikoniveau.
M etoden og dens konkrete anvendelse i forhold til et tolera-
-6
belt 10 livstidsrisikoniveau er nøjere beskrevet i bilag 1.
5.3.3 Anvendelse af risikoestimater angivet i litteraturen
I en række tilfælde vil eksponeringsniveauet svarende til en
-6
10 livstidsrisiko (eller ”unit-risk”-estimater) på forhånd
være beregnet af ekspertgrupper under fx WH O eller US
EPA. For især nyere vurderinger kan det være relevant at
anvende disse værdier som ligeværdigt udgangspunkt på
15
M iljøstyrelsen har tidligere som administrativ praksis anvendt
one-hit metoden. Anvendelse af T 25-metoden vil i forhold til den
medføre lidt højere værdier (skønsmæssigt en faktor 2-4). D enne
forskel skal dog ses i et 10
-6
perspektiv, og må anses som meget
beskeden, og i praksis uden betydning i forbindelse med det til-
stræbte beskyttelsesniveau.
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linie med T 25-metoden ved beregning af T D I og kvalitets-
kriterier.
Argumenterne for at vælge et risikoestimat frem for et andet
kan dels være rent faglige (fx bero på konkrete virkningsme-
kanismer) og dels være mere pragmatiske, idet man også
bør vurdere nødvendigheden af at foretage selvstændige
beregninger af et risikoniveau. For eksempel kan opgaven
være meget omfattende for stoffer med stor datarigdom (fx
PAH -stoffer), hvor en selvstændig vurdering vil kræve ulige
mange resurser og inddragelse af høj faglig ekspertise på
området for at kunne leve op til kvaliteten af en internatio-
nal vurdering.
D erfor vil man i konkrete tilfælde kunne basere kvalitetskri-
terier for kræftfremkaldende stoffer på andre metoder end
T 25 metoden.
Ref er en cer
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier for luft, jord og vand.
European Food Safety Authority (2005). Opinion on a
H armonised Approach for Risk Assessment of C ompounds
Which are both G enotoxic and C arcinogenic.
39
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2259378_1743.png
6 Beregning af kvalitetskriterier for
kemikalier
D ette kapitel beskriver hvorledes kvalitetskriterierne for ke-
mikalier i jord, luft og drikkevand kan beregnes med ud-
gangspunkt i førnævnte T D I-værdier.
Første led i beregningen er en vurdering af, om hele T D I-
værdien eller kun en brøkdel heraf tildeles til beregning af
det konkrete kvalitetskriterium. D ette kan dels være begrun-
det i eksponeringsmæssige overvejelser - den såkaldte allo-
kering, hvor der tages hensyn til evt. andre kilder, der har
betydning for eksponeringen. Eller det kan være begrundet i
øvrige forhold, der kan være afgørende for, om der anven-
des en reduktionsfaktor, så kun en mindre brøkdel af T D I-
værdien anvendes ved beregning af kvalitetskriteriet.
Kapitlet angiver hvilke værdier for medieeksponering der
anvendes ved beregning af kvalitetskriterierne. En mere
uddybet forklaring på valget af disse værdier er givet i bilag
2.
6.1 Gen er el met ode f or ber egn in g af et kval it et skr it e-
r ium
Et sundhedsmæssigt baseret kvalitetskriterium for et stof i
jord, luft eller drikkevand beregnes ud fra den tolerable dag-
lige indtagelse, ved at dividere T D I-værdien med den dagli-
16,17
ge eksponering for det relevante medie WH O/ IPC S . D et
vil sige, at selve beregningen af kvalitetskriteriet ud fra T D I
i princippet er ens for de tre medier, jord, luft og drikkevand
16
WH O/IPC S (1994). Assessing human health risks of chemicals:
D erivation of guidance values for health-based exposure limits.
Environmental H ealth C riteria no. 170. International Programme
on C hemical Safety.
17
WHO/IPC S (1999). Principels for the assessment of risks to
human health from exposure to chemicals. Environmental H ealth
C riteria no. 210. International Programme on C hemical Safety.
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og for alle stoffer, uanset om der foreligger tærskelværdi for
den kritiske effekt eller ej.
Følgende generelle beregningsmetode kan opstilles:
T DI x V x
f
KK
l,j,v
=
__________________________
E
l,j.v
hvor
KK
l,j,v
: kvalitetskriterium for jord, luft eller drikkevand
T D I: angives i mg/ kg legemsvægt/ d
V: legemsvægt i kg
f:
allokeringsfaktor, brøkdel af T D I som ud fra ekspone-
ringsfordeling anvendes til eksponering fra jord, luft eller
drikkevand
3
E
l,j,v
: daglig udsættelse/ forbrug af luft (m /d), jord (kg/d),
eller drikkevand (liter/d).
3
(H vis E
l.j,v
angives i (m /kg lgv/ d), (kg/kg lgv/d), eller (li-
ter/kg lgv/d) udgår V i ovenstående formel).
6.1.2 Anvendelse af TDI
For stoffer hvor der ikke anses at være en tærskelværdi for
effekt, dvs. de genotoksiske kræftfremkaldende stoffer, an-
-6
vendes T D I-værdien (sv.t til en 10 livstidsrisikodosis) di-
rekte til beregning af kvalitetskriteriet.
For andre stoffer, hvor der anses at være en tærskelværdi,
indgår efterfølgende overvejelser vedrørende anvendelse af
en allokeringsfaktor eller reduktionsfaktor.
Allokering
Allokeringsfaktoren ”f” angiver den brøkdel af T D I som
tildeles udsættelsen via det enkelte medie. Ofte tildeles min-
dre end 100% af et kemisk stof til beregning af et kvalitets-
kriterium, da der for en række kemiske stoffer vil være ud-
sættelse gennem andre medier end det enkelte medie jord,
luft og vand. I en række tilfælde vil bidrag gennem forure-
ning af fødevarer eller gennem påvirkning fra indeklimaet
udgøre hovedkilden for en persons udsættelse, og vil der-
med ”lægge beslag på” en betydelig del af T D I-værdien,
hvorfor der kun tildeles en mindre andel til kvalitetskriteriet.
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I de tilfælde hvor bidrag fra andre medier ikke forventes,
fastsættes kvalitetskriterierne som udgangspunkt ved, at hele
T D I allokeres til det pågældende medie. N år det vurderes,
at der foreligger øvrige betydende kilder allokeres som ud-
gangspunkt 10% af T D I til det pågældende medie, med
mindre der er konkret viden om øvrige kilders bidrag, der
siger noget andet. For visse stoffer, hvor langt de største
bidrag kommer fra øvrige kilder, kan der således allokeres
helt ned til kun 1% af T D I (dette er for eksempel gjort for
visse plastblødgørere i forbindelse med et kvalitetskriterium
for drikkevand).
Reduktionsfaktor
I særlige tilfælde kan andre forhold end de rent ekspone-
ringsmæssige betragtninger medføre, at der anvendes en
reduktionsfaktor, således at der kun anvendes en vis brøkdel
af T D I til beregning af kvalitetskriteriet. En sådan faktor
kan efter individuel vurdering komme på tale fx :
-
ved særligt kritiske forhold som persistens og bioakku-
mulering af stoffet,
-
i tilfælde, hvor kvalitetskriteriet er udarbejdet ud fra et
enkelt stofs effekter, men hvor stoffet repræsenterer en
hel stofgruppe, og hvor eksponeringen typisk vil være
karakteriseret ved en blandingseksponering med denne
stofgruppe,
-
i tilfælde hvor der samtidig kan optræde eksponering fra
flere stoffer, og hvor der er formodning om, at der ved
de relevante niveauer vil kunne optræde kombinations-
effekter (fx samvirkende effekter) fra denne blandings-
eksponering.
6.1.3 Eksponeringsbetragtninger
M ålet for eksponeringen i nævneren i brøken til kvalitetskri-
terie-beregningen baseres på standardbetragtninger for dag-
lig udsættelse.
I afsnit 6 i M iljøprojekt N r. 974 (2005) er der foretaget en
opdateret gennemgang af viden om befolkningens udsættel-
se for jord, luft og vand, samt angivet hvilke standardbe-
42
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
tragtninger der anvendes inden for WH O, US EPA og i
EU.
Ud fra hensigten om specifikt at tage hensyn til børns eks-
ponering er der foretaget en revision af den hidtidige prak-
sis. G rundlaget for den reviderede praksis er anført i bilag 2.
6.2 Ber egn in g af l uf t kval it et skr it er iet
Følgende fremgangsmåde anvendes til beregning af luftkva-
litetskriteriet (KK
luft
), når T D I for de(n) kritiske effekt(er)
er fra studier hvor stoffet er givet via munden og angivet i
enheden mg/kg legemsvægt/dag:
KK
luft
T DI x
f
=
──────────
E
luft
hvor
T D I: tolerabel daglig indtagelse (mg/ kg lgv/d)
f:
brøkdel af T D I, der allokeres til udeluften
E
luft
: eksponering luft, standardværdi for dagligt indån-
3
dingsvolumen: 0,5 m /kg lgv/d for 1-5 årige børn.
Følgende fremgangsmåde anvendes, når (nul)effektniveauer
N O(A)EL eller LO(A)EL) for de(n) kritiske effekt(er) er
fra studier hvor stoffet er inhaleret og angivet som en kon-
3
centration i enheden mg/m :
KK
luft
=
TK x
f
f:
allokeringsfaktor
T K: tolerabel koncentration
hvor
TK
N O(A)EC eller LO(A)EC
=
──────────────────────
UF
I
x UF
II
x UF
III
For de fleste typer af systemiske effekter anses det at være
den samlede dosis og ikke stoffets koncentration i luften, der
er af betydning for udvikling af disse effekter. Ved fastsæt-
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
telse af luftkvalitetskriteriet i disse tilfælde foretages en om-
regning af det fastlagte (nul)effektniveau til et gennemsnit-
ligt døgnniveau (kontinuert eksponering) ud fra de i studiets
aktuelle eksponeringsbetingelser. D et vil sige, at der kom-
penseres for, at eksponeringen ikke har foregået i alle døg-
nets timer over en fuld uge. H vis eksponeringen for eksem-
pel er foretaget 6 timer per dag i 5 dage per uge, korrigeres
der med en faktor 6/24 til kontinuert eksponering gennem et
helt døgn og en faktor 5/7 til kontinuert eksponering gen-
nem hele ugen.
For visse lokale effekter (effekter, der optræder lokalt i luft-
vejene samt direkte effekter på hud og øjne) anses det sæd-
vanligvis at være stoffets koncentration i luften og ikke den
samlede dosis som sådan, der er af betydning for udvikling
af disse effekter. For sådanne stoffer kan omregning til en
kontinuert eksponering sædvanligvis udelades fra en konkret
vurdering.
Lugt
N ogle kemiske stoffer har en meget kraftig lugt, og hensyn-
tagen til lugt ved fastsættelse af luftkvalitetskriteriet vil for
mange stoffer (fx en række organiske opløsningsmidler)
medføre lavere luftkvalitetskriterium end det sundhedsbase-
rede luftkvalitetskriterium, idet luftkvalitetskriteriet fastsæt-
tes til 1/3 af 50 %-lugtgrænsen.
Lugtgrænsen for et kemisk stof er generelt defineret som
den koncentration i luften, hvor 50 % af et lugtpanel (kon-
trolleret laboratorieforsøg med bestemmelse af lugtgrænse
med frivillige forsøgspersoner) kan registrere lugten.
Som et luftkvalitetskriterium vurderes en sådan 50 % lugt-
grænse at kunne medføre gener hos en ikke uvæsentligt del
af befolkningen.
I en analyse af en række laboratoriedata, hvor lugtgrænsen
er blevet bestemt for kemiske stoffer, viser det sig, at dosis-
respons sammenhængen generelt er ret stejl for et lugtpanel
(D K-T eknik 2001). For personer, med intakt lugtesans
(svarende til personer, der indgår i et lugtpanel), er der ge-
44
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
nerelt en forholdsvis lille spredning m.h.t. hvornår en lugt
kan opfattes. Ud fra disse data vurderes, at ved et niveau på
1/3 af lugtgrænsen vil maksimalt 1-5% af befolkningen un-
der optimale betingelser kunne fornemme lugt.
Lugtgrænser, der er angivet i litteraturen, kan variere vold-
somt (flere størrelsesordner) D ette skyldes, at metoder til
bestemmelse af lugtgrænser kan variere meget, alt efter hvor
og hvornår de er blevet foretaget, samt at der kan være fore-
taget undersøgelser af forskellige stofkvaliteter, hvor stoffer-
ne ikke er entydigt definerede.
M edmindre lugtgrænsen er bestemt ud fra nye og meget
velbeskrevne metoder, hvor kvalitet og pålidelighed af un-
dersøgelsen kan vurderes, anbefales det at fastsætte luftkva-
litetskriterier på baggrund af lugt fra bestemmelse af lugt-
grænse foretaget af et akkrediteret laboratorium.
6.3 Ber egn in g af jor dkval it et skr it er iet
Følgende fremgangsmåde anvendes ved beregning af jord-
kvalitetskriteriet, når de(n) kritiske effekt(er) er en følge af
gentagen udsættelse:
T DI x V x
f
=
──────────
hvor
E
I, jord
(eller E
H , jord
)
KK
jord
f:
procentdel af T D I, der allokeres til indtagelse af jord
V: legemsvægt, 1-3 årigt barn: 13 kg
E
I,jord
: daglig eksponering (indtagelse) for jord, stan-
dardværdi:
1) 0,0002 kg/d (sv.t. 95-percentilgrænsen) i tilfælde
hvor hele T D I-værdien eller hovedparten af denne
anvendes til beregning af kvalitetskriteriet
2) 0,0001 kg/d (sv.t. medianudsættelse) i tilfælde hvor
-6
T D I er en 10 livstidsrisikodosis for et kræftfrem-
kaldende stof, eller i tilfælde, hvor der anvendes en
mindre del af T D I til jordkvalitetskriteriet
E
H ,jord
: daglig eksponering (hudkontakt) for jord, stan-
dardværdi: 0,001 kg/d for barn.
45
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
2259378_1749.png
E
H ,jord
anvendes i forbindelse med særligt hudgennemtrænge-
lige stoffer, hvor systemisk bidrag fra hudoptag summeres
med det orale bidrag. E
H ,jord
anvendes separat hvis den kriti-
ske effekt er relateret til den direkte hudpåvirkning af foru-
reningskomponenten.
Følgende fremgangsmåde anvendes ved beregning af jord-
kvalitetskriteriet, når den kritiske effekt er akut toksicitet:
KK
jord
TD x V
=
──────
hvor
E
I,jord
(eller E
H , jord
)
T D : tolerabel enkeltdosis
N O(A)EL
akut
eller LO(A)EL
akut
=
──────────────────────
UF
I
x UF
II
x UF
III
hvor
TD
V: legemsvægt, 1-3 årigt barn: 13 kg
E
I
: maksimum enkeltindtag af jord (0,010 kg)
E
H
: maksimal hudkontakt med jord (0,010 kg) (An-
vendes for særligt hudgennemtrængende stoffer).
Ved beregning bør data for optagelse fra mave-tarmkanalen
18
(biotilgængelighed ) så vidt muligt inkluderes, idet de foru-
renende stoffer i visse tilfælde kan binde sig kraftigt til jord-
partikler og derved medføre en reduceret biotilgængelighed.
H vis data ikke foreligger, regnes med samme biotilgænge-
lighed, som i de forsøg, der ligger til grund for T D I-
beregningen (dette kan typisk være forsøg, hvor teststoffet
er opblandet i foderet eller i drikkevandet).
18
”Biotilgængelighed” refererer i denne sammenhæng til det en-
gelske ”bioaccessibility”. Bioaccessibility beskriver den pool af
stoffet, som jorden kan frigive, og den indeholder således også let
bundne former.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Lugt, udseende
Ud over rent sundhedsmæssige aspekter tages der ved fast-
sættelse af jordkvalitetskriteriet hensyn til, at jorden ikke må
lugte eller syne forurenet. D et vil sige, at jorden ikke ved
inspektion må afgive lugt fra forureningen eller se forurenet
ud (klumper af stof(fer) eller misfarvning. D er foreligger
ikke nøjere retningslinier for en sådan subjektiv vurdering.
M ed hensyn til lugt i forbindelse med afdampning henvises
til M iljøprojekt N r. 974 (2005) afsnit 7.4.3, der beskriver
anvendelsen af luftkvalitetskriteriet i forbindelse med af-
dampning af forurenende stoffer fra jord.
6.4 Ber egn in g af dr ikkevan dskval it et skr it er iet
Følgende fremgangsmåde anvendes ved beregning af drik-
kevandskvalitetskriteriet:
T DI x
f
──────────
hvor
E
drikkevand
KK
drikkevand
=
T D I: tolerabelt dagligt indtagelse (mg/ kg lgv/d)
f:
er den procentdel af T D I, der allokeres til indtagelse
af drikkevand
:
E
drikkevand
daglig eksponering for drikkevand, standard-
værdi:
1) 0,08 liter/ kg lgv/d (sv.t. 95-percentilen) for 1-10
årige børn. Anvendes i forbindelse med akutvir-
kende stoffer eller når hovedparten af T D I-værdien
benyttes til beregning af drikkevandskvalitetskriteri-
et.
2) 0,03 liter/ kg lgv/d (sv.t. medianværdi for 1-10 åri-
-6
ge
børn) i tilfælde hvor T D I er en 10 livs-
tidsrisikodosis for et kræftfremkaldende stof, eller i
tilfælde hvor kun en mindre andel af T D I-værdien
benyttes til beregning af drikkevandskvalitetskrite-
riet.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Kemiske stoffer, der er særligt hudoptagelige, vil kunne
optages i en ikke uvæsentlig mængde i forbindelse med
badning, og stoffer, der let fordamper (for eksempel mange
opløsningsmidler), kan især ved brusebadning indåndes
som dampe/aerosoler. Omfanget af disse eksponeringsfor-
mer via brusebadning og karbadning afhænger af, hvor le-
toptageligt stoffet er gennem huden, og i hvor stor udstræk-
ning stoffet frigives ved fordampning fra vandet. D er bør
derfor i konkrete tilfælde (stoffer med høj hudgennemtræn-
gelighed og stoffer med høj flygtighed fra vandfasen), tages
højde for disse bidrag ved fastsættelse af drikkevandskvali-
tetskriteriet, således at den samlede optagelse via drikkevand
og badevand ikke overskrider den del af T D I, som er alloke-
ret til drikkevand.
D er er ikke opstillet konkrete modeller for beregningen af
sådanne bidrag, hvorfor bidragene må vurderes fra sag til
sag under inddragelse af de data og de vurderinger, der er
foretaget for det konkrete stof.
Lugt, smag, udseende
D rikkevandet må ikke lugte, smage eller syne forurenet og
smag, lugt og udseende af drikkevandet har en væsentlig
betydning, også selv om det ikke udgør en sundhedsfare i
relation til indtagelse af drikkevand.
D et vil i nogle tilfælde være lugt, smag, eller udseende, og
ikke stoffets sundhedsmæssige effekter, der er bestemmende
for værdien af drikkevandskvalitetskriteriet.
Lugt- og smagsgrænser, der findes opgivet i litteraturen,
kan variere voldsomt selvom de forskellige undersøgelser er
udført med samme stof. D ette skyldes, at metoder kan vari-
ere meget alt efter hvor, og hvornår de er blevet foretaget.
M edmindre lugt- og smagsgrænsen er bestemt ud fra nye
og meget velbeskrevne metoder, hvor kvalitet og pålidelig-
hed af undersøgelsen kan vurderes, anbefales det, at fastsæt-
telse af drikkevandskvalitetskriterier på baggrund af lugt og
smag foretages ud fra bestemmelse af lugt- og smagsgrænse
foretaget af et akkrediteret laboratorium.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Udgangspunktet for fastsættelse af et lugt- og smagsbaseret
kvalitetskriterium bør være et nul-effekt-niveau (N OEL) i
testpanelet, dvs. den koncentration hvor testpanelet som
helhed ikke kan lugte eller smage stoffet.
Ofte angives lugt- og smagsgrænser i vand på tilsvarende
måde som lugtgrænse i luft, dvs. det niveau, hvor 50 % af et
testpanelet kan lugte/smage stoffet. Angives således lugt-
grænsen i den tilgængelige litteratur som 50 %-grænsen
ganges denne værdi med 1/3 (som beskrevet under luftkva-
litetskriteriet), idet anvendelse af en sådan faktor skønnes at
sikre, at kun en mindre andel af befolkningen vil kunne for-
nemme stoffet ved dette niveau.
Ref er en cer
D K-T eknik (2001). Vurdering af lugttærskelværdier. Rap-
port udarbejdet for M iljøstyrelsen.
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier for luft, jord og vand.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Bilag 1
Kvan t it at iv vur der in g ved ben yt t el se af
T25 ekst r apol at ion smet oden .
Anbefaling af T25-metoden
D er er udviklet forskellige metoder til beregning af, hvor
stor en risiko for udvikling af svulster en given eksponering
for et genotoksisk kræftfremkaldende stof udgør. Ens for
dem alle er at der anvendes en form for statistisk ekstrapola-
tion fra dosisniveauer med kendte eksperimentelle værdier
til de som regel meget lavere dosisniveauer, der oftest er
relevante i relation til den generelle befolknings eksponering
for kemiske stoffer i miljøet. M etoderne beskriver relationen
mellem den administrerede daglige dosis (eller koncentrati-
on) og den resulterende hyppighed af svulster.
Som anført i afsnit 5.3.2. anbefales det at anvende T 25-
ekstrapolering som beskrevet i en baggrundsrapport udar-
bejdet af en arbejdsgruppe i forbindelse med EU´s risiko-
vurderingsarbejde (EU-C ommission 1999).
T 25-metoden er blevet evalueret ved at sammenligne resul-
tater opnået ved denne metode med resultater opnået ved
anvendelse af US EPA´s LM S-metode (Linearised M ulti-
stage M odel) og ved LED
10
metoden, hvor der foretages
lineær ekstrapolation ned i lavdosisområdet ud fra en
benchmark-dosis på 10 % effektniveau (se afsnittene 5.3.2-
4 i M iljøprojekt N r. 974 (2005)). Ved gennemgang af resul-
taterne for lavdosis-estimaterne vurderede man at de er
sammenlignelige.
Ved sammenligning af one-hit metoden og T 25-metoden
vurderes de at medføre sammenlignelige værdier, idet ud-
gangspunktet for begge vurderingerne i princippet er at
anvende laveste dosis med signifikant respons, og herfra
50
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
foretage lineær ekstrapolation ned i lavdosisområdet. I T 25-
metoden divideres med en skaleringsfaktor fra dyr til men-
neske opløftet i
¼
(sv.t. skalering i forhold til stofskiftet),
mens tilsvarende skaleringsfaktor i one-hit metoden er op-
løftet til 1/3 (sv.t. skalering i forhold til overfladeareal). D et-
te forhold alene vil maksimalt bevirke en forskel på de to
metoder på ca. en faktor 2.
Anvendelse af T25-metoden
T 25 defineres som den kroniske dosis (enhed: mg/kg le-
gemsvægt per dag), som vil give 25 % af forsøgsdyrene
svulster i et specifikt væv, efter korrektion for den spontane
hyppighed, inden for den standardiserede levetid af den
pågældende art.
T 25 beregnes med udgangspunkt i et langtidscancerstudie,
hvor den laveste dosis, der giver en signifikant forøgelse af
forsøgsdyr med svulster i et specifikt væv, som udgangs-
punkt anvendes ved beregningen af T 25. Forekomsten af
ondartede og godartede svulster sammenlægges, når de
godartede svulster må mistænkes for at kunne udvikles til
ondartede. H vis der er en højere hyppighed ved en højere
dosis, der giver en lavere T 25, anvendes sidstnævnte, med
mindre der er særlige begrundelser for ikke at tage ud-
gangspunkt i denne. H vis der er flere data- sæt, beregnes
T 25 for det mest relevante datasæt. H vis forskellige datasæt
giver T 25-værdier, som ligger inden for et relativt snævert
interval, anvendes gennemsnittet af disse T 25-værdier. H vis
sidstnævnte procedure ikke anvendes, skal rationalet for
anvendelse af en anden procedure begrundes nøje.
Beregning af T 25 foretages ved at gange dosis D (mg/kg
lgv/dag), hvor signifikant forøget antal svulster forekommer
med faktoren 0,25/p, hvor p er den aktuelle hyppighed af
svulster: T 25 = D x 0,25/p.
Ud fra denne T 25 foretages lineær ekstrapolation ned i lav-
dosisområdet, idet dosis svarende til et givent risikoniveau
beregnes ved simpel forholdsregning. En gennemsnitlig
-6
daglig dosis svarende til en øget livstidsrisiko på 10 kan
således beregnes på følgende måde:
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2259378_1755.png
D osis
(10-6 livstidsrisiko)
= 10 / 0,25 x T 25-dosis
Imidlertid indgår der i beregningerne også dosiskorrektion
med baggrund i en skaleringsfaktor mellem dyr og menne-
sker, og en faktor som angiver andelen af dyrenes levetid,
hvor eksponeringen har fundet sted.
Konkret kan T D I svarende til en 10 livstidsrisiko beregnes
ud fra følgende formel, når T 25 er beregnet ud fra forsøg
med oral eller dermal eksponering hos dyr:
-6
-6
I
t
x [L
e
/ L]
2
x [(T25 x l
e
) / L
e
]
TDI =
0,25 x [W
h
/ W
a
]
0,25
I
t
:
L
e
:
L:
T25:
Den tolerable livstidsrisiko (10
-6
).
Den aktuelle levetid for dyrene.
Den teoretiske gennemsnitslængde af levetiden for dyrene.
Beregnet daglig dosis (mg/kg legemsvægt per dag), der medfører en
25% forøget forekomst af tumorer hos forsøgsdyrene.
l
e
:
Eksponeringstid.
[W
h
/ W
a
]
0,25
: Dosiskorrektion på basis af stofskifte
hvor
W
h
:
Menneskets vægt i kg (sættes oftest til 70 kg).
W
a
:
Gennemsnitsvægt af det pågældende forsøgsdyr (kg).
L, L
e,
l
e
:
H vis eksponeringsvarigheden er kortere end standardleveti-
den for den pågældende art, eller hvis studiet afsluttes inden
standardlevetiden, foretages dosiskorrektion, som beskrevet
i den anførte formel. Standardlevetiden for mus, rotter og
hamstre sættes med mindre andet er angivet for den speci-
fikke stamme til 24 måneder.
Dosis ( T 25)
N år konkrete data ikke specifikt angiver dyrenes legems-
vægt, og dosis i mg/kg lgv/d i forbindelse med dosering
gennem foder eller drikkevand, anvendes følgende værdier i
beregningen:
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2259378_1756.png
Dyreart
Rotte
Mus
Marsvin
Kanin
Hund
Abe
Legemsvægt
(kg)
0,10 (ung)
0,40 (ældre)
0,020
0,75
2,0
10,0
5,0
Indtagelse af
foder
(g/ kg/ dag)
100
50
150
40
30
25
50
Indtagelse af
drikkevand
(ml/ kg/ dag)
75
-
-
-
-
-
(W
h
/W
a
)
Er stoffet givet oralt eller dermalt , foretages der en dosis-
korrektion for forskelle i kropsstørrelse mellem dyr og men-
nesker ved at omregne T 25 til den tilsvarende humane dosis
i mg/kg lgv./dag ved allometrisk skalering på basis af stof-
skiftet (afsnit 4.4.1.2). D enne skalering opnås ved at divide-
0,25
re T 25-dosis med faktoren (W
h
/W
a
)
Ved beregning ud fra inhalationsundersøgelse beregnes den
tolerable indåndingskoncentration T C ved anvendelse af
formlen:
0,25
53
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I
t
x [L
e
/ L]
2
x [(T25 x l
e
) / L
e
]
TC =
0,25
I
t
:
L
e
:
L:
T25:
l
e
:
Den tolerable livstidsrisiko (10
-6
).
Den aktuelle levetid for dyrene.
Den teoretiske gennemsnitslængde af levetiden for dyrene.
Beregnet daglig dosis (mg/m
3
i indåndingsluften), der medfører en
25% forøget forekomst af tumorer hos forsøgsdyrene.
Eksponeringstid.
Ved indsættelse af T 25 anvendes koncentration i indån-
dingsluften og der foretages sædvanligvis omregning til en
gennemsnitligt indåndingskoncentration , hvis forsøget ikke
er udført med kontinuerlig eksponering. D ette gøres ved at
korrigere for antal timer pr. dag og antal dage pr. uge hvor
eksponeringen har fundet sted.
Ref er en cer
EU-C ommission (1999). G uidelines for quantitative risk
characterisation of non-threshold carcinogens in the frame-
work of Existing C hemicals following C ouncil Regulation
(EEC )
793/93. C ommission working G roup on the T echnical
M eetings for Risk Assessment for Existing Substances.
D ocument N O_N L/01/99_Rev.1
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Bilag 2
Baggr un d f or an ven dt e ekspon er in gsvæ dier ved be-
r
r egn in g af kval it et skr it er ier
I denne vejledning ændres praksis med hensyn til de ekspo-
neringsværdier, der anvendes ved beregning af kvalitetskri-
terierne for kemikalier.
T idligere har man i forbindelse med beregning af jordkvali-
tetskriterier som udgangspunkt antaget, at et barn dagligt
indtager 0,2 g jord/d (0,0002 kg/d), mens man ved bereg-
ning af luftkvalitetskriterier har anvendt et scenarie, hvor en
3
voksen person dagligt indånder 20 m luft. Ved beregning af
kvalitetskriterier for kemikalier i drikkevand har udgangs-
punktet været et dagligt indtag på 2 liter vand for en voksen.
Børn
Beskyttelse af børn er de senere år i stigende grad kommet i
fokus, og det har i den forbindelse været debateret i hvilken
udstrækning kvalitetskriterier beregnet ud fra voksnes ud-
sættelse i tilstrækkeligt omfang beskytter børn, da børn i
forhold til deres legemsvægt generelt indtager/ indånder en
større mængde drikkevand/ luft.
I miljøprojekt nr. 589 ”C hildren and the unborn child –
exposure and susceptibility to chemical subtances-” fra
2001, blev der foretaget en detaljeret gennemgang af børns
særlige følsomhed og udsættelsesmønster i forbindelse med
miljøforureninger og kemiske stoffer. I miljøprojektet kon-
kluderes, at der ved fremtidig fastsættelse af kvalitetskriterier
for kemikalier bør tages udgangspunkt i eksponeringsværdi-
er for børn, for at opnå at børn er fuldt omfattet af det be-
skyttelsesniveau, kvalitetskriteriet repræsenterer. D enne
vejledning indarbejder således ønsket om, at principperne
for fastsættelse af kvalitetskriterier tager hensyn til børns
særlige udsættelse.
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Børns udsættelse vil således være udgangspunktet for de fremti-
dige standardværdier for eksponering i forbindelse med jord, luft
og drikkevand.
Standardværdien for børns legemsvægt vil i fremtiden være
13 kg.
Særligt udsatte undergrupper
Almindelig biologisk variation og forskellige former for ad-
færd vil betyde, at nogle grupper vil være mere udsatte end
andre for en given påvirkning via miljøet. D er er således
også med denne vejledning taget stilling til, i hvilken ud-
strækning kvalitetskriterier/grænseværdier for kemikalier skal
tage hensyn til de mere udsatte grupper i befolkningen.
N år kvalitetskriterier for kemikalier beregnes ved at anvende
eksponeringsværdier, der svarer til befolkningsvægtede gen-
nemsnitsværdier eller medianværdier, betyder dette, at ca.
halvdelen af den befolkning, som kvalitetskriteriet skal søge
at beskytte, vil kunne blive udsat for
større
eksponering end
udgangspunktet for beregningen (fx en T D I-værdi). H vis
sigtet med et kvalitetskriterium er, at størstedelen af befolk-
ningen skal være omfattet at det ønskede beskyttelsesniveau,
vil det således være nødvendigt at anvende en øvre fraktil-
værdi for befolkningens udsættelse.
D et skal nævnes, at de standardværdier der hidtil har været
anvendt for børn (jord) og voksne (luft og drikkevand) jf.
beskrivelsen af eksponeringsværdier, svarer til sådanne øvre
percentilgrænser.
Kvalitetskriterier for kemikalier skal fortsat sigte mod at
beskytte flertallet af befolkningen, dvs. også de mere udsatte
undergrupper. I de tilfælde hvor befolkningsfordelingen af
eksponeringerne kendes, vil valg af øvre eksponeringsværdi-
er typisk kunne foretages ved at tage udgangspunkt i værdi-
er svarende til 90- eller 95-percentilerne.
For at sikre særligt udsatte grupper anvendes følgende prin-
cipper :
a ) I situationer, hvor man ved beregning af kvalitetskriteriet
har tildelt hele T DI-værdien, hovedparten eller der er eksakt
56
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2259378_1760.png
viden om størrelsen af udsættelsen via det aktuelle medie, vil det
være nødvendigt at anvende øvre percentilgrænser for ekspone-
ring. Herved sikres at kun en mindre andel af befolkningen vil
blive eksponeret over T DI-niveau.
b)
I andre tilfælde, hvor der anvendes en reduceret T DI-værdi
som følge af anvendelse af en allokeringsfaktor (evt. en særlig
reduktionsfaktor), anvendes derimod medianværdier for udsæt-
telse med mediet. Dette forhold begrundes med, at anvendelse af
en allokeringsfaktor eller reduktionsfaktor sædvanligvs betyder
anvendelse af runde værdier (10 % eller 1% af T DI), som ofte
vil være på ”den sikre side”. I sådanne tilfælde, hvor der i forve-
jen er indbygget en øget grad af sikkerhed, vil det ikke være på-
krævet også at anvende en øvre percentilværdi for eksponering.
Anvendelse af en medianværdi vurderes her, at kunne opfylde
målet om at beskytte størstedelen af befolkningen.
c)
For kræftremkaldende stoffer uden tærskelværdi for effekt
foretages som tidligere nævnt ingen allokering af T DI. I disse
tilfælde anvendes medianværdier for eksponering ved beregning
af kvalitetskriteriet, idet T DI-værdien repræsenterer en daglig
dosis for en befolkningsvægtet gennemsnitlig livstidsrisikoforøgel-
se (en ekstrarisiko på 1 ud af 1 million udsatte over livstid),
hvorfor en gennemsnits-/medianværdi for befolkningens udsæt-
telse må være udgangspunktet.
Luft, daglig standardeksponering
I forbindelse med valg af standardeksponering for luft tages
der udgangspunkt i afsnit 6.1.1 i M iljøprojekt N r. 974
(2005). I dette afsnit vurderes US EPA´s eksponeringsvur-
deringer at udgøre det bedste grundlag. I EU´s risikovurde-
ringprogram for kemiske stoffer henvises ligeledes til de
amerikanske værdier.
Uddrag af tabel 6.1.1
Alder
Børn:
Under 1 år
1 – 2 år
Legemsvægt
(kg)
7.6
13
V
R
– gennemsnit
(m
3
/ dag)
4.5
6.8
V
R
– inaktiv
a
(m
3
/ dag)
2.35
4.16
V
R
- aktiv
(m
3
/ dag)
6.35
9.15
57
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2259378_1761.png
3 – 5 år
6 – 8 år
18
26
8.3
10
4.98
5.95
10.96
13.09
V
R
= Respirations V olumen som henholdsvis gennemsnit, inak-
tivitet og aktivitet.
Værdierne er alders- og kønsopdelte, men angivelserne om-
fatter ikke spredningen (fordelingen) i de enkelte alders-
grupper. D et er således ikke ud fra de forliggende data mu-
ligt at aflæse en 90- eller 95 percentilværdi for eksponerin-
gen af de forskellige aldersgrupper.
Som ovenfor nævnt vil der ved fastsættelsen af luftkvalitets-
kriterier blive taget hensyn til eksponeringen af børn.
Fra tabellen ses, at børn under 1 år i gennemsnit over et
3
3
døgn indånder 4,5 m svarende til 0,59 m /kg lgv/dag, mens
børn i aldersgruppen 1-2 år og 3-5 år indånder henholdsvis
3
3
6,8 m og 8,3 m (svarende til henholdsvis 0,52 og 0,46
3
m /kg lgv/dag). Især de 1-5 årige må anses at være udeakti-
ve.
På denne baggrund vil der ved beregning af luftkvalitetskri-
terier fremover blive anvendt en standardværdi for 1-5 årige
3
børn på 0,5 m luft/ kg lgv.
T il sammenligning kan nævnes at luftkvalitetskriteriet hidtil
er blevet beregnet ud fra et dagligt indåndingsvolumen på
3
0,3 m / kg lgv., idet udgangspunktet her var en voksen per-
3
son (70 kg), der dagligt indåndede 20 m luft.
Jord, daglig standardeksponering
M iljøprojekt N r. 974 (2005) sammenfatter i afsnit 6.1.2 den
seneste viden med hensyn til børns udsættelse for jord samt
anfører forskellige organisationers vurdering.
Ud fra en sammenfattende vurdering kan følgende ekspone-
ringsværdier for børn opstilles:
Eksponeringsvej
Oralt, maksimum enkeltindtag
Eksponeringsværdi
10 g
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Oralt, dagligt gennemsnit
Oralt, 95-percentil
Hudkontakt, dagligt gennemsnit
Hudkontakt, maksimum
0,1 g/ d
0,2 g/ d
1 g/ d
10 g/ d
For børns indtag gennem munden fastsættes jordkvalitets-
kriteriet for akut toksiske stoffer ud fra et enkeltindtag på 10
g jord.
I tilfælde, hvor hele T D I eller hovedparten af T D I anvendes
til beregning af jordkvalitetskriteriet, tages der specifikt hen-
syn til særligt udsatte børn, idet der ved beregning af jord-
kvalitetskriteriet tages udgangspunkt i 95-percentilen for
udsættelse dvs. 0,2 g jord/d for herved at minimere risikoen
for at overskride T D I-værdien.
I andre tilfælde, hvor der kun anvendes en mindre del af
T D I-værdien til jordkvalitetskriteriet, anvendes ved bereg-
ningen af jordkvalitetskriteriet 0,1 g jord/d som et gennem-
sitligt standardindtag.
For kræftfremkaldende stoffer, hvor T D I svarer til en gen-
-6
nemsnitlig 10 livstidsrisikodosis blandt børn, anvendes 0,1
g jord/dag som udgangspunkt for beregning af jordkvalitets-
kriteriet.
Drikkevand, daglig standardeksponering
I M iljøprojekt N r. 974 (2005) i afsnit 6.1.3 gennemgås vi-
den om forskellige aldersgruppers indtagelse af drikkevand,
idet indtagelse både opgives for forskellige aldersgrupper og
fordelingen inden for disse (gennemsnitsværdier og 90-/95
percentiler). Beskrivelse i baggrundsrapporten omfatter
vurdering og anbefalingerne fra US EPA´s Exposure Fac-
tors H andbook.
Baggrundsrapporten henviser i forbindelse med børns ind-
tag af drikkevand til tabel 6.1.3 D , der angiver US EPA´s
anbefalede værdier:
Alder
Gennemsnit
(mean)
50 Percentil
90 Percentil
95 percentil
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Under 1 år
Under 3 år
3 – 5 år
1 – 10 år
0,30 liter/ dag
44 ml/ kg/ dag
0,61 liter/ dag
0,87 liter/ dag
0,74 liter/ dag
35 ml/ kg/ dag
0,24 liter/ dag
35 ml/ kg/ dag
0,65 liter/ dag
102 ml/ kg/ dag
1,5 liter/ dag
1,5 liter/ dag
0,76 liter/ dag
127 ml/ kg/ dag
0,66 liter/ dag
31 ml/ kg/ dag
1,3 liter/ dag
64 ml/ kg/ dag
1,5 liter/ dag
79,4 ml/ kg/ dag
For spædbørn angives medianindtaget at være 35 ml/ kg
lgv/d mens 95-percentilen angives at være på 127 ml/ kg
lgv/d. For børn i aldersgruppen 1-10 år anføres tilsvarende
en medianværdi på 31 ml/kg lgv./d og en 95-percentil på
79,4 ml/kg lgv./d.
Som standardværdi vurderes det mest relevant at anvende
værdien for 1-10 årige børn, idet evt. forskelle i vaner m.h.t.
amning i USA og D anmark kan have stor indflydelse på
drikkevandsindtagelse for spædbørn. Endelig dækker T D I-
begrebet alene moderens direkte eksponering og derved
barnets indirekte udsættelse gennem modermælken, og T D I
er således ikke formelt set beregnet til at dække spædbarnets
direkte udsættelse. G ennemsnitligt er indtagene dog direkte
sammenlignelige.
Ved beregning af drikkevandskvalitetskriteriet, hvor der ved
en given forureningskomponent er foretaget en allokering
på 100 % eller hovedparten af T D I til drikkevandet, eller i
situationer hvor den kritiske effekt er en akut toksisk effekt,
anvendes 95-percentilværdien for 1-10 årige børns indtag,
dvs. et dagligt indtag på 0,08 liter/ kg lgv/d. I disse situatio-
ner, vil drikkevandskvalitetskriteriet således også omfatte
spædbørns direkte udsættelse, idet dette også afspejler ind-
taget for børn under 1 år, som har en høj direkte udsættelse.
Ved beregning i andre situationer, hvor der er foretaget en
allokering på en mindre del af T D I til drikkevandskvalitets-
kriteriet (eller der er anvendt en reduktionsfaktor) anvendes
medianværdien for 1-10-åriges forbrug af drikkevand sv.t.
0,03 liter/ kg lgv/d. Allokeringen vil også betyde at spæd-
børns direkte udsættelse er omfattet af kvalitetskriteriet.
For kræftfremkaldende stoffer, hvor T D I svarer til en gen-
-6
nemsnitlig 10 livstidsrisikodosis blandt børn, anvendes
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0,03 liter/ kg lgv/d som udgangspunkt for beregning af drik-
kevandskvalitetskriteriet.
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Bilag 3
An ven dt e f or kor t el ser
BM D – BenchM ark D osis
D – dag
ED – Eksponerings D osis
EEC – European Economic C ommunity
EU – Europæiske Union
G LP – G ood Laboratory Practice
IARC – International Agency for Research on C ancer
IPC S – International Programme on C hemical Safety
KK – kvalitetskriterie
LED – Linear Ekstrapolations D osis
Lgv – legemsvægt
LM S – Linear M ultistage M odel
LOAEL – Lowest Observed Adverse Effect Level
LOEL – Lowest Observed Effect Level
N OAEL – N o Observed Adverse Effect Level
N OEL – N o Observed Effect Level
OEC D – Organisation for Economic C ooperation and D e-
velopment
PAH – Poly Aromatiske H ydrocarbon
QSAR – Quantitative Structure Activity Relationships
T D I – T olerabel D aglig Indtag (T olerabel D aglig Ekspone-
ring, el. T olerabel D aglig D osis)
T K – T olerabel Koncentration
UF – Usikkerheds Faktor
US EPA – United States Environmental Protection Agency
V
R
– indåndingsvolumen
WH O – World H ealth Organisation
W – Kropsvægt
62
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2259378_1766.png
EEA Report
No 1/2013
Late lessons from early warnings:
science, precaution, innovation
Summary
ISSN 1725-9177
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
2259378_1768.png
EEA Report
No 1/2013
Late lessons from early warnings:
science, precaution, innovation
Summary
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2259378_1769.png
Cover design: EEA
Cover photos © EEA
Layout: EEA/Pia Schmidt
Copyright notice
© EEA, Copenhagen, 2013
Reproduction is authorised, provided the source is acknowledged, save where otherwise stated.
Information about the European Union is available on the Internet. It can be accessed through the Europa
server (www.europa.eu).
Luxembourg: Publications Office of the European Union, 2013
ISBN 978-92-9213-349-8
ISSN 1725-9177
doi:10.2800/70069
Environmental production
This publication is printed according to high environmental standards.
Printed by Rosendahls-Schultz Grafisk
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Both paper qualities are recycled paper and have obtained the ecolabel Nordic Swan.
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Tel.: +45 33 36 71 00
Fax: +45 33 36 71 99
Web: eea.europa.eu
Enquiries: eea.europa.eu/enquiries
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Contents
Contents
Acknowledgements .................................................................................................... 5
Preface ....................................................................................................................... 6
1 Introduction .......................................................................................................... 9
Part A Lessons from health hazards
2 The precautionary principle and false alarms — lessons learned ......................... 12
Steffen Foss Hansen and Joel A. Tickner
3 Lead in petrol 'makes the mind give way' ............................................................ 13
Herbert Needleman and David Gee
4 Too much to swallow: PCE contamination of mains water ................................... 14
David Ozonoff
5 Minamata disease: a challenge for democracy and justice ................................... 15
Takashi Yorifuji, Toshihide Tsuda and Masazumi Harada
6 Beryllium's 'public relations problem' .................................................................. 16
David Michaels and Celeste Monforton
7 Tobacco industry manipulation of research ........................................................ 17
Lisa A. Bero
8 Vinyl chloride: a saga of secrecy .......................................................................... 18
Morando Soffritti, Jennifer Beth Sass, Barry Castleman and David Gee
9 The pesticide DBCP and male infertility ............................................................... 19
Eula Bingham and Celeste Monforton
10 Bisphenol A: contested science, divergent safety evaluations ............................. 20
Andreas Gies and Ana M. Soto
11 DDT: fifty years since
Silent Spring......................................................................
21
Henk Bouwman, Riana Bornman, Henk van den Berg and Henrik Kylin
Part B Emerging lessons from ecosystems
12 Booster biocide antifoulants: is history repeating itself? ..................................... 22
Andrew R. G. Price and James W. Readman
13 Ethinyl oestradiol in the aquatic environment ..................................................... 23
Susan Jobling and Richard Owen
Late lessons from early warnings: science, precaution, innovation
3
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Contents
14 Climate change: science and the precautionary principle..................................... 24
Hartmut Grassl and Bert Metz
15 Floods: lessons about early warning systems ...................................................... 25
Zbigniew W. Kundzewicz
16 Seed-dressing systemic insecticides and honeybees ........................................... 26
Laura Maxim and Jeroen van der Sluijs
17 Ecosystems and managing the dynamics of change ............................................. 27
Jacqueline McGlade and Sybille van den Hove
Part C Emerging issues
18 Late lessons from Chernobyl, early warnings from Fukushima ............................ 28
Paul Dorfman, Aleksandra Fucic and Stephen Thomas
19 Hungry for innovation: from GM crops to agroecology ......................................... 29
David Quist, Jack A. Heinemann, Anne I. Myhr, Iulie Aslaksen and Silvio Funtowicz
20 Invasive alien species: a growing but neglected threat? ..................................... 30
Sarah Brunel, Eladio Fernández-Galiano, Piero Genovesi, Vernon H. Heywood, Christoph
Kueffer and David M. Richardson
21 Mobile phones and brain tumour risk: early warnings, early actions? .................. 31
Lennart Hardell, Michael Carlberg and David Gee
22 Nanotechnology — early lessons from early warnings ......................................... 32
Steffen Foss Hansen, Andrew Maynard, Anders Baun, Joel A. Tickner and Diana M. Bowman
Part D Costs, justice and innovation
23 Understanding and accounting for the costs of inaction ...................................... 33
Mikael Skou Andersen and David Owain Clubb
24 Protecting early warners and late victims............................................................ 34
Carl Cranor
25 Why did business not react with precaution to early warnings? .......................... 35
Marc Le Menestrel and Julian Rode
Part E Implications for science and governance
26 Science for precautionary decision-making ......................................................... 36
Philippe Grandjean
27 More or less precaution?...................................................................................... 37
David Gee
28 In conclusion ....................................................................................................... 38
A full version of the report can be found at:
http://www.eea.europa.eu/publications/late-lessons-2
4
Late lessons from early warnings: science, precaution, innovation
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Acknowledgements
Acknowledgements
This report has been prepared by the European
Environment Agency (EEA) with substantial
contributions from many external authors. The EEA
is particularly grateful to those authors who wrote
the case study chapters.
Originator of the
Late lessons from early warnings
project at the EEA was David Gee.
Acknowledgement is given to the editorial team:
David Gee, Philippe Grandjean, Steffen Foss
Hansen, Sybille van den Hove, Malcolm MacGarvin,
Jock Martin, Gitte Nielsen, David Quist and
David Stanners.
The EEA also thanks advisory board members who
have contributed their experience to the project
over many years: Joan Martinez Alier, Philippe
Bourdeau, Sylvaine Cordier, Sven Dammann,
Michael Depledge, Frans Evers, Silvio Funtowicz,
Thomas Jakl, Martin Krayer von Krauss, Owen
McIntyre, Jerome Ravetz, Nicolas de Sadeleer,
László Somlyódy, Sofia Vaz and Theo Vermeire.
Production support: Mike Asquith, John James
O'Doherty, Peter Saunders, Pia Schmidt and
Bart Ullstein.
Contributing authors: Jeroen Aerts, Maria Albin,
Mikael Skou Andersen, Iulie Aslaksen, Anders
Baun, Constança Belchior, Henk van den Berg,
Lisa A. Bero, Keith Beven, Eula Bingham, Riana
Bornman, Henk Bouwman, Diana M. Bowman,
Sarah Brunel, Michael Carlberg, Argelia Castaño,
Barry Castleman, David Owain Clubb, Charlie
Clutterbuck, Carl Cranor, Paul Dorfman, Eladio
Fernández-Galiano, Gary Fooks, Aleksandra Fucic,
Silvio Funtowicz, David Gee, Piero Genovesi,
Andreas Gies, Anna Gilmore, Philippe Grandjean,
Hartmut Grassl, Tee L. Guidotti, Nigel Haigh,
Steffen Foss Hansen, Mazazumi Harada, Lennart
Hardell, Jack A. Heinemann, Vernon H. Heywood,
Sybille van den Hove, James Huff, Susan Jobling,
Bill Kovarik, Christoph Kueffer, Zbigniew W.
Kundzewicz, Henrik Kylin, Malcolm MacGarvin,
Laura Maxim, Andrew Maynard, Jacqueline
McGlade, Owen McIntyre, Marc Le Menestrel,
Bert Metz, David Michaels, Erik Millstone, Celeste
Monforton, Anne I. Myhr, Herbert Needleman, Joy
Onasch, Richard Owen, David Ozonoff, Andrew
R.G. Price, David Quist, James W. Readman,
Johnny Reker, David M. Richardson, Julian Rode,
Christina Rudén, Jennifer Beth Sass, Richard
Schmuck, Noelle E. Selin, Jeroen van der Sluijs,
Katherine Smith, Morando Soffritti, Ana M. Soto,
Hans von Storch, Stephen Thomas, Joel A. Tickner,
Klement Tockner, Toshihide Tsuda, Pier Vellinga
and Takashi Yorifuji.
Case study chapters have been peer reviewed from a
broad range of perspectives. The EEA would like to
thank all institutions and experts who have given so
generously of their time and knowledge during the
peer review process.
The EEA would also like to thank Domingo Jiménez
Beltrán, Philippe Bourdeau, Jane Keys, Malcolm
MacGarvin, Andy Stirling and Brian Wynne for
being continuing sources of inspiration and ideas
throughout the process of producing both volumes of
Late lessons from early warnings.
The EEA would like to remember, with great
appreciation Poul Harremöes, chairman of the
editorial team for
Late lessons from early warnings
Volume 1, and Masazumi Harada, co-author of
Chapter 5 on Minamata disease, who worked
throughout his career on mercury pollution.
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Preface
Preface
An investment in knowledge pays the best interest
— Benjamin Franklin 'The
Way to Wealth'
(1758).
There is something profoundly wrong with the
way we are living today. There are corrosive
pathologies of inequality all around us — be they
access to a safe environment, healthcare, education
or clean water. These are reinforced by short-term
political actions and a socially divisive language
based on the adulation of wealth. A progressive
response will require not only greater knowledge
about the state of the planet and its resources, but
also an awareness that many aspects will remain
unknown. We will need a more ethical form of
public decision-making based on a language in
which our moral instincts and concerns can be
better expressed. These are the overall aims of
Volume 2 of
Late lessons from early warnings.
Volume 1 of
Late lessons from early warnings
was published at a time when the world was
experiencing an economic slowdown, China had
joined the World Trade Organization and western
Europe was still a 15-member Union. Global grain
production had declined for the third time in four
years due mainly to droughts in North America
and Australia, and the world saw major recalls
of contaminated meat, foot and mouth disease
and bovine spongiform encephalopathy (mad
cow disease). Global temperatures continued to
climb and many bird populations were in decline,
but the United States of America had rejected the
Kyoto Protocol. We were seeing ourselves through
the lens of the first human genome sequence, yet
we were trying to manage chemicals known to
be harmful to humans and ecosystems, through
international conventions and treaties such as the
Basel Convention to deal with toxic waste dumping
in the developing world; the OSPAR/HELCOM
Conventions to reduce the discharges, emissions and
the loss of hazardous substances into the sea and
the Montreal Protocol, to phase out ozone-depleting
substances. The destruction of the World Trade
Center had just happened.
Since then, we have witnessed a period of
extraordinary hubris. Most visibly, the financial
profligacy of the first decade of the century led
inexorably to the crises of 2007–2009 whereby
the major components of the international
financial system were weakened to the extreme by
indebtedness, mispriced products, lax monetary
policies and mis-engineered protection against
risks and uncertainty. The world experienced
more not less volatility. Political systems became
silted up by vested interests and a determination
by citizens to protect assets accumulated in
easier times, and beneath it all lay a deeper
environmental crisis epitomised by climate change
and biodiversity loss.
There was also a collapse of trust, not only in
financial institutions but in big companies, as
they abandoned staff, pensions and health care
schemes. Recent evidence from social psychology
has shown that despite rising levels of education
and innovation in products and services, people
trust only those they know and not strangers. As
Stephen Green said in
Good value: reflections on
money, morality, and an uncertain world
in 2009:
'There has been a massive breakdown of trust:
trust in the financial system, trust in bankers,
trust in business and business leaders, trust
in politicians, trust in the media, trust in the
whole process of globalisation — all have
been severely damaged, in rich countries and
poor countries alike'.
The scientific elites have also been slowly losing
public support. This is in part because of the
growing number of instances of misplaced
certainty about the absence of harm, which has
delayed preventive actions to reduce risks to
human health, despite evidence to the contrary.
Suddenly, our problems have grown into what
Charles W. Churchman in 1967 termed
wicked
problems
— difficult or impossible to solve because
of incomplete, contradictory and changing
requirements, difficult to recognize, resistant
to resolution because of the complexity of their
interdependencies and needing to be tackled not
by one but via many forms of social power. Solving
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Preface
them requires a new combination of hierarchical
power, solidarity and individualism.
What could this mean, for example, for the
100 thousand chemicals currently in commercial use?
To begin with we have more conventions and
treaties in place than a decade ago: the 2004
Rotterdam Convention on the Prior Informed
Consent (PIC) Procedure covering international
trade of 24 pesticides, four severely hazardous
pesticide formulations and 11 industrial chemicals;
the 2004 Stockholm Convention on Persistent
Organic Pollutants to protect human health and the
environment from substances which are highly toxic,
persistent, bio-accumulative and move long distances
in the environment, such as DDT, PCBs, various
industrial chemicals, and a set of unintentional
chemical by-products such as dioxin. But these
conventions only address the top-down hierarchical
approach to power.
At the same time Europe has put in place
legislation to achieve a global regulatory influence
including the EU Cosmetic Directive banning the
use of chemicals known or strongly suspected
of being carcinogens, reproductive toxins, or
mutagens causing cancer, mutation or birth defects;
the EU Restriction of Hazardous Substances
Directive, which restricts the use of hazardous
materials in the manufacture of various types
of electronic and electrical equipment including
lead, mercury, cadmium, hexavalent chromium,
the flame retardents polybrominated biphenyls
and polybrominated diphenyl ethers, and which
encourages the substitution to safe/or safer
alternatives in the electric and electronic equipment
industry; the closely linked 2006 EU Waste
Electrical and Electronic Equipment Directive for
collection, recycling and recovery of electrical
goods; the 2006 Strategic Approach to International
Chemicals Management (SAICM); and the 2007
EU Registration, Evaluation and Authorisation of
Chemicals, widely known as REACH, to assign
greater responsibility to industry to manage
the risks from chemicals and to provide safety
information on substances. The effects of these
regulatory tools are described in different chapters,
but once again point to the main economic actors
rather than communities or individuals.
One thing that has become clearer over the past
decade is that certain chemical substances are
highly stable in nature and can have long-lasting
and wide ranging effects before being broken
down into a harmless form. The risk of a stable
compound is that it can be bio-accumulated in
fatty tissues at concentrations many times higher
than in the surrounding environment. Predators,
such as polar bears, fish and seals, are known
to bio-magnify certain chemicals in even higher
concentrations with devastating consequences
for both humans and ecosystems. So exposure to
toxic chemicals and certain foodstuffs are at risk of
causing harm, especially to vulnerable groups such
as foetuses in the womb or during childhood when
the endocrine system is being actively built. Even
with small dose exposures, the consequences can
in some instances be devastating with problems
ranging from cancer, serious impacts on human
development, chronic diseases and learning
disabilities. Here the power to act could be more
properly set by well-informed individuals and
communities.
The relationship between knowledge and power
lies at the heart of Volume 2. In many chapters,
the implicit links between the sources of scientific
knowledge about pollutants, changes in the
environment and new technologies, and strong
vested interests, both economic and paradigmatic,
are exposed. A number of authors also explore
in greater depth, the short-sightedness of
regulatory science and its role in the identification,
evaluation and governance of natural resources,
physical and chemical hazards. By creating a
better understanding of these normally invisible
aspects, it is hoped that this volume will enable
communities and people to become more effective
stakeholders and participants in the governance of
innovation and economic activities in relation to
the associated risks to humans and the planet.
Much of what we are able to learn from the
histories of past environmental and public health
mistakes is also directly applicable to the better
regulation and governance of global institutions
and financial and economic risks. Robin G.
Collingwood argued in his
Autobiography
(1939),
that:
'History can offer something altogether
different from [scientific] rules, namely
insight. The true function of insight is to
inform people about the present…we study
history in order to see more clearly into the
situation in which we are called upon to act…
the plane on which, ultimately, all problems
arise is the plane of 'real' life: that to which
they are referred for their solution is history.'
In this volume, we go further. Whilst still drawing
lessons from such widely accepted tragedies
as leaded petrol, mercury poisoning in Japan's
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Preface
Minamata Bay and older pesticides which sterilised
many men who used it, we have ventured into the
uncertainties of potential yet contested harm, from
genetically modified products; nanotechnologies;
chemicals such as Bisphenol A; new pesticides
and mobile phones. There is also an examination
of the 80 or so potential 'false positives' where
there had been indications of harm but where it
was subsequently claimed that there were in fact
no risks to prevent: these cases too can provide
information that can help to improve future
decision-making about innovation and emerging
technologies.
A major part of effective decision-making lies in
the way issues are framed. In the case of climate
change, the first order question is whether it is
worth worrying about at all. US Vice President
Al Gore chose to make the question a matter of
choice between believers and sceptics. However,
problems arose when the public was asked to
make a scientific decision when too few people had
the qualifications to make any kind of reasoned
judgement. They were in fact asked to make a false
choice. Instead the question should have been
framed around which areas should people and
governments make decisions and which should be
delegated to experts.
In the end there are few certain and enduring
truths in the ecological and biological sciences, nor
in the economics, psychologies, sociologies and
politics that we use to govern them. One, however,
comes from the work of Elinor Ostrom, a late and
widely missed colleague, who showed from her
work on managing fisheries and ecosystems that
complex problems can be solved if communication
is transparent and open, visions are shared, trust is
high and communities are activated to work from
the bottom-up as well as from the top down.
As we navigate the Anthropocene, the epoch
named in recognition of our impact on the
planet, we will need to encourage more people to
become involved in solving the wicked problems
of our times. Whether through gathering local
information or becoming more aware of the
many uncertainties and unpredictabilities in our
surroundings, the power structures of knowledge
will need to change. And if we are to respond more
responsibly to the early warning signals of change,
we will need to re-design our style of governance
to one which reflects a future defined by the local
and specific rather than only the global and the
average. We hope that Volume 2 of
Late lessons from
early warnings
with its many lessons and insights
can help us all meet such a challenge.
Professor Jacqueline McGlade,
Executive Director
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Introduction
1 Introduction
Why further late lessons from early
warnings?
The 2013
Late lessons from early warnings
report is
the second of its type produced by the European
Environment Agency (EEA) in collaboration with a
broad range of external authors and peer reviewers.
Volume 1 of
Late lessons from early warnings: the
precautionary principle 1896–2000
published in 2001,
looked at the history of a selection of occupational,
public health and environmental hazards and
asked whether we could have been better at taking
action early enough to prevent harm. Twelve key
lessons for better decision-making were drawn
from cases where public policy was formulated
against a background of scientific uncertainty and
'surprises' — and where clear evidence of hazards
to people and the environment was often ignored
(see box on page 11).
The 14 case studies and 12 key lessons from the 2001
report remain highly pertinent today, and underline
four main reasons for a second report. The first
relates to expanding the late lessons approach to
consider long-known, important additional issues
with broad societal implications such as lead in
petrol, mercury, environmental tobacco smoke and
DDT, as well as issues from which lessons have
emerged more recently such as the effects of the
contraceptive pill on feminisation of fish and the
impacts of insecticides on honeybees.
The second concerns filling an acknowledged
gap in the 2001 report, by analysing the issue of
false positives where government regulation was
undertaken based on precaution but later turned
out to be unnecessary. Most of the cases examined
in the
Late lessons from early warnings
reports are
'false negatives' — instances where early warnings
existed but no preventive actions were taken.
The third reason is to address the rapid emergence
of new society-wide challenges such as radiation
from mobile phones, genetically-modified
products, nanotechnologies and invasive alien
species as well as if, how and where precautionary
actions can play a role.
The final reason relates to how precautionary
approaches can help manage the fast-changing,
multiple, systemic challenges the world faces
today, what new insights can be drawn in this
context and how these can underpin opportunities
for sustainable innovations and, supported
by information technologies, greater public
participation in their selection.
Overall approach
As for Volume 1, the approach in Volume 2 has
been to include a wide range of relevant case
studies produced by external authors along with
chapters written by members of the report's
editorial team (see acknowledgements section
for details). The relevant topics for case study
treatment were selected on the basis of advice
from the editor, in collaboration with the editorial
team and an advisory board, members of the
EEA Scientific Committee and the Collegium
Ramazzini (
1
).
The chapters in Volume 2 are grouped into
five parts: A. Lessons from health hazards;
B. Emerging lessons from ecosystems; C. Emerging
issues; D. Costs, justice and innovation; and
E. Implications for science and governance.
The chapters have been written by authors
who, to varying degrees, have had substantial
involvement in the subject area being addressed.
Indeed they would not have been approached if
(
1
) The Collegium Ramazzini is an independent, international academy founded in 1982 by Irving J. Selikoff, Cesare Maltoni and other
eminent scientists. Its mission is to advance the study of occupational and environmental health issues and to be a bridge between
the world of scientific discovery and the social and political centers, which must act on the discoveries of science to protect public
health.
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Introduction
they had not already extensively studied the case
that they were asked to write about. All of them, as
respected experts in their fields and in line with their
professional scientific training, were expected to be
as objective as possible in answering the questions
put to them by EEA. To support this, and to develop
consistency between chapters, the authors were
provided with seven structuring questions to be
followed when building their chapter.
The case studies have been peer-reviewed by
recognised experts in the respective fields who gave
of their time freely and provided their feedback
within a set of editorial guidelines provided by the
EEA.
Scope
The report has been designed, structured and
written in order to, inter alia, help politicians,
policymakers and the public to:
i
understand better the ways in which
scientific
knowledge
is financed, created, evaluated,
ignored, used and misused in taking timely and
precautionary decisions about how to reduce
harms, whilst stimulating benign innovations
and generating useful employment;
learn from some
very expensive 'mistakes'
in the past
so as to help societies make fewer
mistakes now, and in the future, especially with
some of the relatively new, largely unknown,
yet already widespread technologies like
nanotechnology and mobile phones;
Part A of the report commences with an analysis
of 'false positives' showing that these are few and
far between as compared to false negatives and
that carefully designed precautionary actions can
stimulate innovation, even if the risk turns out
not to be real or as serious as initially feared. The
remaining nine chapters address false negatives —
lead in petrol, perchlorethylene contaminated water,
Minamata disease, occupational beryllium disease,
environmental tobacco smoke, vinyl chloride,
dibromochloropropane (DBCP), Bisphenol A and
dichlorodiphenyltrichlorethane (DDT) — from
which three common themes emerge: there was
more than sufficient evidence for much earlier
action; slow and sometimes obstructive behaviour
by businesses whose products endangered
workers, the public and the environment; and the
value of independent scientific research and risk
assessments.
Part B focuses on emerging lessons from the
degradation of natural systems and their wider
implications for society — booster biocides, the pill
and the feminisation of fish, climate change, floods,
insecticides and honeybees as well as ecosystem
resilience more broadly. It considers, like its
predecessor, the issues of scientific evidence as the
basis for action/inaction, the multiple, often complex
factors and feedback loops in play, many of which
are not fully understood, as well as the interfaces
between science, policy and society and how all
actors can move together towards necessary actions
in the context of heightened systemic risks, and
substantial unknowns.
Part C analyses some newly emerging and
large-scale products, technologies and trends, which
potentially offer many benefits but also potentially
much harm to people and ecosystems and thereby
ultimately economic development. Cases addressed
include the Chernobyl and Fukushima nuclear
accidents; genetically modified agricultural crops
and agroecology; the growing threat of invasive
alien species; mobile phones and the risk of brain
tumours; and nanotechnologies. There is often little
science, and very little direct hindsight, to assist in
the management of these emerging technologies but
the lessons from the historical case studies need to
be applied if hazards are to be avoided.
The evidence from the chapters in Part C is that,
by and large, societies are not making the most
use of the costly lessons that can be gleaned
from their histories. A key question is how
this can be improved given the many reasons
identified from the case studies why taking
actions have been delayed including: the novel
ii
iii be aware of less visible, important factors such
as the skewed ways in which the
costs of actions
and inactions
for hazardous technologies
have been estimated, and the role that
some
businesses
have played in ignoring early
warnings and in manufacturing doubt about the
science supporting such warnings;
iv consider how the law, or administrative
arrangements, could be better used to deliver
justice, to those people (and ecosystems) that
have been, or could be, harmed
by poorly
designed, or badly deployed, innovations;
v
explore how best to
engage the public
in
helping to make
strategic choices over
innovations,
and their technological and
social pathways, as well as their involvement
in
ecosystems management
and in long term
monitoring through
citizen science.
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Introduction
and challenging nature of the issues themselves;
poorly or inconsistently evaluated information;
strong opposition by the corporate and scientific
establishments of the day; and the tendency by
the decision making institutions, practices and
cultures to favour the status quo and the short
term perspective. This section also illustrates the
value of bottom up as well as top down approaches
to innovations in ensuring that the directions of
technological pathways, the equitable distributions
of benefits, costs and knowledge ownership, and
the diversity of locally sensitive technological
options are relevant to the food, energy and
ecosystems crises.
The historical chapters illustrate numerous harms
which for the most part have been caused by
irresponsible corporations. This fact, coupled
with shortcomings in how decisions are made by
governments on when to act on early warnings,
and in the law when it comes to compensating
victims of harm, are analysed in three chapters
in Part D of the report. Each chapter analyses the
reasons behind prevailing practice and then goes
on to offer insights, for example, on how cost
calculation methods can be improved; on how
insurance schemes could be used to compensate
future victims of harm; and on the reasons why
businesses frequently ignore early warnings.
The cases in Parts A–D
form the basis for
considering in Part E the governance implications
for science, public policy and public engagement,
and how current practices could be improved
to enable society to maximise the benefits of
innovations while minimising harms. The main
insights are that science could be more relevant for
precautionary decision-making; that the wider use
of the precautionary principle can avert harm and
stimulate innovation; and that the late lessons of
history and precautionary approaches are highly
pertinent to today's multiple and inter-connected
crises — such as those arising from finance,
economics, the use of ecosystems, climate change,
and the use and supply of energy and food.
Finally, many of the historical and recent case
studies illustrate the value of engaging the public
in broadening the knowledge base and stimulating
robust innovations.
Twelve late lessons
Based on the case studies of Volume 1 of
Late lessons from early warnings
(EEA, 2001), twelve key lessons
for better decision-making were drawn:
1
2
3
4
5
6
7
Acknowledge and respond to ignorance, as well as uncertainty and risk, in technology appraisal and public policymaking
Provide adequate long-term environmental and health monitoring and research into early warnings
Identify and work to reduce 'blind spots' and gaps in scientific knowledge
Identify and reduce interdisciplinary obstacles to learning
Ensure that real world conditions are adequately accounted for in regulatory appraisal
Systematically scrutinise the claimed justifications and benefits alongside the potential risks
Evaluate a range of alternative options for meeting needs alongside the option under appraisal, and promote more robust,
diverse and adaptable technologies so as to minimise the costs of surprises and maximise the benefits of innovation
Ensure use of 'lay' and local knowledge, as well as relevant specialist expertise in the appraisal
Take full account of the assumptions and values of different social groups
8
9
10 Maintain the regulatory independence of interested parties while retaining an inclusive approach to information and opinion
gathering
11 Identify and reduce institutional obstacles to learning and action
12 Avoid 'paralysis by analysis' by acting to reduce potential harm when there are reasonable grounds for concern
Source:
EEA, 2001,
Late lessons from early warnings: the precautionary principle 1986–2000,
Environmental issues report
No 22, European Environment Agency.
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Part A — Summary
2 The precautionary principle and false
alarms — lessons learned
Steffen Foss Hansen and Joel A. Tickner
Most of the cases examined in the
Late lessons
from early warnings
reports are 'false negatives'
— instances where early warnings existed but
no preventive actions were taken. In debates
surrounding the precautionary principle it is
often claimed that widespread application of the
principle will lead to a large number of regulatory
false positives — over-regulation of minor risks
and regulation of non-existent risks, often due to
unwarranted public 'fears'. Understanding and
learning from past false positives as well as false
negatives is essential for improving decision-making
about public health and the environment.
This chapter reviews incidents of 'false positives',
where government regulation was undertaken based
on precaution but later turned out to be unnecessary.
In total 88 cases were identified to be alleged false
positives, however, following a detailed analysis
most of them turned out to be either real risks, or
cases where 'the jury is still out', or unregulated
alarms, or risk-risk trade-offs, rather than false
positives.
The analysis revealed four regulatory false
positives: US swine flu, saccharin, food irradiation,
and Southern leaf corn blight. Numerous important
lessons can be learned from each, although there
are few parallels between them in terms of when
and why each risk was falsely believed to be real.
This is a lesson in itself: each risk is unique, as
is the science and politics behind it and hence a
flexible approach is therefore needed, adapted
to the nature of the problem. The costs of the
false positives identified were mainly economic,
although the actions taken to address swine flu
in 1976 did lead to some unintended deaths and
human suffering, and diverted resources from
other potentially serious health risks. Determining
the net costs of mistaken regulatory action,
however, requires a complete assessment of the
impacts of the regulation, including the costs and
benefits of using alternative technologies and
approaches.
Overall, the analysis shows that fear of false
positives is misplaced and should not be a rationale
for avoiding precautionary actions where warranted.
False positives are few and far between as
compared to false negatives and carefully designed
precautionary actions can stimulate innovation, even
if the risk turns out not to be real or as serious as
initially feared. There is a need for new approaches
to characterising and preventing complex risks
that move debate from the 'problem' sphere to the
'solutions' sphere. By learning from the lessons in
this chapter, more effective preventive decisions can
be made in the future.
The scarcity of genuine false positives compared
to the large number of 'mistaken false positives'
could partly be the result of a deliberate strategy
in risk communication. Several references and
leaked documents have shown that some regulated
parties have consciously recruited reputable
scientists, media experts and politicians to call on
if their products are linked to a possible hazard.
Manufacturing doubt, disregarding scientific
evidence of risks and claiming over-regulation
appear to be a deliberate strategy for some industry
groups and think tanks to undermine precautionary
decision-making.
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Part A — Summary
3 Lead in petrol 'makes the mind give
way'
Herbert Needleman and David Gee
This chapter addresses the widespread use of
lead in petrol. It focuses on the period 1925–2005,
when leaded petrol was first widely marketed in
the US and then spread to the rest of the world
before being gradually phased out from the 1970s.
In Europe, the Aarhus Protocol (www.unece.org/
env/pp/treatytext.html) initiated the phase-out of
leaded petrol in the period 1998–2005.
The neurotoxic effects of lead were recognised as
far back as Roman times. And in 1925, at the 'one
day trial' of leaded petrol in the US, many experts
warned of the likely health impacts of adding lead
to petrol. Yet, despite the availability of an equally
effective alcohol additive which was assessed
by experts to be cleaner, the leaded route to fuel
efficiency was chosen in the US and then exported to
the rest of the world.
For several decades after the introduction of leaded
petrol, virtually no independent research was
carried out and the main source of information was
industry and industry-sponsored researchers. Not
until the 1960s and 1970s did independent scientists
from outside this group show, for example, that
body burdens of lead arising from human activities
were not 'normal', as industry claimed, but were
hundreds of times higher than before the industrial
revolution and were therefore likely to be harmful.
At its peak in the mid-1970s, leaded petrol released
about 200 000 tonnes of lead into the atmosphere
annually in both the US and Europe. Following
the subsequent phase-out, blood lead levels in
children (the most sensitive group exposed) quickly
fell, in line with the decrease in air concentrations.
The lessons nevertheless remain relevant globally
today. Although nearly all countries worldwide
had phased out leaded petrol by 2012, lead
concentrations in soils and sediments remain high.
Meanwhile, electronic wastes containing lead and
other contaminants also cause elevated blood lead
levels.
Supplementary panel texts focus on the events
leading up to the US choice of leaded petrol as
the primary fuel source in 1925 and more recent
accounts of EU policymaking on lead in petrol and
the road to phase-outs in Germany and the United
Kingdom.
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Part A — Summary
4 Too much to swallow: PCE
contamination of mains water
David Ozonoff
PCE (perchlorethylene, also known as 'perc' or
tetrachloroethylene), was used in the production of
plastic linings for drinking water distribution pipes
in the late 1960s and 1970s. This new and relatively
untested type of distribution pipe was used in over
700 miles of New England's water distribution
systems. Not until 1976 was it discovered that
PCE had been leaching into the water from the
pipe lining, causing widespread contamination of
water supplies that still today require continuous
remediation.
Before the pipes were put into production there
was a substantial amount of scientific information
available about the potential hazards of PCE. This
did not include current concerns about PCE's
carcinogenicity, teratogenicity and other health
consequences of relatively low-level exposure
upper most among today's concerns, but many
early warnings suggested the need for caution in
introducing PCE-based mains pipe linings.
PCE had been used to treat hookworm and data
on side effects were in the literature, while later
a variety of occupational users were studied,
including aircraft workers, small companies in
countries where biological monitoring was required,
and dry-cleaning firms. Several environmental
studies were also conducted to see if drinking
water contaminated with PCE or its close relative,
TCE (trichloroethylene), was associated with
cancer. Results were mixed and the chemical
industry consistently denied that PCE was a human
carcinogen.
This case study explores the early (pre 1970)
history researching the toxicity of the chemical. It
also focuses on the failure of one manufacturer,
Johns-Manville Corporation, to recognise the
warning signals about using a suspected toxic
substance. It examines why a new product was
deployed without thought to the public health
consequences and why evidence of the potential
hazard was ignored.
The science has not been hidden. It has been
ineffective in guiding and catalysing action.
Whether the problem is a failed duty of care or
a lack of clarity about what evidence will trigger
action, the contemporary argument over how to
interpret the scientific evidence is irresolvable
within science itself. There are no overarching
criteria from the philosophy of science that can
dictate a solution.
This chapter also includes two supplementary texts.
A panel that analyses the differences between the
conclusions of risk assessments based on the same
data, focusing in particular on assessments of PCE
and TCE. A further panel describes the opportunities
to switch to wet-cleaning technologies to reduce the
current use of PCE in dry cleaning.
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Part A — Summary
5 Minamata disease: a challenge for
democracy and justice
Takashi Yorifuji, Toshihide Tsuda and Masazumi Harada
Minamata disease, which can induce lethal or
severely debilitating mental and physical effects,
was caused by methylmercury-contaminated
effluent released into Minamata Bay by Chisso,
Japan's largest chemical manufacturer. It resulted
in widespread suffering among those who
unknowingly ate the contaminated fish. This chapter
documents the story in three phases.
The disease first came to prominence in the 1950s.
It was officially identified in 1956 and attributed to
factory effluent but the government took no action
to stop contamination or prohibit fish consumption.
Chisso knew it was discharging methylmercury
and could have known that it was the likely active
factor but it chose not to collaborate and actively
hindered research. The government concurred,
prioritising industrial growth over public health.
In 1968 Chisso stopped using the process that
caused methylmercury pollution and the Japanese
government then conceded that methylmercury was
the etiologic agent of Minamata disease.
The second part of the story addresses the discovery
that methylmercury is transferred across the
placenta to affect the development of unborn
children, resulting in serious mental and physical
problems in later life. Experts missed this at first
because of a medical consensus that such transfer
across the placenta was impossible.
The third phase focuses on the battle for
compensation. Initially, Chisso gave token
'sympathy money' under very limited criteria. In
1971 the Japanese government adopted a more
generous approach but after claims and costs soared
a more restrictive definition was introduced in
1977, justified by controversial 'expert opinions'.
Legal victories for the victims subsequently made
the government's position untenable and a political
solution was reached in 1995–1996. In 2003, the
'expert opinions' were shown to be flawed and the
Supreme Court declared the definition invalid in
2004.
In September 2011 there were 2 273 officially
recognised patients. Still, the continuing failure
to investigate which areas and communities were
affected means that the financial settlement's
geographic and temporal scope is still not properly
determined. Alongside deep-seated issues with
respect to transparency in decision-making and
information sharing, this indicates that Japan
still faces a fundamental democratic deficit in its
handling of manmade disasters.
This chapter is followed by three short updates
on the effects of mercury poisoning since
Minamata; on attempts to contain it, including
the 2009 global agreement to phase mercury out
of economic activity; and on the need for better
information about contaminant exposures to
enable policymakers to make informed choices that
balance the benefits of fish consumption against the
assumed adverse effects of low-level methylmercury
exposures.
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Part A — Summary
6 Beryllium's 'public relations problem'
David Michaels and Celeste Monforton
Scores of workers employed in nuclear weapons
production have been diagnosed with chronic
beryllium disease (CBD), a progressive and
irreversible inflammatory lung disease. This chapter
presents a history of knowledge and public policy
about preventing beryllium-related disease, focusing
primarily on the United States beryllium industry's
role in shaping US regulatory policy.
Over several decades increasingly compelling
evidence accumulated that CBD was associated
with beryllium exposure at levels below the existing
regulatory standard. The beryllium industry had a
strong financial incentive to challenge the data and
decided to be proactive in shaping interpretation
of scientific literature on beryllium's health effects.
It hired public relations and 'product defence'
consulting firms to refute evidence that the standard
was inadequate. When the scientific evidence
became so great that it was no longer credible to
deny that workers developed CBD at permitted
exposure levels, the beryllium industry responded
with a new rationale to delay promulgation of a
new, more protective exposure limit.
This case study underscores the importance of
considering the hazards from toxic materials
throughout the entire product life cycle. While
primary producers of beryllium products may be
able to control exposures in their own facilities, it is
unlikely that many secondary users and recyclers
have the expertise, resources and knowledge
necessary to prevent beryllium disease in exposed
workers and residents in nearby communities.
The primary lessons of this chapter are widely
applicable to many environmental health
controversies. In particular, it illustrates the practice
of 'manufacturing uncertainty' — a strategy used
by some polluters and manufacturers of hazardous
products to prevent or delay regulation or victim
compensation.
This chapter is followed by an analysis of the
rationale for corporate behaviour in the regulation
of beryllium. It is argued that the availability of
occasional and limited opportunities for companies
to change course without suffering onerous
consequences would encourage them to rethink their
position and create an obligation on shareholders
to take the responsible course. Although this may
be perceived as letting them 'get away with it', the
end result may be better public policy and corporate
responsibility.
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Part A — Summary
7 Tobacco industry manipulation of
research
Lisa A. Bero
This chapter differs in some ways from the others
in Volume 2 of
Late lessons from early warnings.
The
history of 'second hand', 'passive' or 'environmental
tobacco smoke' (ETS), to which non-smokers are
exposed overlaps with the history of active smoking.
Those affected include the partners and children of
smokers, and the bartenders and other workers who
have to work in smoky environments.
The focus in this chapter is on the strategies used
by the tobacco industry to deny, downplay, distort
and dismiss the growing evidence that, like active
smoking, ETS causes lung cancer and other effects
in non-smokers. It does not address the history
of scientific knowledge about tobacco and how it
was used or not used to reduce lung cancer and
other harmful effects of tobacco smoke. There is
much literature on this and a table at the end of the
chapter summarises the main dates in the evolution
of knowledge in this area.
The chapter concentrates on the 'argumentation'
that was used to accept, or reject, the growing
scientific evidence of harm. Who generated
and financed the science used to refute data on
adverse health effects? What were the motivations?
What kind of science and information, tools and
assumptions were used to refute data on the
adverse health of tobacco?
The release of millions of internal tobacco industry
documents due to law suits in the US has given
insights into the inner workings of the tobacco
industry and revealed their previously hidden
involvement in manipulating research. However,
this insight is not available for most corporate
sectors. The chapter discusses the possibilities of 'full
disclosure' of funding sources and special interests
in research and risk assessment in order to secure
independence and prevent bias towards particular
viewpoints.
While smoking bans are now being introduced
in more and more countries, other industries
are drawing inspiration from tobacco company
strategies, seeking to maintain doubt about
harm in order to keep hazardous products in the
marketplace.
The chapter also includes a summary of the tobacco
industry's role in shaping risk assessment in the US
and Europe to serve its own interests.
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Part A — Summary
8 Vinyl chloride: a saga of secrecy
Morando Soffritti, Jennifer Beth Sass, Barry Castleman and David Gee
This chapter is about how early warnings in the
1950s and 1960s concerning the short-term harm of
vinyl chloride (VC) to the skin and bones of workers,
and to the livers of laboratory animals, were initially
hidden from other workers and regulators. This
was despite some early misgivings by company
experts whose advice was initially ignored by their
employers. This pattern was repeated when the
later, more devastating news of a rare liver cancer
in workers was revealed by long-term animal
studies and by an attentive and concerned company
physician.
Unlike many other histories, however, this story
features a very prompt response from the global
chemical industry to the publication of the liver
cancer evidence, a response that included funding
cancer testing and later compliance with a large
reduction in the permissible exposure limits. The
case also provides early evidence of reproductive
effects of vinyl chloride monomer (VCM).
Other features of this story presage the later and
common responses of the corporate world to
heightened public awareness and pressure from
non-governmental organisations (NGOs) and trade
unions, including greatly exaggerated estimates of
the likely costs of complying with tighter pollution
controls; a frequent mismatch between the position
of the trade association and that of many, more
progressive companies within the association; but
also some relatively quick corporate responses to
public, NGO and regulatory pressure.
The chapter also features two legal aspects, which,
though more common in the US, are also valuable
for Europeans. First, the potentially positive role that
judicial review of regulatory proposals can play in
providing a societal judgement about the behaviour
of corporations. This can embrace not just moral
judgements but also judgements about the state of
the science and what society should do with it.
Second, the role that document discovery in
legal compensation cases can play in revealing
the real and until then secret activities of
corporations. Any proposals to promote justice
for victims of environmental and health harms
via no fault administrative arrangements need
to be accompanied by other measures to extract
information about corporate behaviour.
The chapter is followed by a panel analysing the
value of animal testing for identifying carcinogens.
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Part A — Summary
9 The pesticide DBCP and male infertility
Eula Bingham and Celeste Monforton
Dibromochloropropane (DBCP) is a pesticide used
against nematodes (roundworms or threadworms)
that damage pineapples, bananas and other tropical
fruits. It was introduced into US agriculture
in 1955 and approved for use as a fumigant in
1964. By 1961 laboratory experiments had shown
that it made the testicles of rodents shrink and
significantly reduced the quantity and quality of
sperm. Nonetheless, the compound was widely
marketed and became a commercial success.
In 1977, workers at a production plant became
worried that they were unable to father children.
An emergency study by a US government agency
discovered that in many cases the workers were
suffering from deficient or absent sperm. While
controls were improved at US facilities, the product
continued to be marketed and sprayed in Latin
America, the Philippines, some African countries,
and elsewhere.
By the 1990s, tens of thousands of plantation
workers in these countries had allegedly suffered
adverse reproductive effects from DBCP use.
The story continues today with contentious
legal claims for compensation, contamination of
drinking water and industry attempts to prevent
a Swedish documentary on the issue from being
screened.
This chapter looks at the knowledge available
about the hazards and the actions taken, or not
taken, to avert them. The DBCP story is significant
as it is the first clear example of reproductive
damage to workers who manufactured and used a
synthetic chemical. This is one of many examples
supporting the growing concerns about increasing
rates of reproductive and developmental disease,
and about the endocrine disrupting chemicals that
seem to be playing a role in these disorders.
Protecting production workers, users, consumers
and the environment from chemicals that may
damage reproduction demands closer integration
of scientific disciplines, as well as government
action. The lessons of DBCP may help in
ensuring timely protection from harm, based on
precautionary approaches to scientific evidence.
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Part A — Summary
10 Bisphenol A: contested science,
divergent safety evaluations
Andreas Gies and Ana M. Soto
Bisphenol A (BPA) is currently one of the world's
best-selling chemicals and primarily used to make
polycarbonate plastics. It is widely used in common
products such as baby bottles, household electronics,
medical devices and coatings on food containers. BPA
is known to mimic the female hormone oestrogen and
has been found to leach from the materials where it is
used.
Studies have suggested that even exposure to low
doses of BPA may cause endocrine disrupting
effects. As with other hormones, it appears that an
organism is most sensitive during development but
that effects are often not observed until much later
in the lifecycle. This means that at the time when the
effects become detectable, the chemical exposure has
vanished. This makes it extremely difficult to link
exposure to effects in humans.
This chapter maps some of the findings in studies of
rodents and humans. It also discusses the challenges
of evaluating scientific findings in a field where
industry-sponsored studies and independent
scientific research seem to deviate strongly. The
authors offer suggestions for ways to uncouple
financial interests from scientific research and testing.
A widely used and dispersed industrial chemical
like Bisphenol A is a controversial example
of an endocrine disrupting substance that
has implications for policymakers. Different
approaches to risk assessment for BPA by US and
European authorities are presented. It throws light
on the ways in which similar evidence is evaluated
differently in different risk assessments and
presents challenges for applying the precautionary
principle.
The intense discussion and scientific work on BPA
have slowly contributed to a process of improving
test strategies. While traditional toxicology has
relied on a monotonic increasing dose-response
relationship as evidence that the effect is caused by
the test agent, studies on BPA and other endocrine
disruptor chemicals (EDCs) have demonstrated the
limitations of this approach and adjustments have
been made in some cases.
It has also been widely accepted that effects
cannot be predicted by simply thinking of BPA as
a weak oestrogen and extrapolating from what is
observed for more potent endogenous oestrogens.
This lesson is particularly evident in the intense
pharmaceutical interest in selective oestrogen
response modifiers (SERMs).
The chapter is followed by a panel analysing the
value of animal testing for identifying carcinogens.
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Part A — Summary
11 DDT: fifty years since
Silent Spring
Henk Bouwman, Riana Bornman, Henk van den Berg and Henrik Kylin
'There was a strange stillness. The birds for example
— where had they gone? Many people spoke about
them, puzzled and disturbed. The feeding stations
in the backyards were deserted. The few birds seen
anywhere were moribund: they trembled violently
and could not fly. It was a spring without voices
... only silence lay over the fields and woods and
marsh.'
The book
Silent Spring
by Rachel Carson is mainly
about the impacts of chemicals (in particular
dichlorodiphenyltrichlorethane also known as DDT)
on the environment and human health. Indeed, the
close association between humans and birds remains
very apt. Representing the only two warm-blooded
groups of life on Earth, mammals and birds share
the same environments and threats.
Carson's claim that she lived in 'an era dominated
by industry, in which the right to make a dollar at
whatever cost is seldom challenged' still resonates
strongly with the problems that societies face all
over the world. One chapter heading, 'The obligation
to endure', derived from the French biologist and
philosopher Jean Rostand's famous observation that,
'the obligation to endure gives us the right to know'.
United States President John F. Kennedy responded
to the challenge posed by Carson by investigating
DDT, leading to its complete ban in the US. The
ban was followed by a range of institutions and
regulations concerned with environmental issues in
the US and elsewhere, driven by public demand for
knowledge and protection.
DDT was the primary tool used in the first global
malaria eradication programme during the 1950s
and 1960s. The insecticide is sprayed on the inner
walls and ceilings of houses. Malaria has been
successfully eliminated from many regions but
remains endemic in large parts of the world.
DDT remains one of the 12 insecticides — and
the only organochlorine compound — currently
recommended by the World Health Organization
(WHO), and under the Stockholm Convention
on Persistent Organic Pollutants, countries may
continue to use DDT. Global annual use of DDT
for disease vector control is estimated at more than
5 000 tonnes.
It is clear that the social conscience awakened by
Rachel Carson 50 years ago gave momentum to a
groundswell of actions and interventions that are
slowly but steadily making inroads at myriad levels.
Chapter 17 of her book, 'The other road' reminds the
reader of the opportunities that should have been
seized much earlier. With more than 10 % of bird
species worldwide now threatened in one way or
another, it is clear that we missed early warnings
or failed to act on them. Will we continue to miss
signposts to 'other roads'? Are our obligations to
endure met by our rights to know? As Carson said
50 years ago: 'The choice, after all, is ours to make.'
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Part B — Summary
12 Booster biocide antifoulants: is history
repeating itself?
Andrew R. G. Price and James W. Readman
Tributyltin (TBT) was widely used as an effective
antifouling agent in paints for ships and boats until
the European Community restricted its use in 1989
because of its proven harm to the environment
and shellfisheries. Thereafter, booster biocides
were introduced to enhance the performance of
antifouling paints. They were believed to be less
damaging to aquatic life than TBT. Subsequently,
however, it has been established that booster
biocides can also create significant environmental
risks.
This chapter outlines the background to booster
biocide use, the early warnings about their potential
physiological and ecological impacts on non-target
species, and the actions taken in response. The
science that set some alarm bells ringing is described,
along with lessons that could influence the future of
an industry still searching for less environmentally
invasive solutions.
Booster biocide antifouling agents threaten a variety
of habitats — from coral reefs and seagrass beds
to open moorings — within the EU and globally.
Their primarily herbicidal properties mean that
coral zooxanthellae, phytoplankton and periphyton
are particularly vulnerable. Compared to TBT, an
antifouling agent with a quite specific action, booster
biocides have more broad-spectrum impacts. The
wider ecological effect of shifting to booster biocides
remain poorly understood but of considerable
concern because they may affect the base of marine
food chains.
From a toxicological viewpoint, booster
biocides do not threaten to have endocrine
disrupting properties similar to TBTs. At current
environmental concentrations, however, some
can damage primary producers and some are
persistent. While legislation has been introduced
to control their use, the rigour of regulations varies
between countries. These geographical disparities
need to be addressed, and future biocidal products
and novel approaches to antifouling should be
better appraised.
For policymakers, the challenge is to protect
non-target biological communities from selective
change resulting from booster biocide use.
Persistence, bioaccumulative and toxic (PBT) criteria
can be used to evaluate the relative potential impact
from the available biocides, and consequently
target appropriate legislation. Nevertheless,
lateral thinking, aiming to identify novel materials
and strategies to address antifouling, could pay
dividends in the future.
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Part B — Summary
13 Ethinyl oestradiol in the aquatic
environment
Susan Jobling and Richard Owen
Many decades of research have shown that when
released to the environment, a group of hormones
known as oestrogens, both synthetic and naturally
occurring, can have serious impacts on wildlife. This
includes the development of intersex characteristics
in male fish, which diminishes fertility and
fecundity. Although often sublethal, such impacts
may be permanent and irreversible.
This chapter describes the scientific evidence
and regulatory debates concerning one of these
oestrogens, ethinyloestradiol (EE2), an active
ingredient in the birth control pill. First developed
in 1938, it is released to the aquatic environment
via wastewater treatment plants. Although it is
now clear that wildlife species are exposed to and
impacted by a cocktail of endocrine disrupting
chemicals, there is also reasonable scientific certainty
that EE2 plays a significant role, and at vanishingly
low levels in the environment.
In 2004 the Environment Agency of England and
Wales accepted this, judging the evidence sufficient
to warrant consideration of risk management.
In 2012, nearly 75 years after its synthesis, the
European Commission proposed to regulate EE2
as a EU-wide 'priority substance' under the Water
Framework Directive (the primary legislation for
protecting and conserving European water bodies).
This proposal was subsequently amended, delaying
any decision on a regulatory 'environmental quality
standard' until at least 2016.
This is in part because control of EE2 will come
at a significant price. Complying with proposed
regulatory limits in the environment means
removing very low (part per trillion) levels of EE2
from wastewater effluents at considerable expense.
Is this a price we are willing to pay? Or will the
price of precautionary action be simply too high
— a pill too bitter to swallow? To what extent is
society, which has enjoyed decades of flexible
fertility and will also ultimately pay for the control
and management of its unintended consequences,
involved in this decision? And what could this mean
for the many thousands of other pharmaceuticals
that ubiquitously infiltrate our environment and
which could have sublethal effects on aquatic
animals at similarly low levels?
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Part B — Summary
14 Climate change: science and the
precautionary principle
Hartmut Grassl and Bert Metz
The first scientifically credible early warning
about the possible dangers of climate change
due to carbon dioxide (CO
2
) emissions from
burning fossil fuels came in 1897. While the basic
physical principles of global warming are simple,
however, the more detailed science of climate
change is exceedingly complicated. Even now,
more than a hundred years since the first early
warning, many important details of climate change
cannot be predicted with certainty. It is therefore
unsurprising that the science of climate change and
questions about the true value of burning fossil
fuels have fostered sustained scientific and political
controversy.
When the first volume of
Late lessons from early
warnings
was drafted there appeared to be too
much legitimate controversy about climate change
for the issue to be included. A case study could
have led to arguments that distracted attention
from the valuable and robust lessons from more
established issues such as asbestos, polychlorinated
biphenyls (PCBs), chlorofluorocarbons (CFCs) and
the ozone-hole, X-rays and acid rain. This decision
was taken despite the then widespread acceptance
that 'the balance of evidence suggests a discernible
human influence on global climate' (Contribution
of
Working Group I to the Second Assessment Report of
the Intergovernmental Panel on Climate Change,
IPCC,
1995).
Over a decade later and after two more reviews by
the Intergovernmental Panel on Climate Change
(IPCC) of a much greater volume of climate change
science it seemed appropriate to include climate
change in this volume, despite some continuing
controversy. The evidence that human activities
are having a dangerous impact on the climate has
strengthened since 1995. By 2007, the IPCC was able
to conclude with 'very high confidence that the global
net effect of human activities since 1750 has been
one of warming'. Given the size and irreversibility
(on human time scales) of many of the harmful effects
of human-induced climate change, there is an urgent
need for action to reduce CO
2
emissions and other
greenhouse gases. Some contrarian views persist,
however, as the authors illustrate.
This chapter summarises the history of growing
knowledge about human-induced climate
change and of the main actions, or inactions that
accompanied it. Like many other chapters, it
reflects the lifelong commitment of both authors
to trying to understand and mitigate the effects of
human-induced climate change. It concludes with
some lessons and insights that are relevant to many
other environmental and health issues.
Also included is a panel text describing how the
IPCC's approach to assessing uncertainty evolved
between its first to its fifth assessment reports.
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Part B — Summary
15 Floods: lessons about early warning
systems
Zbigniew W. Kundzewicz
Floods are an increasingly acute problem. Intense
precipitation has become more frequent and more
intense, growing manmade pressure has increased
the magnitude of floods that result from any level
of precipitation, and flawed decisions about the
location of human infrastructure have increased the
flood loss potential.
Unlike most other case studies presented in this
report, this chapter focuses on flooding as a
phenomenon and the requirements for effective
early warning systems, rather than addressing
a particular event and the lessons that can be
learned.
Flooding cannot be wholly prevented. The
occurrence of a flood need not be considered a
'failure' and, conversely, minimisation of losses
may constitute a 'success'. There are lessons to
be learned from every flood and it is important
to use them in preparing for the next flood. Once
we accept that no flood protection measures can
guarantee complete safety, a general change of
paradigm is needed to reduce human vulnerability
to floods. The attitude of 'living with floods' and
accommodating them in planning seems more
sustainable than hopelessly striving to eradicate
them.
Flood forecasting and warning systems fail because
links in the chain perform poorly or fail completely.
A single weak point in a system that otherwise
contains excellent components may render the
overall system performance unsatisfactory.
A successful system requires sufficient integration
of components and collaboration and coordination
between multiple institutions.
The chapter deals primarily with the challenges of
fluvial (river) floods. It is complemented by three
short supplementary texts. The first highlights
the complex, dynamic and diverse ecosystems of
river floodplains, which are often degraded during
construction of flood defences. Despite their huge
economic value, near-natural floodplains are
among the most threatened ecosystems globally.
The second discusses uncertainties in anticipating
rainfall patterns and intensity, and their
relationship to flood levels during extreme flows.
Such uncertainties present challenges for scientists
and decision-makers alike.
The third addresses the increasing risks of coastal
flooding due to factors such as climate change and
sea-level rise, and reviews European experience
with precautionary action.
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Part B — Summary
16 Seed-dressing systemic insecticides and
honeybees
Laura Maxim and Jeroen van der Sluijs
In 1994 French beekeepers began to report alarming
signs. During summer, many honeybees did not
return to the hives. Honeybees gathered close
together in small groups on the ground or hovered,
disoriented, in front of the hive and displayed
abnormal foraging behaviour. These signs were
accompanied by winter losses.
Evidence pointed to Bayer's seed-dressing systemic
insecticide Gaucho
®
, which contains the active
substance imidacloprid. This chapter presents
the historical evolution of evidence on the risks
of Gaucho
®
to honeybees in sunflower and maize
seed-dressing in France, and analyses the actions in
response to the accumulating evidence regarding
these risks.
The social processes that ultimately lead to
application of the precautionary principle for
the ban of Gaucho
®
in sunflower and maize
seed-dressing are described, with a focus on the
ways in which scientific findings were used by
stakeholders and decision-makers to influence
policy during the controversy.
Public scientists were in a difficult position in this
case. The results of their work were central to a
social debate with high economic and political
stakes. In certain cases their work was not judged
according to its scientific merit but based on
whether or not it supported the positions of some
stakeholders. This situation tested the ability and
courage of researchers to withstand pressure and
continue working on imidacloprid.
Other European countries also suspended
neonicotinoid seed-dressing insecticides. Evidence
of the toxicity of neonicotinoids present in the dust
emitted during sowing of coated seeds supported
such decisions. Most important, the French case
highlighted the major weaknesses of regulatory
risk assessment and marketing authorisation of
pesticides, and particularly neonicotinoids. These
insights were recently confirmed by work by the
European Food Safety Authority.
From this case study eight lessons are drawn about
governance of controversies related to chemical
risks. The study is followed by two additional
texts. A first panel presents Bayer Crop Science's
comments on the analysis in this chapter. A second
contains the authors' response to the Bayer
comments.
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Part B — Summary
17 Ecosystems and managing the
dynamics of change
Jacqueline McGlade and Sybille van den Hove
A decade after Rachel Carson's
Silent Spring
was
published, describing the toxic legacy of the
twentieth century, Annie Dillard in her Pulitzer
prize winning book
Pilgrim at Tinker Creek,
opened up a different way of looking at the
world. It presaged a twenty first century in which
the global economy would be based on a more
thorough understanding of nature, its functioning
and material wealth. Wholly descriptive, yet
increasingly relevant, her book captured the very
essence of what this chapter is about: that amongst
the observations which routinely help to predict
the evolution of the natural world are the seeds of
surprise — surprise of the unusual and surprise
as a portent of future change. Our systemic failure
to anticipate such surprises forms the core of this
chapter. A series of case studies from fisheries,
forests, savannah and aquatic systems are used to
underline how early warnings about changes in
these natural systems emerged but were not used.
The chapter highlights how the division of
knowledge into political, disciplinary and
geographic silos has led to the 'recurring
nightmares' of short-term interests outcompeting
long-term vision; situations where competition
replaces co-operation; fragmentation of values
and interest; fragmentation of authority and
responsibility; and fragmentation of information
and knowledge leading to inadequate solutions
or even additional problems. In addition, the
lack of institutional fit has often confounded the
effectiveness of the stewardship of ecosystem
services, and led to unexpected surprises, excessive
rent seeking and high transaction costs.
Using counterfactual thinking (i.e. the dependence
of
whether, when
and
how
one event occurs on
whether, when
and
how
another event occurs and the
possible alteration of events), built around the four
interconnected concepts of
planetary boundaries,
tipping points, panarchy
and
resilience,
the chapter
provides an analytical lens through which to
explore why many of the warning signals were
not seen. The chapter concludes by suggesting
why ecosystems are likely to be even more at risk
in the future and why we will need to observe
and interpret the dynamics of both nature and
institutions ever more closely if we are to avoid
sudden irreversible ecological changes.
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Part C — Summary
18 Late lessons from Chernobyl, early
warnings from Fukushima
Paul Dorfman, Aleksandra Fucic and Stephen Thomas
The nuclear accident at Fukushima in Japan occurred
almost exactly 25 years after the Chernobyl nuclear
accident in 1986. Analysis of each provides valuable
late and early lessons that could prove helpful to
decision-makers and the public as plans are made
to meet the energy demands of the coming decades
while responding to the growing environmental costs
of climate change and the need to ensure energy
security in a politically unstable world.
This chapter explores some key aspects of the
Chernobyl and Fukushima accidents, the radiation
releases, their effects and their implications for
any construction of new nuclear plants in Europe.
There are also lessons to be learned about nuclear
construction costs, liabilities, future investments
and risk assessment of foreseeable and unexpected
events that affect people and the environment.
Since health consequences may start to arise from
the Fukushima accident and be documented over
the next 5–40 years, a key lesson to be learned
concerns the multifactorial nature of the event. In
planning future radiation protection, preventive
measures and bio-monitoring of exposed
populations, it will be of great importance to
integrate the available data on both cancer and
non-cancer diseases following overexposure to
ionising radiation; adopt a complex approach to
interpreting data, considering the impacts of age,
gender and geographical dispersion of affected
individuals; and integrate the evaluation of latency
periods between exposure and disease diagnosis
development for each cancer type.
Given the degree of uncertainty and complexity
attached to even the most tightly framed and
rigorous nuclear risk assessment, attempts to
weight the magnitude of accident by the expected
probability of occurrence have proven problematic,
since these essentially theoretical calculations
can only be based on sets of pre-conditioning
assumptions. This is not an arcane philosophical
point but rather a very practical issue with
significant implications for the proper management
of nuclear risk. With its failure to plan for the
cascade of unexpected beyond design-base
accidents, the regulatory emphasis on risk-based
probabilistic assessment has proven very limited.
An urgent reappraisal of this approach and its
real-life application seems overdue.
Whatever one's view of the risks and benefits of
nuclear energy, it is clear that the possibility of
catastrophic accidents and consequent economic
liabilities must be factored into the policy and
regulatory decision-making process. In the context
of current collective knowledge on nuclear risks,
planned pan-European liability regimes will need
significant re-evaluation.
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Part C — Summary
19 Hungry for innovation: from GM crops
to agroecology
David A. Quist, Jack A. Heinemann, Anne I. Myhr, Iulie Aslaksen and Silvio Funtowicz
Innovation's potential to deliver food security
and solve other agriculture-related problems is
high on the agenda of virtually all nations. This
chapter looks at two different examples of food and
agricultural innovation: genetically modified (GM)
crops and agroecological methods, which illustrate
how different innovation strategies affect future
agricultural and social options.
GM crops are well suited to high-input
monoculture agricultural systems that are highly
productive but largely unsustainable in their
reliance on external, non-renewable inputs.
Intellectual property rights granted for GM crops
often close down, rather than open up further
innovation potential, and stifle investment into a
broader diversity of innovations allowing a greater
distribution of their benefits.
Science-based agroecological methods are
participatory in nature and designed to fit within
the dynamics underpinning the multifunctional
role of agriculture in producing food, enhancing
biodiversity and ecoystem services, and providing
security to communities. They are better suited to
agricultural systems that aim to deliver sustainable
food security than high external input approaches.
They do, however, require a broader range of
incentives and supportive frameworks to succeed.
Both approaches raise the issue of the governance
of innovation within agriculture and more generally
within societies.
The chapter explores the consequences of a
'top-down transfer of technology' approach
in addressing the needs of poor farmers. Here
innovation is often framed in terms of economic
growth in a competitive global economy, a focus
that may conflict with efforts to reduce or reverse
environmental damage caused by existing models
of agriculture, or even deter investment into socially
responsible innovation.
Another option explored is a 'bottom-up' approach,
using and building upon resources already
available: local people, their knowledge, needs,
aspirations and indigenous natural resources. The
bottom-up approach may also involve the public
as a key actor in decisions about the design of food
systems, particularly as it relates to food quality,
health, and social and environmental sustainability.
Options are presented for how best to answer
consumer calls for food quality, sustainability and
social equity in a wide sense, while responding to
health and environmental concerns and securing
livelihoods in local small-scale agriculture. If we
fail to address the governance of innovation in
food, fibre and fuel production now, then current
indications are that we will design agriculture to fail.
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Part C — Summary
20 Invasive alien species: a growing but
neglected threat?
Sarah Brunel, Eladio Fernández-Galiano, Piero Genovesi, Vernon H. Heywood, Christoph Kueffer and
David M. Richardson
Biological invasions are one of the five major causes
of biodiversity loss as global human travel and
trade have moved, and continue to move, thousands
of species between and across continents. Some
species of alien origin have a high probability of
unrestrained growth which can ultimately lead to
environmental damage.
An alien species — animal, plant or microorganism
— is one that has been introduced, as a result of
human activity, either accidentally or deliberately,
to an area it could not have reached on its own.
A common definition of the term 'invasive'
focuses on its (negative) impact, while other
definitions consider only rate of spread and exclude
considerations of impact.
Despite the growing amount of legislation being
adopted at the global scale, biological invasions
continue to grow at a rapid rate, with no indication
yet of any saturation effect. Decision-making in this
area is very challenging. The overall complexity
of the problem, its interdisciplinarity, the scientific
uncertainties and the large number of stakeholders
that need to be informed and involved, together
demand governance actions that are difficult to see
emerging at the regional scale (as in the EU), let
alone globally.
It is widely agreed that preventing biological
invasions or tackling them at a very early stage
is the most efficient and cost-effective approach.
Harmless species can be confused with harmful
invasive species, however, leading to a waste of
resources. Even more seriously, harmful invaders
can be mistaken for innocuous species — so-called
'invaders in disguise' — and no appropriate action
may be taken to counter the threats they pose.
Even with a very good risk assessment system, new
outbreaks of invasive alien species could still occur,
necessitating a system of rapid early warning
and effective eradication response. The decision
on where to draw the line on the acceptable
environmental risks versus the introduction of
new species or new communities that may carry
invasive alien species then becomes a value
judgement.
There is lively debate within the scientific
community regarding the most appropriate
strategies for managing invasive alien species.
Governments and institutions charged with making
decisions have access to considerable knowledge
on the topic, but the lack of rules of interactions
between multiple parties regularly thwarts effective
decision-making.
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Part C — Summary
21 Mobile phones and brain tumour risk:
early warnings, early actions?
Lennart Hardell, Michael Carlberg and David Gee
In 2011 the World Health Organization's
International Agency for Research on Cancer (IARC)
categorised the radiation fields from mobile phones
and other devices that emit similar non-ionizing
electromagnetic fields (EMFs), as a Group 2B
i.e. 'possible' human carcinogen. Nine years earlier
IARC gave the same classification to the magnetic
fields from overhead electric power lines.
The IARC decision on mobile phones was
principally based on two sets of case-control human
studies of possible links between mobile phone use
and brain tumours: the IARC Interphone study
and the Hardell group studies from Sweden. Both
provided complementary and generally mutually
supportive results. This chapter gives an account
of the studies by these two groups — and others
coming to different conclusions — as well as reviews
and discussions leading up to the IARC decision
in 2011. The chapter also describes how different
groups have interpreted the authoritative IARC
evaluation very differently.
There are by now several meta-analyses and reviews
on mobile phones and brain tumours, which
describe the challenges of doing epidemiology on
this issue, the methodological limitations of the
major studies published so far and the difficulties of
interpreting their results.
It has been suggested that national incidence data
on brain tumours could be used to qualify or
disqualify the association between mobile phones
and brain tumours observed in the case-control
studies. However, in addition to methodological
shortcomings, there might be other factors that
influence the overall incidence rate such as changes
in exposure to other risk factors for brain tumours
that are unknown in descriptive studies. Cancer
incidence depends on initiation, promotion and
progression of the disease. As the mechanism for
radiofrequency electromagnetic fields carcinogenesis
is unclear, it supports the view that descriptive data
on brain tumour incidence is of limited value.
The chapter points to mobile phone industry inertia
in considering the various studies and taking the
IARC carcinogenic classification into account and
a failings from the media in providing the public
with robust and consistent information on potential
health risks. The IARC carcinogenic classification
also appears not to have had any significant impact
on governments' perceptions of their responsibilities
to protect public health from this widespread source
of radiation.
The benefits of mobile telecommunications are
many but such benefits need to be accompanied
by consideration of the possibility of widespread
harms. Precautionary actions now to reduce head
exposures would limit the size and seriousness of
any brain tumour risk that may exist. Reducing
exposures may also help to reduce the other possible
harms that are not considered in this case study.
Evidence is increasing that workers with heavy
long-term use of wireless phones who develop
glioma or acoustic neuroma should be compensated.
The first case in the world was established on
12 October 2012. The Italian Supreme Court affirmed
a previous ruling that the Insurance Body for Work
(INAIL) must grant worker's compensation to a
businessman who had used wireless phones for
12 years and developed a neuroma in the brain.
Late lessons from early warnings: science, precaution, innovation
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Part C — Summary
22 Nanotechnology — early lessons from
early warnings
Steffen Foss Hansen, Andrew Maynard, Anders Baun, Joel A. Tickner and Diana M. Bowman
Nanotechnology is the latest in a long series of
technologies heralded as ushering in a new era of
technology-driven prosperity. Current and future
applications of nanotechnology are expected to lead
to substantial societal and environmental benefits,
increasing economic development and employment,
generating better materials at lower environmental
costs, and offering new ways to diagnose and treat
medical conditions. Nevertheless, as new materials
based on nanoscale engineering move from the lab
to the marketplace, have we learnt the lessons of
past 'wonder technologies' or are we destined to
repeat past mistakes?
This chapter first introduces nanotechnology,
clarifies the terminology of nanomaterials and
describes current uses of these unique materials.
Some of the early warning signs of possible adverse
impacts of some nanomaterials are summarised,
along with regulatory responses of some
governments. Inspired by the EEA's first volume
of
Late lessons from early warnings,
the chapter looks
critically at what lessons can already be learned,
notwithstanding nanotechnology's immaturity.
Nanotechnology development has occurred in
the absence of clear design rules for chemists and
materials developers on how to integrate health,
safety and environmental concerns into design.
The emerging area of 'green nanotechnology' offers
promise for the future with its focus on preventive
design. To gain traction, however, it is important
that research on the sustainability of materials
is funded at levels significant enough to identify
early warnings, and that regulatory systems
provide incentives for safer and sustainable
materials.
Political decision-makers have yet to address many
of the shortcomings in legislation, research and
development, and limitations in risk assessment,
management and governance of nanotechnologies
and other emerging technologies. As a result,
there remains a developmental environment that
hinders the adoption of precautionary yet socially
and economically responsive strategies in the field
of nanotechnology. If left unresolved, this could
hamper society's ability to ensure responsible
development of nanotechnologies.
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Part D — Summary
23 Understanding and accounting for the
costs of inaction
Mikael Skou Andersen and David Owain Clubb
In political decision-making processes, the burden
of proof is often distributed such that policymakers
only respond to early warning signals from
environmental hazards once the costs of inaction
have been estimated.
This chapter revisits some key environmental issues
for which estimates of costs of inaction have been
carefully developed over many years of research.
The aim is to consider the methodological challenges
involved in producing estimates that are credible
and appropriate rather than present specific
estimates for these costs.
The case studies also provide insights into how
early warning signals might provide a basis
for estimating the costs of inaction, when the
science base is less consolidated. For example,
the case of nitrates in drinking water illustrates
that a precautionary approach to the costs of
inaction is quite conceivable. The phase-out of
ozone-depleting substances, where early-warning
scientists successfully alerted the world to the
damaging effects of chlorofluorocarbons (CFCs),
provides another important case because additional
impacts for global warming actually cause the
costs of inaction to be considerably higher than
initially believed. This is a reminder that figures
for the costs of inaction have often been grossly
underestimated.
Finally, in the case of air pollution, making use of
different estimates for mortality risk avoidance will
help decision-makers to see that there are higher-
and lower-bound estimates for the costs of inaction.
Even if the lower-bound estimates are perhaps too
conservative, with a bias towards health effects, they
will in many situations encourage more rather than
less abatement effort. Reducing emission loads will
also tend to bring relief for the intangible assets of
biodiversity and nature.
Making the best use of environmental science and
modelling helps to make environmental protection
and precaution a priority. Producing cost estimates
should not be left to economists alone, but should
rather be seen as a starting point for a broader
discussion, featuring also the relevant expertise
in health, ecology, demography, modelling and
science. Well researched estimates, based on
interdisciplinary collaboration, can strengthen
some of those scattered and diffuse interests, which
during the ordinary processes of policy-making
have difficulty making their voices heard.
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Part D — Summary
24 Protecting early warners and late
victims
Carl Cranor
Many
Late lessons from early warnings
chapters
provide examples of early warning scientists who
were harassed for bringing inconvenient truths
about impending harm to the attention of the
public and regulators. There is also some evidence
that young scientists are being discouraged from
entering controversial fields for fear of such
harassment. In addition, where warnings have been
ignored and damage has ensued, it has often proven
difficult in the past to achieve prompt and fair
compensation for the victims. Some ideas for reform,
building on some current institutional models are
explored here.
This chapter first explores the idea of extending
whistleblowing laws to help encourage and protect
early-warning scientists and others who identify
evidence of impending harm. Complementary
measures, such as greater involvement of
professional societies and the use of recognition
awards, as for example in Germany, could also be
helpful.
Next, the chapter explores improved mechanisms
for compensating victims of pollution and
contamination. The chapter on the Minamata Bay
disaster provides an extreme example of long
delays in getting adequate compensation for the
victims of methylmercury poisoning. It was almost
fifty years, between 1956 and 2004, before the
victims attained equitable levels of compensation
and legal recognition of responsibility. Other case
studies illustrate similar examples of long delays in
receiving adequate compensation.
Options are examined for providing justice to any
future victims of those emerging technologies
such as nanotechnology, genetically modified
crops and mobile phone use, which currently can
provide broad public benefits but potentially at a
cost to small groups of victims. The potential for
widespread exposure and uncertain science could
justify 'no-fault' administrative schemes that provide
more efficient and equitable redress in situations
where the benefit of scientific doubt would be
given to victims. The use of anticipatory assurance
bonds to help minimise and meet the costs of future
environmental damage from large scale technologies
is also explored.
A supplementary panel text describes cases of
asbestos and mesothelioma, where the senior
courts in the United Kingdom have developed
innovative ways of dealing with both joint and
several liability, and the foreseeability of subsequent
asbestos cancers, after the initial recognition of
the respiratory disease, asbestosis. Such legal
developments in the field of personal injury could
illustrate the future direction of long-tail liability in
both environmental damage and personal injury.
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Part D — Summary
25 Why did business not react with
precaution to early warnings?
Marc Le Menestrel and Julian Rode
In the past, companies have frequently neglected
early warning signals about potential hazards for
human health or the environment associated with
their products or operations. This chapter reviews
and analyses relevant interdisciplinary literature
and prominent case studies — in particular those
documented in both volumes of
Late lessons from
early warnings
— and identifies main factors
responsible for the disregard of early warning
signals.
The chapter shows how economic motives often
drive non-precautionary business decisions. In
virtually all reviewed cases it was perceived to
be profitable for industries to continue using
potentially harmful products or operations.
However, decisions are also influenced by a complex
mix of epistemological, regulatory, cultural and
psychological aspects. For instance, characteristics of
the research environment and the regulatory context
can provide business actors with opportunities
to enter into 'political actions' to deny or even
suppress early warning signals. Also, business
decision-makers face psychological barriers to
awareness and acceptance of the conflicts of values
and interests entailed by early warning signals.
Cultural business context may further contribute to
the denial of conflicts of values.
The chapter concludes with a set of reflections
on how to support more precautionary business
decision making. A prominent policy response to
the conflicting interests of business and society
is introducing regulations that attempt to steer
business rationality towards internalising external
effects. Innovative solutions such as assurance
bonding should be considered.
There is a need to better understand and expose
why business actors do not respond voluntarily to
early warning signals with precautionary actions.
Blaming business, in particular with hindsight,
tends to be common reaction that may not always
be constructive. It often misses the complex or
even contradictory set of motives and drivers that
business actors face.
Public institutions could support progressive
business by analysing and publically disclosing
the dilemmas and temptations entailed by early
warning signals, for example for different industries
and for the specific societal and regulatory context
of decisions. Rigorous and explicit exposition of
the dilemmas will create further incentives for
responsible actors to share and communicate their
precautionary responses.
An additional reflection centres on the role of
political actions of business actors, in particular
those actions aimed at suppressing early warning
signals. Regulatory efforts that make the political
actions of business more transparent can help
to sustain a sound balance of power, thereby
maintaining our ability to benefit from early
warning signals and reducing the likelihood of
health and environmental hazards.
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Part E — Summary
26 Science for precautionary
decision-making
Philippe Grandjean
The goals of academic researchers may differ
from those of regulatory agencies responsible for
protecting the environment. Thus, research must
take into account issues such as feasibility, merit and
institutional agendas, which may lead to inflexibility
and inertia.
A large proportion of academic research on
environmental hazards therefore seems to focus
on a small number of well studied environmental
chemicals, such as metals. Research on
environmental hazards should therefore to a greater
extent consider poorly known problems, especially
the potential hazards about which new information
is in particular need.
Misinterpretation may occur when results
published in scientific journals are expressed in
hedged language. For example, a study that fails to
document with statistical significance the presence
of a hazard is often said to be negative, and the
results may be misinterpreted as evidence that
a hazard is absent. Such erroneous conclusions
are inspired by science traditions, which demand
meticulous and repeated examination before a
hypothesis can be said to be substantiated.
For prioritising needs for action, research
should instead focus on identifying the possible
magnitude of potential hazards. Research is always
affected by uncertainties and many of them can
blur a real association between an environmental
hazard and its adverse effects, thereby resulting
in an underestimated risk. Environmental health
research therefore needs to address the following
question: are we sufficiently confident that this
exposure to a potential hazard leads to adverse
effects serious enough to initiate transparent and
democratic procedures to decide on appropriate
intervention?
The choice of research topics must consider
societal needs for information on poorly known
and potentially dangerous risks. The research
should be complementary and extend current
knowledge, rather than being repetitive for
verification purposes, as required by the
traditional science paradigm. Research findings
should be openly available and reported so that
they inform judgments concerning the possible
magnitude of suspected environmental hazards,
thereby facilitating precautionary and timely
decision-making.
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Part E — Summary
27 More or less precaution?
David Gee
Despite its presence in a growing body of EU and
national legislation and case law, the application
of the precautionary principle has been strongly
opposed by vested interests who perceive short term
economic costs from its use. There is also intellectual
resistance from scientists who fail to acknowledge
that scientific ignorance and uncertainty, are
excessively attached to conventional scientific
paradigms, and who wait for very high strengths
of evidence before accepting causal links between
exposure to stressors and harm.
The chapter focuses on some of the key issues that
are relevant to a more common understanding of the
precautionary principle and to its wider application.
These include different and confusing definitions of
the precautionary principle and of related concepts
such as prevention, risk, uncertainty, variability and
ignorance; common myths about the meaning of the
precautionary principle; different approaches to the
handling of scientific complexity and uncertainty;
and the use of different strengths of evidence for
different purposes.
The context for applying the precautionary
principle also involves considering the 'knowledge
to ignorance' ratio for the agent in focus: the
precautionary principle is particularly relevant
where the ratio of knowledge to ignorance is low, as
with emerging technologies.
A working definition of the precautionary principle
is presented that aims to overcome some of the
difficulties with other definitions, such as their use
of triple negatives; a failure to address the context
of use of the precautionary principle; no reference
to the need for case specific strengths of evidence to
justify precaution; and overly narrow interpretations
of the pros and cons of action or inaction.
The chapter also points to the need for greater
public engagement in the process of framing and
decision-making about both upstream innovations
and their downstream hazards, including the
specification of the 'high level of protection' required
by the EU treaty. A precautionary and participatory
framework for risk analysis is proposed, along with
some 'criteria for action' to complement criteria for
causation.
The capacity to foresee and forestall disasters,
especially when such action is opposed by powerful
economic and political interests, appears to be
limited, as the case studies in
Late lesson from early
warnings
illustrate. The chapter argues that with
more humility in the face of uncertainty, ignorance
and complexity, and wider public engagement,
societies could heed the lessons of past experience
and use the precautionary principle, to anticipate
and minimise many future hazards, whilst
stimulating innovation. Such an approach would
also encourage more participatory risk analysis;
more realistic and transparent systems science;
and more socially relevant and diverse innovations
designed to meet the needs of people and
ecosystems.
Late lessons from early warnings: science, precaution, innovation
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Part E — Summary
28 In conclusion
The first volume of
Late lessons from early warnings
highlighted the difficulties of balancing precaution
with technological innovation and ended with a call
to action for policymakers. How much progress has
been made since then?
First, there is growing evidence that precautionary
measures do not stifle innovation, but instead can
encourage it, in particular when supported by smart
regulation or well-designed tax changes. Not only
has the body of knowledge become richer since
2001, but also the number of stakeholders involved
in decision-making has become larger and more
diverse. There has also been increasing attention
to communicating scientific uncertainty, especially
in the fields of climate change, food safety, and
emerging risks.
However, there has been less progress in other areas:
for example, many of the political and scientific
'bureaucratic silos' still remain, despite frequent
calls for policy integration and inter-departmental
coordination. This has led to the unintended
destruction of stocks of natural capital in some
parts of the world and in other instances, the
global spread of technologies, despite warnings of
impending hazards. The result has been widespread
damage, with most polluters still not paying the full
costs of pollution.
Yet, more encouragingly, new transformative
approaches are emerging to manage the systemic
and interconnected challenges the world faces
e.g. economic/financial, climate/energy, ecosystems/
food. These relate, inter alia, to the increasing use
of digital communications and networking by
consumers, citizens and shareholders to demand
and foster increased participation, more social
responsibility, greater levels of accountability and
higher transparency, especially in determining
future pathways for energy and food production.
There is a greater understanding of the complexity
of the environment, of scientific ignorance
and uncertainties, the irreversibility of many
harmful impacts and on the broader risks to
the long term interests of society if political and
financial institutions remain unchanged. Also
some corporations are fundamentally embracing
sustainable development objectives in their business
models and activities.
The case studies across both volumes of
Late lessons
from early warnings
cover a diverse range of chemical
and technological innovations, and highlight a
number of systemic problems. These include a lack
of institutional and other mechanisms to respond
to early warning signals; a lack of ways to correct
market failures either caused by misleading market
prices or where costs and risks to society and nature
are not properly internalised; and the fact that key
decisions on innovation pathways are made by those
with vested interests and/or by a limited number of
people on behalf of many. The insights and lessons
drawn from the case histories certainly provide the
seeds for some of the answers. They also provide
knowledge for a series of key actions that are
outlined below.
Of course, many questions remain. For example:
how can the precautionary principle be used
further to support decision-making in the face
of uncertainties and the inevitable surprises that
come from complex systems?; how can societies
avoid a lack of 'perfect' knowledge being used as
a justification for inaction in the face of 'plausible'
evidence of serious harm?; how can conflicting
interests be balanced during the phases of
development and use?; and how can the benefits
of products and technologies be more equitably
distributed?
Reduce delays between early warnings
and actions
The majority of the case studies in
Late lessons
from early warnings
Volumes 1 and 2 illustrate
that if the precautionary principle had been
applied on the basis of early warnings, justified
by 'reasonable grounds for concern' many lives
would have been saved and much damage to
ecosystems avoided. It is therefore very important
that large scale emerging technologies, such as
biotechnologies, nanotechnologies and information
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Part E — Summary
and communication technologies, apply the
precautionary principle based on the experiences and
lessons learned from these and other case studies.
Precautionary actions can be seen to stimulate rather
than hinder innovation; they certainly do not lead to
excessive false alarms. As the analysis in Volume 2
shows, of 88 cases of claimed 'false positives', where
hazards were wrongly regulated as potential risks,
only four were genuine false alarms. The frequency
and scale of harm from the mainly 'false negative'
case studies indicate that shifting public policy
towards avoiding harm, even at the cost of some
false alarms, would seem to be worthwhile, given the
asymmetrical costs of being wrong in terms of acting
or not acting based on credible early warnings.
However, the speed and scale of today's
technological innovations can inhibit timely action.
This is often because by the time clear evidence
of harm has been established, the technology
has been modified, thereby allowing claims of
safety to be subsequently re-asserted. Even where
the technological change has been marginal, the
large, often global, scale of investment can lead to
widespread technological lock-in, which is then
difficult and expensive to alter.
These features of current technological innovation
strengthen the case for taking early warning signals
more seriously and acting on lower strengths
of evidence than those normally used to reach
'scientific causality'. Most of the historical case
studies show that by the time such strong evidence
of causality becomes available, the harm to people
and ecosystems has become more diverse and
widespread than when first identified, and may
even have been caused by much lower exposures
than those initially considered dangerous.
The case studies have also shown that there are
many barriers to precautionary action, including:
the short-term nature of most political and financial
horizons; the existence of technological monopolies;
the conservative nature of the sciences involved,
including the separate 'silos' within which they
operate; the power of some stakeholders; and the
cultural and institutional circumstances of public
policymaking that often favour the status quo.
practical consequences for minimising harm. Much
of the harm described in Volumes 1 and 2, such
as cancers or species decline, is caused by several
co-causal factors acting either independently or
together. For example, the reduction of intelligence
in children can be linked to lead in petrol, mercury
and polychlorinated biphenyls (PCBs) as well as
to socio-economic factors; bee colony collapse can
be linked to viruses, climate change and nicotinoid
pesticides; and climate change itself is caused
by many complex and inter-linked chemical and
physical processes.
In some cases, such as foetal or fish exposures,
it is the timing of the exposure to a stressor that
causes the harm, not necessarily the amount; the
harm may also be caused or exacerbated by other
stressors acting in a particular timed sequence. In
other cases, such as radiation and some chemicals
such as bisphenol A (BPA), low exposures can be
more harmful than high exposures; and in others,
such as asbestos with tobacco, and some endocrine
disrupting substances, the harmful effects of
mixtures can be greater than from each separate
stressor. There are also varying susceptibilities
to the same stressors in different people, species
and ecosystems, depending on pre-existing stress
levels, genetics and epigenetics. This variation can
lead to differences in thresholds or tipping point
exposures, above which harm becomes apparent in
some exposed groups or ecosystems but not others.
Indeed there are some harmful effects which occur
only at the level of the system, such as a bee colony,
which cannot be predicted from analysing a single
part of the system, such as an individual bee.
Our increased knowledge of complex biological
and ecological systems has also revealed that
certain harmful substances, such as polychlorinated
biphenyls (PCBs) and dichlorodiphenyltrichlorethane
(DDT) can move around the world via a range of
biogeochemical and physical processes and then
accumulate in organisms and ecosystems many
thousands of kilometres away.
The practical implications of these observations
are threefold. First, it is very difficult to establish
very strong evidence that a single substance or
stressor 'causes' harm to justify timely actions to
avoid harm; in many cases only reasonable evidence
of co-causality will be available. Second, a lack
of consistency between research results is not a
strong reason for dismissing possible causal links:
inconsistency is to be expected from complexity.
Third, while reducing harmful exposure to one
co-causal factor may not necessarily lead to a large
reduction in the overall harm caused by many other
Acknowledge complexity when dealing
with multiple effects and thresholds
Increasing scientific knowledge has shown that the
causal links between stressors and harm are more
complex than was previously thought and this has
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Part E — Summary
factors, in some cases the removal of just one link
in the chain of multi-causality could reduce much
harm.
A more holistic and multi-disciplinary systems
science is needed to analyse and manage the causal
complexity of the systems in which we live.
that grossly simplify reality rather than using
long-term observations and trend data of biological
and ecological systems. These approaches have
sometimes led to the production of false positives.
More importantly the governance of scientific
ignorance and unknown unknowns has been
neglected.
Finally, many case studies highlight the problems
faced by early warning scientists who have been
harassed for their pioneering work, including bans
on speaking out or publishing, loss of funding,
legal or other threats, and demotion. One obvious
conclusion is that scientists in these situations
should receive better protection either via an
extension of 'whistle blowing' and discrimination
laws, or by independent acknowledgement of the
value of their work.
Rethink and enrich environment and
health research
Environment and health research overly focuses
on well-known rather than unknown hazards at
the expense of emerging issues and their potential
impacts. For example the ten most well-known
substances, such as lead and mercury, account for
about half of all articles on chemical substances
published in the main environmental journals
over the last decade. Over the past decade,
public research funding in the European Union
on nanotechnology, biotechnology as well as
Information and Communications Technology
(ICT) is heavily biased towards product
development with about 1 % being spent on
their potential hazards. A more equal division of
funding between known and emerging issues, and
between products and their hazards, would enrich
science and help avoid future harm to people and
ecosystems and to the long term economic success
of those technologies.
Funding more holistic systems science would
also help achieve a greater integration among
the different branches of science and counteract
problems such as: peer review predominantly within
and not across disciplines; short-term interests
outcompeting long-term vision; competition
replacing cooperation because of conflicts of interest;
contradictions amongst paradigms; fragmentation
of values and authority; as well as fragmentation
of information and knowledge. These can all
lead to inferior solutions and provide increased
opportunities for those with vested interests to
manufacture doubt.
Scientific methods can also be improved. For
example, much higher strengths of evidence are
required overall before causality is accepted,
compared to the evidence being used to assert
safety. The assertion that there is
no evidence of
harm
is then often assumed to be
evidence of no
harm,
even though the relevant research is missing.
Historically there has been an over-reliance on the
statistical significance of point estimates compared
to confidence limits based on multiple sampling.
There has also been a bias towards using models
Improve the quality and value of risk
assessments
The majority of the case studies in
Late lessons
from early warnings
indicate that risk assessment
approaches need to better embrace the realities
of causal and systems complexity (rather than
use a narrow conception of 'risk') with the
inevitable features of ignorance, indeterminacy
and contingency. In a number of case studies, for
example BPA, where low doses are more harmful
than high doses, or tributyltin antifoulants (TBT)
and synthetic oestrogen diethylstilboestrol (DES)
where the timing of the dose is what makes it
harmful, simplistic assumptions are inadequate.
Variability in exposures and varying susceptibilities
in populations and species exposed also need to be
more realistically factored into risk assessments.
This is equally true for technological risk
assessments. As the Fukushima Investigation
Committee concluded in 2011:
'…the accidents present us with crucial lessons
on how we should be prepared for 'incidents
beyond assumptions'. With its failure to plan
for the cascade effects beyond design–base
accidents 'the regulatory emphasis on risk
based probabilistic risk assessment has proven
very limited'.
In other words, narrow risk assessment approaches
are now outstripped by the realities which they
cannot address, recognise and communicate. Too
often this contributes to the effective denial of those
risks that do not fit the risk assessment frame. It
is therefore urgent that risk assessment practices
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Part E — Summary
be transformed to make them broader-based,
more inclusive, transparent and accountable.
There should also be more communication on the
diversity of scientific views, especially on emerging
issues where ignorance and uncertainties are high
and genuine differences of scientific interpretations
are likely, desirable, and defensible. In this sense,
recognising the pedigree of knowledge, i.e. the
consistency of views amongst peers and the level
of convergence coming from different branches of
research, is essential for effective decision making
and action to support the wellbeing of people and
the environment.
The case studies show that evaluations of evidence
in risk assessments can be improved by including
a wide range of stakeholders when framing the
risks and options agenda; broadening the scope and
membership of evaluation committees; increasing
the transparency of committee approaches and
methods, particularly in identifying uncertainties
and ignorance; and ensuring their independence
from undue influence through using appropriate
funding sources and applying robust policies on
conflicts of interest.
Public confidence would be increased if all the
evidence used in risk assessments was made
publicly accessible and open to independent
verification, including data submitted by industries
to authorities.
As experiences from mercury, nuclear accidents,
leaded petrol, mobile phones, BPA, and bees
show, there can be a significant divergence in the
evaluations of the same, or very similar, scientific
evidence by different risk assessment committees.
In such instances, differences in the choice of
paradigm, assumptions, criteria for accepting
evidence, weights placed on different types of
evidence, and how uncertainties were handled, all
need to be explained. Risk assessors and decision
makers also need to be aware that complexity and
uncertainty have sometimes been misused to shift
the focus away from precautionary actions by
'manufacturing doubt' and by waiting for 'sound
science' approaches that were originally developed
by the tobacco industry to delay action.
this framework, governments have at least three
roles: providing direction by putting in place smart
regulations and consistent market signals; ensuring
that the distributional consequences of innovations
are balanced between risks and rewards across
society, fostering a diversity of innovations so that
the wider interests of society; and take precedence
over narrower interests.
Numerous case studies show that decisions to act
without precaution often come from businesses.
There are, however, several impediments to
businesses acting in a precautionary manner,
including a focus on short-term economic value
for shareholders alongside psychological factors
that lead to a so-called 'ethical blindness' or a
'self-serving bias' whereby people largely interpret
ambiguous situations in their own interests.
Governments and businesses could collaborate more
with citizens on publicly disclosing the potential
value conflicts entailed in acting on early warning
signals. A culture of transparency can in turn
promote positive business attitudes and innovations.
Involving the public can also help in choosing
between those innovation pathways to the future; on
prioritising relevant public research; on providing
data and information in support of monitoring and
early warnings; improving risk assessments; on
striking appropriate trade-offs between innovations
and plausible health and environmental harms; and,
making decisions about risk-risk trade-offs.
Correcting market failures using the
polluter pays and prevention principles
When evidence of initial harm emerges, the costs
should be internalised retroactively into the prices
of polluting products, via taxes and charges, in
line with the polluter pays principle and emerging
practice across the world. The revenues could then
be devoted partly to stimulating research into less
hazardous alternatives, and partly to reform tax
systems by reducing taxes and charges on 'societal
goods' like employment.
The pollution taxes/charges would rise or fall in line
with new scientific knowledge about increasing/
decreasing harm, and this would help to level the
playing field for less-polluting alternative products.
Tax shifts from employment to pollution and the
inefficient use of resources can bring multiple
benefits such as increased employment, a stimulus
to innovation, a more stable tax base in the light of
expected demographic changes, and a more efficient
tax collection system.
Foster cooperation between business,
government and citizens
Policy formulation should start from a broad
concept of technological innovation to include
non-technological, social, institutional,
organisational and behavioural innovation. In
Late lessons from early warnings: science, precaution, innovation
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Part E — Summary
More broadly, firms and governments need to extend
their economic accounting systems to incorporate the
full impacts of their activities on people's health and
on ecosystems. Governments need to anticipate this
in their policies, by providing the right blend of fiscal
instruments to both protect the public and ensure that
firms internalise the true costs of potential harm.
A number of case studies also demonstrate the
long time lags between evidence of harm and the
additional injustice and time of forcing victims
to pursue their cases through civil compensation
claims. Prompt and anticipatory no-fault
compensation schemes and assurance bonds, could
be set up and financed in advance of potential
harm by the industries that are producing novel
and large-scale technologies, thereby helping to
offset any potential market failure. Such schemes
can also be designed to increase the incentives for
innovating companies to carry out more
a priori
research into the identification and elimination of
hazards.
act to transform our ways of thinking and of doing,
and urgently so in the face of
unprecedented global
changes, challenges and opportunities.
Many lessons
have been learnt, yet have not been acted upon.
Any
calls for action will need to reflect on today's global
socio-economic setting and support, among other
things, the drive to:
• rebalance the prioritisation of economic and
financial capital over social, human and natural
capitals through the broader application of the
policy principles of precaution, prevention and
polluter-pays, and environmental accounting;
• broaden the nature of evidence and public
engagement in choices about key innovation
pathways by directing scientific efforts more
towards dealing with complex, systemic
challenges and unknowns and complementing
this with professional, lay, local and traditional
knowledge; and,
• build greater adaptability and resilience in
governance systems to deal with multiple
systemic threats and surprises, through
strengthening institutional structures and
deploying information technologies in support
of the concept of responsible information and
dialogues.
The governance of innovation will remain at the
level of good intentions unless it is translated
into innovations in science practices, institutional
arrangements and public engagements as well as
transformations in prevailing business attitudes,
practice and influence. These are the tasks that lie
ahead.
Governance of innovation and innovation
in governance
The
Late lessons from early warnings
reports
demonstrate the complexities of developing not
only the right kind of science and knowledge but
also handling the interactions between the many
actors and institutions involved — governments,
policymakers, businesses, entrepreneurs, scientists,
civil society representatives, citizens and the media.
Alongside many other analyses produced across
the world today, the reports also stress the need to
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In memory of Masazumi Harada,
1935–2012
Shocked by their miserable lives, Harada devoted
himself to the study of the disease from that time.
Harada published a thesis on congenital Minamata
disease in 1964. The work had a significant impact
as it disproved the conventional belief at the
time that the placenta does not pass poisons. He
received an award from the Japanese Society of
Psychiatry and Neurology for the thesis in 1965.
He then established the Open Research Center
for Minamata Studies at the university in 2005,
becoming the center's head. He continued to
lead the disease's research from non-medical
perspectives as well. Harada visited Brazil, China
and native Indian communities in Canada to
discover those suspected of suffering from the
disease.
Author of many books, Harada wrote 'Minamata
Byo' (Minamata Disease), which raised awareness
on the issue around the world.
Masazumi Harada, a physician involved for
many years in the study of the mercury poisoning
Minamata disease, died in June 2012 of acute
myelocytic leukemia at his home in Kumamoto
City. He was 77.
Harada conducted medical examinations on the
disease's sufferers for the first time in the summer
of 1961 in Minamata city in Kumamoto Prefecture
while he was a student at Kumamoto University's
graduate school.
Dr. Masazumi Harada first came to
Asubpeeschoseewagong (Grassy Narrows) and
Wabaseemoong (White Dog) First Nations in
Canada in the early 1970s. Harada's death comes
at the end of River Run 2012, five days of actions
by members and supporters of Grassy Narrows in
Toronto, who are seeking to have Minamata disease
recognized in Canada and Ontario. Harada's final
report for the Grassy Narrows community was
released on 4 June 2012 after 30 years of research,
showing mercury deposited in the river by the
Dryden paper mill in the 1970s is impacting those
who were not yet born when the dumping ceased.
Late lessons from early warnings: science, precaution, innovation
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In memory of Poul Harremoës,
1934–2003
1971. He was a key participant in numerous settings,
including the first Scientific Committee of the
European Environment Agency from 1995.
He had a civil engineering degree from the Technical
University of Denmark. He specialised early on in
geo-technics and constructed dams on the Faroe
Islands. While teaching geo-technics he wrote a
textbook that was used for more than 40 years.
However, he was able to quickly change his research
direction and develop new areas of excellence. So,
for example, he got a grant to study at Berkeley,
California, from where he received a M.Sc. degree in
environmental engineering.
In 1972, he became professor in environmental
engineering at the Technical University of Denmark
where he originally worked with wastewater
discharge to the sea and the biological processes of
wastewater treatment. He became a world leading
scientist in the theories of biofilms for removal
of organics and nitrogen from wastewater before
turning to sewer design and modelling. In 2000, Poul
was awarded the
Heineken prize for Environmental
Sciences
for his contributions to the theory of
biofilm kinetics in relation to biological waste water
treatment and for his successful organisation of the
international scientific community in water pollution
research and control.
As a result of his work with sewers and storm water
he went into the area of risk analysis and the role of
the precautionary principle. In a short time he became
an international expert in this field and was highly
demanded for lectures in all parts of the world. A key
outcome of his interest was his contributions as
chairman of the editorial team for the first volume of
Late lessons from early warnings
published in 2001.
Poul Harremoës was a key player in environmental
issues in Denmark and internationally for more than
30 years until his death, at 69, in 2003. In that time,
those who worked closely with him benefited from
a continuous, almost daily flow of excellent ideas for
new research projects.
He was a member of the Danish Pollution Council,
which prepared the first framework national law
on environmental protection and advised on the
establishment of a Ministry of Environment from
44
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European Environment Agency
Late lessons from early warnings: science, precaution, innovation —
Summary
2013 — 44 pp. — 21 x 29.7 cm
ISBN 978-92-9213-349-8
doi:10.2800/70069
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TH-AL-13-001-EN-C
doi:10.2800/70069
European Environment Agency
Kongens Nytorv 6
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Denmark
Tel.: +45 33 36 71 00
Fax: +45 33 36 71 99
Web: eea.europa.eu
Enquiries: eea.europa.eu/enquiries
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Metoder til fastsættelse af
kvalitetskriterier for kemiske stoffer i
jord, luft og drikkevand med henblik
på at beskytte sundheden
Vejl edn in g f r a Mil jøst yr el sen
Nr. 5
2006
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Indhold
FORORD
1
IN D LED N IN G
5
7
1.1 H
VAD ER KVALIT ET SKRIT ERIER
7
1.1.1 Formål med fastsættelse af kvalitetskriterier for
kemikalier
7
1.1.2 Generelle principper for fastsættelse af
kvalitetskriterier for kemikalier
9
1.2 V
EJLED N IN G EN S OPBYG N IN G OG IN D HOLD
10
1.3 Æ
N D RIN G ER I FORHOLD T IL T ID LIG ERE PRAKSIS
12
R
EFEREN C ER
13
2 D AT AG RUN D LAG FOR VURD ERIN G AF
FARLIG H ED
2.1 D
AT A FRA M EN N ESKER
2.2 D
YREEKSPERIM EN T ELLE UN D ERSØG ELSER
2.3 A
N D RE T YPER D AT A
2.4 I
N D HEN T N IN G AF D AT A
R
EFEREN C ER
3 FARLIG H ED SVURD ERIN G OG
FARLIG H ED SKARAKT ERISERIN G
3.1
D
OSIS
-
EFFEKT OG D OSIS
-
RESPON S
20
21
22
24
24
25
26
26
27
27
29
SAM M EN HÆ N G E
3.2 F
AST SÆ T T ELSE AF N UL
-
EFFEKT N IVEAU OG
LAVEST E EFFEKT N IVEAU
3.3 B
EN C HM ARK
-
M ET OD EN
3.4 U
D PEG N IN G AF KRIT ISK EFFEKT
3.5 R
ELEVAN S AF VISSE EFFEKT ER I FORSØG SD YR
R
EFEREN C ER
14
14
16
17
18
19
20
4 BEREG N IN G AF T D I FOR ST OFFER M ED
T Æ RSKELVÆ RD I
4.1 T D I-
BEG REBET
4.2 A
N VEN D ELSE AF USIKKERHED SFAKT ORER
4.2.1
Usikkerhedsfaktor I
4.2.2
Usikkerhedsfaktor II
3
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4.2.3
4.2.4
Usikkerhedsfaktor III
Samlet usikkerhedsfaktor
R
EFEREN C ER
5 BEREG N IN G AF T D I FOR
KRÆ FT FREM KALD EN D E ST OFFER
5.1
29
32
33
34
K
RÆ FT FREM KALD EN D E ST OFFER M ED OG UD EN
T Æ RSKELVÆ RD I
34
5.2 V
URD ERIN G AF KRÆFT FREM KALD EN D E EFFEKT
35
5.3 B
EREG N IN G AF
T D I
FOR KRÆFT FREM KALD EN D E
ST OFFER UD EN T ÆRSKELVÆRD I
37
5.3.1
T olerabelt risikoniveau
37
5.3.2
M etode til beregning af T DI og livstidsrisiko 37
5.3.3
Anvendelse af risikoestimater angivet i litteraturen38
R
EFEREN C ER
39
6 BEREG N IN G AF KVALIT ET SKRIT ERIER FOR
KEM IKALIER
40
6.1 G
EN EREL M ET OD E FOR BEREG N IN G AF ET
40
6.1.2 Anvendelse af T DI
41
6.1.3 Eksponeringsbetragtninger
42
6.2 B
EREG N IN G AF LUFT KVALIT ET SKRIT ERIET
43
6.3 B
EREG N IN G AF JORD KVALIT ET SKRIT ERIET
45
6.4 B
EREG N IN G AF D RIKKEVAN D SKVALIT ET SKRIT ERIET
47
R
EFEREN C ER
49
KVALIT ET SKRIT ERIUM
BILAG 1
K
VAN T IT AT IV VURD ERIN G VED BEN YT T ELSE AF
T 25
EKST RAPOLAT ION SM ET OD EN
.
Anbefaling af T 25-metoden
Anvendelse af T 25-metoden
R
EFEREN C ER
BILAG 2
B
AG G RUN D FOR AN VEN D T E EKSPON ERIN G SVÆRD IER
VED BEREG N IN G AF KVALIT ET SKRIT ERIER
50
50
50
51
54
55
55
57
58
59
62
62
Luft, daglig standardeksponering
Jord, daglig standardeksponering
Drikkevand, daglig standardeksponering
BILAG 3
A
N VEN D T E FORKORT ELSER
4
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Forord
Principperne for vurdering og fastsættelse af kvalitetskriteri-
er for kemikalier med henblik på at beskytte sundheden er
1
beskrevet tidligere . M en i forbindelse med M iljøministerens
redegørelse om jordforureningsloven i 2003, besluttede re-
geringen at nedsætte en arbejdsgruppe, som fik til opgave at
”vurdere,
hvorvidt de sundhedsmæssige kvalitetskriterier ligger
på det rigtige niveau i relation til international praksis, samt
give forslag til ændringer.
Arbejdsgruppen udpegede en række politiske valg, der ind-
går i principperne for fastsættelse af kvalitetskriterier. På
den baggrund blev der i december 2005 indgået en aftale
mellem M iljøministeren og et bredt udsnit af Folketingets
partier, som bl.a. fastlægger følgende
generelle principper
for fastsættelsen
af forebyggende kriterier :
H ovedparten af befolkningen skal fortsat beskyttes (dvs.
hensyntagen til særligt udsatte skal også inddrages).
D er skal tages specifikt hensyn til børn.
Det fastholdes, at der højst anvendes en samlet
usikkerhedsfaktor på 10.000, når resultater fra dy-
reforsøg overføres til mennesker.
-6
D er accepteres fortsat en livstidsrisiko på 10 .
D enne vejledning indarbejder disse principper og gennem-
går de metoder, som skal anvendes ved fastsættelse kvali-
tetskriterier for jord, luft og drikkevand med henblik på at
2
beskytte sundheden .
1
M iljøstyrelsens Vejledning nr. 1 ”Sundhedsmæssig vurdering af
kemiske stoffer i drikkevand ”, 1992, og i bilag til M iljøstyrelsens
Vejledning nr. 6, 1990 ”Begrænsning af luftforurening fra virk-
somheder” samt i M iljøprojekt nr. 12, 1995 ”T oksikologiske kva-
litetskriterier for jord og drikkevand”.
2
Principper for fastsættelse af kvalitetskriterier med henblik på at
beskytte miljøet er tilsvarende beskrevet i M iljøstyrelsens vejled-
5
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Vejledningen henvender sig til centrale og lokale myndighe-
der, herunder embedslægeinstitutionerne, konsulenter, råd-
givere og virksomheder.
M iljøstyrelsen fastsætter løbende kvalitetskriterier for kon-
krete kemiske stoffer i jord, luft og drikkevand med henblik
på at beskytte sundheden, jf. M iljøbeskyttelsesloven § 14,
stk. 1,. Kvalitetskriterierne bliver fastsat på baggrund af
videnskabelige rapporter og efter drøftelse i en styregruppe
med deltagelse af bl.a. Fødevarestyrelsen, Arbejdstilsynet og
Sundhedsstyrelsen.
D enne vejledning og detaljeringsgraden, ikke mindst i den
3
tilhørende faglige rapport , skal give grundlag for større
forståelse for, hvordan kvalitetskriterier skal udarbejdes.
Kvalitetskriterierne anvendes dels til at vurdere alvoren af
en allerede given forurening, og dels når myndighederne
stiller krav i forbindelse med udledning af konkrete stoffer til
omgivelserne.
ning nr. 4 (2004): Principper for fastsættelse af vandkvalitetskrite-
rier for stoffer i overfladevand.
3
M iljøprojekt N r. 974, M iljøstyrelsen (2005). Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik på
fastsættelse af kvalitetskriterier for luft, jord og vand. Rapporten er
udarbejdet af Institut for Fødevaresikkerhed og Ernæring, Føde-
varedirektoratet (nu D anmarks Fødevareforskning) i samarbejde
med M iljøstyrelsen.
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1 Indledning
1.1 Hvad er kval it et skr it er ier
1.1.1 Formål med fastsættelse af kvalitetskriterier for kemikali-
er
D enne vejledning beskriver den administrative praksis ved
fastsættelse af kvalitetskriterier for kemikalier med henblik
på at beskytte sundheden.
Kvalitetskriterier danner basis for en række vurderinger af
administrativ karakter, som vedrører både jord, luft og drik-
kevand.
M ålsætningen ved fastsættelsen af kvalitetskriterier for ke-
mikalier er, at de skal medvirke til
at forebygge forurening og
skader på sundheden.
Kvalitetskriterierne ses som et element
i lovens overordnede politiske målsætning om at oppebære
et højt beskyttelsesniveau for befolkningens sundhed og
sikre en bæredygtig udvikling, herunder fremme af renere
teknologi.
Kvalitetskriterierne angiver et højt beskyttelsesniveau, hvor
ingen effekt kan forventes, selv ved udsættelse gennem et
helt liv, eller hvis der er tale om et stof uden tærskelværdi,
en teoretisk forøget risiko for kræft hos én ud af en million
mennesker, som er udsat for stoffer gennem et helt liv på 70
år.
Kvalitetskriterierne bruges af myndighederne i forbindelse
med vurdering af alvoren af et givet forureningsniveau. D et
kan være relevant, hvis der er tale om en eksisterende foru-
rening (fortidens synder), eller hvis der skal fastsættes krav-
værdier for udledning af konkrete stoffer i miljøet (forebyg-
gende). For begge situationer kan andre forhold end de
sundhedsmæssige spille ind, såsom baggrundsniveauer og
tekniske/økonomiske overvejelser. Ved indsatsen i forhold til
eksisterende forureninger kan der også være behov for at
7
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vurdere, hvad der er sundhedsmæssigt forsvarligt, når der
tages hensyn til overordnede samfundsmæssige prioriterin-
ger. M ed udgangspunkt i de sundhedsmæssigt fastsatte kva-
litetskriterier udarbejdes således en række administrativt
fastsatte kriterier.
Eksempler på administrative kriterier som er baseret på kva-
litetskriterier er:
1. Luftkvalitetskriteriet anvendes som udgangspunkt til at
fastsætte bidrags værdier (B-værdier), der anvendes i
forbindelse med regulering af virksomheders udslip af
kemiske stoffer til udeluften.
2. Luftkvalitetskriteriet anvendes til at vurdere afdamp-
ning af kemiske stoffer fra jordforureninger. D et an-
vendes også ved kortlægning og offentlig oprydning af
forurenede grunde.
3. Jordkvalitetskriterier anvendes som udgangspunkt ved
fastsættelse af administrative kriterier, der anvendes ved
de lokale myndigheders kortlægning af forurenede
grunde og i forbindelse med vurderinger af arealanven-
delse, samt ved offentlig oprydning af forurenede
4
grunde
.
4. Jordkvalitetskriteriet anvendes endvidere som udgangs-
punktet for fastsættelse af afskæringskriteriet for visse
immobile stoffer. Afskæringskriteriet anvendes ved let-
tere forurenede områder som skillelinie mellem det ni-
veau, hvor det er nødvendigt at fjerne jorden og det ni-
veau, hvor det er tilstrækkeligt at iværksætte særlige
forholdsregler i forbindelse med følsom anvendelse af
områderne, som fx private haver eller børneinstitutio-
ner.
5. D rikkevandskvalitetskriteriet anvendes af de centrale og
decentrale myndigheder i forbindelse med håndtering
af konkrete sager med kemisk forurening af drikkevand,
som et supplement til de kravværdier, der er fastsat i
bekendtgørelsen om vandkvalitet.
6. D rikkevandskvalitetskriterierne anvendes som ud-
gangspunkt ved fastsættelse af grundvandskvalitetskri-
terier i tilknytning til nedsivning fra jordforureninger,
Kvalitetskriterierne omfatter normalt ikke en vurdering af om
arealer kan anvendes til dyrkning af nytteplanter eller til afgræs-
ning for husdyr.
4
8
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idet grundvandet skal være af en kvalitet, så de fastsatte
drikkevandskrav/ -kvalitetskriterier kan overholdes.
D er eksisterer en række vejledninger og lister, som nærmere
beskriver baggrunden for, hvordan et kvalitetskriterium kan
5
anvendes.
1.1.2 Generelle principper for fastsættelse af kvalitetskriterier
for kemikalier
Kvalitetskriterierne fastsættes på et niveau, hvor udsættelse
gennem et helt liv ikke fører til skadevirkninger i befolknin-
gen. D e fastsættes på baggrund af den eksisterende viden og
under hensyntagen til de mangler, der ligger i datagrundla-
get.
For at minimere risici for skadelig påvirkning af befolknin-
gen indgår beskyttelse af særligt følsomme grupper fx børn,
gravide, syge, ældre og svækkede ved fastsættelse af kvali-
tetskriterier.
Viden om et kemisk stofs sundhedsskadelige egenskaber og
om bestemte befolkningsgruppers særlige følsomhed er
sjældent så eksakt, at der kan fastsættes et kvalitetskriterium,
der præcist definerer skillelinien (hvis en sådan overhovedet
findes) mellem et ufarligt og farligt niveau. Kvalitetskriteri-
erne kan således ikke opfattes som en streg i sandet, hvor
enhver overskridelse er farlig. Ved fastsættelse af kvalitets-
kriterier for kemikalier skal anvendes en forsigtighedstil-
gang, da målet er at sikre et højt beskyttelsesniveau for alle
ved udsættelse over et helt liv.
Et kvalitetskriterium skal således opfattes som en sikker-
hedsgrænse og ikke en faregrænse. En overskridelse er ”det
gule lys”, som advarer om, at her er noget, som måske kan
blive et reelt problem.
Luftvejledningen, M iljøstyrelsens Vejledning nr. 2, 2001; Op-
rydning på forurenede lokaliteter
5
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1.2 Vejl edn in gen s opbygn in g og in dh ol d
Vejledningen udstikker retningslinier for den faglige risiko-
vurdering og for de metoder/ principper der anvendes.
D ernæst beskrives proceduren for beregning af kvalitetskri-
terierne (se figur 1).
D ata-og litteratursøgning
Farlighedsvurdering og
farlighedskarakterisering;
identifikation af kritisk
effekt
Stoffer med tærskel-
værdi: T D I ud fra
N OAEL for den
kritiske effekt; anven-
delse af usikkerheds-
Stoffer uden tærskel-
værdi: Beregning af
T D I svarende til en
tolerabel livstidsrisiko-
dosis.
Beregning af kvalitetskriterie
med udgangspunkt i T D I-
værdi og eksponeringsværdi
for de aktuelle medier.
Figur 1.
Fr emgan gsmåden ved ber egn in g af kval it et skr it er ium
(TDI=Tol er abel Dagl igt In dt ag)
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D et videnskabelige grundlag for fastsættelse af sundheds-
mæssigt baserede kvalitetskriterier for kemiske stoffer i jord,
luft og drikkevand består af en farlighedsvurdering, en do-
sis-respons (effekt) vurdering (farlighedskarakterisering),
samt en eksponeringsvurdering. Farlighedsvurderingen og
farlighedskarakteriseringen tager udgangspunkt i undersø-
gelser af det pågældende stofs toksikologiske effekter i men-
nesker og i dyr.
I kapitel 2 omtales
Datagrundlaget
som anvendes som ud-
gangspunkt for arbejdet. D ata hentes primært fra internati-
onale og nationale dokumenter, via litteratursøgning i inter-
nationale databaser, samt fra originalartikler.
Kapitel 3 behandler de faglige metoder, der anvendes i for-
bindelse med farlighedsvurderingen og farlighedskarakteri-
seringen. D osis-effekt og dosis-responssammenhænge og
udpegning af N OAEL (N o Observed Adverse Effect Level)
og LOAEL (Lowest Observed Adverse Effect Level) be-
skrives.
I kapitel 4 beskrives hvordan farlighedskarakteriseringen
udmunder i udpegning af en kritisk effekt, som danner ud-
gangspunkt for fastsættelse af en
tolerabel daglig indtagelse,
T DI.
H er omtales, hvordan anvendelsen af usikkerhedsfak-
torer indgår i beregningerne.
I kapitel 5 omtales, hvordan T D I beregnes for kræftfrem-
kaldende stoffer uden tærskelværdi. Risikoniveauet for
T D I-værdien defineres, og der gives retningslinier med
hensyn til valg af metode til, hvordan beregningen af dette
risikoniveau foretages.
Kapitel 6 beskriver, hvordan den videre beregning af kvali-
tetskriterier for kemiske stoffer i jord, luft og drikkevand
foretages ud fra de fastsatte T D I-værdier. I bilag 2 til vej-
ledningen omtales rationalet for at anvende konkrete stan-
dardbetragtninger m.h.t. personers udsættelse for forure-
ninger gennem jord, luft og drikkevand. Endvidere omtales
hvilke andre faktorer (fx hensyntagen til lugt eller smag)
end de rent sundhedsmæssige, der i visse tilfælde kan have
indflydelse på kvalitetskriteriet.
11
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1.3 Æ dr in ger i f or h ol d t il t idl iger e pr aksis
n
Ved fastsættelsen af kvalitetskriterier anvendes der interna-
tionalt anerkendte principper. I denne forbindelse skal
fremhæves de principper og metoder, der er beskrevet i to
6,7
publikationer af WH O/ IPC S om udarbejdelsen af vejle-
dende grænseværdier og risikovurdering af kemisk udsættel-
8,9
se. WH O´s publikationer omhandlende risikovurdering og
fastsættelse af vejledende grænseværdier for en række kemi-
ske stoffer i drikkevand og luft har også indgået i arbejdet.
På tilsvarende vis er der en tæt sammenhæng med de prin-
cipper og metoder, der anvendes i forbindelse med EU´s
10
risikovurderingsprogram for kemiske stoffer .
På visse områder indebærer denne vejledning, at den hidti-
dige praksis for fastsættelse af kvalitetskriterier justeres. D et-
te gælder fx for beregning af kvalitetskriterier for kemikalier
i luft og drikkevand, idet der nu som udgangspunkt anven-
des standardværdier for børns udsættelse (se kapitel 6 og
bilag 2).
I forbindelse med ekstrapolering af tolerabelt risikoniveau
for genotoksiske kræftfremkaldende stoffer (dvs. kræftfrem-
kaldende stoffer hvor der ikke anses at være en tærskelværdi
for effekt), anvendes lineær ekstrapolation ud fra den så-
6
WH O/IPC S (1994). Assessing human health risks of chemicals:
D erivation of guidance values for health-based exposure limits.
Environmental H ealth C riteria no. 170. International Programme
on C hemical Safety.
7
WHO/IPC S (1999). Principals for the assessment of risks to
human health from exposure to chemicals. Environmental H ealth
C riteria no. 210. International Programme on C hemical Safety.
8
WHO (1996). G uidelines for drinking-water quality 2
nd
edition,
vol 2. H ealth C riteria and other supporting information. Interna-
tional Programme on C hemical Safety.
9
WHO (2000). Air Quality G uidelines for Europe, 2
nd
edition.
WH O Regional Publications, European Series, no. 91.
10
EEC (2003). T echnical G uidance D ocument in support of
C ommission D irective 93/67/EEC on risk assessment for new
notified substances and C ommission Regulation (EC ) N o.
1488/94 on risk assessment for existing substances and D irective
98/8/EC of the European Parliament and of the C ouncil concern-
ing the placing of biocidal products on the market.
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2259378_1826.png
kaldte T 25- metode udviklet i forbindelse med EU´s risiko-
vurderingsprogram (kapitel 5).
H vis datagrundlaget er til stede, anbefales det at anvende
benchmark-metoden ved fastsættelse af T D I (kapitel 3).
D et skal bemærkes, at denne vejledning anvender begrebet
usikkerhedsfaktorer, hvor man tidligere anvendte begrebet
sikkerhedsfaktorer. D els beskriver ordet
usikkerhed
i højere
grad faktorernes anvendelse, idet de netop tager højde for
usikkerheder. D els imødegås den misforståelse, at en stor
sikkerhedsfaktor for et stof medfører større sikkerhed for
dette stof i forhold til en lille anvendt sikkerhedsfaktor for et
andet stof. Faktorerne anvendes derimod for at opnå et ens-
artet beskyttelsesniveau, og størrelsen af faktorerne afspejler
usikkerheder som følge af usikker viden og manglende data-
grundlag.
D e angivne metoder i vejledningen anvendes fremover ved
fastsættelse af kvalitetskriterier.
D e ændringer der er sket i forhold til tidligere praksis bety-
der ikke, at de eksisterende kvalitetskriterier skal ”laves om”,
idet anvendelse af de nye metoder ikke vurderes at påvirke
beskyttesesniveauet væsentligt. N år et kvalitetskriterium
tages op til revurdering bør dette ske både m.h.t. til revur-
dering af de sundhedsmæssige data og af de eksponerings-
mæssige forhold. En revurdering foretages derfor fuldt ud
med alle de vurderingsmæssige og beregningsmæssige faser,
der er beskrevet i vejledningen.
Ref er en cer
Bekendtgørelse af Lov om miljøbeskyttelse (M iljøbeskyttel-
sesloven). Lovbekendtgørelse nr. 753 af 25. august 2001.
M iljøstyrelsen (1991). Orientering om ny miljøbeskyttelses-
lov. Orientering nr. 6, 1991.
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2 Datagrundlag for vurdering af far-
lighed
Fastsættelse af kvalitetskriterier for et kemisk stof sker på
baggrund af eksisterende viden om stoffets sundhedsskade-
lige egenskaber.
Kvalitetskriterierne fastsættes med henblik på beskyttelse af
menneskers sundhed, og det ideelle datagrundlag for fast-
sættelse af et kvalitetskriterium er derfor viden, hvor menne-
sker har været udsat for det konkrete stof. For langt de fleste
kemiske stoffer er der kun begrænset viden om veldefineret
udsættelse og effekter hos mennesker, og kvalitetetskrite-
rierne vil som oftest være baseret på viden opnået fra dyre-
11
forsøg med mere veldefineret udsættelse eller
in vitro
data .
For en mere detaljeret beskrivelse af nedenstående afsnit
henvises til kapitel 2, M iljøprojekt N r. 974 (2005).
2.1 Dat a f r a men n esker
Fordelen ved at anvende data, hvor mennesker har været
udsat for et kemisk stof, er, at man undgår at skulle overføre
data fra dyreforsøg, og estimere hvad en tilsvarende udsæt-
telse betyder hos mennesker. Erfaringer med menneskers
udsættelse kan stamme fra en række forskellige typer under-
søgelser og afrapporteringer, der groft kan deles op på føl-
gende måde:
-
-
-
case reports og kliniske undersøgelser
befolkningsundersøgelser (fx arbejdsmiljø eller udvalgte dele
af befolkningen)
undersøgelser af frivillige forsøgspersoner
11
D ata fra reagensglasforsøg.
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Ved
case reports og kliniske undersøgelser
opnås data fra for-
giftningstilfælde eller erfaringer fra undersøgelser i klinik-
ken, hvor personer fx i behandlingsøjemed udsættes for
stoffer for at vurdere eventuelle allergiske reaktioner. For-
delen ved disse typer data er, at man her umiddelbart kan se
en sammenhæng mellem udsættelse og (akutte) effekter.
I
befolkningsundersøgelser
vurderes en større gruppe af men-
nesker mere systematisk med hensyn til sammenhængen
mellem udsættelse og sundhedsskader. D isse undersøgelser
kan fx omfatte sundhedsovervågning af særlige grupper i
arbejdsmiljøet, hvor personerne er karakteriseret ved en
særlig udsættelse, eller man kan undersøge, om der hos per-
soner, der har udviklet nogle konkrete sygdomme, er nogle
fælles karakteristika med hensyn til kemiske påvirkninger.
Fordelen ved at anvende data fra denne type undersøgelser
er, at man er meget tæt på den målgruppe, man ønsker at
beskytte med kvalitetskriterierne. Samtidig ses effekterne i
sammenhæng med den dagligdag, som mennesker nu en-
gang fungerer i, hvor man udsættes for en kompleks blan-
ding af livsstilsfaktorer og miljøfaktorer. Ulempen er, at det
ofte er vanskeligt at vurdere omfanget af udsættelsen af en
given komponent, og at det pga. mange andre samvirkende
faktorer kan være svært at påvise sammenhænge, som kan
være sløret af al ”støjen” fra andre faktorer. Ligesom under-
søgelserne kun sjældent kan dokumentere en årsags-
virkningssammenhæng, vil de også kun uhyre sjældent kun-
ne anvendes til at dokumentere manglende sammenhæng,
dvs. frikende stoffer.
I
undersøgelser med frivillige forsøgspersoner
udsætter man i
reglen forsøgspersonerne i en kortere varighed for et kon-
kret stof for at vurdere effekterne. D isse undersøgelser er
meget sammenlignelige med dyreforsøg, hvor man tilsva-
rende har en meget veldefineret udsættelse. D e naturlige og
etiske begrænsninger ved disse undersøgelser betyder, at der
hos mennesker kun kan undersøges for lettere grader af
akutte effekter og i sammenhæng med kortere tids forsøgs-
udsættelse. Endvidere er forsøgspersonerne sjældent særligt
følsomme, som visse undergrupper i befolkningen kan være.
M an skal være meget opmærksom på det etiske aspekt
m.h.t. anvendelse af frivillige forsøgspersoner. I forbindelse
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med vurdering af konkrete humane undersøgelser i risiko-
vurderingssammenhæng, bør anvendelsen af disse data vur-
deres nøje såvel ud fra etiske som kvalitetsmæssige hensyn.
Især ældre undersøgelser kan være udført under stærkt kriti-
sable forhold og med store undersøgelsesmæssige mangler.
Kvalitetskriterier for kemikalier fastsættes ud fra eksisteren-
de data, og det frarådes generelt at igangsætte humanforsøg
for at opnå øget viden om konkrete stoffers skadelige effek-
ter.
2.2 Dyr eeksper imen t el l e un der søgel ser
For de fleste kemiske stoffer foreligger der ikke data fra
menneskers udsættelse, hvorfor kvalitetskriterier hyppigst
baseres på data fra dyreeksperimentelle undersøgelser.
Resultaterne fra dyreforsøgene anvendes således som model
og anvendes til at forudsige hvilke effekter, der kan forven-
tes hos mennesker. D yreeksperimentelle data kan også be-
nyttes som supplement til humane data, der ikke er entydi-
ge, eller til at udpege de aktive stoffer, når mennesker har
været udsat og reageret over for blandinger af stoffer.
Fordelene ved dyreforsøg er, at der er tale om standardise-
rede forsøgsbetingelser, og at der er mulighed for at afsløre
væsentlig flere effekter hos forsøgsdyr end hos mennesker,
da organer og væv kan undersøges efter forsøgets afslut-
ning. D er er også mulighed for at undersøge virkningsme-
kanismer og detaljerede dosis-effekt og dosis-
responssammenhænge for enkeltstoffer.
Ideelt set ønskes der ved fastsættelsen af kvalitetskriterier for
et kemikalie et fuldt datasæt bestående af dyreeksperimen-
telle undersøgelser til vurdering af en række toksikologiske
egenskaber: T oksikokinetik (optagelse og udskillelse), akut
toksicitet, irritation, sensibilisering (allergi), toksicitet ved
gentagen administration af stoffet, mutagenicitet og geno-
toksicitet (påvirkning af arvematerialet), kræftfremkaldende
effekter, samt effekter på reproduktion og fosterudvikling.
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2259378_1830.png
D yreforsøg har imidlertid også begrænsninger, da nogle
effekter kan være vanskelige at afsløre fx lettere grader af
slimhindeirritation i øjne og luftveje, lettere grader af på-
virkning af centralnervesystemet og visse typer nerveskader.
Endelig kan nogle dyrearter udvikle artspecifikke effekter
over for visse stoffer, hvor relevansen i forhold til udsættelse
af mennesker er meget omdiskuteret (se afsnit 3).
D et er endvidere vigtigt at vurdere kvaliteten af de dy-
reeksperimentelle undersøgelser, der anvendes som ud-
gangspunkt for fastsættelse af kvalitetskriterier. Undersøgel-
ser af høj kvalitet, som er udført efter eller på niveau med
OEC D ´s eller EU´s retningslinier for forsøgsdyrstestning,
bør foretrækkes. Ved risikovurderingen i forbindelse med
fastsættelse af kvalitetskriterier er der dog ikke nogle formel-
le kvalitetskrav til undersøgelserne, idet en lang række un-
dersøgelser i den videnskabelige litteratur ofte vil være ud-
ført i forskningsøjemed uden at undersøgelserne er udført
efter en officiel forsøgsguideline eller i overensstemmelse
12
med G LP-reglerne. Sådanne undersøgelser, der ofte er
kvalitetssikret i peer-reviewede tidsskrifter, kan indeholde
væsentlig information. Forsøgets kvalitet og validitet må i de
aktuelle tilfælde vurderes, og der tages stilling til om forsø-
get kan være af betydning ved fastsættelse af et kvalitetskri-
terium.
På baggrund af de etiske aspekter ved dyreforsøg arbejdes
der internationalt med at udvikle alternative
in vitro
meto-
der.
2.3 An dr e t yper dat a
Ud over forsøg på levende dyr foreligger der ofte undersø-
gelser der er udført på udtagne organer, væv eller isolerede
celler. D isse
in vitro
metoder finder især anvendelse til vur-
dering af stoffers toksiske effekt på organ-/celleniveau sær-
ligt m.h.t. mutagene og genotoksiske effekter.
12
G LP står for G ood Laboratory Practice, og er et regelsæt ud-
viklet af OEC D for at sikre kvaliteteten af undersøgelserne.
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2259378_1831.png
N ormalt kan
in vitro
forsøg ikke anvendes til at fastlægge
tærskel for effekt (N OAEL e.l.), men de vil indgå i bedøm-
melsen af stoffets farlighed. In vitro-data kan således styrke
mistanken om skadeeffekter og derved påvirke valget af
usikkerhedsfaktorer (se afsnit 4).
Ved mangel på data for et konkret stof kan data fra nært
beslægtede stoffer indgå i vurderingen ud fra betragtninger
om kemisk strukturlighed og sammenfaldende effekter. Så-
danne data kan have indflydelse på den rent kvalitative, men
også i visse tilfælde i den kvantitative vurdering, hvis det
konkret vurderes, at der er grundlag for meget snævert kob-
lede analogislutninger.
Endvidere kan der udføres en mere systematisk analyse ved-
rørende kvantitative struktur-aktivitets relationer (engelsk:
Quantitative Structure Activity Relationships – QSARs).
Anvendelse af denne form for computerbaserede modeller
har i en række tilfælde vist sig som et alternativ til dyrefor-
søg med henblik på forudsigelse af toksikologiske egenska-
13
ber (M ST 2001 ). Vurderingerne kan sjældent anvendes
som udgangspunkt for beregning af kvalitetskriteriet, men
vil i visse tilfælde kunne anvendes til styrkelse af mistanken
om konkrete effekter. QSAR vil således kunne påvirke val-
get af usikkerhedsfaktorer ved beregning af kvalitetskriteriet.
2.4 In dh en t n in g af dat a
Som udgangspunkt for udarbejdelse af kvalitetskriterier
anvendes i udstrakt grad internationalt anerkendte stofmo-
nografier og dokumenter, hvor det aktuelle stof er vurderet
og beskrevet m.h.t. dets sundhedsskadelige effekter. En
række af disse værker (kilder) er nævnt i afsnit 2.5.1 i M il-
jøprojekt N r. 974 (2005) . Sådanne dokumenter, der ofte er
baseret på en grundig faglig vurdering ved en særlig nedsat
ekspertgruppe, vil typisk kunne anvendes til at udpege de
relevante undersøgelser og data, der skal anvendes til den
videre beregning af kvalitetetskriteriet. D et anbefales gene-
13
M iljøstyrelsen (2001). Report on the advisory list for selfclassi-
fication of dangerous substances. Environmental Project N o. 636
2001. http://www.mst.dk/udgiv/publications/2001/87-7944-694-
9/html/
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relt, at data, der skal danne udgangspunkt for beregning af
kvalitetskriteriet, altid hjemskaffes som originallitteratur til
vurdering af den konkrete undersøgelses kvalitet og rele-
vans.
Endvidere søges i en række relevante databaser (se afsnit
2.5.2 i den faglige rapport). Sådanne søgninger er især rele-
vante, hvis en international stofmonografi for det konkrete
stof ikke foreligger, eller hvis vurderingen ligger nogle år
tilbage.
For visse stoffer kan man komme ud for at datasøgning
giver så ringe resultat, at der ikke er tilstrækkeligt data-
grundlag til at foretage en vurdering af stoffet. For eksempel
hvis der kun er akutte studier til rådighed, eller ingen studier
fastlægger N O(A)EL/LO(A)EL.
Ref er en cer
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier i jord, luft og drikkevand.
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3 Farlighedsvurdering og farligheds-
karakterisering
Farlighedsvurderingen og farlighedskarakteriseringen har til
formål at beskrive stoffets farlige egenskaber. D er opstilles i
videst muligt omfang dosis-effekt og dosis-respons sam-
menhænge, der danner baggrund for identifikation af den
kritiske effekt. D en kritiske effekt er den effekt, der anses for
at være den afgørende ved den sundhedsmæssige vurdering.
N uleffekt niveauet (evt. laveste effektniveau) for denne ef-
fekt anvendes til beregning af T D I (tolerabelt dagligt indtag/
tolerabelt daglig eksponering), som i den videre proces be-
nyttes til beregning af kvalitetskriteriet.
3.1 Dosis-ef f ekt og dosis-r espon s sammen h æ ge
n
Udsættelse for et kemisk stof kan medføre forskellige typer
effekter afhængig af eksponeringsvej, eksponeringens stør-
relse og varighed. Lettere grader af effekter kan være forbi-
gående genevirkninger i form af fx slimhindeirritation, mens
alvorlige effekter kan være dødeligt forløbende akutte for-
giftninger eller udvikling af kroniske sygdomme som kræft.
En længerevarende dyreeksperimentel undersøgelse vil såle-
des kunne give viden om forskellige typer effekter ved for-
skellige eksponeringsniveauer (dosis-effekt), og om hvor
lang tid det tager, før de optræder i forhold til eksponerin-
gen.
Yderligere vil man fra undersøgelsen kunne se, hvor stor en
andel af de doserede dyr der er ramt af effekten (dosis-
respons). Visse effekter kan være opdelt i forskellige svær-
hedsgrader eller stadier, hvor der så for hver af disse kan
foreligge dosis-responssammenhænge.
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2259378_1834.png
Figur 1 Eksempler på dosisrespons-sammenhænge
Ovenstående figur viser, hvordan dosisrepons-kurver for
forskellige effekter kan optegnes ud fra konkrete forsøgsdata
med forskellige eksponeringsniveauer og observerede effek-
ter ved disse (markeret med krydser). Kurve a angiver fx
dosis-respons forløbet for luftvejsirritation hos forsøgsdyre-
ne, og er her karakteriseret ved at være meget stejl (alle dyr
påvirkes inden for et forholdsvist lille dosisinterval, dvs. lille
spredning i følsomhed). Kurve b angiver forekomsten af
kræftsvulster og viser en dosisrespons sammenhæng ved
højere eksponeringsniveauer, og beskriver en noget fladere
dosis-respons sammenhæng (dvs. dyrenes følsomhed over
for udvikling af kræft er mere spredt). N OAEL-
markeringerne på figuren repræsenterer eksponeringsni-
veauer, hvor der ikke blev fundet statistisk signifikant flere
dyr i eksponeringsgruppen end i kontrolgruppen, der udvik-
ler den pågældende effekt, mens LOAEL-værdierne repræ-
senterer det laveste eksponeringsniveau, der har medført en
signifikant forøget forekomst af effekten.
D en faglige baggrundsrapport (M iljøprojekt N r. 974 (2005)
) angiver i afsnit 3.1 mere detaljerede beskrivelser og tolk-
ningen af forskellige dosis-respons forløb.
3.2 Fast sæ t el se af n ul -ef f ekt n iveau og l avest e ef -
t
f ekt n iveau
For langt de fleste typer effekter vurderes der at være en
tærskelværdi, der adskiller effektniveauer fra ikke-
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effektniveauer, dvs. eksponeringen skal overskride en vis
tærskelværdi før dosis er tilstrækkelig til at udløse effekt.
N iveauet umiddelbart under denne teoretiske tærskelværdi
betegnes nuleffektniveauet, der er den højeste dosis, der ikke
medfører effekt. D osisniveauet umiddelbart over tærskel-
værdien betegnes laveste effektniveau, da dette er det laveste
dosisniveau, der lige netop udløser effekten.
I praksis anvendes for nuleffektniveauet det såkaldte
no ob-
served adverse effect level, N OAEL,
der er den højeste af de i
forsøget anvendte doser, hvor der i et konkret forsøg ikke er
observeret
den givne effekt. For laveste effekt-niveau anven-
des det såkaldte
lowest observed adverse effect level, LOAEL,
der er den laveste dosis i forsøget hvor der er observeret den
givne effekt.
I litteraturen anvendes betegnelserne N OAEL og N OEL
(no
observed effect level)
samt LOAEL og LOEL (lowest
ob-
served effect level).
N år betegnelserne anvendes korrekt, er
det for at sondre mellem om de effektniveauer eller nul-
effektniveauer der beskrives, er i forhold til
skadelige (adver-
se)
effekter eller effekter generelt, hvor også lettere grader af
effekter som påvirkning af enzymniveauer og andre effekter
af ikke direkte skadelig karakter er omfattet.
M an må dog være opmærksom på, at denne skelnen mellem
skadelige og ikke-skadelige effekter i mange tilfælde ikke er
gjort konsekvent i litteraturen, og at betegnelserne ofte be-
nyttes i flæng. D et kan således i konkrete tilfælde være van-
skeligt at afgøre, hvor grænsen går for, om en effekt skal
tolkes som skadelig eller ej, og dermed om et LOEL snarere
skal tolkes som et LOAEL.
Se endvidere afsnit 3.2 i den faglige rapport (1).
3.3 Ben ch mar k-met oden
N O(A)EL/ LO(A)EL metoden til udpegning af et ekspone-
ringsniveau er afhængig af, hvilke eksponeringsniveauer
man har valgt ved udførelse af et forsøg, og i nogle tilfælde
har man måske ikke engang fundet et N O(A)EL. D ette har
medført, at en nyere metode, benchmark-metoden, visse
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steder har vundet indpas i forbindelse med risikovurderin-
ger, idet der ikke anvendes en N O(A)EL eller LO(A)EL
men en benchmark-dosis for den videre beregning af T D I.
Ved denne metode foretages en computerbaseret modelle-
ring af dosis-responskurven ud fra de tilgængelige data. På
dosis-respons kurven findes ED
5
– eller ED
10
-niveauet (dvs.
det eksponeringsniveau, der medfører respons hos 5% eller
10% af de eksponerede). D enne dosis vælges derpå som
udgangspunkt (benchmark-dosis, BM D
5
eller BM D
10
) for
den videre beregning på tilsvarende måde som man anven-
der en N O(A)EL- eller LO(A)EL-værdi.
M etoden anvendes af de canadiske miljømyndigheder og af
US EPA, og også af WH O i forbindelse med ”Air quality
G uidelines for Europe” (2). WH O angiver i denne forbin-
delse, at en BM D
5
ud fra en gennemsnitsbetragtning kan
sammenlignes med et N O(A)EL, mens en BM D
10
kan
sammenlignes med et LO(A)EL.
WH O omtaler også anvendelsen af benchmark-metoden
som en alternativ metode i forbindelse med publikation om
risikovurdering fra 1999 (3) og i forbindelse med publikati-
on om fastsættelse af vejledende grænseværdier fra 1994
(4).
På nuværende tidspunkt haves der kun sparsom erfaring
med anvendelsen af metoden herhjemme. Som det faglige
miljøprojekt anfører, kan benchmark-metoden ikke umid-
delbart anvendes for alle typer data, og metoden kræver for
de relevante effektområder, hvor den kan anvendes, ofte
flere dosis-niveauer end der sædvanligvis haves.
Benchmark-metoden er, når der foreligger tilstrækkelige
data, et supplement til den traditionelle N O(A)EL/
LO(A)EL metode i forbindelse med fastsættelse af kvali-
tetskriterier. Uanset hvilken metode man vælger, bør man
vurdere og begrunde den fra gang til gang, dvs. man bør
referere til og begrunde de anvendte beregningsmetoder
eller henvise til de originalreferencer, hvor den benyttede
benchmark-dosis er beregnet.
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3.4 Udpegn in g af kr it isk ef f ekt
Ved den samlede vurdering af dosis-effekt og dosis-respons
sammenhænge foretages udpegning af den kritiske effekt
samt udpegning af den N O(A)EL/ LO(A)EL værdi (evt.
benchmarkdosis), der vurderes som mest relevant ved fast-
sættelse af kvalitetskriteriet. Ofte, men ikke nødvendigvis, vil
dette være den laveste N O(A)EL/ LO(A)EL værdi, der er
rapporteret vedrørende en skadelig effekt eller potentielt
skadelig effekt.
Ved udpegning af den kritiske effekt vurderes relevansen af
eksponeringsmåden (eksponeringsvejen i en given undersø-
gelse) i forhold til eksponeringsvejen for det medie (jord,
luft eller vand) kvalitetskriteriet skal udarbejdes for. Alvor-
ligheden af forskellige effekter sammenholdes i forhold til,
hvor langt de ligger fra hinanden i eksponeringsniveau. D et
vurderes fx om en alvorlig effekt kan være en følge af min-
dre alvorlige effekter, som således kan ses som en forløber
og indikator for udvikling af en egentlig skadeeffekt. Endvi-
dere vurderes i det konkrete tilfælde, om der optræder visse
artsspecifikke effekter hos forsøgsdyrene, og om dokumen-
tationen er tilstrækkelig til, at disse fund kan vurderes at
være irrelevante i forhold til mennesker (se afsnit 3.5).
Ved tvivlstilfælde om udpegning af kritisk effekt og
N O(A)EL/LO(A)EL værdi kan det være nødvendigt at
udpege flere N O(A)ELs/LO(A)ELs for de potentielt kriti-
ske effekter og anvende disse sideløbende ved den efterføl-
gende beregning af T D I/ kvalitetskriterier. D ette er for at
vurdere, hvordan anvendelse af usikkerhedsfaktorer og
andre beregningsmæssige forhold får indflydelse på kvali-
tetskriteriet, når der anvendes forskellige udgangspunkter
m.h.t. kritisk effekt og N O(A)EL/LO(A)EL.
3.5 Rel evan s af visse ef f ekt er i f or søgsdyr
Som udgangspunkt anvendes dyremodeller som troværdige
modeller ved forudsigelse af stoffets egenskaber hos menne-
sker. Visse effekter, der optræder i forsøgsdyr, har vist sig at
være tæt knyttet til bestemte dyrearter. I tilfælde, hvor der
foreligger dokumentation for at effekterne alene er forårsa-
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get af en sådan artsspecifik virkningsmåde, anses disse for at
være af meget begrænset relevans ved den videre vurdering
af stoffet.
Især inden for kræftområdet har man fundet flere typer
svulster (tumorer), hvor relevansen i forhold til mennesker i
de enkelte tilfælde bør vurderes nøjere. I M iljøprojekt N r.
974 (2005) er en række af disse beskrevet i afsnit 3.7.
Ref er en cer
(1) M iljøprojekt N r. 974 (2005). Principper for sundheds-
mæssig vurdering af kemiske stoffer med henblik på fastsæt-
telse af kvalitetskriterier for luft, jord og vand.
(2) WH O (2000). Air Quality G uidelines for Europe.
WH O regional Publications, European Series, N o. 91.
(3) WH O (1999). Principles for the assessment of risks to
human health from exposure to chemicals. Environmental
H ealth C riteria 210. International Programme on C hemical
Safety.
(4) WH O (1994). Assessing human health risks of chemi-
cals: derivation of guidance values for health-based expo-
sure limits. Environmental H ealth C riteria 170. Interna-
tional Programme on C hemical Safety.
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4 Beregning af TDI for stoffer med
tærskelværdi
4.1 TDI-begr ebet
D et sidste trin i farlighedskarakteriseringen er beregning af
tolerabelt dagligt indtag,
T DI (eller
tolerabel koncentration,
T K ).
Ved beregning for stoffer, hvor der anses at være en
nedre tærskel for effekt anvendes usikkerhedsfaktorer:
N O(A)EL
T DI (T K ) =
a

UF
I
x UF
II
x UF
III
Alternativt kan et LO(A)EL eller en Benchmark-dosis BM D
x
anvendes, se afsnit 3.3.
D en tolerable daglige indtagelse (T D I) er et udtryk for den
daglige gennemsnitsdosis (fra alle kilder), som befolkningen
vurderes at kunne udsættes for (tolerere) gennem et helt
livsforløb, uden at der forventes at opstå sundhedsskadelige
effekter.
T D I angives sædvanligvis i enheden mg/kg legemsvægt per
dag.
Analogt til T D I kan betegnelsen tolerabel koncentration
(T K) defineres som den koncentration af et stof i jord, luft
eller drikkevand som befolkningen vurderes at kunne udsæt-
tes for (tolerere) gennem et helt livsforløb, uden at der for-
ventes at opstå sundhedsskadelige effekter. T K angives fx i
3
enheden mg/m (luft), mg/l (drikkevand), eller i mg/kg
(jord).
For nogle stoffer er det nødvendigt at fastsætte en PT WI –
værdi (Provisional T olerable Weekly Intake – PT WI), der
angiver det tolerable ugentlige indtag, i stedet for T D I.
PT WI benyttes sædvanligvis over for stoffer, hvor det er
a
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vigtigt at understrege, at det er den samlede eksponering
over længere tid, der er af betydning for forekomst af effek-
ter (fx bly og cadmium).
Begrundelse for anvendelse af usikkerhedsfaktorer omtales
kort nedenfor, idet en mere detaljeret beskrivelse er givet i
M iljøprojekt N r. 974 (2005) afsnit 4.4
4.2 An ven del se af usikker h edsf akt or er
I kommentarerne til M iljøbeskyttelsesloven angives at ”M il-
jøministeriet ved udstedelse af regler og vejledninger kan
operere med fx sikkerhedsfaktorer ved fastsættelse af græn-
seværdier eller retningslinier for forureningsmæssige bereg-
ninger på de områder, hvor der ikke foreligger et tilstrække-
ligt eksakt vidensgrundlag”
T idligere har man anvendt begrebet sikkerhedsfaktorer. D et
har imidlertid vist sig, at denne betegnelse kan misforstås,
således at man forventer større sikkerhed, jo større sikker-
hedsfaktor der anvendes. D ette er ikke i overensstemmelse
med, hvordan faktorerne anvendes, idet de benyttes for at
tage hensyn til usikkerheder og manglende viden i data-
grundlaget, dvs. jo større usikkerhed jo større faktor. Ved
brugen af disse faktorer tilstræbes det, at der opnås et ensar-
tet beskyttelsesniveau udtrykt ved T D I-værdien. På denne
baggrund er det derfor mere korrekt at anvende betegnelsen
usikkerhedsfaktorer.
Også i udenlandsk litteratur anvendes forskellige termer for
denne faktor fx: safety factor, uncertainty factor, Sicher-
heitsfaktor, assessment factor, bedömningsfaktor.
N edenfor angives hvilke elementer og hensyn, der indgår i
de tre usikkerhedsfaktorer.
4.2.1 Usikkerhedsfaktor I
Usikkerhedsfaktor I (UF
I
) anvendes for at tage højde for, at
mennesker kan være mere følsomme over for et givent stof
end forsøgsdyr. D enne faktor har historisk været sat til 10.
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Ekstrapolation af data fra dyr til mennesker kan opfattes
som omhandlende to forskellige aspekter:
1) korrektion af dosis for forskelle i kropsstørrelse mel-
lem forsøgsdyr og mennesker, såkaldt allometrisk
skalering, og
2) andre former for forskelle mellem forsøgsdyr og
mennesker, som ikke nødvendigvis afspejles i forskelle-
ne i kropsstørrelse.
M iljøprojekt N r. 974 (2005) har gennemgået den eksiste-
rende viden og understøtter, at der fortsat som udgangs-
punkt anvendes en standardværdi på 10 for UF
I
, hvilket
også er i overensstemmelse med international praksis, når
dosis hos dyr omsættes til human dosis med samme enhed.
H vis der foreligger veldokumenteret viden om toksikokine-
tiske og/eller toksikodynamiske forskelle mellem det givne
forsøgsdyr og mennesker, anbefales det at tage udgangs-
punkt i denne viden med henblik på fastsættelse af en data-
specifik faktor i stedet for anvendelse af en standardværdi
på 10. I den forbindelse kan 10-faktoren evt. opdeles i un-
derfaktorer, hvor størrelsen af disse ”delfaktorer” må vurde-
res konkret fra gang til gang.
Ved beregning af tolerabel koncentration (T K), hvor ud-
gangspunktet er dyreforsøg, hvor eksponeringen foregår via
inhalation, bør ekstrapolering til humaneksponering ved
inhalation foretages direkte ud fra eksponeringsniveauet
3
angivet i mg stof /m (omregnet til kontinuerlig gennem-
snitskoncentration per dag), frem for at foretage omregning
fra indåndet dosis til mg/kg lgv/d for forsøgsdyrene. Ved at
anvende indåndingskoncentrationen direkte svarer dette til
at doseringen foretages i forhold til stofskiftet, hvilket anses
for at være den mest relevante metode, når der skal korrige-
res for forskelle i kropsstørrelse. Anvendelse af en UF
I
skal
ses i lyset heraf og bør derfor i denne situation ligge lavere
0,5
end 10. En værdi på en halv tierpotens (10 ) kan som ud-
gangspunkt anvendes til resterende forskelle m.h.t. artsfor-
skelle i kinetik og dynamik, medmindre konkrete data tilsi-
ger højere eller lavere værdi.
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D er bør i videst muligt omfang tages hensyn til en række
mætningsfænomener (fx mætning af absorption, metabo-
lisme eller udskillelse), der kan forekomme i dyreforsøg ved
høj dosering, idet disse mætningsfænomener ofte ikke vil
være relevante ved lavere miljømæssigt relevante niveauer. I
sådanne tilfælde bør der om muligt omregnes til ”effektiv”
dosis/ koncentration som dyrene har været udsat for.
4.2.2 Usikkerhedsfaktor II
Usikkerhedsfaktor II (UF
II
) anvendes for at tage højde for,
at nogle individer i befolkningen kan være mere følsomme
over for et givent stof end den generelle befolkning (for
eksempel børn, gravide, ældre, svækkede, kronisk syge).
D enne faktor har oftest været sat til 10. Forskellene i føl-
somhed skyldes den biologiske variation, der findes mellem
mennesker. Faktorer som alder, køn, graviditet, genotype,
helbred, og livsstil kan være medvirkende til en øget biolo-
gisk følsomhed, som afspejler dels forskelle i toksikokinetik
og dels i toksikodynamik.
M iljøprojekt N r. 974 (2005) henviser til en række analyser,
der har vurderet variationen mellem mennesker og dermed
størrelsen af UF
II
. Sammenfattende understøtter disse ana-
lyser anvendelse af en standardværdi på 10 for denne varia-
tion.
D enne usikkerhedsfaktor skal derfor som udgangpunkt sæt-
tes til 10. En alternativ værdi kan anvendes, hvis udgangs-
punktet for N O(A)EL/LO/A)EL værdien specifikt er relate-
ret til data for særligt følsomme personer eller den kritiske
effekt er en effekt, hvor man har særligt kendskab til variati-
onsbredden i følsomhed.
4.2.3 Usikkerhedsfaktor III
Usikkerhedsfaktor III (UF
III
) anvendes for at tage højde for
manglende kvalitet og relevans af de tilgængelige data. I
relation til fastsættelse af kvalitetskriterier i jord, luft og
drikkevand har denne faktor typisk varieret fra 1 til 100
afhængigt af datagrundlaget for de pågældende stoffer.
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I UF
III
indgår bl.a. følgende elementer :
•
kvaliteten af datasættet (fx ekstrapolation fra subkronisk
nuleffektniveau til kronisk nuleffektniveau),,
•
ekstrapolation fra en eksponeringsvej til en anden (”rou-
te to route” ekstrapolation fx omregning fra oral dosis til
inhalationsdosis),
•
ekstrapolation fra LO(A)EL til N O(A)EL,
•
og alvorligheden af effekterne (fx kræftfremkaldende
effekter).
D et er ikke muligt at pege på en specifik størrelsesorden for
en standardværdi, hverken for de enkelte delelementer af
UF
III
eller for den samlede UF
III
.
D er henvises til M iljøprojekt N r. 974 (2005) for en nærme-
re beskrivelse af UF
III
i rapportens afsnit 4.4.3.
N edenfor anføres mere kortfattet retningslinierne for fast-
sættelse af UF
III
.
K valitet og relevans af data
UF
III
skal tage højde for, om der er kvalitetsmæssige eller
datamæssige mangler. Vurdering af kvalitet, omfatter vurde-
ring af om de enkelte undersøgelser (og især undersøgelser-
ne der refererer til de kritiske effekter og effektniveauer) er
udført og afrapporteret på en måde, så resultaterne anses
for relevante og pålidelige. Selve omfanget af datasættet
vurderes for data vedrørende alle relevante effektområder i
relation til kortvarig og langvarig eksponering, og det vurde-
res om der i datasættet er væsentlige mangler i forhold til
vurdering af kritisk effekt og estimering af T D I. En faktor
på 1 anvendes ved datasæt, som vurderes at være fuldt til-
strækkeligt for det givne stof, mens der ved mindre eller
større mangler har været anbefalet faktorer i størrelsesorde-
nen 3-10. I visse tilfælde med store mangler kan en faktor
på helt op til 100 komme på tale. Fastlæggelse af UF
III
må
ofte baseres på en ekspertvurdering og foretages under hen-
syntagen til det enkelte stofs toksikologiske profil.
Et særligt aspekt, er manglende viden om børn og ufødtes
følsomhed for konkrete kemiske påvirkninger. For at beskyt-
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
te børn og ufødte er det vigtigt ved fastsættelse af UF
III
at
vurdere om der er tilstrækkelig viden om disse forhold ud
fra reproduktionsforsøg og flergenerationsforsøg. Er disse
forhold ikke tilstrækkeligt belyst bør mangel på data have
indflydelse på valget af UF
III
. Størrelsen af en sådan delfak-
tor må ses i sammenhæng med stoffets toksikologiske profil
og hvilke øvrige data, der haves.
Ekstrapolation fra en eksponeringsvej til en anden
Ved mangel på data for den relevante eksponeringsvej kan
det blive nødvendigt at foretage en “route-to-route” ekstra-
polation. D e analyser, der er foretaget med hensyn til eks-
trapolation fra oralt N O(A)EL til et N O(A)EC ved inhala-
tion, peger generelt på, at en ekstrapoleret værdi ofte vil
være væsentligt højere end en observeret værdi (dvs toksici-
teten undervurderes). D et modsatte gør sig generelt gæl-
dende når der ekstrapoleres fra oralt N O(A)EL til
N O(A)EL ved hudkontakt, hvor den ekstrapolerede værdi
ofte vil være lavere end en observeret værdi (dvs. toksicite-
ten overvurderes). D er kan imidlertid ikke peges på en kon-
kret størrelse for usikkerhedsfaktor III ved disse ekstrapola-
tioner, der hviler på et meget usikkert grundlag. Vurderin-
gen af om en ”route-to route” ekstrapolation skal foretages,
og i hvilken udstrækning der skal anvendes en usikkerheds-
faktor i tilknytning hertil, må bero på en ekspertvurdering i
det konkrete tilfælde.
For stoffer, hvor der kun findes subakutte eller subkroniske
undersøgelser, er det ikke muligt at fastsætte et N O(A)EL
for livstidseksponering, som generelt må forventes at ligge
lavere. D er har været foretaget flere analyser af forholdet
mellem N OAELs og LOAELs opnået i studier af forskellige
eksponeringsvarigheder. M ed baggrund i disse synes der at
være belæg for en usikkerhedsfaktor af størrelsesorden mi-
nimum 10. En af de nyere analyser har således vist, at en
faktor på 10 vil være tilstrækkelig i knap 90% af tilfældene,
når der var tale om ekstrapolation fra subkroniske data,
mens der ved ekstrapolation fra subakutte data skulle an-
vendes en væsentlig højere faktor (> 20).
Ved ekstrapolation fra LO(A)EL til N O(A)EL kan der ikke
peges på en generel faktorstørrelse, som afspejler en generel
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usikkerhed. Praksis inden for området og de tilgængelige
analyser af problemstillingen peger på, at en værdi omkring
en faktor 10 i langt de fleste tilfælde er tilstrækkelig. Vurde-
ringen må imidlertid bero på en ekspertvurdering i hvert
enkelt tilfælde.
M ed baggrund i vægtning af ovenstående aspekter anvendes
en UF
III
på 10 som udgangspunkt. D enne værdi kan så kor-
rigeres, når der er grundlag for dette i konkrete tilfælde.
D enne problemstilling kan i visse situationer omgås, når det
ud fra data er muligt at beregne en benchmark-dosis, såle-
des at denne anvendes i stedet for LO(A)EL-værdien.
Alvorligheden af effekter
D et har været praksis ved fastsættelse af kvalitetskriterier, at
særligt alvorlige effekter (fx kræftfremkaldende effekt eller
fosterbeskadigende effekter) afspejles i usikkerhedsfaktor
III. D et gælder især i de tilfælde, hvor den alvorlige effekt
optræder ved lave dosisniveauer. H er kan anvendes
en ekstra
faktor
på op til 10 for at tage hensyn til dette. For at få den
endelige værdi for UF
III
ganger man de enkelte værdier
sammen.
Sammenfattende kan det konkluderes, at det ikke er muligt
at sætte en standardværdi for en samlet UF
III
. Usikkerheder-
ne inden for de forskellige områder må vægtes, når der tages
stilling til en samlet faktor for UF
III
, da en multiplikation af
mange delfaktorer i UF
III
kan give en meget høj værdi, og i
visse tilfælde give et skævt billede af det samlede vi-
dengrundlag og kvaliteten heraf. Fastsættelse af UF
III
bør
således i høj grad bero på en ekspertvurdering, hvor valget
af faktoren og elementerne heri tydeligt begrundes.
4.2.4 Samlet usikkerhedsfaktor
Ved beregning af T D I divideres N O(A)EL evt. LO(A)EL
med de tre usikkerhedsfaktorer, der således ganges sammen.
Ved multiplikation af UF
I
, UF
II
og UF
III
bør der imidlertid
tages stilling til størrelsen af den samlede usikkerhedsfaktor,
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og der bør foretages en overordnet vurdering i forhold til
det givne datasæt.
En meget stor usikkerhedsfaktor, der kan medføre en meget
lille T D I-værdi, betyder ikke nødvendigvis, at stoffet er lige
så potent eller farligt som andre, mere velkendte stoffer med
tilsvarende lave T D I-værdi. D en beregnede lave værdi må
snarere ses som en følge af store usikkerheder i datagrund-
laget. En samlet usikkerhedsfaktor på 10.000 og derover,
bør derfor ikke anvendes.
Ref er en cer
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier for luft, jord og vand.
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2259378_1847.png
5 Beregning af TDI for kræftfremkal-
dende stoffer
5.1 Kr æ t f r emkal den de st of f er med og uden t æ skel -
f
r
væ di
r
Kræftfremkaldende stoffer anses for at kunne deles op i to
grupper grundet deres virkningsmekanisme. D en ene grup-
pe består af stoffer, der virker kræftfremkaldende som følge
af evnen til at påvirke cellernes delings- og differentierings-
hastighed. D ette kan ske gennem direkte eller indirekte på-
virkning af cellernes receptorer. For sådanne stoffer antages
der at være en nedre tærskelværdi for denne effekt. D erfor
kan T D I beregnes ved hjælp af usikkerhedsfaktorer, som
omtalt i forrige afsnit.
D en anden gruppe af kræftfremkaldende stoffer virker gen-
nem kemisk interaktion med cellernes arvemasse, og den
kræftfremkaldende effekt vurderes at være en følge af stof-
fets beskadigelse af cellernes arveanlæg (muta-
gen/genotoksisk aktivitet). For disse stoffer anses der ikke at
være et nedre eksponeringsniveau uden øget risiko for ska-
devirkninger. For sådanne stoffer anvendes ikke usikker-
hedsfaktorer ved beregning af T D I. I stedet beregnes T D I
ved hjælp af en matematisk modelberegning, hvor man på
forhånd definerer et risikoniveau man vil acceptere, og be-
regner så hvilken udsættelse, som giver denne risiko.
Ved vurdering af kræftfremkaldende effekt er det således af
stor betydning, om det kræftfremkaldende stof falder ind
under den ene eller den anden kategori. D er findes stoffer,
som både er genotoksiske – dvs. kræftfremkaldende uden
tærskel for effekt, og kræftfremkaldende ved andre meka-
nismer, hvor der anses at være en tærskel. Ved vurdering af
denne type stoffer, kræver det en ekspertvurdering at afgø-
re, om de data der ligger til grund, bedst giver grundlag for
at vurdere stoffet som tilhørende den ene eller anden kate-
gori. D er har således i EU været arbejdet på at udvikle
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2259378_1848.png
nærmere vejledning i hvordan disse typer stoffer kan vurde-
14
res .
5.2 Vur der in g af kr æ t f r emkal den de ef f ekt
f
EU, WH O IARC (International Agency for Research on
C ancer) og US EPA anvender en række forholdsvis sam-
menlignelige procedurer/ kriterier ved vurdering af, om et
stof skal i kategorien ”kræftfremkaldende”. Stofferne ind-
placeres i forskellige underkategorier alt efter dokumentati-
onens omfang, og under hensyntagen til om dokumentatio-
nen stammer fra humandata eller dyredata.
Yderligere indgår der i vurderingerne også stillingtagen til
virkningsmekanismer, fx om stoffer virker gennem en mu-
tagen/ genotoksisk mekanisme. I EU´s klassificeringssystem
for kemiske stoffer er der også kriterier for, hvornår et stof
skal kategoriseres som ”mutagent”.
Principperne for inddeling af kræftfremkaldende stoffer i
kategorier er mere udførligt beskrevet i M iljøprojekt N r. 974
(2005) afsnit 3.6.
Ved vurdering af et stofs kræftfremkaldende effekt i forbin-
delse med risikokarakterisering og beregning af kvalitetskri-
terier tages der så vidt muligt udgangspunkt i de ovennævn-
te vurderinger, idet der suppleres med opdateret viden fra
litteraturen. D et vurderes om der er dokumentation for at
den kræftfremkaldende effekt er en følge af genotoksisk
virkning, og om stoffet derfor skal betragtes som værende
uden en nedre tærskel for effekt.
H vis data taler for, at stoffet virker gennem en ikke-
genotoksisk mekanisme, anses stoffet for at besidde en tær-
skelværdi for skadelig effekt. For en række stoffer vil data og
viden vedrørende virkningsmekanisme være meget mangel-
fuld, og det kan være vanskeligt at sondre, om stoffet skal
betragtes som værende enten med eller uden tærskelværdi.
Sådanne tvivlstilfælde kan bedst håndteres ved at betragte
14
European Food Safety Authority (2005). Opinion on a H armo-
nised Approach for Risk Assessment of Compounds Which are
both G enotoxic and C arcinogenic.
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stoffet som havende en tærskelværdi, og i den forbindelse
anvende en øget usikkerhedsfaktor (UF
III
) for at tage hensyn
til usikkerheden om eksistensen af en tærskelværdi.
D er bør således være et vist datagrundlag, der peger hen
mod en genotoksisk mekanisme, før stoffet vurderes efter en
model uden nedre grænse.
Ved vurderingen af kræftfremkaldende effekt tages stilling
til om den er knyttet til bestemte eksponeringsveje, og om
disse er relevante i forbindelse med et kvalitetskriterium for
stoffet i jord, luft eller drikkevand.
Visse kræftformer kan være forsøgsdyrsspecifikke, og når
sådanne kræftfund kan dokumenteres som ikke-relevante i
human sammenhæng, tillægges disse fund kun begrænset
vægt (se afsnit 3.5).
Ved vurderinger i relation til kvalitetskriterier tages der alene
stilling til om stoffet skal betragtes som kræftfremkaldende,
og om stoffet ud fra dets virkningsmekanisme skal anses for
at have en tærskelværdi eller ej. D er foretages således ikke
en mere detaljeret indplacering i forskellige kategorier i for-
hold til dokumentationens art og omfang, dvs. der inddeles
ikke i kategorier for humane og dyreeksperimentelle kræft-
fremkaldende stoffer.
Et stof, som på baggrund af dokumentationen indplaceres i
EU’s C arc1 eller C arc 2, i IARC ’s gruppe 1 eller gruppe
2A/2B, og/eller i US EPA’s gruppe A eller B1/B2, vil som
udgangspunkt medføre, at stoffet betragtes som kræftfrem-
kaldende, med mindre der er nyere undersøgelser eller vel-
underbyggede informationer og fortolkninger af data, der
taler imod en sådan vurdering.
T ilsvarende gælder stoffer, som er opført på Arbejdstilsy-
nets liste over stoffer, som anses for at være kræftfremkal-
dende. D et skal dog understreges, at stoffer, som hverken er
vurderet af EU, IARC og/eller US EPA eller er indplaceret i
en lavere kategori (EU C arc3, IARC gruppe 3 og/eller US
EPA gruppe C /D ), godt kan blive betragtet som kræftfrem-
kaldende i relation til fastsættelse af kvalitetskriterier for
kemikalier i jord, luft og drikkevand, hvis der er velunder-
byggede data, der taler for det. D et kan for eksempel være i
36
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
tilfælde af, at der er publiceret nye undersøgelser siden en
eventuel vurdering er foretaget af EU, IARC og/eller US
EPA, eller der kan være stor kemisk strukturlighed med
andre kendte kræftfremkaldende stoffer. I sidstnævnte til-
fælde kan QSAR-modellering indgå som supplerende støtte
for vurderingen.
5.3 Ber egn in g af TDI f or kr æ t f r emkal den de st of f er
f
uden t æ skel væ di
r
r
5.3.1 Tolerabelt risikoniveau
T D I-værdien for kræftfremkaldende stoffer uden tærskel-
værdi fastsættes til en værdi, der repræsenterer et accepteret
risikoniveau for udvikling af kræft. D enne værdi har traditi-
-6
onelt været fastsat til en 10 livstidsrisiko, og vil også med
udsendelse af denne vejledning være det ønskede risikoni-
veau.
Konkret betyder dette, at man med udgangspunkt i human-
data eller dyreforsøg, hvor den kræftfremkaldende effekt er
påvist, ved hjælp af matematisk modellering estimerer dosis-
respons kurvens forløb så langt ned i lav-
-6
eksponeringsområdet, at en eksponering svarende til en 10
livstidsrisiko kan beregnes. T D I er således den daglige gen-
nemsnitseksponering, der ud fra
teoretiske beregninger
svarer
til en forøget risiko for cancer på 1 ud af en million menne-
sker, som er udsat for stoffet gennem en hel livstid.
5.3.2 Metode til beregning af TDI og livstidsrisiko
D er er udviklet forskellige metoder til beregning af, hvor
stor en risiko for udvikling af svulster en given eksponering
for et genotoksisk kræftfremkaldende stof udgør. For alle
metoder gælder, at der anvendes en eller anden form for
matematisk ekstrapolation fra dosisniveauer med de kendte
eksperimentelle værdier for forekomsten af svulster til de
som regel meget lavere dosisniveauer, der svarer til en fore-
komst hos 1 ud af en million. M etoderne beskriver relatio-
nen mellem den daglige eksponering (udtrykt som dosis
37
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
2259378_1851.png
eller koncentration) og den sammenhørende sandsynlighed
for udvikling af svulster.
Beskrivelse af forskellige metoder og sammenligning mellem
disse fremgår af M iljøprojekt N r. 974 (2005) afsnit 5.3 og
5.4.
D en foretrukne metode til fastsættelse af T D I er T 25-
metoden, som også anvendes i EU-regi. D en baserer sig
ligesom one-hit metoden på lineær ekstrapolation med ud-
gangspunkt i laveste dosisniveau, hvor der optræder signifi-
15
kant forøget antal svulster .
M etoden er en simplificeret lineær metode med udgangs-
punkt i en beregnet T 25-dosis. T 25-dosis defineres i denne
sammenhæng som den kroniske eksponering (enhed: mg/kg
3
legemsvægt per dag eller mg/m ), som vil give 25% af for-
søgsdyrene svulster i et specifikt væv, efter korrektion for
den spontane hyppighed, indenfor den standardiserede le-
vetid for den pågældende dyreart. M ed udgangspunkt i
denne T 25-dosis foretages lineær ekstrapolation ved simpel
forholdsregning ned til en dosis, der svarer til et tolerabelt
risikoniveau.
M etoden og dens konkrete anvendelse i forhold til et tolera-
-6
belt 10 livstidsrisikoniveau er nøjere beskrevet i bilag 1.
5.3.3 Anvendelse af risikoestimater angivet i litteraturen
I en række tilfælde vil eksponeringsniveauet svarende til en
-6
10 livstidsrisiko (eller ”unit-risk”-estimater) på forhånd
være beregnet af ekspertgrupper under fx WH O eller US
EPA. For især nyere vurderinger kan det være relevant at
anvende disse værdier som ligeværdigt udgangspunkt på
15
M iljøstyrelsen har tidligere som administrativ praksis anvendt
one-hit metoden. Anvendelse af T 25-metoden vil i forhold til den
medføre lidt højere værdier (skønsmæssigt en faktor 2-4). D enne
forskel skal dog ses i et 10
-6
perspektiv, og må anses som meget
beskeden, og i praksis uden betydning i forbindelse med det til-
stræbte beskyttelsesniveau.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
linie med T 25-metoden ved beregning af T D I og kvalitets-
kriterier.
Argumenterne for at vælge et risikoestimat frem for et andet
kan dels være rent faglige (fx bero på konkrete virkningsme-
kanismer) og dels være mere pragmatiske, idet man også
bør vurdere nødvendigheden af at foretage selvstændige
beregninger af et risikoniveau. For eksempel kan opgaven
være meget omfattende for stoffer med stor datarigdom (fx
PAH -stoffer), hvor en selvstændig vurdering vil kræve ulige
mange resurser og inddragelse af høj faglig ekspertise på
området for at kunne leve op til kvaliteten af en internatio-
nal vurdering.
D erfor vil man i konkrete tilfælde kunne basere kvalitetskri-
terier for kræftfremkaldende stoffer på andre metoder end
T 25 metoden.
Ref er en cer
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier for luft, jord og vand.
European Food Safety Authority (2005). Opinion on a
H armonised Approach for Risk Assessment of C ompounds
Which are both G enotoxic and C arcinogenic.
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2259378_1853.png
6 Beregning af kvalitetskriterier for
kemikalier
D ette kapitel beskriver hvorledes kvalitetskriterierne for ke-
mikalier i jord, luft og drikkevand kan beregnes med ud-
gangspunkt i førnævnte T D I-værdier.
Første led i beregningen er en vurdering af, om hele T D I-
værdien eller kun en brøkdel heraf tildeles til beregning af
det konkrete kvalitetskriterium. D ette kan dels være begrun-
det i eksponeringsmæssige overvejelser - den såkaldte allo-
kering, hvor der tages hensyn til evt. andre kilder, der har
betydning for eksponeringen. Eller det kan være begrundet i
øvrige forhold, der kan være afgørende for, om der anven-
des en reduktionsfaktor, så kun en mindre brøkdel af T D I-
værdien anvendes ved beregning af kvalitetskriteriet.
Kapitlet angiver hvilke værdier for medieeksponering der
anvendes ved beregning af kvalitetskriterierne. En mere
uddybet forklaring på valget af disse værdier er givet i bilag
2.
6.1 Gen er el met ode f or ber egn in g af et kval it et skr it e-
r ium
Et sundhedsmæssigt baseret kvalitetskriterium for et stof i
jord, luft eller drikkevand beregnes ud fra den tolerable dag-
lige indtagelse, ved at dividere T D I-værdien med den dagli-
16,17
ge eksponering for det relevante medie WH O/ IPC S . D et
vil sige, at selve beregningen af kvalitetskriteriet ud fra T D I
i princippet er ens for de tre medier, jord, luft og drikkevand
16
WH O/IPC S (1994). Assessing human health risks of chemicals:
D erivation of guidance values for health-based exposure limits.
Environmental H ealth C riteria no. 170. International Programme
on C hemical Safety.
17
WHO/IPC S (1999). Principels for the assessment of risks to
human health from exposure to chemicals. Environmental H ealth
C riteria no. 210. International Programme on C hemical Safety.
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og for alle stoffer, uanset om der foreligger tærskelværdi for
den kritiske effekt eller ej.
Følgende generelle beregningsmetode kan opstilles:
T DI x V x
f
KK
l,j,v
=
__________________________
E
l,j.v
hvor
KK
l,j,v
: kvalitetskriterium for jord, luft eller drikkevand
T D I: angives i mg/ kg legemsvægt/ d
V: legemsvægt i kg
f:
allokeringsfaktor, brøkdel af T D I som ud fra ekspone-
ringsfordeling anvendes til eksponering fra jord, luft eller
drikkevand
3
E
l,j,v
: daglig udsættelse/ forbrug af luft (m /d), jord (kg/d),
eller drikkevand (liter/d).
3
(H vis E
l.j,v
angives i (m /kg lgv/ d), (kg/kg lgv/d), eller (li-
ter/kg lgv/d) udgår V i ovenstående formel).
6.1.2 Anvendelse af TDI
For stoffer hvor der ikke anses at være en tærskelværdi for
effekt, dvs. de genotoksiske kræftfremkaldende stoffer, an-
-6
vendes T D I-værdien (sv.t til en 10 livstidsrisikodosis) di-
rekte til beregning af kvalitetskriteriet.
For andre stoffer, hvor der anses at være en tærskelværdi,
indgår efterfølgende overvejelser vedrørende anvendelse af
en allokeringsfaktor eller reduktionsfaktor.
Allokering
Allokeringsfaktoren ”f” angiver den brøkdel af T D I som
tildeles udsættelsen via det enkelte medie. Ofte tildeles min-
dre end 100% af et kemisk stof til beregning af et kvalitets-
kriterium, da der for en række kemiske stoffer vil være ud-
sættelse gennem andre medier end det enkelte medie jord,
luft og vand. I en række tilfælde vil bidrag gennem forure-
ning af fødevarer eller gennem påvirkning fra indeklimaet
udgøre hovedkilden for en persons udsættelse, og vil der-
med ”lægge beslag på” en betydelig del af T D I-værdien,
hvorfor der kun tildeles en mindre andel til kvalitetskriteriet.
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I de tilfælde hvor bidrag fra andre medier ikke forventes,
fastsættes kvalitetskriterierne som udgangspunkt ved, at hele
T D I allokeres til det pågældende medie. N år det vurderes,
at der foreligger øvrige betydende kilder allokeres som ud-
gangspunkt 10% af T D I til det pågældende medie, med
mindre der er konkret viden om øvrige kilders bidrag, der
siger noget andet. For visse stoffer, hvor langt de største
bidrag kommer fra øvrige kilder, kan der således allokeres
helt ned til kun 1% af T D I (dette er for eksempel gjort for
visse plastblødgørere i forbindelse med et kvalitetskriterium
for drikkevand).
Reduktionsfaktor
I særlige tilfælde kan andre forhold end de rent ekspone-
ringsmæssige betragtninger medføre, at der anvendes en
reduktionsfaktor, således at der kun anvendes en vis brøkdel
af T D I til beregning af kvalitetskriteriet. En sådan faktor
kan efter individuel vurdering komme på tale fx :
-
ved særligt kritiske forhold som persistens og bioakku-
mulering af stoffet,
-
i tilfælde, hvor kvalitetskriteriet er udarbejdet ud fra et
enkelt stofs effekter, men hvor stoffet repræsenterer en
hel stofgruppe, og hvor eksponeringen typisk vil være
karakteriseret ved en blandingseksponering med denne
stofgruppe,
-
i tilfælde hvor der samtidig kan optræde eksponering fra
flere stoffer, og hvor der er formodning om, at der ved
de relevante niveauer vil kunne optræde kombinations-
effekter (fx samvirkende effekter) fra denne blandings-
eksponering.
6.1.3 Eksponeringsbetragtninger
M ålet for eksponeringen i nævneren i brøken til kvalitetskri-
terie-beregningen baseres på standardbetragtninger for dag-
lig udsættelse.
I afsnit 6 i M iljøprojekt N r. 974 (2005) er der foretaget en
opdateret gennemgang af viden om befolkningens udsættel-
se for jord, luft og vand, samt angivet hvilke standardbe-
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
tragtninger der anvendes inden for WH O, US EPA og i
EU.
Ud fra hensigten om specifikt at tage hensyn til børns eks-
ponering er der foretaget en revision af den hidtidige prak-
sis. G rundlaget for den reviderede praksis er anført i bilag 2.
6.2 Ber egn in g af l uf t kval it et skr it er iet
Følgende fremgangsmåde anvendes til beregning af luftkva-
litetskriteriet (KK
luft
), når T D I for de(n) kritiske effekt(er)
er fra studier hvor stoffet er givet via munden og angivet i
enheden mg/kg legemsvægt/dag:
KK
luft
T DI x
f
=
──────────
E
luft
hvor
T D I: tolerabel daglig indtagelse (mg/ kg lgv/d)
f:
brøkdel af T D I, der allokeres til udeluften
E
luft
: eksponering luft, standardværdi for dagligt indån-
3
dingsvolumen: 0,5 m /kg lgv/d for 1-5 årige børn.
Følgende fremgangsmåde anvendes, når (nul)effektniveauer
N O(A)EL eller LO(A)EL) for de(n) kritiske effekt(er) er
fra studier hvor stoffet er inhaleret og angivet som en kon-
3
centration i enheden mg/m :
KK
luft
=
TK x
f
f:
allokeringsfaktor
T K: tolerabel koncentration
hvor
TK
N O(A)EC eller LO(A)EC
=
──────────────────────
UF
I
x UF
II
x UF
III
For de fleste typer af systemiske effekter anses det at være
den samlede dosis og ikke stoffets koncentration i luften, der
er af betydning for udvikling af disse effekter. Ved fastsæt-
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
telse af luftkvalitetskriteriet i disse tilfælde foretages en om-
regning af det fastlagte (nul)effektniveau til et gennemsnit-
ligt døgnniveau (kontinuert eksponering) ud fra de i studiets
aktuelle eksponeringsbetingelser. D et vil sige, at der kom-
penseres for, at eksponeringen ikke har foregået i alle døg-
nets timer over en fuld uge. H vis eksponeringen for eksem-
pel er foretaget 6 timer per dag i 5 dage per uge, korrigeres
der med en faktor 6/24 til kontinuert eksponering gennem et
helt døgn og en faktor 5/7 til kontinuert eksponering gen-
nem hele ugen.
For visse lokale effekter (effekter, der optræder lokalt i luft-
vejene samt direkte effekter på hud og øjne) anses det sæd-
vanligvis at være stoffets koncentration i luften og ikke den
samlede dosis som sådan, der er af betydning for udvikling
af disse effekter. For sådanne stoffer kan omregning til en
kontinuert eksponering sædvanligvis udelades fra en konkret
vurdering.
Lugt
N ogle kemiske stoffer har en meget kraftig lugt, og hensyn-
tagen til lugt ved fastsættelse af luftkvalitetskriteriet vil for
mange stoffer (fx en række organiske opløsningsmidler)
medføre lavere luftkvalitetskriterium end det sundhedsbase-
rede luftkvalitetskriterium, idet luftkvalitetskriteriet fastsæt-
tes til 1/3 af 50 %-lugtgrænsen.
Lugtgrænsen for et kemisk stof er generelt defineret som
den koncentration i luften, hvor 50 % af et lugtpanel (kon-
trolleret laboratorieforsøg med bestemmelse af lugtgrænse
med frivillige forsøgspersoner) kan registrere lugten.
Som et luftkvalitetskriterium vurderes en sådan 50 % lugt-
grænse at kunne medføre gener hos en ikke uvæsentligt del
af befolkningen.
I en analyse af en række laboratoriedata, hvor lugtgrænsen
er blevet bestemt for kemiske stoffer, viser det sig, at dosis-
respons sammenhængen generelt er ret stejl for et lugtpanel
(D K-T eknik 2001). For personer, med intakt lugtesans
(svarende til personer, der indgår i et lugtpanel), er der ge-
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
nerelt en forholdsvis lille spredning m.h.t. hvornår en lugt
kan opfattes. Ud fra disse data vurderes, at ved et niveau på
1/3 af lugtgrænsen vil maksimalt 1-5% af befolkningen un-
der optimale betingelser kunne fornemme lugt.
Lugtgrænser, der er angivet i litteraturen, kan variere vold-
somt (flere størrelsesordner) D ette skyldes, at metoder til
bestemmelse af lugtgrænser kan variere meget, alt efter hvor
og hvornår de er blevet foretaget, samt at der kan være fore-
taget undersøgelser af forskellige stofkvaliteter, hvor stoffer-
ne ikke er entydigt definerede.
M edmindre lugtgrænsen er bestemt ud fra nye og meget
velbeskrevne metoder, hvor kvalitet og pålidelighed af un-
dersøgelsen kan vurderes, anbefales det at fastsætte luftkva-
litetskriterier på baggrund af lugt fra bestemmelse af lugt-
grænse foretaget af et akkrediteret laboratorium.
6.3 Ber egn in g af jor dkval it et skr it er iet
Følgende fremgangsmåde anvendes ved beregning af jord-
kvalitetskriteriet, når de(n) kritiske effekt(er) er en følge af
gentagen udsættelse:
T DI x V x
f
=
──────────
hvor
E
I, jord
(eller E
H , jord
)
KK
jord
f:
procentdel af T D I, der allokeres til indtagelse af jord
V: legemsvægt, 1-3 årigt barn: 13 kg
E
I,jord
: daglig eksponering (indtagelse) for jord, stan-
dardværdi:
1) 0,0002 kg/d (sv.t. 95-percentilgrænsen) i tilfælde
hvor hele T D I-værdien eller hovedparten af denne
anvendes til beregning af kvalitetskriteriet
2) 0,0001 kg/d (sv.t. medianudsættelse) i tilfælde hvor
-6
T D I er en 10 livstidsrisikodosis for et kræftfrem-
kaldende stof, eller i tilfælde, hvor der anvendes en
mindre del af T D I til jordkvalitetskriteriet
E
H ,jord
: daglig eksponering (hudkontakt) for jord, stan-
dardværdi: 0,001 kg/d for barn.
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2259378_1859.png
E
H ,jord
anvendes i forbindelse med særligt hudgennemtrænge-
lige stoffer, hvor systemisk bidrag fra hudoptag summeres
med det orale bidrag. E
H ,jord
anvendes separat hvis den kriti-
ske effekt er relateret til den direkte hudpåvirkning af foru-
reningskomponenten.
Følgende fremgangsmåde anvendes ved beregning af jord-
kvalitetskriteriet, når den kritiske effekt er akut toksicitet:
KK
jord
TD x V
=
──────
hvor
E
I,jord
(eller E
H , jord
)
T D : tolerabel enkeltdosis
N O(A)EL
akut
eller LO(A)EL
akut
=
──────────────────────
UF
I
x UF
II
x UF
III
hvor
TD
V: legemsvægt, 1-3 årigt barn: 13 kg
E
I
: maksimum enkeltindtag af jord (0,010 kg)
E
H
: maksimal hudkontakt med jord (0,010 kg) (An-
vendes for særligt hudgennemtrængende stoffer).
Ved beregning bør data for optagelse fra mave-tarmkanalen
18
(biotilgængelighed ) så vidt muligt inkluderes, idet de foru-
renende stoffer i visse tilfælde kan binde sig kraftigt til jord-
partikler og derved medføre en reduceret biotilgængelighed.
H vis data ikke foreligger, regnes med samme biotilgænge-
lighed, som i de forsøg, der ligger til grund for T D I-
beregningen (dette kan typisk være forsøg, hvor teststoffet
er opblandet i foderet eller i drikkevandet).
18
”Biotilgængelighed” refererer i denne sammenhæng til det en-
gelske ”bioaccessibility”. Bioaccessibility beskriver den pool af
stoffet, som jorden kan frigive, og den indeholder således også let
bundne former.
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Lugt, udseende
Ud over rent sundhedsmæssige aspekter tages der ved fast-
sættelse af jordkvalitetskriteriet hensyn til, at jorden ikke må
lugte eller syne forurenet. D et vil sige, at jorden ikke ved
inspektion må afgive lugt fra forureningen eller se forurenet
ud (klumper af stof(fer) eller misfarvning. D er foreligger
ikke nøjere retningslinier for en sådan subjektiv vurdering.
M ed hensyn til lugt i forbindelse med afdampning henvises
til M iljøprojekt N r. 974 (2005) afsnit 7.4.3, der beskriver
anvendelsen af luftkvalitetskriteriet i forbindelse med af-
dampning af forurenende stoffer fra jord.
6.4 Ber egn in g af dr ikkevan dskval it et skr it er iet
Følgende fremgangsmåde anvendes ved beregning af drik-
kevandskvalitetskriteriet:
T DI x
f
──────────
hvor
E
drikkevand
KK
drikkevand
=
T D I: tolerabelt dagligt indtagelse (mg/ kg lgv/d)
f:
er den procentdel af T D I, der allokeres til indtagelse
af drikkevand
:
E
drikkevand
daglig eksponering for drikkevand, standard-
værdi:
1) 0,08 liter/ kg lgv/d (sv.t. 95-percentilen) for 1-10
årige børn. Anvendes i forbindelse med akutvir-
kende stoffer eller når hovedparten af T D I-værdien
benyttes til beregning af drikkevandskvalitetskriteri-
et.
2) 0,03 liter/ kg lgv/d (sv.t. medianværdi for 1-10 åri-
-6
ge
børn) i tilfælde hvor T D I er en 10 livs-
tidsrisikodosis for et kræftfremkaldende stof, eller i
tilfælde hvor kun en mindre andel af T D I-værdien
benyttes til beregning af drikkevandskvalitetskrite-
riet.
47
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Kemiske stoffer, der er særligt hudoptagelige, vil kunne
optages i en ikke uvæsentlig mængde i forbindelse med
badning, og stoffer, der let fordamper (for eksempel mange
opløsningsmidler), kan især ved brusebadning indåndes
som dampe/aerosoler. Omfanget af disse eksponeringsfor-
mer via brusebadning og karbadning afhænger af, hvor le-
toptageligt stoffet er gennem huden, og i hvor stor udstræk-
ning stoffet frigives ved fordampning fra vandet. D er bør
derfor i konkrete tilfælde (stoffer med høj hudgennemtræn-
gelighed og stoffer med høj flygtighed fra vandfasen), tages
højde for disse bidrag ved fastsættelse af drikkevandskvali-
tetskriteriet, således at den samlede optagelse via drikkevand
og badevand ikke overskrider den del af T D I, som er alloke-
ret til drikkevand.
D er er ikke opstillet konkrete modeller for beregningen af
sådanne bidrag, hvorfor bidragene må vurderes fra sag til
sag under inddragelse af de data og de vurderinger, der er
foretaget for det konkrete stof.
Lugt, smag, udseende
D rikkevandet må ikke lugte, smage eller syne forurenet og
smag, lugt og udseende af drikkevandet har en væsentlig
betydning, også selv om det ikke udgør en sundhedsfare i
relation til indtagelse af drikkevand.
D et vil i nogle tilfælde være lugt, smag, eller udseende, og
ikke stoffets sundhedsmæssige effekter, der er bestemmende
for værdien af drikkevandskvalitetskriteriet.
Lugt- og smagsgrænser, der findes opgivet i litteraturen,
kan variere voldsomt selvom de forskellige undersøgelser er
udført med samme stof. D ette skyldes, at metoder kan vari-
ere meget alt efter hvor, og hvornår de er blevet foretaget.
M edmindre lugt- og smagsgrænsen er bestemt ud fra nye
og meget velbeskrevne metoder, hvor kvalitet og pålidelig-
hed af undersøgelsen kan vurderes, anbefales det, at fastsæt-
telse af drikkevandskvalitetskriterier på baggrund af lugt og
smag foretages ud fra bestemmelse af lugt- og smagsgrænse
foretaget af et akkrediteret laboratorium.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Udgangspunktet for fastsættelse af et lugt- og smagsbaseret
kvalitetskriterium bør være et nul-effekt-niveau (N OEL) i
testpanelet, dvs. den koncentration hvor testpanelet som
helhed ikke kan lugte eller smage stoffet.
Ofte angives lugt- og smagsgrænser i vand på tilsvarende
måde som lugtgrænse i luft, dvs. det niveau, hvor 50 % af et
testpanelet kan lugte/smage stoffet. Angives således lugt-
grænsen i den tilgængelige litteratur som 50 %-grænsen
ganges denne værdi med 1/3 (som beskrevet under luftkva-
litetskriteriet), idet anvendelse af en sådan faktor skønnes at
sikre, at kun en mindre andel af befolkningen vil kunne for-
nemme stoffet ved dette niveau.
Ref er en cer
D K-T eknik (2001). Vurdering af lugttærskelværdier. Rap-
port udarbejdet for M iljøstyrelsen.
M iljøstyrelsen (2005). M iljøprojekt N r. 974. Principper for
sundhedsmæssig vurdering af kemiske stoffer med henblik
på fastsættelse af kvalitetskriterier for luft, jord og vand.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Bilag 1
Kvan t it at iv vur der in g ved ben yt t el se af
T25 ekst r apol at ion smet oden .
Anbefaling af T25-metoden
D er er udviklet forskellige metoder til beregning af, hvor
stor en risiko for udvikling af svulster en given eksponering
for et genotoksisk kræftfremkaldende stof udgør. Ens for
dem alle er at der anvendes en form for statistisk ekstrapola-
tion fra dosisniveauer med kendte eksperimentelle værdier
til de som regel meget lavere dosisniveauer, der oftest er
relevante i relation til den generelle befolknings eksponering
for kemiske stoffer i miljøet. M etoderne beskriver relationen
mellem den administrerede daglige dosis (eller koncentrati-
on) og den resulterende hyppighed af svulster.
Som anført i afsnit 5.3.2. anbefales det at anvende T 25-
ekstrapolering som beskrevet i en baggrundsrapport udar-
bejdet af en arbejdsgruppe i forbindelse med EU´s risiko-
vurderingsarbejde (EU-C ommission 1999).
T 25-metoden er blevet evalueret ved at sammenligne resul-
tater opnået ved denne metode med resultater opnået ved
anvendelse af US EPA´s LM S-metode (Linearised M ulti-
stage M odel) og ved LED
10
metoden, hvor der foretages
lineær ekstrapolation ned i lavdosisområdet ud fra en
benchmark-dosis på 10 % effektniveau (se afsnittene 5.3.2-
4 i M iljøprojekt N r. 974 (2005)). Ved gennemgang af resul-
taterne for lavdosis-estimaterne vurderede man at de er
sammenlignelige.
Ved sammenligning af one-hit metoden og T 25-metoden
vurderes de at medføre sammenlignelige værdier, idet ud-
gangspunktet for begge vurderingerne i princippet er at
anvende laveste dosis med signifikant respons, og herfra
50
 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
foretage lineær ekstrapolation ned i lavdosisområdet. I T 25-
metoden divideres med en skaleringsfaktor fra dyr til men-
neske opløftet i
¼
(sv.t. skalering i forhold til stofskiftet),
mens tilsvarende skaleringsfaktor i one-hit metoden er op-
løftet til 1/3 (sv.t. skalering i forhold til overfladeareal). D et-
te forhold alene vil maksimalt bevirke en forskel på de to
metoder på ca. en faktor 2.
Anvendelse af T25-metoden
T 25 defineres som den kroniske dosis (enhed: mg/kg le-
gemsvægt per dag), som vil give 25 % af forsøgsdyrene
svulster i et specifikt væv, efter korrektion for den spontane
hyppighed, inden for den standardiserede levetid af den
pågældende art.
T 25 beregnes med udgangspunkt i et langtidscancerstudie,
hvor den laveste dosis, der giver en signifikant forøgelse af
forsøgsdyr med svulster i et specifikt væv, som udgangs-
punkt anvendes ved beregningen af T 25. Forekomsten af
ondartede og godartede svulster sammenlægges, når de
godartede svulster må mistænkes for at kunne udvikles til
ondartede. H vis der er en højere hyppighed ved en højere
dosis, der giver en lavere T 25, anvendes sidstnævnte, med
mindre der er særlige begrundelser for ikke at tage ud-
gangspunkt i denne. H vis der er flere data- sæt, beregnes
T 25 for det mest relevante datasæt. H vis forskellige datasæt
giver T 25-værdier, som ligger inden for et relativt snævert
interval, anvendes gennemsnittet af disse T 25-værdier. H vis
sidstnævnte procedure ikke anvendes, skal rationalet for
anvendelse af en anden procedure begrundes nøje.
Beregning af T 25 foretages ved at gange dosis D (mg/kg
lgv/dag), hvor signifikant forøget antal svulster forekommer
med faktoren 0,25/p, hvor p er den aktuelle hyppighed af
svulster: T 25 = D x 0,25/p.
Ud fra denne T 25 foretages lineær ekstrapolation ned i lav-
dosisområdet, idet dosis svarende til et givent risikoniveau
beregnes ved simpel forholdsregning. En gennemsnitlig
-6
daglig dosis svarende til en øget livstidsrisiko på 10 kan
således beregnes på følgende måde:
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2259378_1865.png
D osis
(10-6 livstidsrisiko)
= 10 / 0,25 x T 25-dosis
Imidlertid indgår der i beregningerne også dosiskorrektion
med baggrund i en skaleringsfaktor mellem dyr og menne-
sker, og en faktor som angiver andelen af dyrenes levetid,
hvor eksponeringen har fundet sted.
Konkret kan T D I svarende til en 10 livstidsrisiko beregnes
ud fra følgende formel, når T 25 er beregnet ud fra forsøg
med oral eller dermal eksponering hos dyr:
-6
-6
I
t
x [L
e
/ L]
2
x [(T25 x l
e
) / L
e
]
TDI =
0,25 x [W
h
/ W
a
]
0,25
I
t
:
L
e
:
L:
T25:
Den tolerable livstidsrisiko (10
-6
).
Den aktuelle levetid for dyrene.
Den teoretiske gennemsnitslængde af levetiden for dyrene.
Beregnet daglig dosis (mg/kg legemsvægt per dag), der medfører en
25% forøget forekomst af tumorer hos forsøgsdyrene.
l
e
:
Eksponeringstid.
[W
h
/ W
a
]
0,25
: Dosiskorrektion på basis af stofskifte
hvor
W
h
:
Menneskets vægt i kg (sættes oftest til 70 kg).
W
a
:
Gennemsnitsvægt af det pågældende forsøgsdyr (kg).
L, L
e,
l
e
:
H vis eksponeringsvarigheden er kortere end standardleveti-
den for den pågældende art, eller hvis studiet afsluttes inden
standardlevetiden, foretages dosiskorrektion, som beskrevet
i den anførte formel. Standardlevetiden for mus, rotter og
hamstre sættes med mindre andet er angivet for den speci-
fikke stamme til 24 måneder.
Dosis ( T 25)
N år konkrete data ikke specifikt angiver dyrenes legems-
vægt, og dosis i mg/kg lgv/d i forbindelse med dosering
gennem foder eller drikkevand, anvendes følgende værdier i
beregningen:
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2259378_1866.png
Dyreart
Rotte
Mus
Marsvin
Kanin
Hund
Abe
Legemsvægt
(kg)
0,10 (ung)
0,40 (ældre)
0,020
0,75
2,0
10,0
5,0
Indtagelse af
foder
(g/ kg/ dag)
100
50
150
40
30
25
50
Indtagelse af
drikkevand
(ml/ kg/ dag)
75
-
-
-
-
-
(W
h
/W
a
)
Er stoffet givet oralt eller dermalt , foretages der en dosis-
korrektion for forskelle i kropsstørrelse mellem dyr og men-
nesker ved at omregne T 25 til den tilsvarende humane dosis
i mg/kg lgv./dag ved allometrisk skalering på basis af stof-
skiftet (afsnit 4.4.1.2). D enne skalering opnås ved at divide-
0,25
re T 25-dosis med faktoren (W
h
/W
a
)
Ved beregning ud fra inhalationsundersøgelse beregnes den
tolerable indåndingskoncentration T C ved anvendelse af
formlen:
0,25
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2259378_1867.png
I
t
x [L
e
/ L]
2
x [(T25 x l
e
) / L
e
]
TC =
0,25
I
t
:
L
e
:
L:
T25:
l
e
:
Den tolerable livstidsrisiko (10
-6
).
Den aktuelle levetid for dyrene.
Den teoretiske gennemsnitslængde af levetiden for dyrene.
Beregnet daglig dosis (mg/m
3
i indåndingsluften), der medfører en
25% forøget forekomst af tumorer hos forsøgsdyrene.
Eksponeringstid.
Ved indsættelse af T 25 anvendes koncentration i indån-
dingsluften og der foretages sædvanligvis omregning til en
gennemsnitligt indåndingskoncentration , hvis forsøget ikke
er udført med kontinuerlig eksponering. D ette gøres ved at
korrigere for antal timer pr. dag og antal dage pr. uge hvor
eksponeringen har fundet sted.
Ref er en cer
EU-C ommission (1999). G uidelines for quantitative risk
characterisation of non-threshold carcinogens in the frame-
work of Existing C hemicals following C ouncil Regulation
(EEC )
793/93. C ommission working G roup on the T echnical
M eetings for Risk Assessment for Existing Substances.
D ocument N O_N L/01/99_Rev.1
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Bilag 2
Baggr un d f or an ven dt e ekspon er in gsvæ dier ved be-
r
r egn in g af kval it et skr it er ier
I denne vejledning ændres praksis med hensyn til de ekspo-
neringsværdier, der anvendes ved beregning af kvalitetskri-
terierne for kemikalier.
T idligere har man i forbindelse med beregning af jordkvali-
tetskriterier som udgangspunkt antaget, at et barn dagligt
indtager 0,2 g jord/d (0,0002 kg/d), mens man ved bereg-
ning af luftkvalitetskriterier har anvendt et scenarie, hvor en
3
voksen person dagligt indånder 20 m luft. Ved beregning af
kvalitetskriterier for kemikalier i drikkevand har udgangs-
punktet været et dagligt indtag på 2 liter vand for en voksen.
Børn
Beskyttelse af børn er de senere år i stigende grad kommet i
fokus, og det har i den forbindelse været debateret i hvilken
udstrækning kvalitetskriterier beregnet ud fra voksnes ud-
sættelse i tilstrækkeligt omfang beskytter børn, da børn i
forhold til deres legemsvægt generelt indtager/ indånder en
større mængde drikkevand/ luft.
I miljøprojekt nr. 589 ”C hildren and the unborn child –
exposure and susceptibility to chemical subtances-” fra
2001, blev der foretaget en detaljeret gennemgang af børns
særlige følsomhed og udsættelsesmønster i forbindelse med
miljøforureninger og kemiske stoffer. I miljøprojektet kon-
kluderes, at der ved fremtidig fastsættelse af kvalitetskriterier
for kemikalier bør tages udgangspunkt i eksponeringsværdi-
er for børn, for at opnå at børn er fuldt omfattet af det be-
skyttelsesniveau, kvalitetskriteriet repræsenterer. D enne
vejledning indarbejder således ønsket om, at principperne
for fastsættelse af kvalitetskriterier tager hensyn til børns
særlige udsættelse.
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 L 42 - 2020-21 - Bilag 1: Høringssvar og høringsnotater, fra klima-, energi- og forsyningsministeren
Børns udsættelse vil således være udgangspunktet for de fremti-
dige standardværdier for eksponering i forbindelse med jord, luft
og drikkevand.
Standardværdien for børns legemsvægt vil i fremtiden være
13 kg.
Særligt udsatte undergrupper
Almindelig biologisk variation og forskellige former for ad-
færd vil betyde, at nogle grupper vil være mere udsatte end
andre for en given påvirkning via miljøet. D er er således
også med denne vejledning taget stilling til, i hvilken ud-
strækning kvalitetskriterier/grænseværdier for kemikalier skal
tage hensyn til de mere udsatte grupper i befolkningen.
N år kvalitetskriterier for kemikalier beregnes ved at anvende
eksponeringsværdier, der svarer til befolkningsvægtede gen-
nemsnitsværdier eller medianværdier, betyder dette, at ca.
halvdelen af den befolkning, som kvalitetskriteriet skal søge
at beskytte, vil kunne blive udsat for
større
eksponering end
udgangspunktet for beregningen (fx en T D I-værdi). H vis
sigtet med et kvalitetskriterium er, at størstedelen af befolk-
ningen skal være omfattet at det ønskede beskyttelsesniveau,
vil det således være nødvendigt at anvende en øvre fraktil-
værdi for befolkningens udsættelse.
D et skal nævnes, at de standardværdier der hidtil har været
anvendt for børn (jord) og voksne (luft og drikkevand) jf.
beskrivelsen af eksponeringsværdier, svarer til sådanne øvre
percentilgrænser.
Kvalitetskriterier for kemikalier skal fortsat sigte mod at
beskytte flertallet af befolkningen, dvs. også de mere udsatte
undergrupper. I de tilfælde hvor befolkningsfordelingen af
eksponeringerne kendes, vil valg af øvre eksponeringsværdi-
er typisk kunne foretages ved at tage udgangspunkt i værdi-
er svarende til 90- eller 95-percentilerne.
For at sikre særligt udsatte grupper anvendes følgende prin-
cipper :
a ) I situationer, hvor man ved beregning af kvalitetskriteriet
har tildelt hele T DI-værdien, hovedparten eller der er eksakt
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2259378_1870.png
viden om størrelsen af udsættelsen via det aktuelle medie, vil det
være nødvendigt at anvende øvre percentilgrænser for ekspone-
ring. Herved sikres at kun en mindre andel af befolkningen vil
blive eksponeret over T DI-niveau.
b)
I andre tilfælde, hvor der anvendes en reduceret T DI-værdi
som følge af anvendelse af en allokeringsfaktor (evt. en særlig
reduktionsfaktor), anvendes derimod medianværdier for udsæt-
telse med mediet. Dette forhold begrundes med, at anvendelse af
en allokeringsfaktor eller reduktionsfaktor sædvanligvs betyder
anvendelse af runde værdier (10 % eller 1% af T DI), som ofte
vil være på ”den sikre side”. I sådanne tilfælde, hvor der i forve-
jen er indbygget en øget grad af sikkerhed, vil det ikke være på-
krævet også at anvende en øvre percentilværdi for eksponering.
Anvendelse af en medianværdi vurderes her, at kunne opfylde
målet om at beskytte størstedelen af befolkningen.
c)
For kræftremkaldende stoffer uden tærskelværdi for effekt
foretages som tidligere nævnt ingen allokering af T DI. I disse
tilfælde anvendes medianværdier for eksponering ved beregning
af kvalitetskriteriet, idet T DI-værdien repræsenterer en daglig
dosis for en befolkningsvægtet gennemsnitlig livstidsrisikoforøgel-
se (en ekstrarisiko på 1 ud af 1 million udsatte over livstid),
hvorfor en gennemsnits-/medianværdi for befolkningens udsæt-
telse må være udgangspunktet.
Luft, daglig standardeksponering
I forbindelse med valg af standardeksponering for luft tages
der udgangspunkt i afsnit 6.1.1 i M iljøprojekt N r. 974
(2005). I dette afsnit vurderes US EPA´s eksponeringsvur-
deringer at udgøre det bedste grundlag. I EU´s risikovurde-
ringprogram for kemiske stoffer henvises ligeledes til de
amerikanske værdier.
Uddrag af tabel 6.1.1
Alder
Børn:
Under 1 år
1 – 2 år
Legemsvægt
(kg)
7.6
13
V
R
– gennemsnit
(m
3
/ dag)
4.5
6.8
V
R
– inaktiv
a
(m
3
/ dag)
2.35
4.16
V
R
- aktiv
(m
3
/ dag)
6.35
9.15
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2259378_1871.png
3 – 5 år
6 – 8 år
18
26
8.3
10
4.98
5.95
10.96
13.09
V
R
= Respirations V olumen som henholdsvis gennemsnit, inak-
tivitet og aktivitet.
Værdierne er alders- og kønsopdelte, men angivelserne om-
fatter ikke spredningen (fordelingen) i de enkelte alders-
grupper. D et er således ikke ud fra de forliggende data mu-
ligt at aflæse en 90- eller 95 percentilværdi for eksponerin-
gen af de forskellige aldersgrupper.
Som ovenfor nævnt vil der ved fastsættelsen af luftkvalitets-
kriterier blive taget hensyn til eksponeringen af børn.
Fra tabellen ses, at børn under 1 år i gennemsnit over et
3
3
døgn indånder 4,5 m svarende til 0,59 m /kg lgv/dag, mens
børn i aldersgruppen 1-2 år og 3-5 år indånder henholdsvis
3
3
6,8 m og 8,3 m (svarende til henholdsvis 0,52 og 0,46
3
m /kg lgv/dag). Især de 1-5 årige må anses at være udeakti-
ve.
På denne baggrund vil der ved beregning af luftkvalitetskri-
terier fremover blive anvendt en standardværdi for 1-5 årige
3
børn på 0,5 m luft/ kg lgv.
T il sammenligning kan nævnes at luftkvalitetskriteriet hidtil
er blevet beregnet ud fra et dagligt indåndingsvolumen på
3
0,3 m / kg lgv., idet udgangspunktet her var en voksen per-
3
son (70 kg), der dagligt indåndede 20 m luft.
Jord, daglig standardeksponering
M iljøprojekt N r. 974 (2005) sammenfatter i afsnit 6.1.2 den
seneste viden med hensyn til børns udsættelse for jord samt
anfører forskellige organisationers vurdering.
Ud fra en sammenfattende vurdering kan følgende ekspone-
ringsværdier for børn opstilles:
Eksponeringsvej
Oralt, maksimum enkeltindtag
Eksponeringsværdi
10 g
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2259378_1872.png
Oralt, dagligt gennemsnit
Oralt, 95-percentil
Hudkontakt, dagligt gennemsnit
Hudkontakt, maksimum
0,1 g/ d
0,2 g/ d
1 g/ d
10 g/ d
For børns indtag gennem munden fastsættes jordkvalitets-
kriteriet for akut toksiske stoffer ud fra et enkeltindtag på 10
g jord.
I tilfælde, hvor hele T D I eller hovedparten af T D I anvendes
til beregning af jordkvalitetskriteriet, tages der specifikt hen-
syn til særligt udsatte børn, idet der ved beregning af jord-
kvalitetskriteriet tages udgangspunkt i 95-percentilen for
udsættelse dvs. 0,2 g jord/d for herved at minimere risikoen
for at overskride T D I-værdien.
I andre tilfælde, hvor der kun anvendes en mindre del af
T D I-værdien til jordkvalitetskriteriet, anvendes ved bereg-
ningen af jordkvalitetskriteriet 0,1 g jord/d som et gennem-
sitligt standardindtag.
For kræftfremkaldende stoffer, hvor T D I svarer til en gen-
-6
nemsnitlig 10 livstidsrisikodosis blandt børn, anvendes 0,1
g jord/dag som udgangspunkt for beregning af jordkvalitets-
kriteriet.
Drikkevand, daglig standardeksponering
I M iljøprojekt N r. 974 (2005) i afsnit 6.1.3 gennemgås vi-
den om forskellige aldersgruppers indtagelse af drikkevand,
idet indtagelse både opgives for forskellige aldersgrupper og
fordelingen inden for disse (gennemsnitsværdier og 90-/95
percentiler). Beskrivelse i baggrundsrapporten omfatter
vurdering og anbefalingerne fra US EPA´s Exposure Fac-
tors H andbook.
Baggrundsrapporten henviser i forbindelse med børns ind-
tag af drikkevand til tabel 6.1.3 D , der angiver US EPA´s
anbefalede værdier:
Alder
Gennemsnit
(mean)
50 Percentil
90 Percentil
95 percentil
59
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Under 1 år
Under 3 år
3 – 5 år
1 – 10 år
0,30 liter/ dag
44 ml/ kg/ dag
0,61 liter/ dag
0,87 liter/ dag
0,74 liter/ dag
35 ml/ kg/ dag
0,24 liter/ dag
35 ml/ kg/ dag
0,65 liter/ dag
102 ml/ kg/ dag
1,5 liter/ dag
1,5 liter/ dag
0,76 liter/ dag
127 ml/ kg/ dag
0,66 liter/ dag
31 ml/ kg/ dag
1,3 liter/ dag
64 ml/ kg/ dag
1,5 liter/ dag
79,4 ml/ kg/ dag
For spædbørn angives medianindtaget at være 35 ml/ kg
lgv/d mens 95-percentilen angives at være på 127 ml/ kg
lgv/d. For børn i aldersgruppen 1-10 år anføres tilsvarende
en medianværdi på 31 ml/kg lgv./d og en 95-percentil på
79,4 ml/kg lgv./d.
Som standardværdi vurderes det mest relevant at anvende
værdien for 1-10 årige børn, idet evt. forskelle i vaner m.h.t.
amning i USA og D anmark kan have stor indflydelse på
drikkevandsindtagelse for spædbørn. Endelig dækker T D I-
begrebet alene moderens direkte eksponering og derved
barnets indirekte udsættelse gennem modermælken, og T D I
er således ikke formelt set beregnet til at dække spædbarnets
direkte udsættelse. G ennemsnitligt er indtagene dog direkte
sammenlignelige.
Ved beregning af drikkevandskvalitetskriteriet, hvor der ved
en given forureningskomponent er foretaget en allokering
på 100 % eller hovedparten af T D I til drikkevandet, eller i
situationer hvor den kritiske effekt er en akut toksisk effekt,
anvendes 95-percentilværdien for 1-10 årige børns indtag,
dvs. et dagligt indtag på 0,08 liter/ kg lgv/d. I disse situatio-
ner, vil drikkevandskvalitetskriteriet således også omfatte
spædbørns direkte udsættelse, idet dette også afspejler ind-
taget for børn under 1 år, som har en høj direkte udsættelse.
Ved beregning i andre situationer, hvor der er foretaget en
allokering på en mindre del af T D I til drikkevandskvalitets-
kriteriet (eller der er anvendt en reduktionsfaktor) anvendes
medianværdien for 1-10-åriges forbrug af drikkevand sv.t.
0,03 liter/ kg lgv/d. Allokeringen vil også betyde at spæd-
børns direkte udsættelse er omfattet af kvalitetskriteriet.
For kræftfremkaldende stoffer, hvor T D I svarer til en gen-
-6
nemsnitlig 10 livstidsrisikodosis blandt børn, anvendes
60
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kevandskvalitetskriteriet.
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Bilag 3
An ven dt e f or kor t el ser
BM D – BenchM ark D osis
D – dag
ED – Eksponerings D osis
EEC – European Economic C ommunity
EU – Europæiske Union
G LP – G ood Laboratory Practice
IARC – International Agency for Research on C ancer
IPC S – International Programme on C hemical Safety
KK – kvalitetskriterie
LED – Linear Ekstrapolations D osis
Lgv – legemsvægt
LM S – Linear M ultistage M odel
LOAEL – Lowest Observed Adverse Effect Level
LOEL – Lowest Observed Effect Level
N OAEL – N o Observed Adverse Effect Level
N OEL – N o Observed Effect Level
OEC D – Organisation for Economic C ooperation and D e-
velopment
PAH – Poly Aromatiske H ydrocarbon
QSAR – Quantitative Structure Activity Relationships
T D I – T olerabel D aglig Indtag (T olerabel D aglig Ekspone-
ring, el. T olerabel D aglig D osis)
T K – T olerabel Koncentration
UF – Usikkerheds Faktor
US EPA – United States Environmental Protection Agency
V
R
– indåndingsvolumen
WH O – World H ealth Organisation
W – Kropsvægt
62
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Generelt
Et helt grundlæggende princip i risikovurdering af miljøtoksiner er adskillelse af
risikovurdering og risikohåndtering.
Et grundlæggende princip er endvidere at Risikovurderingen skal foretages
foretages stricte på videnskabeligt grundlag, uden indflydelse af fra politiske
eller økonomiske interesser. På EU-niveau er dette bagrunden for oprettelsen
af de Europæiske argenturer, herunder EFSA og EEA.
EFSA og EEA foretager vurderinger uden indflydelse fra de politiske lag i EU, og
der er strenge krav til de eksterne eksperter argenturerne anvender for at sikre
mod inhabilitet, i form af politiske eller økonomiske interesser. Således indgår
eksempelvis ingen eksperter med relationer til industri-interessenter.
Når EU kommisionen støtter sig til vurdering fra en lille NGO (ICNIRP), frem for
vurderinger foretaget af EEA, bryder de herved med den normale praksis i EU.
Endvidere er størstedelen af medlemmerne i ICNIRP fysikere, og derfor ikke
fageksperter i forhold til biologiske effekter. Endelig er der ikke en tilsvarende
sikkerhed for inhabilitet, som normalt sikres i argenturernes vurderinger.
EEA har blandt andet i rapporten Late lessons fra 2013 anbefalet at
forsigtighedsprincippet tages i anvendelse i forhold til Radiofrekvent
Elektromagnetisk stråling. Citat (s. 38-39):
It is therefore very important that large scale
emerging technologies, such as biotechnologies, nanotechnologies and information and communication
technologies, apply the precautionary principle based on the experiences and lessons learned from these and
other case studies.
Dette dokument beskriver hvordan EFSA mener den videnskabelige evidens
bør vurderes:
https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2017.4971
https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/sp.efsa.2020.EN-1843
(inhabilitet=impartiality)
I forhold til risikovurdering vil der altid være data gaps, og der vil altid være
modstridende videnskabelige resultater.
http://www.efsa.europa.eu/en/methodology/guidance
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Som det fremgår af EFSAs dokumenter, er det en alvorlig fejl hvis der kræves
absolut bevis for effekt, herunder når ICNIRP eksempelvis afviser den meget
omfattende forskning som viser non-thermale biologiske effekter, med den
begrundelse mekanismen bag ikke fuldstændig forstået.
Som det fremgår af EFSAs dokumenter, er det derfor afgørende at den gruppe
forskere der udvælges til at vurdere evidensen er habile, og eventuelle
inhabilitet tages meget alvorlig. Dette er en af Agenturernes hovedopgaver.
Nationale vurderinger og myndighedernes håndtering
De nationale myndigheder (i DK SSI, FVST og MST) kan foretage risikovurdering
dels på vurderinger fra de Europæiske Argenturer, men kan også tage
risikovurderinger foretaget af nationale eksperter i betragtning. De nationale
risikovurderinger skal igen foretages af forskere, som ikke har økonomiske eller
politiske interesser, og der vil normalt være tale om eksperter på danske
universiteter. På Fødevareområdet foretages sådanne risikovurderinger af
Fødevareinstituttet DTU, mens Miljøstyrelsen får vurderinger fra flere af
universiteterne.
Ligesom i EU, blev risikovurdering og risikohåndtering adskilt i Danmark ved
udgangen af 2006, hvor sektorforskningsinstitutionerne (under ministerierne)
blev adskilt fra myndighederne og langt ind under universiteterne. Forskerne
har siden ikke været underlagt de myndigheder de rådgiver (med undtagelse af
SSI).
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https://www.eea.europa.eu/about-us
EEA
The European Environment Agency (EEA) is an agency of the European Union, whose task is
to provide sound, independent information on the environment. The EEA aims to support
sustainable development by helping to achieve significant and measurable improvement in
Europe's environment, through the provision of timely, targeted, relevant and reliable
information to policymaking agents and the public.
The European environment information and observation network (Eionet)
is a partnership
network of the EEA and its member and cooperating countries. Through Eionet, the EEA
brings together environmental information from individual countries concentrating on the
delivery of timely, nationally validated, high-quality data.
This knowledge is made widely available through the EEA website and forms the basis of
both thematic and integrated environmental assessments. This information serves to
support environmental management processes, environmental policymaking and
assessment, as well as citizen participation.
Rapport:
Late lessons from early warnings: science, precaution, innovation
https://www.eea.europa.eu/publications/late-lessons-2
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Kilde:
https://mst.dk/kemi/kemikalier/graensevaerdier-og-kvalitetskriterier/
Grænseværdier og kvalitetskriterier
Hver dag bliver vi mennesker udsat for et stort antal kemiske stoffer. Det
kan for eksempel ske gennem maden vi spiser, luften vi indånder, eller
vandet vi drikker. For at beskytte mennesker og miljø mod uacceptable
mængder af kemikalier, fastsætter Miljøstyrelsen grænseværdier - i form
af de såkaldte kvalitetskriterier - for mange stoffer.
Sundheds-kvalitetskriterier
Sundhedskvalitetskriteriene bliver brugt til at beskytte mennesker mod forurening fra
de mange kemikalier, som vi bruger og bliver udsat for i hverdagen. Se bl.a.
grænseværdier for luft, jord og vand, datablade samt baggrundsrapporter.
Miljø-kvalitetskriterier for forurenende stoffer i vandmiljøet
Miljøstyrelsen fastsætter kvalitetskriterier for forurenende stoffer i vandmiljøet (søer,
vandløb og havet). Kvalitetskriterierne bliver fastsat på baggrund af kemiske stoffers
effekter på de dyr og planter, der lever i vandet. Få digital adgang til information om
pt. 164 stoffer fordelt på 148 datablade.
https://mst.dk/kemi/kemikalier/graensevaerdier-og-kvalitetskriterier/sundhedskvalitetskriterier/
Sundhedskvalitetskriterier
Vi bruger mange kemikalier i vores hverdag. Derfor er det nødvendigt at beskytte mennesker
og miljø mod forurening fra disse. Til det formål bliver der fastsat grænseværdier - de
såkaldte kvalitetskriterier - for, hvilke koncentrationer af kemikalier, der må være i jord, luft,
spildevand og drikkevand.
Om grænseværdier
Grænseværdier bliver brugt til at beskytte mennesker og miljø mod forurening fra de mange
kemikalier, som vi bruger og bliver udsat for i hverdagen.
Grænseværdier for luft
Grænseværdier for kemikalier i luft bliver brugt til at begrænse og forebygge luftforurening
fra virksomheder, energiproduktion og affaldsforbrænding.
Grænseværdier for jord
Grænseværdier for kemikalier i jord bliver brugt, når man skal vurdere forurenet jord, rydde
op på forurenede grunde, og når man skal rådgive personer, der bor på lettere forurenede
grunde.
Grænseværdier for vand
Grænseværdier for kemikalier i grundvand og drikkevand bliver fastsat, så vores drikkevand
er sundhedsmæssigt forsvarligt at drikke, ser rent ud og er uden farve, smag eller lugt.
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Datablade for stoffer med luftkvalitetskriterier og B-værdier
Her finder du en liste over stoffer, hvor der i forbindelse med fastsættelsen af
kvalitetskriterier for luft og deraf følgende B-værdier er udarbejdet et datablad over stoffets
sundhedseffekter mv.
Baggrundsrapporter (kriteriedokumenter) for stoffer med luftkvalitetskriterier
Her finder du en liste over stoffer, hvor der i forbindelse med fastsættelsen af
kvalitetskriterier for luft er udarbejdet en baggrundsrapport.
Datablade for stoffer med jord- og drikkevandskvalitetskriterier
Her finder du en liste over stoffer, hvor der i forbindelse med fastsættelsen af
kvalitetskriterier for jord og/eller drikkevand er udarbejdet et datablad over stoffets
sundhedseffekter mv.
Baggrundsrapporter (kriteriedokumenter) for stoffer med jord- eller
drikkevandskvalitetskriterier
Her finder du en liste over stoffer, hvor der i forbindelse med fastsættelsen af
kvalitetskriterier for jord eller drikkevand er udarbejdet en baggrundsrapport.
https://mst.dk/kemi/kemikalier/graensevaerdier-og-
kvalitetskriterier/sundhedskvalitetskriterier/baggrundsrapporter-for-stoffer-med-jord-eller-
drikkevandskvalitetskriterier/
https://www2.mst.dk/Udgiv/publikationer/2006/87-7052-182-4/pdf/87-7052-182-4.pdf
Kvalitetskriterier for miljøfarlige forurenende stoffer i
vandmiljøet
Miljøstyrelsen fastsætter kvalitetskriterier for forurenende stoffer i
vandmiljøet (søer, vandløb og havet). Kvalitetskriterierne bliver fastsat på
baggrund af kemiske stoffers effekter på de dyr og planter, der lever i
vandet.
Miljøkvalitetskriterierne udgør den højeste koncentration af et forurenende stof, hvor
myndighederne vurderer, at det ikke giver skader på vandmiljøet. Kvalitetskriterierne
for vandmiljøet er baggrund for de lovmæssigt fastsatte miljøkvalitetskrav, som ligger
til grund for at begrænse spildevandsudledninger til vandmiljøet.
De lovfastsatte miljøkvalitetskrav fremgår af bekendtgørelse nr. 1625 af 19. december
2017 om fastlæggelse af miljømål for vandløb, søer, overgangsvande, kystvande og
grundvand,
se den på retsinformations hjemmeside.
Nedenfor findes en liste over stoffer, hvor der i forbindelse med fastsættelsen af
kvalitetskriterier for vand og/eller sediment og biota, er udarbejdet et datablad over
stoffets miljøeffekter mv.
Databladene fremstår med varierende layout, forord og logo grundet tidspunktet for
udarbejdelsen, og alle indeholder relevante informationer om kemikaliets fysisk-
kemiske egenskaber, giftighed og fastsættelse af miljøkvalitetskriterier.
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I databladene henvises til det vejledningsmateriale, som ligger til grund for
udarbejdelsen. Det drejer sig om relevant vejledning fra Miljøstyrelsen samt EU-
kommissionens vejledning
”Guidance document No. 27 Technical Guidance for
Deriving Environmetal Quality Standards”,
som har gennemgået opdateringer, hvilket
afspejles i databladene i forhold til miljøkvalitetskriteriernes udarbejdelse, samt for
hvilke matricer (vand, sediment og biota), der er fastsat miljøkvalitetskriterier for.
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EEA Report
No 1/2013
Late lessons from early warnings:
science, precaution, innovation
Summary
ISSN 1725-9177
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EEA Report
No 1/2013
Late lessons from early warnings:
science, precaution, innovation
Summary
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Cover design: EEA
Cover photos © EEA
Layout: EEA/Pia Schmidt
Copyright notice
© EEA, Copenhagen, 2013
Reproduction is authorised, provided the source is acknowledged, save where otherwise stated.
Information about the European Union is available on the Internet. It can be accessed through the Europa
server (www.europa.eu).
Luxembourg: Publications Office of the European Union, 2013
ISBN 978-92-9213-349-8
ISSN 1725-9177
doi:10.2800/70069
Environmental production
This publication is printed according to high environmental standards.
Printed by Rosendahls-Schultz Grafisk
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Tel.: +45 33 36 71 00
Fax: +45 33 36 71 99
Web: eea.europa.eu
Enquiries: eea.europa.eu/enquiries
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Contents
Contents
Acknowledgements .................................................................................................... 5
Preface ....................................................................................................................... 6
1 Introduction .......................................................................................................... 9
Part A Lessons from health hazards
2 The precautionary principle and false alarms — lessons learned ......................... 12
Steffen Foss Hansen and Joel A. Tickner
3 Lead in petrol 'makes the mind give way' ............................................................ 13
Herbert Needleman and David Gee
4 Too much to swallow: PCE contamination of mains water ................................... 14
David Ozonoff
5 Minamata disease: a challenge for democracy and justice ................................... 15
Takashi Yorifuji, Toshihide Tsuda and Masazumi Harada
6 Beryllium's 'public relations problem' .................................................................. 16
David Michaels and Celeste Monforton
7 Tobacco industry manipulation of research ........................................................ 17
Lisa A. Bero
8 Vinyl chloride: a saga of secrecy .......................................................................... 18
Morando Soffritti, Jennifer Beth Sass, Barry Castleman and David Gee
9 The pesticide DBCP and male infertility ............................................................... 19
Eula Bingham and Celeste Monforton
10 Bisphenol A: contested science, divergent safety evaluations ............................. 20
Andreas Gies and Ana M. Soto
11 DDT: fifty years since
Silent Spring......................................................................
21
Henk Bouwman, Riana Bornman, Henk van den Berg and Henrik Kylin
Part B Emerging lessons from ecosystems
12 Booster biocide antifoulants: is history repeating itself? ..................................... 22
Andrew R. G. Price and James W. Readman
13 Ethinyl oestradiol in the aquatic environment ..................................................... 23
Susan Jobling and Richard Owen
Late lessons from early warnings: science, precaution, innovation
3
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Contents
14 Climate change: science and the precautionary principle..................................... 24
Hartmut Grassl and Bert Metz
15 Floods: lessons about early warning systems ...................................................... 25
Zbigniew W. Kundzewicz
16 Seed-dressing systemic insecticides and honeybees ........................................... 26
Laura Maxim and Jeroen van der Sluijs
17 Ecosystems and managing the dynamics of change ............................................. 27
Jacqueline McGlade and Sybille van den Hove
Part C Emerging issues
18 Late lessons from Chernobyl, early warnings from Fukushima ............................ 28
Paul Dorfman, Aleksandra Fucic and Stephen Thomas
19 Hungry for innovation: from GM crops to agroecology ......................................... 29
David Quist, Jack A. Heinemann, Anne I. Myhr, Iulie Aslaksen and Silvio Funtowicz
20 Invasive alien species: a growing but neglected threat? ..................................... 30
Sarah Brunel, Eladio Fernández-Galiano, Piero Genovesi, Vernon H. Heywood, Christoph
Kueffer and David M. Richardson
21 Mobile phones and brain tumour risk: early warnings, early actions? .................. 31
Lennart Hardell, Michael Carlberg and David Gee
22 Nanotechnology — early lessons from early warnings ......................................... 32
Steffen Foss Hansen, Andrew Maynard, Anders Baun, Joel A. Tickner and Diana M. Bowman
Part D Costs, justice and innovation
23 Understanding and accounting for the costs of inaction ...................................... 33
Mikael Skou Andersen and David Owain Clubb
24 Protecting early warners and late victims............................................................ 34
Carl Cranor
25 Why did business not react with precaution to early warnings? .......................... 35
Marc Le Menestrel and Julian Rode
Part E Implications for science and governance
26 Science for precautionary decision-making ......................................................... 36
Philippe Grandjean
27 More or less precaution?...................................................................................... 37
David Gee
28 In conclusion ....................................................................................................... 38
A full version of the report can be found at:
http://www.eea.europa.eu/publications/late-lessons-2
4
Late lessons from early warnings: science, precaution, innovation
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Acknowledgements
Acknowledgements
This report has been prepared by the European
Environment Agency (EEA) with substantial
contributions from many external authors. The EEA
is particularly grateful to those authors who wrote
the case study chapters.
Originator of the
Late lessons from early warnings
project at the EEA was David Gee.
Acknowledgement is given to the editorial team:
David Gee, Philippe Grandjean, Steffen Foss
Hansen, Sybille van den Hove, Malcolm MacGarvin,
Jock Martin, Gitte Nielsen, David Quist and
David Stanners.
The EEA also thanks advisory board members who
have contributed their experience to the project
over many years: Joan Martinez Alier, Philippe
Bourdeau, Sylvaine Cordier, Sven Dammann,
Michael Depledge, Frans Evers, Silvio Funtowicz,
Thomas Jakl, Martin Krayer von Krauss, Owen
McIntyre, Jerome Ravetz, Nicolas de Sadeleer,
László Somlyódy, Sofia Vaz and Theo Vermeire.
Production support: Mike Asquith, John James
O'Doherty, Peter Saunders, Pia Schmidt and
Bart Ullstein.
Contributing authors: Jeroen Aerts, Maria Albin,
Mikael Skou Andersen, Iulie Aslaksen, Anders
Baun, Constança Belchior, Henk van den Berg,
Lisa A. Bero, Keith Beven, Eula Bingham, Riana
Bornman, Henk Bouwman, Diana M. Bowman,
Sarah Brunel, Michael Carlberg, Argelia Castaño,
Barry Castleman, David Owain Clubb, Charlie
Clutterbuck, Carl Cranor, Paul Dorfman, Eladio
Fernández-Galiano, Gary Fooks, Aleksandra Fucic,
Silvio Funtowicz, David Gee, Piero Genovesi,
Andreas Gies, Anna Gilmore, Philippe Grandjean,
Hartmut Grassl, Tee L. Guidotti, Nigel Haigh,
Steffen Foss Hansen, Mazazumi Harada, Lennart
Hardell, Jack A. Heinemann, Vernon H. Heywood,
Sybille van den Hove, James Huff, Susan Jobling,
Bill Kovarik, Christoph Kueffer, Zbigniew W.
Kundzewicz, Henrik Kylin, Malcolm MacGarvin,
Laura Maxim, Andrew Maynard, Jacqueline
McGlade, Owen McIntyre, Marc Le Menestrel,
Bert Metz, David Michaels, Erik Millstone, Celeste
Monforton, Anne I. Myhr, Herbert Needleman, Joy
Onasch, Richard Owen, David Ozonoff, Andrew
R.G. Price, David Quist, James W. Readman,
Johnny Reker, David M. Richardson, Julian Rode,
Christina Rudén, Jennifer Beth Sass, Richard
Schmuck, Noelle E. Selin, Jeroen van der Sluijs,
Katherine Smith, Morando Soffritti, Ana M. Soto,
Hans von Storch, Stephen Thomas, Joel A. Tickner,
Klement Tockner, Toshihide Tsuda, Pier Vellinga
and Takashi Yorifuji.
Case study chapters have been peer reviewed from a
broad range of perspectives. The EEA would like to
thank all institutions and experts who have given so
generously of their time and knowledge during the
peer review process.
The EEA would also like to thank Domingo Jiménez
Beltrán, Philippe Bourdeau, Jane Keys, Malcolm
MacGarvin, Andy Stirling and Brian Wynne for
being continuing sources of inspiration and ideas
throughout the process of producing both volumes of
Late lessons from early warnings.
The EEA would like to remember, with great
appreciation Poul Harremöes, chairman of the
editorial team for
Late lessons from early warnings
Volume 1, and Masazumi Harada, co-author of
Chapter 5 on Minamata disease, who worked
throughout his career on mercury pollution.
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Preface
Preface
An investment in knowledge pays the best interest
— Benjamin Franklin 'The
Way to Wealth'
(1758).
There is something profoundly wrong with the
way we are living today. There are corrosive
pathologies of inequality all around us — be they
access to a safe environment, healthcare, education
or clean water. These are reinforced by short-term
political actions and a socially divisive language
based on the adulation of wealth. A progressive
response will require not only greater knowledge
about the state of the planet and its resources, but
also an awareness that many aspects will remain
unknown. We will need a more ethical form of
public decision-making based on a language in
which our moral instincts and concerns can be
better expressed. These are the overall aims of
Volume 2 of
Late lessons from early warnings.
Volume 1 of
Late lessons from early warnings
was published at a time when the world was
experiencing an economic slowdown, China had
joined the World Trade Organization and western
Europe was still a 15-member Union. Global grain
production had declined for the third time in four
years due mainly to droughts in North America
and Australia, and the world saw major recalls
of contaminated meat, foot and mouth disease
and bovine spongiform encephalopathy (mad
cow disease). Global temperatures continued to
climb and many bird populations were in decline,
but the United States of America had rejected the
Kyoto Protocol. We were seeing ourselves through
the lens of the first human genome sequence, yet
we were trying to manage chemicals known to
be harmful to humans and ecosystems, through
international conventions and treaties such as the
Basel Convention to deal with toxic waste dumping
in the developing world; the OSPAR/HELCOM
Conventions to reduce the discharges, emissions and
the loss of hazardous substances into the sea and
the Montreal Protocol, to phase out ozone-depleting
substances. The destruction of the World Trade
Center had just happened.
Since then, we have witnessed a period of
extraordinary hubris. Most visibly, the financial
profligacy of the first decade of the century led
inexorably to the crises of 2007–2009 whereby
the major components of the international
financial system were weakened to the extreme by
indebtedness, mispriced products, lax monetary
policies and mis-engineered protection against
risks and uncertainty. The world experienced
more not less volatility. Political systems became
silted up by vested interests and a determination
by citizens to protect assets accumulated in
easier times, and beneath it all lay a deeper
environmental crisis epitomised by climate change
and biodiversity loss.
There was also a collapse of trust, not only in
financial institutions but in big companies, as
they abandoned staff, pensions and health care
schemes. Recent evidence from social psychology
has shown that despite rising levels of education
and innovation in products and services, people
trust only those they know and not strangers. As
Stephen Green said in
Good value: reflections on
money, morality, and an uncertain world
in 2009:
'There has been a massive breakdown of trust:
trust in the financial system, trust in bankers,
trust in business and business leaders, trust
in politicians, trust in the media, trust in the
whole process of globalisation — all have
been severely damaged, in rich countries and
poor countries alike'.
The scientific elites have also been slowly losing
public support. This is in part because of the
growing number of instances of misplaced
certainty about the absence of harm, which has
delayed preventive actions to reduce risks to
human health, despite evidence to the contrary.
Suddenly, our problems have grown into what
Charles W. Churchman in 1967 termed
wicked
problems
— difficult or impossible to solve because
of incomplete, contradictory and changing
requirements, difficult to recognize, resistant
to resolution because of the complexity of their
interdependencies and needing to be tackled not
by one but via many forms of social power. Solving
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Preface
them requires a new combination of hierarchical
power, solidarity and individualism.
What could this mean, for example, for the
100 thousand chemicals currently in commercial use?
To begin with we have more conventions and
treaties in place than a decade ago: the 2004
Rotterdam Convention on the Prior Informed
Consent (PIC) Procedure covering international
trade of 24 pesticides, four severely hazardous
pesticide formulations and 11 industrial chemicals;
the 2004 Stockholm Convention on Persistent
Organic Pollutants to protect human health and the
environment from substances which are highly toxic,
persistent, bio-accumulative and move long distances
in the environment, such as DDT, PCBs, various
industrial chemicals, and a set of unintentional
chemical by-products such as dioxin. But these
conventions only address the top-down hierarchical
approach to power.
At the same time Europe has put in place
legislation to achieve a global regulatory influence
including the EU Cosmetic Directive banning the
use of chemicals known or strongly suspected
of being carcinogens, reproductive toxins, or
mutagens causing cancer, mutation or birth defects;
the EU Restriction of Hazardous Substances
Directive, which restricts the use of hazardous
materials in the manufacture of various types
of electronic and electrical equipment including
lead, mercury, cadmium, hexavalent chromium,
the flame retardents polybrominated biphenyls
and polybrominated diphenyl ethers, and which
encourages the substitution to safe/or safer
alternatives in the electric and electronic equipment
industry; the closely linked 2006 EU Waste
Electrical and Electronic Equipment Directive for
collection, recycling and recovery of electrical
goods; the 2006 Strategic Approach to International
Chemicals Management (SAICM); and the 2007
EU Registration, Evaluation and Authorisation of
Chemicals, widely known as REACH, to assign
greater responsibility to industry to manage
the risks from chemicals and to provide safety
information on substances. The effects of these
regulatory tools are described in different chapters,
but once again point to the main economic actors
rather than communities or individuals.
One thing that has become clearer over the past
decade is that certain chemical substances are
highly stable in nature and can have long-lasting
and wide ranging effects before being broken
down into a harmless form. The risk of a stable
compound is that it can be bio-accumulated in
fatty tissues at concentrations many times higher
than in the surrounding environment. Predators,
such as polar bears, fish and seals, are known
to bio-magnify certain chemicals in even higher
concentrations with devastating consequences
for both humans and ecosystems. So exposure to
toxic chemicals and certain foodstuffs are at risk of
causing harm, especially to vulnerable groups such
as foetuses in the womb or during childhood when
the endocrine system is being actively built. Even
with small dose exposures, the consequences can
in some instances be devastating with problems
ranging from cancer, serious impacts on human
development, chronic diseases and learning
disabilities. Here the power to act could be more
properly set by well-informed individuals and
communities.
The relationship between knowledge and power
lies at the heart of Volume 2. In many chapters,
the implicit links between the sources of scientific
knowledge about pollutants, changes in the
environment and new technologies, and strong
vested interests, both economic and paradigmatic,
are exposed. A number of authors also explore
in greater depth, the short-sightedness of
regulatory science and its role in the identification,
evaluation and governance of natural resources,
physical and chemical hazards. By creating a
better understanding of these normally invisible
aspects, it is hoped that this volume will enable
communities and people to become more effective
stakeholders and participants in the governance of
innovation and economic activities in relation to
the associated risks to humans and the planet.
Much of what we are able to learn from the
histories of past environmental and public health
mistakes is also directly applicable to the better
regulation and governance of global institutions
and financial and economic risks. Robin G.
Collingwood argued in his
Autobiography
(1939),
that:
'History can offer something altogether
different from [scientific] rules, namely
insight. The true function of insight is to
inform people about the present…we study
history in order to see more clearly into the
situation in which we are called upon to act…
the plane on which, ultimately, all problems
arise is the plane of 'real' life: that to which
they are referred for their solution is history.'
In this volume, we go further. Whilst still drawing
lessons from such widely accepted tragedies
as leaded petrol, mercury poisoning in Japan's
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Preface
Minamata Bay and older pesticides which sterilised
many men who used it, we have ventured into the
uncertainties of potential yet contested harm, from
genetically modified products; nanotechnologies;
chemicals such as Bisphenol A; new pesticides
and mobile phones. There is also an examination
of the 80 or so potential 'false positives' where
there had been indications of harm but where it
was subsequently claimed that there were in fact
no risks to prevent: these cases too can provide
information that can help to improve future
decision-making about innovation and emerging
technologies.
A major part of effective decision-making lies in
the way issues are framed. In the case of climate
change, the first order question is whether it is
worth worrying about at all. US Vice President
Al Gore chose to make the question a matter of
choice between believers and sceptics. However,
problems arose when the public was asked to
make a scientific decision when too few people had
the qualifications to make any kind of reasoned
judgement. They were in fact asked to make a false
choice. Instead the question should have been
framed around which areas should people and
governments make decisions and which should be
delegated to experts.
In the end there are few certain and enduring
truths in the ecological and biological sciences, nor
in the economics, psychologies, sociologies and
politics that we use to govern them. One, however,
comes from the work of Elinor Ostrom, a late and
widely missed colleague, who showed from her
work on managing fisheries and ecosystems that
complex problems can be solved if communication
is transparent and open, visions are shared, trust is
high and communities are activated to work from
the bottom-up as well as from the top down.
As we navigate the Anthropocene, the epoch
named in recognition of our impact on the
planet, we will need to encourage more people to
become involved in solving the wicked problems
of our times. Whether through gathering local
information or becoming more aware of the
many uncertainties and unpredictabilities in our
surroundings, the power structures of knowledge
will need to change. And if we are to respond more
responsibly to the early warning signals of change,
we will need to re-design our style of governance
to one which reflects a future defined by the local
and specific rather than only the global and the
average. We hope that Volume 2 of
Late lessons from
early warnings
with its many lessons and insights
can help us all meet such a challenge.
Professor Jacqueline McGlade,
Executive Director
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Introduction
1 Introduction
Why further late lessons from early
warnings?
The 2013
Late lessons from early warnings
report is
the second of its type produced by the European
Environment Agency (EEA) in collaboration with a
broad range of external authors and peer reviewers.
Volume 1 of
Late lessons from early warnings: the
precautionary principle 1896–2000
published in 2001,
looked at the history of a selection of occupational,
public health and environmental hazards and
asked whether we could have been better at taking
action early enough to prevent harm. Twelve key
lessons for better decision-making were drawn
from cases where public policy was formulated
against a background of scientific uncertainty and
'surprises' — and where clear evidence of hazards
to people and the environment was often ignored
(see box on page 11).
The 14 case studies and 12 key lessons from the 2001
report remain highly pertinent today, and underline
four main reasons for a second report. The first
relates to expanding the late lessons approach to
consider long-known, important additional issues
with broad societal implications such as lead in
petrol, mercury, environmental tobacco smoke and
DDT, as well as issues from which lessons have
emerged more recently such as the effects of the
contraceptive pill on feminisation of fish and the
impacts of insecticides on honeybees.
The second concerns filling an acknowledged
gap in the 2001 report, by analysing the issue of
false positives where government regulation was
undertaken based on precaution but later turned
out to be unnecessary. Most of the cases examined
in the
Late lessons from early warnings
reports are
'false negatives' — instances where early warnings
existed but no preventive actions were taken.
The third reason is to address the rapid emergence
of new society-wide challenges such as radiation
from mobile phones, genetically-modified
products, nanotechnologies and invasive alien
species as well as if, how and where precautionary
actions can play a role.
The final reason relates to how precautionary
approaches can help manage the fast-changing,
multiple, systemic challenges the world faces
today, what new insights can be drawn in this
context and how these can underpin opportunities
for sustainable innovations and, supported
by information technologies, greater public
participation in their selection.
Overall approach
As for Volume 1, the approach in Volume 2 has
been to include a wide range of relevant case
studies produced by external authors along with
chapters written by members of the report's
editorial team (see acknowledgements section
for details). The relevant topics for case study
treatment were selected on the basis of advice
from the editor, in collaboration with the editorial
team and an advisory board, members of the
EEA Scientific Committee and the Collegium
Ramazzini (
1
).
The chapters in Volume 2 are grouped into
five parts: A. Lessons from health hazards;
B. Emerging lessons from ecosystems; C. Emerging
issues; D. Costs, justice and innovation; and
E. Implications for science and governance.
The chapters have been written by authors
who, to varying degrees, have had substantial
involvement in the subject area being addressed.
Indeed they would not have been approached if
(
1
) The Collegium Ramazzini is an independent, international academy founded in 1982 by Irving J. Selikoff, Cesare Maltoni and other
eminent scientists. Its mission is to advance the study of occupational and environmental health issues and to be a bridge between
the world of scientific discovery and the social and political centers, which must act on the discoveries of science to protect public
health.
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Introduction
they had not already extensively studied the case
that they were asked to write about. All of them, as
respected experts in their fields and in line with their
professional scientific training, were expected to be
as objective as possible in answering the questions
put to them by EEA. To support this, and to develop
consistency between chapters, the authors were
provided with seven structuring questions to be
followed when building their chapter.
The case studies have been peer-reviewed by
recognised experts in the respective fields who gave
of their time freely and provided their feedback
within a set of editorial guidelines provided by the
EEA.
Scope
The report has been designed, structured and
written in order to, inter alia, help politicians,
policymakers and the public to:
i
understand better the ways in which
scientific
knowledge
is financed, created, evaluated,
ignored, used and misused in taking timely and
precautionary decisions about how to reduce
harms, whilst stimulating benign innovations
and generating useful employment;
learn from some
very expensive 'mistakes'
in the past
so as to help societies make fewer
mistakes now, and in the future, especially with
some of the relatively new, largely unknown,
yet already widespread technologies like
nanotechnology and mobile phones;
Part A of the report commences with an analysis
of 'false positives' showing that these are few and
far between as compared to false negatives and
that carefully designed precautionary actions can
stimulate innovation, even if the risk turns out
not to be real or as serious as initially feared. The
remaining nine chapters address false negatives —
lead in petrol, perchlorethylene contaminated water,
Minamata disease, occupational beryllium disease,
environmental tobacco smoke, vinyl chloride,
dibromochloropropane (DBCP), Bisphenol A and
dichlorodiphenyltrichlorethane (DDT) — from
which three common themes emerge: there was
more than sufficient evidence for much earlier
action; slow and sometimes obstructive behaviour
by businesses whose products endangered
workers, the public and the environment; and the
value of independent scientific research and risk
assessments.
Part B focuses on emerging lessons from the
degradation of natural systems and their wider
implications for society — booster biocides, the pill
and the feminisation of fish, climate change, floods,
insecticides and honeybees as well as ecosystem
resilience more broadly. It considers, like its
predecessor, the issues of scientific evidence as the
basis for action/inaction, the multiple, often complex
factors and feedback loops in play, many of which
are not fully understood, as well as the interfaces
between science, policy and society and how all
actors can move together towards necessary actions
in the context of heightened systemic risks, and
substantial unknowns.
Part C analyses some newly emerging and
large-scale products, technologies and trends, which
potentially offer many benefits but also potentially
much harm to people and ecosystems and thereby
ultimately economic development. Cases addressed
include the Chernobyl and Fukushima nuclear
accidents; genetically modified agricultural crops
and agroecology; the growing threat of invasive
alien species; mobile phones and the risk of brain
tumours; and nanotechnologies. There is often little
science, and very little direct hindsight, to assist in
the management of these emerging technologies but
the lessons from the historical case studies need to
be applied if hazards are to be avoided.
The evidence from the chapters in Part C is that,
by and large, societies are not making the most
use of the costly lessons that can be gleaned
from their histories. A key question is how
this can be improved given the many reasons
identified from the case studies why taking
actions have been delayed including: the novel
ii
iii be aware of less visible, important factors such
as the skewed ways in which the
costs of actions
and inactions
for hazardous technologies
have been estimated, and the role that
some
businesses
have played in ignoring early
warnings and in manufacturing doubt about the
science supporting such warnings;
iv consider how the law, or administrative
arrangements, could be better used to deliver
justice, to those people (and ecosystems) that
have been, or could be, harmed
by poorly
designed, or badly deployed, innovations;
v
explore how best to
engage the public
in
helping to make
strategic choices over
innovations,
and their technological and
social pathways, as well as their involvement
in
ecosystems management
and in long term
monitoring through
citizen science.
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Introduction
and challenging nature of the issues themselves;
poorly or inconsistently evaluated information;
strong opposition by the corporate and scientific
establishments of the day; and the tendency by
the decision making institutions, practices and
cultures to favour the status quo and the short
term perspective. This section also illustrates the
value of bottom up as well as top down approaches
to innovations in ensuring that the directions of
technological pathways, the equitable distributions
of benefits, costs and knowledge ownership, and
the diversity of locally sensitive technological
options are relevant to the food, energy and
ecosystems crises.
The historical chapters illustrate numerous harms
which for the most part have been caused by
irresponsible corporations. This fact, coupled
with shortcomings in how decisions are made by
governments on when to act on early warnings,
and in the law when it comes to compensating
victims of harm, are analysed in three chapters
in Part D of the report. Each chapter analyses the
reasons behind prevailing practice and then goes
on to offer insights, for example, on how cost
calculation methods can be improved; on how
insurance schemes could be used to compensate
future victims of harm; and on the reasons why
businesses frequently ignore early warnings.
The cases in Parts A–D
form the basis for
considering in Part E the governance implications
for science, public policy and public engagement,
and how current practices could be improved
to enable society to maximise the benefits of
innovations while minimising harms. The main
insights are that science could be more relevant for
precautionary decision-making; that the wider use
of the precautionary principle can avert harm and
stimulate innovation; and that the late lessons of
history and precautionary approaches are highly
pertinent to today's multiple and inter-connected
crises — such as those arising from finance,
economics, the use of ecosystems, climate change,
and the use and supply of energy and food.
Finally, many of the historical and recent case
studies illustrate the value of engaging the public
in broadening the knowledge base and stimulating
robust innovations.
Twelve late lessons
Based on the case studies of Volume 1 of
Late lessons from early warnings
(EEA, 2001), twelve key lessons
for better decision-making were drawn:
1
2
3
4
5
6
7
Acknowledge and respond to ignorance, as well as uncertainty and risk, in technology appraisal and public policymaking
Provide adequate long-term environmental and health monitoring and research into early warnings
Identify and work to reduce 'blind spots' and gaps in scientific knowledge
Identify and reduce interdisciplinary obstacles to learning
Ensure that real world conditions are adequately accounted for in regulatory appraisal
Systematically scrutinise the claimed justifications and benefits alongside the potential risks
Evaluate a range of alternative options for meeting needs alongside the option under appraisal, and promote more robust,
diverse and adaptable technologies so as to minimise the costs of surprises and maximise the benefits of innovation
Ensure use of 'lay' and local knowledge, as well as relevant specialist expertise in the appraisal
Take full account of the assumptions and values of different social groups
8
9
10 Maintain the regulatory independence of interested parties while retaining an inclusive approach to information and opinion
gathering
11 Identify and reduce institutional obstacles to learning and action
12 Avoid 'paralysis by analysis' by acting to reduce potential harm when there are reasonable grounds for concern
Source:
EEA, 2001,
Late lessons from early warnings: the precautionary principle 1986–2000,
Environmental issues report
No 22, European Environment Agency.
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Part A — Summary
2 The precautionary principle and false
alarms — lessons learned
Steffen Foss Hansen and Joel A. Tickner
Most of the cases examined in the
Late lessons
from early warnings
reports are 'false negatives'
— instances where early warnings existed but
no preventive actions were taken. In debates
surrounding the precautionary principle it is
often claimed that widespread application of the
principle will lead to a large number of regulatory
false positives — over-regulation of minor risks
and regulation of non-existent risks, often due to
unwarranted public 'fears'. Understanding and
learning from past false positives as well as false
negatives is essential for improving decision-making
about public health and the environment.
This chapter reviews incidents of 'false positives',
where government regulation was undertaken based
on precaution but later turned out to be unnecessary.
In total 88 cases were identified to be alleged false
positives, however, following a detailed analysis
most of them turned out to be either real risks, or
cases where 'the jury is still out', or unregulated
alarms, or risk-risk trade-offs, rather than false
positives.
The analysis revealed four regulatory false
positives: US swine flu, saccharin, food irradiation,
and Southern leaf corn blight. Numerous important
lessons can be learned from each, although there
are few parallels between them in terms of when
and why each risk was falsely believed to be real.
This is a lesson in itself: each risk is unique, as
is the science and politics behind it and hence a
flexible approach is therefore needed, adapted
to the nature of the problem. The costs of the
false positives identified were mainly economic,
although the actions taken to address swine flu
in 1976 did lead to some unintended deaths and
human suffering, and diverted resources from
other potentially serious health risks. Determining
the net costs of mistaken regulatory action,
however, requires a complete assessment of the
impacts of the regulation, including the costs and
benefits of using alternative technologies and
approaches.
Overall, the analysis shows that fear of false
positives is misplaced and should not be a rationale
for avoiding precautionary actions where warranted.
False positives are few and far between as
compared to false negatives and carefully designed
precautionary actions can stimulate innovation, even
if the risk turns out not to be real or as serious as
initially feared. There is a need for new approaches
to characterising and preventing complex risks
that move debate from the 'problem' sphere to the
'solutions' sphere. By learning from the lessons in
this chapter, more effective preventive decisions can
be made in the future.
The scarcity of genuine false positives compared
to the large number of 'mistaken false positives'
could partly be the result of a deliberate strategy
in risk communication. Several references and
leaked documents have shown that some regulated
parties have consciously recruited reputable
scientists, media experts and politicians to call on
if their products are linked to a possible hazard.
Manufacturing doubt, disregarding scientific
evidence of risks and claiming over-regulation
appear to be a deliberate strategy for some industry
groups and think tanks to undermine precautionary
decision-making.
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Part A — Summary
3 Lead in petrol 'makes the mind give
way'
Herbert Needleman and David Gee
This chapter addresses the widespread use of
lead in petrol. It focuses on the period 1925–2005,
when leaded petrol was first widely marketed in
the US and then spread to the rest of the world
before being gradually phased out from the 1970s.
In Europe, the Aarhus Protocol (www.unece.org/
env/pp/treatytext.html) initiated the phase-out of
leaded petrol in the period 1998–2005.
The neurotoxic effects of lead were recognised as
far back as Roman times. And in 1925, at the 'one
day trial' of leaded petrol in the US, many experts
warned of the likely health impacts of adding lead
to petrol. Yet, despite the availability of an equally
effective alcohol additive which was assessed
by experts to be cleaner, the leaded route to fuel
efficiency was chosen in the US and then exported to
the rest of the world.
For several decades after the introduction of leaded
petrol, virtually no independent research was
carried out and the main source of information was
industry and industry-sponsored researchers. Not
until the 1960s and 1970s did independent scientists
from outside this group show, for example, that
body burdens of lead arising from human activities
were not 'normal', as industry claimed, but were
hundreds of times higher than before the industrial
revolution and were therefore likely to be harmful.
At its peak in the mid-1970s, leaded petrol released
about 200 000 tonnes of lead into the atmosphere
annually in both the US and Europe. Following
the subsequent phase-out, blood lead levels in
children (the most sensitive group exposed) quickly
fell, in line with the decrease in air concentrations.
The lessons nevertheless remain relevant globally
today. Although nearly all countries worldwide
had phased out leaded petrol by 2012, lead
concentrations in soils and sediments remain high.
Meanwhile, electronic wastes containing lead and
other contaminants also cause elevated blood lead
levels.
Supplementary panel texts focus on the events
leading up to the US choice of leaded petrol as
the primary fuel source in 1925 and more recent
accounts of EU policymaking on lead in petrol and
the road to phase-outs in Germany and the United
Kingdom.
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Part A — Summary
4 Too much to swallow: PCE
contamination of mains water
David Ozonoff
PCE (perchlorethylene, also known as 'perc' or
tetrachloroethylene), was used in the production of
plastic linings for drinking water distribution pipes
in the late 1960s and 1970s. This new and relatively
untested type of distribution pipe was used in over
700 miles of New England's water distribution
systems. Not until 1976 was it discovered that
PCE had been leaching into the water from the
pipe lining, causing widespread contamination of
water supplies that still today require continuous
remediation.
Before the pipes were put into production there
was a substantial amount of scientific information
available about the potential hazards of PCE. This
did not include current concerns about PCE's
carcinogenicity, teratogenicity and other health
consequences of relatively low-level exposure
upper most among today's concerns, but many
early warnings suggested the need for caution in
introducing PCE-based mains pipe linings.
PCE had been used to treat hookworm and data
on side effects were in the literature, while later
a variety of occupational users were studied,
including aircraft workers, small companies in
countries where biological monitoring was required,
and dry-cleaning firms. Several environmental
studies were also conducted to see if drinking
water contaminated with PCE or its close relative,
TCE (trichloroethylene), was associated with
cancer. Results were mixed and the chemical
industry consistently denied that PCE was a human
carcinogen.
This case study explores the early (pre 1970)
history researching the toxicity of the chemical. It
also focuses on the failure of one manufacturer,
Johns-Manville Corporation, to recognise the
warning signals about using a suspected toxic
substance. It examines why a new product was
deployed without thought to the public health
consequences and why evidence of the potential
hazard was ignored.
The science has not been hidden. It has been
ineffective in guiding and catalysing action.
Whether the problem is a failed duty of care or
a lack of clarity about what evidence will trigger
action, the contemporary argument over how to
interpret the scientific evidence is irresolvable
within science itself. There are no overarching
criteria from the philosophy of science that can
dictate a solution.
This chapter also includes two supplementary texts.
A panel that analyses the differences between the
conclusions of risk assessments based on the same
data, focusing in particular on assessments of PCE
and TCE. A further panel describes the opportunities
to switch to wet-cleaning technologies to reduce the
current use of PCE in dry cleaning.
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Part A — Summary
5 Minamata disease: a challenge for
democracy and justice
Takashi Yorifuji, Toshihide Tsuda and Masazumi Harada
Minamata disease, which can induce lethal or
severely debilitating mental and physical effects,
was caused by methylmercury-contaminated
effluent released into Minamata Bay by Chisso,
Japan's largest chemical manufacturer. It resulted
in widespread suffering among those who
unknowingly ate the contaminated fish. This chapter
documents the story in three phases.
The disease first came to prominence in the 1950s.
It was officially identified in 1956 and attributed to
factory effluent but the government took no action
to stop contamination or prohibit fish consumption.
Chisso knew it was discharging methylmercury
and could have known that it was the likely active
factor but it chose not to collaborate and actively
hindered research. The government concurred,
prioritising industrial growth over public health.
In 1968 Chisso stopped using the process that
caused methylmercury pollution and the Japanese
government then conceded that methylmercury was
the etiologic agent of Minamata disease.
The second part of the story addresses the discovery
that methylmercury is transferred across the
placenta to affect the development of unborn
children, resulting in serious mental and physical
problems in later life. Experts missed this at first
because of a medical consensus that such transfer
across the placenta was impossible.
The third phase focuses on the battle for
compensation. Initially, Chisso gave token
'sympathy money' under very limited criteria. In
1971 the Japanese government adopted a more
generous approach but after claims and costs soared
a more restrictive definition was introduced in
1977, justified by controversial 'expert opinions'.
Legal victories for the victims subsequently made
the government's position untenable and a political
solution was reached in 1995–1996. In 2003, the
'expert opinions' were shown to be flawed and the
Supreme Court declared the definition invalid in
2004.
In September 2011 there were 2 273 officially
recognised patients. Still, the continuing failure
to investigate which areas and communities were
affected means that the financial settlement's
geographic and temporal scope is still not properly
determined. Alongside deep-seated issues with
respect to transparency in decision-making and
information sharing, this indicates that Japan
still faces a fundamental democratic deficit in its
handling of manmade disasters.
This chapter is followed by three short updates
on the effects of mercury poisoning since
Minamata; on attempts to contain it, including
the 2009 global agreement to phase mercury out
of economic activity; and on the need for better
information about contaminant exposures to
enable policymakers to make informed choices that
balance the benefits of fish consumption against the
assumed adverse effects of low-level methylmercury
exposures.
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Part A — Summary
6 Beryllium's 'public relations problem'
David Michaels and Celeste Monforton
Scores of workers employed in nuclear weapons
production have been diagnosed with chronic
beryllium disease (CBD), a progressive and
irreversible inflammatory lung disease. This chapter
presents a history of knowledge and public policy
about preventing beryllium-related disease, focusing
primarily on the United States beryllium industry's
role in shaping US regulatory policy.
Over several decades increasingly compelling
evidence accumulated that CBD was associated
with beryllium exposure at levels below the existing
regulatory standard. The beryllium industry had a
strong financial incentive to challenge the data and
decided to be proactive in shaping interpretation
of scientific literature on beryllium's health effects.
It hired public relations and 'product defence'
consulting firms to refute evidence that the standard
was inadequate. When the scientific evidence
became so great that it was no longer credible to
deny that workers developed CBD at permitted
exposure levels, the beryllium industry responded
with a new rationale to delay promulgation of a
new, more protective exposure limit.
This case study underscores the importance of
considering the hazards from toxic materials
throughout the entire product life cycle. While
primary producers of beryllium products may be
able to control exposures in their own facilities, it is
unlikely that many secondary users and recyclers
have the expertise, resources and knowledge
necessary to prevent beryllium disease in exposed
workers and residents in nearby communities.
The primary lessons of this chapter are widely
applicable to many environmental health
controversies. In particular, it illustrates the practice
of 'manufacturing uncertainty' — a strategy used
by some polluters and manufacturers of hazardous
products to prevent or delay regulation or victim
compensation.
This chapter is followed by an analysis of the
rationale for corporate behaviour in the regulation
of beryllium. It is argued that the availability of
occasional and limited opportunities for companies
to change course without suffering onerous
consequences would encourage them to rethink their
position and create an obligation on shareholders
to take the responsible course. Although this may
be perceived as letting them 'get away with it', the
end result may be better public policy and corporate
responsibility.
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Part A — Summary
7 Tobacco industry manipulation of
research
Lisa A. Bero
This chapter differs in some ways from the others
in Volume 2 of
Late lessons from early warnings.
The
history of 'second hand', 'passive' or 'environmental
tobacco smoke' (ETS), to which non-smokers are
exposed overlaps with the history of active smoking.
Those affected include the partners and children of
smokers, and the bartenders and other workers who
have to work in smoky environments.
The focus in this chapter is on the strategies used
by the tobacco industry to deny, downplay, distort
and dismiss the growing evidence that, like active
smoking, ETS causes lung cancer and other effects
in non-smokers. It does not address the history
of scientific knowledge about tobacco and how it
was used or not used to reduce lung cancer and
other harmful effects of tobacco smoke. There is
much literature on this and a table at the end of the
chapter summarises the main dates in the evolution
of knowledge in this area.
The chapter concentrates on the 'argumentation'
that was used to accept, or reject, the growing
scientific evidence of harm. Who generated
and financed the science used to refute data on
adverse health effects? What were the motivations?
What kind of science and information, tools and
assumptions were used to refute data on the
adverse health of tobacco?
The release of millions of internal tobacco industry
documents due to law suits in the US has given
insights into the inner workings of the tobacco
industry and revealed their previously hidden
involvement in manipulating research. However,
this insight is not available for most corporate
sectors. The chapter discusses the possibilities of 'full
disclosure' of funding sources and special interests
in research and risk assessment in order to secure
independence and prevent bias towards particular
viewpoints.
While smoking bans are now being introduced
in more and more countries, other industries
are drawing inspiration from tobacco company
strategies, seeking to maintain doubt about
harm in order to keep hazardous products in the
marketplace.
The chapter also includes a summary of the tobacco
industry's role in shaping risk assessment in the US
and Europe to serve its own interests.
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Part A — Summary
8 Vinyl chloride: a saga of secrecy
Morando Soffritti, Jennifer Beth Sass, Barry Castleman and David Gee
This chapter is about how early warnings in the
1950s and 1960s concerning the short-term harm of
vinyl chloride (VC) to the skin and bones of workers,
and to the livers of laboratory animals, were initially
hidden from other workers and regulators. This
was despite some early misgivings by company
experts whose advice was initially ignored by their
employers. This pattern was repeated when the
later, more devastating news of a rare liver cancer
in workers was revealed by long-term animal
studies and by an attentive and concerned company
physician.
Unlike many other histories, however, this story
features a very prompt response from the global
chemical industry to the publication of the liver
cancer evidence, a response that included funding
cancer testing and later compliance with a large
reduction in the permissible exposure limits. The
case also provides early evidence of reproductive
effects of vinyl chloride monomer (VCM).
Other features of this story presage the later and
common responses of the corporate world to
heightened public awareness and pressure from
non-governmental organisations (NGOs) and trade
unions, including greatly exaggerated estimates of
the likely costs of complying with tighter pollution
controls; a frequent mismatch between the position
of the trade association and that of many, more
progressive companies within the association; but
also some relatively quick corporate responses to
public, NGO and regulatory pressure.
The chapter also features two legal aspects, which,
though more common in the US, are also valuable
for Europeans. First, the potentially positive role that
judicial review of regulatory proposals can play in
providing a societal judgement about the behaviour
of corporations. This can embrace not just moral
judgements but also judgements about the state of
the science and what society should do with it.
Second, the role that document discovery in
legal compensation cases can play in revealing
the real and until then secret activities of
corporations. Any proposals to promote justice
for victims of environmental and health harms
via no fault administrative arrangements need
to be accompanied by other measures to extract
information about corporate behaviour.
The chapter is followed by a panel analysing the
value of animal testing for identifying carcinogens.
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Part A — Summary
9 The pesticide DBCP and male infertility
Eula Bingham and Celeste Monforton
Dibromochloropropane (DBCP) is a pesticide used
against nematodes (roundworms or threadworms)
that damage pineapples, bananas and other tropical
fruits. It was introduced into US agriculture
in 1955 and approved for use as a fumigant in
1964. By 1961 laboratory experiments had shown
that it made the testicles of rodents shrink and
significantly reduced the quantity and quality of
sperm. Nonetheless, the compound was widely
marketed and became a commercial success.
In 1977, workers at a production plant became
worried that they were unable to father children.
An emergency study by a US government agency
discovered that in many cases the workers were
suffering from deficient or absent sperm. While
controls were improved at US facilities, the product
continued to be marketed and sprayed in Latin
America, the Philippines, some African countries,
and elsewhere.
By the 1990s, tens of thousands of plantation
workers in these countries had allegedly suffered
adverse reproductive effects from DBCP use.
The story continues today with contentious
legal claims for compensation, contamination of
drinking water and industry attempts to prevent
a Swedish documentary on the issue from being
screened.
This chapter looks at the knowledge available
about the hazards and the actions taken, or not
taken, to avert them. The DBCP story is significant
as it is the first clear example of reproductive
damage to workers who manufactured and used a
synthetic chemical. This is one of many examples
supporting the growing concerns about increasing
rates of reproductive and developmental disease,
and about the endocrine disrupting chemicals that
seem to be playing a role in these disorders.
Protecting production workers, users, consumers
and the environment from chemicals that may
damage reproduction demands closer integration
of scientific disciplines, as well as government
action. The lessons of DBCP may help in
ensuring timely protection from harm, based on
precautionary approaches to scientific evidence.
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Part A — Summary
10 Bisphenol A: contested science,
divergent safety evaluations
Andreas Gies and Ana M. Soto
Bisphenol A (BPA) is currently one of the world's
best-selling chemicals and primarily used to make
polycarbonate plastics. It is widely used in common
products such as baby bottles, household electronics,
medical devices and coatings on food containers. BPA
is known to mimic the female hormone oestrogen and
has been found to leach from the materials where it is
used.
Studies have suggested that even exposure to low
doses of BPA may cause endocrine disrupting
effects. As with other hormones, it appears that an
organism is most sensitive during development but
that effects are often not observed until much later
in the lifecycle. This means that at the time when the
effects become detectable, the chemical exposure has
vanished. This makes it extremely difficult to link
exposure to effects in humans.
This chapter maps some of the findings in studies of
rodents and humans. It also discusses the challenges
of evaluating scientific findings in a field where
industry-sponsored studies and independent
scientific research seem to deviate strongly. The
authors offer suggestions for ways to uncouple
financial interests from scientific research and testing.
A widely used and dispersed industrial chemical
like Bisphenol A is a controversial example
of an endocrine disrupting substance that
has implications for policymakers. Different
approaches to risk assessment for BPA by US and
European authorities are presented. It throws light
on the ways in which similar evidence is evaluated
differently in different risk assessments and
presents challenges for applying the precautionary
principle.
The intense discussion and scientific work on BPA
have slowly contributed to a process of improving
test strategies. While traditional toxicology has
relied on a monotonic increasing dose-response
relationship as evidence that the effect is caused by
the test agent, studies on BPA and other endocrine
disruptor chemicals (EDCs) have demonstrated the
limitations of this approach and adjustments have
been made in some cases.
It has also been widely accepted that effects
cannot be predicted by simply thinking of BPA as
a weak oestrogen and extrapolating from what is
observed for more potent endogenous oestrogens.
This lesson is particularly evident in the intense
pharmaceutical interest in selective oestrogen
response modifiers (SERMs).
The chapter is followed by a panel analysing the
value of animal testing for identifying carcinogens.
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Part A — Summary
11 DDT: fifty years since
Silent Spring
Henk Bouwman, Riana Bornman, Henk van den Berg and Henrik Kylin
'There was a strange stillness. The birds for example
— where had they gone? Many people spoke about
them, puzzled and disturbed. The feeding stations
in the backyards were deserted. The few birds seen
anywhere were moribund: they trembled violently
and could not fly. It was a spring without voices
... only silence lay over the fields and woods and
marsh.'
The book
Silent Spring
by Rachel Carson is mainly
about the impacts of chemicals (in particular
dichlorodiphenyltrichlorethane also known as DDT)
on the environment and human health. Indeed, the
close association between humans and birds remains
very apt. Representing the only two warm-blooded
groups of life on Earth, mammals and birds share
the same environments and threats.
Carson's claim that she lived in 'an era dominated
by industry, in which the right to make a dollar at
whatever cost is seldom challenged' still resonates
strongly with the problems that societies face all
over the world. One chapter heading, 'The obligation
to endure', derived from the French biologist and
philosopher Jean Rostand's famous observation that,
'the obligation to endure gives us the right to know'.
United States President John F. Kennedy responded
to the challenge posed by Carson by investigating
DDT, leading to its complete ban in the US. The
ban was followed by a range of institutions and
regulations concerned with environmental issues in
the US and elsewhere, driven by public demand for
knowledge and protection.
DDT was the primary tool used in the first global
malaria eradication programme during the 1950s
and 1960s. The insecticide is sprayed on the inner
walls and ceilings of houses. Malaria has been
successfully eliminated from many regions but
remains endemic in large parts of the world.
DDT remains one of the 12 insecticides — and
the only organochlorine compound — currently
recommended by the World Health Organization
(WHO), and under the Stockholm Convention
on Persistent Organic Pollutants, countries may
continue to use DDT. Global annual use of DDT
for disease vector control is estimated at more than
5 000 tonnes.
It is clear that the social conscience awakened by
Rachel Carson 50 years ago gave momentum to a
groundswell of actions and interventions that are
slowly but steadily making inroads at myriad levels.
Chapter 17 of her book, 'The other road' reminds the
reader of the opportunities that should have been
seized much earlier. With more than 10 % of bird
species worldwide now threatened in one way or
another, it is clear that we missed early warnings
or failed to act on them. Will we continue to miss
signposts to 'other roads'? Are our obligations to
endure met by our rights to know? As Carson said
50 years ago: 'The choice, after all, is ours to make.'
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Part B — Summary
12 Booster biocide antifoulants: is history
repeating itself?
Andrew R. G. Price and James W. Readman
Tributyltin (TBT) was widely used as an effective
antifouling agent in paints for ships and boats until
the European Community restricted its use in 1989
because of its proven harm to the environment
and shellfisheries. Thereafter, booster biocides
were introduced to enhance the performance of
antifouling paints. They were believed to be less
damaging to aquatic life than TBT. Subsequently,
however, it has been established that booster
biocides can also create significant environmental
risks.
This chapter outlines the background to booster
biocide use, the early warnings about their potential
physiological and ecological impacts on non-target
species, and the actions taken in response. The
science that set some alarm bells ringing is described,
along with lessons that could influence the future of
an industry still searching for less environmentally
invasive solutions.
Booster biocide antifouling agents threaten a variety
of habitats — from coral reefs and seagrass beds
to open moorings — within the EU and globally.
Their primarily herbicidal properties mean that
coral zooxanthellae, phytoplankton and periphyton
are particularly vulnerable. Compared to TBT, an
antifouling agent with a quite specific action, booster
biocides have more broad-spectrum impacts. The
wider ecological effect of shifting to booster biocides
remain poorly understood but of considerable
concern because they may affect the base of marine
food chains.
From a toxicological viewpoint, booster
biocides do not threaten to have endocrine
disrupting properties similar to TBTs. At current
environmental concentrations, however, some
can damage primary producers and some are
persistent. While legislation has been introduced
to control their use, the rigour of regulations varies
between countries. These geographical disparities
need to be addressed, and future biocidal products
and novel approaches to antifouling should be
better appraised.
For policymakers, the challenge is to protect
non-target biological communities from selective
change resulting from booster biocide use.
Persistence, bioaccumulative and toxic (PBT) criteria
can be used to evaluate the relative potential impact
from the available biocides, and consequently
target appropriate legislation. Nevertheless,
lateral thinking, aiming to identify novel materials
and strategies to address antifouling, could pay
dividends in the future.
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Part B — Summary
13 Ethinyl oestradiol in the aquatic
environment
Susan Jobling and Richard Owen
Many decades of research have shown that when
released to the environment, a group of hormones
known as oestrogens, both synthetic and naturally
occurring, can have serious impacts on wildlife. This
includes the development of intersex characteristics
in male fish, which diminishes fertility and
fecundity. Although often sublethal, such impacts
may be permanent and irreversible.
This chapter describes the scientific evidence
and regulatory debates concerning one of these
oestrogens, ethinyloestradiol (EE2), an active
ingredient in the birth control pill. First developed
in 1938, it is released to the aquatic environment
via wastewater treatment plants. Although it is
now clear that wildlife species are exposed to and
impacted by a cocktail of endocrine disrupting
chemicals, there is also reasonable scientific certainty
that EE2 plays a significant role, and at vanishingly
low levels in the environment.
In 2004 the Environment Agency of England and
Wales accepted this, judging the evidence sufficient
to warrant consideration of risk management.
In 2012, nearly 75 years after its synthesis, the
European Commission proposed to regulate EE2
as a EU-wide 'priority substance' under the Water
Framework Directive (the primary legislation for
protecting and conserving European water bodies).
This proposal was subsequently amended, delaying
any decision on a regulatory 'environmental quality
standard' until at least 2016.
This is in part because control of EE2 will come
at a significant price. Complying with proposed
regulatory limits in the environment means
removing very low (part per trillion) levels of EE2
from wastewater effluents at considerable expense.
Is this a price we are willing to pay? Or will the
price of precautionary action be simply too high
— a pill too bitter to swallow? To what extent is
society, which has enjoyed decades of flexible
fertility and will also ultimately pay for the control
and management of its unintended consequences,
involved in this decision? And what could this mean
for the many thousands of other pharmaceuticals
that ubiquitously infiltrate our environment and
which could have sublethal effects on aquatic
animals at similarly low levels?
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Part B — Summary
14 Climate change: science and the
precautionary principle
Hartmut Grassl and Bert Metz
The first scientifically credible early warning
about the possible dangers of climate change
due to carbon dioxide (CO
2
) emissions from
burning fossil fuels came in 1897. While the basic
physical principles of global warming are simple,
however, the more detailed science of climate
change is exceedingly complicated. Even now,
more than a hundred years since the first early
warning, many important details of climate change
cannot be predicted with certainty. It is therefore
unsurprising that the science of climate change and
questions about the true value of burning fossil
fuels have fostered sustained scientific and political
controversy.
When the first volume of
Late lessons from early
warnings
was drafted there appeared to be too
much legitimate controversy about climate change
for the issue to be included. A case study could
have led to arguments that distracted attention
from the valuable and robust lessons from more
established issues such as asbestos, polychlorinated
biphenyls (PCBs), chlorofluorocarbons (CFCs) and
the ozone-hole, X-rays and acid rain. This decision
was taken despite the then widespread acceptance
that 'the balance of evidence suggests a discernible
human influence on global climate' (Contribution
of
Working Group I to the Second Assessment Report of
the Intergovernmental Panel on Climate Change,
IPCC,
1995).
Over a decade later and after two more reviews by
the Intergovernmental Panel on Climate Change
(IPCC) of a much greater volume of climate change
science it seemed appropriate to include climate
change in this volume, despite some continuing
controversy. The evidence that human activities
are having a dangerous impact on the climate has
strengthened since 1995. By 2007, the IPCC was able
to conclude with 'very high confidence that the global
net effect of human activities since 1750 has been
one of warming'. Given the size and irreversibility
(on human time scales) of many of the harmful effects
of human-induced climate change, there is an urgent
need for action to reduce CO
2
emissions and other
greenhouse gases. Some contrarian views persist,
however, as the authors illustrate.
This chapter summarises the history of growing
knowledge about human-induced climate
change and of the main actions, or inactions that
accompanied it. Like many other chapters, it
reflects the lifelong commitment of both authors
to trying to understand and mitigate the effects of
human-induced climate change. It concludes with
some lessons and insights that are relevant to many
other environmental and health issues.
Also included is a panel text describing how the
IPCC's approach to assessing uncertainty evolved
between its first to its fifth assessment reports.
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Part B — Summary
15 Floods: lessons about early warning
systems
Zbigniew W. Kundzewicz
Floods are an increasingly acute problem. Intense
precipitation has become more frequent and more
intense, growing manmade pressure has increased
the magnitude of floods that result from any level
of precipitation, and flawed decisions about the
location of human infrastructure have increased the
flood loss potential.
Unlike most other case studies presented in this
report, this chapter focuses on flooding as a
phenomenon and the requirements for effective
early warning systems, rather than addressing
a particular event and the lessons that can be
learned.
Flooding cannot be wholly prevented. The
occurrence of a flood need not be considered a
'failure' and, conversely, minimisation of losses
may constitute a 'success'. There are lessons to
be learned from every flood and it is important
to use them in preparing for the next flood. Once
we accept that no flood protection measures can
guarantee complete safety, a general change of
paradigm is needed to reduce human vulnerability
to floods. The attitude of 'living with floods' and
accommodating them in planning seems more
sustainable than hopelessly striving to eradicate
them.
Flood forecasting and warning systems fail because
links in the chain perform poorly or fail completely.
A single weak point in a system that otherwise
contains excellent components may render the
overall system performance unsatisfactory.
A successful system requires sufficient integration
of components and collaboration and coordination
between multiple institutions.
The chapter deals primarily with the challenges of
fluvial (river) floods. It is complemented by three
short supplementary texts. The first highlights
the complex, dynamic and diverse ecosystems of
river floodplains, which are often degraded during
construction of flood defences. Despite their huge
economic value, near-natural floodplains are
among the most threatened ecosystems globally.
The second discusses uncertainties in anticipating
rainfall patterns and intensity, and their
relationship to flood levels during extreme flows.
Such uncertainties present challenges for scientists
and decision-makers alike.
The third addresses the increasing risks of coastal
flooding due to factors such as climate change and
sea-level rise, and reviews European experience
with precautionary action.
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Part B — Summary
16 Seed-dressing systemic insecticides and
honeybees
Laura Maxim and Jeroen van der Sluijs
In 1994 French beekeepers began to report alarming
signs. During summer, many honeybees did not
return to the hives. Honeybees gathered close
together in small groups on the ground or hovered,
disoriented, in front of the hive and displayed
abnormal foraging behaviour. These signs were
accompanied by winter losses.
Evidence pointed to Bayer's seed-dressing systemic
insecticide Gaucho
®
, which contains the active
substance imidacloprid. This chapter presents
the historical evolution of evidence on the risks
of Gaucho
®
to honeybees in sunflower and maize
seed-dressing in France, and analyses the actions in
response to the accumulating evidence regarding
these risks.
The social processes that ultimately lead to
application of the precautionary principle for
the ban of Gaucho
®
in sunflower and maize
seed-dressing are described, with a focus on the
ways in which scientific findings were used by
stakeholders and decision-makers to influence
policy during the controversy.
Public scientists were in a difficult position in this
case. The results of their work were central to a
social debate with high economic and political
stakes. In certain cases their work was not judged
according to its scientific merit but based on
whether or not it supported the positions of some
stakeholders. This situation tested the ability and
courage of researchers to withstand pressure and
continue working on imidacloprid.
Other European countries also suspended
neonicotinoid seed-dressing insecticides. Evidence
of the toxicity of neonicotinoids present in the dust
emitted during sowing of coated seeds supported
such decisions. Most important, the French case
highlighted the major weaknesses of regulatory
risk assessment and marketing authorisation of
pesticides, and particularly neonicotinoids. These
insights were recently confirmed by work by the
European Food Safety Authority.
From this case study eight lessons are drawn about
governance of controversies related to chemical
risks. The study is followed by two additional
texts. A first panel presents Bayer Crop Science's
comments on the analysis in this chapter. A second
contains the authors' response to the Bayer
comments.
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Part B — Summary
17 Ecosystems and managing the
dynamics of change
Jacqueline McGlade and Sybille van den Hove
A decade after Rachel Carson's
Silent Spring
was
published, describing the toxic legacy of the
twentieth century, Annie Dillard in her Pulitzer
prize winning book
Pilgrim at Tinker Creek,
opened up a different way of looking at the
world. It presaged a twenty first century in which
the global economy would be based on a more
thorough understanding of nature, its functioning
and material wealth. Wholly descriptive, yet
increasingly relevant, her book captured the very
essence of what this chapter is about: that amongst
the observations which routinely help to predict
the evolution of the natural world are the seeds of
surprise — surprise of the unusual and surprise
as a portent of future change. Our systemic failure
to anticipate such surprises forms the core of this
chapter. A series of case studies from fisheries,
forests, savannah and aquatic systems are used to
underline how early warnings about changes in
these natural systems emerged but were not used.
The chapter highlights how the division of
knowledge into political, disciplinary and
geographic silos has led to the 'recurring
nightmares' of short-term interests outcompeting
long-term vision; situations where competition
replaces co-operation; fragmentation of values
and interest; fragmentation of authority and
responsibility; and fragmentation of information
and knowledge leading to inadequate solutions
or even additional problems. In addition, the
lack of institutional fit has often confounded the
effectiveness of the stewardship of ecosystem
services, and led to unexpected surprises, excessive
rent seeking and high transaction costs.
Using counterfactual thinking (i.e. the dependence
of
whether, when
and
how
one event occurs on
whether, when
and
how
another event occurs and the
possible alteration of events), built around the four
interconnected concepts of
planetary boundaries,
tipping points, panarchy
and
resilience,
the chapter
provides an analytical lens through which to
explore why many of the warning signals were
not seen. The chapter concludes by suggesting
why ecosystems are likely to be even more at risk
in the future and why we will need to observe
and interpret the dynamics of both nature and
institutions ever more closely if we are to avoid
sudden irreversible ecological changes.
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Part C — Summary
18 Late lessons from Chernobyl, early
warnings from Fukushima
Paul Dorfman, Aleksandra Fucic and Stephen Thomas
The nuclear accident at Fukushima in Japan occurred
almost exactly 25 years after the Chernobyl nuclear
accident in 1986. Analysis of each provides valuable
late and early lessons that could prove helpful to
decision-makers and the public as plans are made
to meet the energy demands of the coming decades
while responding to the growing environmental costs
of climate change and the need to ensure energy
security in a politically unstable world.
This chapter explores some key aspects of the
Chernobyl and Fukushima accidents, the radiation
releases, their effects and their implications for
any construction of new nuclear plants in Europe.
There are also lessons to be learned about nuclear
construction costs, liabilities, future investments
and risk assessment of foreseeable and unexpected
events that affect people and the environment.
Since health consequences may start to arise from
the Fukushima accident and be documented over
the next 5–40 years, a key lesson to be learned
concerns the multifactorial nature of the event. In
planning future radiation protection, preventive
measures and bio-monitoring of exposed
populations, it will be of great importance to
integrate the available data on both cancer and
non-cancer diseases following overexposure to
ionising radiation; adopt a complex approach to
interpreting data, considering the impacts of age,
gender and geographical dispersion of affected
individuals; and integrate the evaluation of latency
periods between exposure and disease diagnosis
development for each cancer type.
Given the degree of uncertainty and complexity
attached to even the most tightly framed and
rigorous nuclear risk assessment, attempts to
weight the magnitude of accident by the expected
probability of occurrence have proven problematic,
since these essentially theoretical calculations
can only be based on sets of pre-conditioning
assumptions. This is not an arcane philosophical
point but rather a very practical issue with
significant implications for the proper management
of nuclear risk. With its failure to plan for the
cascade of unexpected beyond design-base
accidents, the regulatory emphasis on risk-based
probabilistic assessment has proven very limited.
An urgent reappraisal of this approach and its
real-life application seems overdue.
Whatever one's view of the risks and benefits of
nuclear energy, it is clear that the possibility of
catastrophic accidents and consequent economic
liabilities must be factored into the policy and
regulatory decision-making process. In the context
of current collective knowledge on nuclear risks,
planned pan-European liability regimes will need
significant re-evaluation.
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Part C — Summary
19 Hungry for innovation: from GM crops
to agroecology
David A. Quist, Jack A. Heinemann, Anne I. Myhr, Iulie Aslaksen and Silvio Funtowicz
Innovation's potential to deliver food security
and solve other agriculture-related problems is
high on the agenda of virtually all nations. This
chapter looks at two different examples of food and
agricultural innovation: genetically modified (GM)
crops and agroecological methods, which illustrate
how different innovation strategies affect future
agricultural and social options.
GM crops are well suited to high-input
monoculture agricultural systems that are highly
productive but largely unsustainable in their
reliance on external, non-renewable inputs.
Intellectual property rights granted for GM crops
often close down, rather than open up further
innovation potential, and stifle investment into a
broader diversity of innovations allowing a greater
distribution of their benefits.
Science-based agroecological methods are
participatory in nature and designed to fit within
the dynamics underpinning the multifunctional
role of agriculture in producing food, enhancing
biodiversity and ecoystem services, and providing
security to communities. They are better suited to
agricultural systems that aim to deliver sustainable
food security than high external input approaches.
They do, however, require a broader range of
incentives and supportive frameworks to succeed.
Both approaches raise the issue of the governance
of innovation within agriculture and more generally
within societies.
The chapter explores the consequences of a
'top-down transfer of technology' approach
in addressing the needs of poor farmers. Here
innovation is often framed in terms of economic
growth in a competitive global economy, a focus
that may conflict with efforts to reduce or reverse
environmental damage caused by existing models
of agriculture, or even deter investment into socially
responsible innovation.
Another option explored is a 'bottom-up' approach,
using and building upon resources already
available: local people, their knowledge, needs,
aspirations and indigenous natural resources. The
bottom-up approach may also involve the public
as a key actor in decisions about the design of food
systems, particularly as it relates to food quality,
health, and social and environmental sustainability.
Options are presented for how best to answer
consumer calls for food quality, sustainability and
social equity in a wide sense, while responding to
health and environmental concerns and securing
livelihoods in local small-scale agriculture. If we
fail to address the governance of innovation in
food, fibre and fuel production now, then current
indications are that we will design agriculture to fail.
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Part C — Summary
20 Invasive alien species: a growing but
neglected threat?
Sarah Brunel, Eladio Fernández-Galiano, Piero Genovesi, Vernon H. Heywood, Christoph Kueffer and
David M. Richardson
Biological invasions are one of the five major causes
of biodiversity loss as global human travel and
trade have moved, and continue to move, thousands
of species between and across continents. Some
species of alien origin have a high probability of
unrestrained growth which can ultimately lead to
environmental damage.
An alien species — animal, plant or microorganism
— is one that has been introduced, as a result of
human activity, either accidentally or deliberately,
to an area it could not have reached on its own.
A common definition of the term 'invasive'
focuses on its (negative) impact, while other
definitions consider only rate of spread and exclude
considerations of impact.
Despite the growing amount of legislation being
adopted at the global scale, biological invasions
continue to grow at a rapid rate, with no indication
yet of any saturation effect. Decision-making in this
area is very challenging. The overall complexity
of the problem, its interdisciplinarity, the scientific
uncertainties and the large number of stakeholders
that need to be informed and involved, together
demand governance actions that are difficult to see
emerging at the regional scale (as in the EU), let
alone globally.
It is widely agreed that preventing biological
invasions or tackling them at a very early stage
is the most efficient and cost-effective approach.
Harmless species can be confused with harmful
invasive species, however, leading to a waste of
resources. Even more seriously, harmful invaders
can be mistaken for innocuous species — so-called
'invaders in disguise' — and no appropriate action
may be taken to counter the threats they pose.
Even with a very good risk assessment system, new
outbreaks of invasive alien species could still occur,
necessitating a system of rapid early warning
and effective eradication response. The decision
on where to draw the line on the acceptable
environmental risks versus the introduction of
new species or new communities that may carry
invasive alien species then becomes a value
judgement.
There is lively debate within the scientific
community regarding the most appropriate
strategies for managing invasive alien species.
Governments and institutions charged with making
decisions have access to considerable knowledge
on the topic, but the lack of rules of interactions
between multiple parties regularly thwarts effective
decision-making.
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Part C — Summary
21 Mobile phones and brain tumour risk:
early warnings, early actions?
Lennart Hardell, Michael Carlberg and David Gee
In 2011 the World Health Organization's
International Agency for Research on Cancer (IARC)
categorised the radiation fields from mobile phones
and other devices that emit similar non-ionizing
electromagnetic fields (EMFs), as a Group 2B
i.e. 'possible' human carcinogen. Nine years earlier
IARC gave the same classification to the magnetic
fields from overhead electric power lines.
The IARC decision on mobile phones was
principally based on two sets of case-control human
studies of possible links between mobile phone use
and brain tumours: the IARC Interphone study
and the Hardell group studies from Sweden. Both
provided complementary and generally mutually
supportive results. This chapter gives an account
of the studies by these two groups — and others
coming to different conclusions — as well as reviews
and discussions leading up to the IARC decision
in 2011. The chapter also describes how different
groups have interpreted the authoritative IARC
evaluation very differently.
There are by now several meta-analyses and reviews
on mobile phones and brain tumours, which
describe the challenges of doing epidemiology on
this issue, the methodological limitations of the
major studies published so far and the difficulties of
interpreting their results.
It has been suggested that national incidence data
on brain tumours could be used to qualify or
disqualify the association between mobile phones
and brain tumours observed in the case-control
studies. However, in addition to methodological
shortcomings, there might be other factors that
influence the overall incidence rate such as changes
in exposure to other risk factors for brain tumours
that are unknown in descriptive studies. Cancer
incidence depends on initiation, promotion and
progression of the disease. As the mechanism for
radiofrequency electromagnetic fields carcinogenesis
is unclear, it supports the view that descriptive data
on brain tumour incidence is of limited value.
The chapter points to mobile phone industry inertia
in considering the various studies and taking the
IARC carcinogenic classification into account and
a failings from the media in providing the public
with robust and consistent information on potential
health risks. The IARC carcinogenic classification
also appears not to have had any significant impact
on governments' perceptions of their responsibilities
to protect public health from this widespread source
of radiation.
The benefits of mobile telecommunications are
many but such benefits need to be accompanied
by consideration of the possibility of widespread
harms. Precautionary actions now to reduce head
exposures would limit the size and seriousness of
any brain tumour risk that may exist. Reducing
exposures may also help to reduce the other possible
harms that are not considered in this case study.
Evidence is increasing that workers with heavy
long-term use of wireless phones who develop
glioma or acoustic neuroma should be compensated.
The first case in the world was established on
12 October 2012. The Italian Supreme Court affirmed
a previous ruling that the Insurance Body for Work
(INAIL) must grant worker's compensation to a
businessman who had used wireless phones for
12 years and developed a neuroma in the brain.
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Part C — Summary
22 Nanotechnology — early lessons from
early warnings
Steffen Foss Hansen, Andrew Maynard, Anders Baun, Joel A. Tickner and Diana M. Bowman
Nanotechnology is the latest in a long series of
technologies heralded as ushering in a new era of
technology-driven prosperity. Current and future
applications of nanotechnology are expected to lead
to substantial societal and environmental benefits,
increasing economic development and employment,
generating better materials at lower environmental
costs, and offering new ways to diagnose and treat
medical conditions. Nevertheless, as new materials
based on nanoscale engineering move from the lab
to the marketplace, have we learnt the lessons of
past 'wonder technologies' or are we destined to
repeat past mistakes?
This chapter first introduces nanotechnology,
clarifies the terminology of nanomaterials and
describes current uses of these unique materials.
Some of the early warning signs of possible adverse
impacts of some nanomaterials are summarised,
along with regulatory responses of some
governments. Inspired by the EEA's first volume
of
Late lessons from early warnings,
the chapter looks
critically at what lessons can already be learned,
notwithstanding nanotechnology's immaturity.
Nanotechnology development has occurred in
the absence of clear design rules for chemists and
materials developers on how to integrate health,
safety and environmental concerns into design.
The emerging area of 'green nanotechnology' offers
promise for the future with its focus on preventive
design. To gain traction, however, it is important
that research on the sustainability of materials
is funded at levels significant enough to identify
early warnings, and that regulatory systems
provide incentives for safer and sustainable
materials.
Political decision-makers have yet to address many
of the shortcomings in legislation, research and
development, and limitations in risk assessment,
management and governance of nanotechnologies
and other emerging technologies. As a result,
there remains a developmental environment that
hinders the adoption of precautionary yet socially
and economically responsive strategies in the field
of nanotechnology. If left unresolved, this could
hamper society's ability to ensure responsible
development of nanotechnologies.
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Part D — Summary
23 Understanding and accounting for the
costs of inaction
Mikael Skou Andersen and David Owain Clubb
In political decision-making processes, the burden
of proof is often distributed such that policymakers
only respond to early warning signals from
environmental hazards once the costs of inaction
have been estimated.
This chapter revisits some key environmental issues
for which estimates of costs of inaction have been
carefully developed over many years of research.
The aim is to consider the methodological challenges
involved in producing estimates that are credible
and appropriate rather than present specific
estimates for these costs.
The case studies also provide insights into how
early warning signals might provide a basis
for estimating the costs of inaction, when the
science base is less consolidated. For example,
the case of nitrates in drinking water illustrates
that a precautionary approach to the costs of
inaction is quite conceivable. The phase-out of
ozone-depleting substances, where early-warning
scientists successfully alerted the world to the
damaging effects of chlorofluorocarbons (CFCs),
provides another important case because additional
impacts for global warming actually cause the
costs of inaction to be considerably higher than
initially believed. This is a reminder that figures
for the costs of inaction have often been grossly
underestimated.
Finally, in the case of air pollution, making use of
different estimates for mortality risk avoidance will
help decision-makers to see that there are higher-
and lower-bound estimates for the costs of inaction.
Even if the lower-bound estimates are perhaps too
conservative, with a bias towards health effects, they
will in many situations encourage more rather than
less abatement effort. Reducing emission loads will
also tend to bring relief for the intangible assets of
biodiversity and nature.
Making the best use of environmental science and
modelling helps to make environmental protection
and precaution a priority. Producing cost estimates
should not be left to economists alone, but should
rather be seen as a starting point for a broader
discussion, featuring also the relevant expertise
in health, ecology, demography, modelling and
science. Well researched estimates, based on
interdisciplinary collaboration, can strengthen
some of those scattered and diffuse interests, which
during the ordinary processes of policy-making
have difficulty making their voices heard.
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Part D — Summary
24 Protecting early warners and late
victims
Carl Cranor
Many
Late lessons from early warnings
chapters
provide examples of early warning scientists who
were harassed for bringing inconvenient truths
about impending harm to the attention of the
public and regulators. There is also some evidence
that young scientists are being discouraged from
entering controversial fields for fear of such
harassment. In addition, where warnings have been
ignored and damage has ensued, it has often proven
difficult in the past to achieve prompt and fair
compensation for the victims. Some ideas for reform,
building on some current institutional models are
explored here.
This chapter first explores the idea of extending
whistleblowing laws to help encourage and protect
early-warning scientists and others who identify
evidence of impending harm. Complementary
measures, such as greater involvement of
professional societies and the use of recognition
awards, as for example in Germany, could also be
helpful.
Next, the chapter explores improved mechanisms
for compensating victims of pollution and
contamination. The chapter on the Minamata Bay
disaster provides an extreme example of long
delays in getting adequate compensation for the
victims of methylmercury poisoning. It was almost
fifty years, between 1956 and 2004, before the
victims attained equitable levels of compensation
and legal recognition of responsibility. Other case
studies illustrate similar examples of long delays in
receiving adequate compensation.
Options are examined for providing justice to any
future victims of those emerging technologies
such as nanotechnology, genetically modified
crops and mobile phone use, which currently can
provide broad public benefits but potentially at a
cost to small groups of victims. The potential for
widespread exposure and uncertain science could
justify 'no-fault' administrative schemes that provide
more efficient and equitable redress in situations
where the benefit of scientific doubt would be
given to victims. The use of anticipatory assurance
bonds to help minimise and meet the costs of future
environmental damage from large scale technologies
is also explored.
A supplementary panel text describes cases of
asbestos and mesothelioma, where the senior
courts in the United Kingdom have developed
innovative ways of dealing with both joint and
several liability, and the foreseeability of subsequent
asbestos cancers, after the initial recognition of
the respiratory disease, asbestosis. Such legal
developments in the field of personal injury could
illustrate the future direction of long-tail liability in
both environmental damage and personal injury.
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Part D — Summary
25 Why did business not react with
precaution to early warnings?
Marc Le Menestrel and Julian Rode
In the past, companies have frequently neglected
early warning signals about potential hazards for
human health or the environment associated with
their products or operations. This chapter reviews
and analyses relevant interdisciplinary literature
and prominent case studies — in particular those
documented in both volumes of
Late lessons from
early warnings
— and identifies main factors
responsible for the disregard of early warning
signals.
The chapter shows how economic motives often
drive non-precautionary business decisions. In
virtually all reviewed cases it was perceived to
be profitable for industries to continue using
potentially harmful products or operations.
However, decisions are also influenced by a complex
mix of epistemological, regulatory, cultural and
psychological aspects. For instance, characteristics of
the research environment and the regulatory context
can provide business actors with opportunities
to enter into 'political actions' to deny or even
suppress early warning signals. Also, business
decision-makers face psychological barriers to
awareness and acceptance of the conflicts of values
and interests entailed by early warning signals.
Cultural business context may further contribute to
the denial of conflicts of values.
The chapter concludes with a set of reflections
on how to support more precautionary business
decision making. A prominent policy response to
the conflicting interests of business and society
is introducing regulations that attempt to steer
business rationality towards internalising external
effects. Innovative solutions such as assurance
bonding should be considered.
There is a need to better understand and expose
why business actors do not respond voluntarily to
early warning signals with precautionary actions.
Blaming business, in particular with hindsight,
tends to be common reaction that may not always
be constructive. It often misses the complex or
even contradictory set of motives and drivers that
business actors face.
Public institutions could support progressive
business by analysing and publically disclosing
the dilemmas and temptations entailed by early
warning signals, for example for different industries
and for the specific societal and regulatory context
of decisions. Rigorous and explicit exposition of
the dilemmas will create further incentives for
responsible actors to share and communicate their
precautionary responses.
An additional reflection centres on the role of
political actions of business actors, in particular
those actions aimed at suppressing early warning
signals. Regulatory efforts that make the political
actions of business more transparent can help
to sustain a sound balance of power, thereby
maintaining our ability to benefit from early
warning signals and reducing the likelihood of
health and environmental hazards.
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Part E — Summary
26 Science for precautionary
decision-making
Philippe Grandjean
The goals of academic researchers may differ
from those of regulatory agencies responsible for
protecting the environment. Thus, research must
take into account issues such as feasibility, merit and
institutional agendas, which may lead to inflexibility
and inertia.
A large proportion of academic research on
environmental hazards therefore seems to focus
on a small number of well studied environmental
chemicals, such as metals. Research on
environmental hazards should therefore to a greater
extent consider poorly known problems, especially
the potential hazards about which new information
is in particular need.
Misinterpretation may occur when results
published in scientific journals are expressed in
hedged language. For example, a study that fails to
document with statistical significance the presence
of a hazard is often said to be negative, and the
results may be misinterpreted as evidence that
a hazard is absent. Such erroneous conclusions
are inspired by science traditions, which demand
meticulous and repeated examination before a
hypothesis can be said to be substantiated.
For prioritising needs for action, research
should instead focus on identifying the possible
magnitude of potential hazards. Research is always
affected by uncertainties and many of them can
blur a real association between an environmental
hazard and its adverse effects, thereby resulting
in an underestimated risk. Environmental health
research therefore needs to address the following
question: are we sufficiently confident that this
exposure to a potential hazard leads to adverse
effects serious enough to initiate transparent and
democratic procedures to decide on appropriate
intervention?
The choice of research topics must consider
societal needs for information on poorly known
and potentially dangerous risks. The research
should be complementary and extend current
knowledge, rather than being repetitive for
verification purposes, as required by the
traditional science paradigm. Research findings
should be openly available and reported so that
they inform judgments concerning the possible
magnitude of suspected environmental hazards,
thereby facilitating precautionary and timely
decision-making.
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Part E — Summary
27 More or less precaution?
David Gee
Despite its presence in a growing body of EU and
national legislation and case law, the application
of the precautionary principle has been strongly
opposed by vested interests who perceive short term
economic costs from its use. There is also intellectual
resistance from scientists who fail to acknowledge
that scientific ignorance and uncertainty, are
excessively attached to conventional scientific
paradigms, and who wait for very high strengths
of evidence before accepting causal links between
exposure to stressors and harm.
The chapter focuses on some of the key issues that
are relevant to a more common understanding of the
precautionary principle and to its wider application.
These include different and confusing definitions of
the precautionary principle and of related concepts
such as prevention, risk, uncertainty, variability and
ignorance; common myths about the meaning of the
precautionary principle; different approaches to the
handling of scientific complexity and uncertainty;
and the use of different strengths of evidence for
different purposes.
The context for applying the precautionary
principle also involves considering the 'knowledge
to ignorance' ratio for the agent in focus: the
precautionary principle is particularly relevant
where the ratio of knowledge to ignorance is low, as
with emerging technologies.
A working definition of the precautionary principle
is presented that aims to overcome some of the
difficulties with other definitions, such as their use
of triple negatives; a failure to address the context
of use of the precautionary principle; no reference
to the need for case specific strengths of evidence to
justify precaution; and overly narrow interpretations
of the pros and cons of action or inaction.
The chapter also points to the need for greater
public engagement in the process of framing and
decision-making about both upstream innovations
and their downstream hazards, including the
specification of the 'high level of protection' required
by the EU treaty. A precautionary and participatory
framework for risk analysis is proposed, along with
some 'criteria for action' to complement criteria for
causation.
The capacity to foresee and forestall disasters,
especially when such action is opposed by powerful
economic and political interests, appears to be
limited, as the case studies in
Late lesson from early
warnings
illustrate. The chapter argues that with
more humility in the face of uncertainty, ignorance
and complexity, and wider public engagement,
societies could heed the lessons of past experience
and use the precautionary principle, to anticipate
and minimise many future hazards, whilst
stimulating innovation. Such an approach would
also encourage more participatory risk analysis;
more realistic and transparent systems science;
and more socially relevant and diverse innovations
designed to meet the needs of people and
ecosystems.
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Part E — Summary
28 In conclusion
The first volume of
Late lessons from early warnings
highlighted the difficulties of balancing precaution
with technological innovation and ended with a call
to action for policymakers. How much progress has
been made since then?
First, there is growing evidence that precautionary
measures do not stifle innovation, but instead can
encourage it, in particular when supported by smart
regulation or well-designed tax changes. Not only
has the body of knowledge become richer since
2001, but also the number of stakeholders involved
in decision-making has become larger and more
diverse. There has also been increasing attention
to communicating scientific uncertainty, especially
in the fields of climate change, food safety, and
emerging risks.
However, there has been less progress in other areas:
for example, many of the political and scientific
'bureaucratic silos' still remain, despite frequent
calls for policy integration and inter-departmental
coordination. This has led to the unintended
destruction of stocks of natural capital in some
parts of the world and in other instances, the
global spread of technologies, despite warnings of
impending hazards. The result has been widespread
damage, with most polluters still not paying the full
costs of pollution.
Yet, more encouragingly, new transformative
approaches are emerging to manage the systemic
and interconnected challenges the world faces
e.g. economic/financial, climate/energy, ecosystems/
food. These relate, inter alia, to the increasing use
of digital communications and networking by
consumers, citizens and shareholders to demand
and foster increased participation, more social
responsibility, greater levels of accountability and
higher transparency, especially in determining
future pathways for energy and food production.
There is a greater understanding of the complexity
of the environment, of scientific ignorance
and uncertainties, the irreversibility of many
harmful impacts and on the broader risks to
the long term interests of society if political and
financial institutions remain unchanged. Also
some corporations are fundamentally embracing
sustainable development objectives in their business
models and activities.
The case studies across both volumes of
Late lessons
from early warnings
cover a diverse range of chemical
and technological innovations, and highlight a
number of systemic problems. These include a lack
of institutional and other mechanisms to respond
to early warning signals; a lack of ways to correct
market failures either caused by misleading market
prices or where costs and risks to society and nature
are not properly internalised; and the fact that key
decisions on innovation pathways are made by those
with vested interests and/or by a limited number of
people on behalf of many. The insights and lessons
drawn from the case histories certainly provide the
seeds for some of the answers. They also provide
knowledge for a series of key actions that are
outlined below.
Of course, many questions remain. For example:
how can the precautionary principle be used
further to support decision-making in the face
of uncertainties and the inevitable surprises that
come from complex systems?; how can societies
avoid a lack of 'perfect' knowledge being used as
a justification for inaction in the face of 'plausible'
evidence of serious harm?; how can conflicting
interests be balanced during the phases of
development and use?; and how can the benefits
of products and technologies be more equitably
distributed?
Reduce delays between early warnings
and actions
The majority of the case studies in
Late lessons
from early warnings
Volumes 1 and 2 illustrate
that if the precautionary principle had been
applied on the basis of early warnings, justified
by 'reasonable grounds for concern' many lives
would have been saved and much damage to
ecosystems avoided. It is therefore very important
that large scale emerging technologies, such as
biotechnologies, nanotechnologies and information
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Part E — Summary
and communication technologies, apply the
precautionary principle based on the experiences and
lessons learned from these and other case studies.
Precautionary actions can be seen to stimulate rather
than hinder innovation; they certainly do not lead to
excessive false alarms. As the analysis in Volume 2
shows, of 88 cases of claimed 'false positives', where
hazards were wrongly regulated as potential risks,
only four were genuine false alarms. The frequency
and scale of harm from the mainly 'false negative'
case studies indicate that shifting public policy
towards avoiding harm, even at the cost of some
false alarms, would seem to be worthwhile, given the
asymmetrical costs of being wrong in terms of acting
or not acting based on credible early warnings.
However, the speed and scale of today's
technological innovations can inhibit timely action.
This is often because by the time clear evidence
of harm has been established, the technology
has been modified, thereby allowing claims of
safety to be subsequently re-asserted. Even where
the technological change has been marginal, the
large, often global, scale of investment can lead to
widespread technological lock-in, which is then
difficult and expensive to alter.
These features of current technological innovation
strengthen the case for taking early warning signals
more seriously and acting on lower strengths
of evidence than those normally used to reach
'scientific causality'. Most of the historical case
studies show that by the time such strong evidence
of causality becomes available, the harm to people
and ecosystems has become more diverse and
widespread than when first identified, and may
even have been caused by much lower exposures
than those initially considered dangerous.
The case studies have also shown that there are
many barriers to precautionary action, including:
the short-term nature of most political and financial
horizons; the existence of technological monopolies;
the conservative nature of the sciences involved,
including the separate 'silos' within which they
operate; the power of some stakeholders; and the
cultural and institutional circumstances of public
policymaking that often favour the status quo.
practical consequences for minimising harm. Much
of the harm described in Volumes 1 and 2, such
as cancers or species decline, is caused by several
co-causal factors acting either independently or
together. For example, the reduction of intelligence
in children can be linked to lead in petrol, mercury
and polychlorinated biphenyls (PCBs) as well as
to socio-economic factors; bee colony collapse can
be linked to viruses, climate change and nicotinoid
pesticides; and climate change itself is caused
by many complex and inter-linked chemical and
physical processes.
In some cases, such as foetal or fish exposures,
it is the timing of the exposure to a stressor that
causes the harm, not necessarily the amount; the
harm may also be caused or exacerbated by other
stressors acting in a particular timed sequence. In
other cases, such as radiation and some chemicals
such as bisphenol A (BPA), low exposures can be
more harmful than high exposures; and in others,
such as asbestos with tobacco, and some endocrine
disrupting substances, the harmful effects of
mixtures can be greater than from each separate
stressor. There are also varying susceptibilities
to the same stressors in different people, species
and ecosystems, depending on pre-existing stress
levels, genetics and epigenetics. This variation can
lead to differences in thresholds or tipping point
exposures, above which harm becomes apparent in
some exposed groups or ecosystems but not others.
Indeed there are some harmful effects which occur
only at the level of the system, such as a bee colony,
which cannot be predicted from analysing a single
part of the system, such as an individual bee.
Our increased knowledge of complex biological
and ecological systems has also revealed that
certain harmful substances, such as polychlorinated
biphenyls (PCBs) and dichlorodiphenyltrichlorethane
(DDT) can move around the world via a range of
biogeochemical and physical processes and then
accumulate in organisms and ecosystems many
thousands of kilometres away.
The practical implications of these observations
are threefold. First, it is very difficult to establish
very strong evidence that a single substance or
stressor 'causes' harm to justify timely actions to
avoid harm; in many cases only reasonable evidence
of co-causality will be available. Second, a lack
of consistency between research results is not a
strong reason for dismissing possible causal links:
inconsistency is to be expected from complexity.
Third, while reducing harmful exposure to one
co-causal factor may not necessarily lead to a large
reduction in the overall harm caused by many other
Acknowledge complexity when dealing
with multiple effects and thresholds
Increasing scientific knowledge has shown that the
causal links between stressors and harm are more
complex than was previously thought and this has
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Part E — Summary
factors, in some cases the removal of just one link
in the chain of multi-causality could reduce much
harm.
A more holistic and multi-disciplinary systems
science is needed to analyse and manage the causal
complexity of the systems in which we live.
that grossly simplify reality rather than using
long-term observations and trend data of biological
and ecological systems. These approaches have
sometimes led to the production of false positives.
More importantly the governance of scientific
ignorance and unknown unknowns has been
neglected.
Finally, many case studies highlight the problems
faced by early warning scientists who have been
harassed for their pioneering work, including bans
on speaking out or publishing, loss of funding,
legal or other threats, and demotion. One obvious
conclusion is that scientists in these situations
should receive better protection either via an
extension of 'whistle blowing' and discrimination
laws, or by independent acknowledgement of the
value of their work.
Rethink and enrich environment and
health research
Environment and health research overly focuses
on well-known rather than unknown hazards at
the expense of emerging issues and their potential
impacts. For example the ten most well-known
substances, such as lead and mercury, account for
about half of all articles on chemical substances
published in the main environmental journals
over the last decade. Over the past decade,
public research funding in the European Union
on nanotechnology, biotechnology as well as
Information and Communications Technology
(ICT) is heavily biased towards product
development with about 1 % being spent on
their potential hazards. A more equal division of
funding between known and emerging issues, and
between products and their hazards, would enrich
science and help avoid future harm to people and
ecosystems and to the long term economic success
of those technologies.
Funding more holistic systems science would
also help achieve a greater integration among
the different branches of science and counteract
problems such as: peer review predominantly within
and not across disciplines; short-term interests
outcompeting long-term vision; competition
replacing cooperation because of conflicts of interest;
contradictions amongst paradigms; fragmentation
of values and authority; as well as fragmentation
of information and knowledge. These can all
lead to inferior solutions and provide increased
opportunities for those with vested interests to
manufacture doubt.
Scientific methods can also be improved. For
example, much higher strengths of evidence are
required overall before causality is accepted,
compared to the evidence being used to assert
safety. The assertion that there is
no evidence of
harm
is then often assumed to be
evidence of no
harm,
even though the relevant research is missing.
Historically there has been an over-reliance on the
statistical significance of point estimates compared
to confidence limits based on multiple sampling.
There has also been a bias towards using models
Improve the quality and value of risk
assessments
The majority of the case studies in
Late lessons
from early warnings
indicate that risk assessment
approaches need to better embrace the realities
of causal and systems complexity (rather than
use a narrow conception of 'risk') with the
inevitable features of ignorance, indeterminacy
and contingency. In a number of case studies, for
example BPA, where low doses are more harmful
than high doses, or tributyltin antifoulants (TBT)
and synthetic oestrogen diethylstilboestrol (DES)
where the timing of the dose is what makes it
harmful, simplistic assumptions are inadequate.
Variability in exposures and varying susceptibilities
in populations and species exposed also need to be
more realistically factored into risk assessments.
This is equally true for technological risk
assessments. As the Fukushima Investigation
Committee concluded in 2011:
'…the accidents present us with crucial lessons
on how we should be prepared for 'incidents
beyond assumptions'. With its failure to plan
for the cascade effects beyond design–base
accidents 'the regulatory emphasis on risk
based probabilistic risk assessment has proven
very limited'.
In other words, narrow risk assessment approaches
are now outstripped by the realities which they
cannot address, recognise and communicate. Too
often this contributes to the effective denial of those
risks that do not fit the risk assessment frame. It
is therefore urgent that risk assessment practices
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Part E — Summary
be transformed to make them broader-based,
more inclusive, transparent and accountable.
There should also be more communication on the
diversity of scientific views, especially on emerging
issues where ignorance and uncertainties are high
and genuine differences of scientific interpretations
are likely, desirable, and defensible. In this sense,
recognising the pedigree of knowledge, i.e. the
consistency of views amongst peers and the level
of convergence coming from different branches of
research, is essential for effective decision making
and action to support the wellbeing of people and
the environment.
The case studies show that evaluations of evidence
in risk assessments can be improved by including
a wide range of stakeholders when framing the
risks and options agenda; broadening the scope and
membership of evaluation committees; increasing
the transparency of committee approaches and
methods, particularly in identifying uncertainties
and ignorance; and ensuring their independence
from undue influence through using appropriate
funding sources and applying robust policies on
conflicts of interest.
Public confidence would be increased if all the
evidence used in risk assessments was made
publicly accessible and open to independent
verification, including data submitted by industries
to authorities.
As experiences from mercury, nuclear accidents,
leaded petrol, mobile phones, BPA, and bees
show, there can be a significant divergence in the
evaluations of the same, or very similar, scientific
evidence by different risk assessment committees.
In such instances, differences in the choice of
paradigm, assumptions, criteria for accepting
evidence, weights placed on different types of
evidence, and how uncertainties were handled, all
need to be explained. Risk assessors and decision
makers also need to be aware that complexity and
uncertainty have sometimes been misused to shift
the focus away from precautionary actions by
'manufacturing doubt' and by waiting for 'sound
science' approaches that were originally developed
by the tobacco industry to delay action.
this framework, governments have at least three
roles: providing direction by putting in place smart
regulations and consistent market signals; ensuring
that the distributional consequences of innovations
are balanced between risks and rewards across
society, fostering a diversity of innovations so that
the wider interests of society; and take precedence
over narrower interests.
Numerous case studies show that decisions to act
without precaution often come from businesses.
There are, however, several impediments to
businesses acting in a precautionary manner,
including a focus on short-term economic value
for shareholders alongside psychological factors
that lead to a so-called 'ethical blindness' or a
'self-serving bias' whereby people largely interpret
ambiguous situations in their own interests.
Governments and businesses could collaborate more
with citizens on publicly disclosing the potential
value conflicts entailed in acting on early warning
signals. A culture of transparency can in turn
promote positive business attitudes and innovations.
Involving the public can also help in choosing
between those innovation pathways to the future; on
prioritising relevant public research; on providing
data and information in support of monitoring and
early warnings; improving risk assessments; on
striking appropriate trade-offs between innovations
and plausible health and environmental harms; and,
making decisions about risk-risk trade-offs.
Correcting market failures using the
polluter pays and prevention principles
When evidence of initial harm emerges, the costs
should be internalised retroactively into the prices
of polluting products, via taxes and charges, in
line with the polluter pays principle and emerging
practice across the world. The revenues could then
be devoted partly to stimulating research into less
hazardous alternatives, and partly to reform tax
systems by reducing taxes and charges on 'societal
goods' like employment.
The pollution taxes/charges would rise or fall in line
with new scientific knowledge about increasing/
decreasing harm, and this would help to level the
playing field for less-polluting alternative products.
Tax shifts from employment to pollution and the
inefficient use of resources can bring multiple
benefits such as increased employment, a stimulus
to innovation, a more stable tax base in the light of
expected demographic changes, and a more efficient
tax collection system.
Foster cooperation between business,
government and citizens
Policy formulation should start from a broad
concept of technological innovation to include
non-technological, social, institutional,
organisational and behavioural innovation. In
Late lessons from early warnings: science, precaution, innovation
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Part E — Summary
More broadly, firms and governments need to extend
their economic accounting systems to incorporate the
full impacts of their activities on people's health and
on ecosystems. Governments need to anticipate this
in their policies, by providing the right blend of fiscal
instruments to both protect the public and ensure that
firms internalise the true costs of potential harm.
A number of case studies also demonstrate the
long time lags between evidence of harm and the
additional injustice and time of forcing victims
to pursue their cases through civil compensation
claims. Prompt and anticipatory no-fault
compensation schemes and assurance bonds, could
be set up and financed in advance of potential
harm by the industries that are producing novel
and large-scale technologies, thereby helping to
offset any potential market failure. Such schemes
can also be designed to increase the incentives for
innovating companies to carry out more
a priori
research into the identification and elimination of
hazards.
act to transform our ways of thinking and of doing,
and urgently so in the face of
unprecedented global
changes, challenges and opportunities.
Many lessons
have been learnt, yet have not been acted upon.
Any
calls for action will need to reflect on today's global
socio-economic setting and support, among other
things, the drive to:
• rebalance the prioritisation of economic and
financial capital over social, human and natural
capitals through the broader application of the
policy principles of precaution, prevention and
polluter-pays, and environmental accounting;
• broaden the nature of evidence and public
engagement in choices about key innovation
pathways by directing scientific efforts more
towards dealing with complex, systemic
challenges and unknowns and complementing
this with professional, lay, local and traditional
knowledge; and,
• build greater adaptability and resilience in
governance systems to deal with multiple
systemic threats and surprises, through
strengthening institutional structures and
deploying information technologies in support
of the concept of responsible information and
dialogues.
The governance of innovation will remain at the
level of good intentions unless it is translated
into innovations in science practices, institutional
arrangements and public engagements as well as
transformations in prevailing business attitudes,
practice and influence. These are the tasks that lie
ahead.
Governance of innovation and innovation
in governance
The
Late lessons from early warnings
reports
demonstrate the complexities of developing not
only the right kind of science and knowledge but
also handling the interactions between the many
actors and institutions involved — governments,
policymakers, businesses, entrepreneurs, scientists,
civil society representatives, citizens and the media.
Alongside many other analyses produced across
the world today, the reports also stress the need to
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In memory of Masazumi Harada,
1935–2012
Shocked by their miserable lives, Harada devoted
himself to the study of the disease from that time.
Harada published a thesis on congenital Minamata
disease in 1964. The work had a significant impact
as it disproved the conventional belief at the
time that the placenta does not pass poisons. He
received an award from the Japanese Society of
Psychiatry and Neurology for the thesis in 1965.
He then established the Open Research Center
for Minamata Studies at the university in 2005,
becoming the center's head. He continued to
lead the disease's research from non-medical
perspectives as well. Harada visited Brazil, China
and native Indian communities in Canada to
discover those suspected of suffering from the
disease.
Author of many books, Harada wrote 'Minamata
Byo' (Minamata Disease), which raised awareness
on the issue around the world.
Masazumi Harada, a physician involved for
many years in the study of the mercury poisoning
Minamata disease, died in June 2012 of acute
myelocytic leukemia at his home in Kumamoto
City. He was 77.
Harada conducted medical examinations on the
disease's sufferers for the first time in the summer
of 1961 in Minamata city in Kumamoto Prefecture
while he was a student at Kumamoto University's
graduate school.
Dr. Masazumi Harada first came to
Asubpeeschoseewagong (Grassy Narrows) and
Wabaseemoong (White Dog) First Nations in
Canada in the early 1970s. Harada's death comes
at the end of River Run 2012, five days of actions
by members and supporters of Grassy Narrows in
Toronto, who are seeking to have Minamata disease
recognized in Canada and Ontario. Harada's final
report for the Grassy Narrows community was
released on 4 June 2012 after 30 years of research,
showing mercury deposited in the river by the
Dryden paper mill in the 1970s is impacting those
who were not yet born when the dumping ceased.
Late lessons from early warnings: science, precaution, innovation
43
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In memory of Poul Harremoës,
1934–2003
1971. He was a key participant in numerous settings,
including the first Scientific Committee of the
European Environment Agency from 1995.
He had a civil engineering degree from the Technical
University of Denmark. He specialised early on in
geo-technics and constructed dams on the Faroe
Islands. While teaching geo-technics he wrote a
textbook that was used for more than 40 years.
However, he was able to quickly change his research
direction and develop new areas of excellence. So,
for example, he got a grant to study at Berkeley,
California, from where he received a M.Sc. degree in
environmental engineering.
In 1972, he became professor in environmental
engineering at the Technical University of Denmark
where he originally worked with wastewater
discharge to the sea and the biological processes of
wastewater treatment. He became a world leading
scientist in the theories of biofilms for removal
of organics and nitrogen from wastewater before
turning to sewer design and modelling. In 2000, Poul
was awarded the
Heineken prize for Environmental
Sciences
for his contributions to the theory of
biofilm kinetics in relation to biological waste water
treatment and for his successful organisation of the
international scientific community in water pollution
research and control.
As a result of his work with sewers and storm water
he went into the area of risk analysis and the role of
the precautionary principle. In a short time he became
an international expert in this field and was highly
demanded for lectures in all parts of the world. A key
outcome of his interest was his contributions as
chairman of the editorial team for the first volume of
Late lessons from early warnings
published in 2001.
Poul Harremoës was a key player in environmental
issues in Denmark and internationally for more than
30 years until his death, at 69, in 2003. In that time,
those who worked closely with him benefited from
a continuous, almost daily flow of excellent ideas for
new research projects.
He was a member of the Danish Pollution Council,
which prepared the first framework national law
on environmental protection and advised on the
establishment of a Ministry of Environment from
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European Environment Agency
Late lessons from early warnings: science, precaution, innovation —
Summary
2013 — 44 pp. — 21 x 29.7 cm
ISBN 978-92-9213-349-8
doi:10.2800/70069
How to obtain EU publications
Publications for sale:
•
via EU Bookshop (http://bookshop.europa.eu);
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from your bookseller by quoting the title, the publisher and/or ISBN number;
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by contacting one of our sales agents directly. You can obtain their contact
details on the Internet (http://bookshop.europa.eu) or by sending a fax to
+352 2929-42758.
Free publications:
•
via EU Bookshop (http://bookshop.europa.eu);
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at the European Commission's representations or delegations. You can obtain
their contact details on the Internet (http://ec.europa.eu) or by sending a fax
to +352 2929-42758.
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TH-AL-13-001-EN-C
doi:10.2800/70069
European Environment Agency
Kongens Nytorv 6
1050 Copenhagen K
Denmark
Tel.: +45 33 36 71 00
Fax: +45 33 36 71 99
Web: eea.europa.eu
Enquiries: eea.europa.eu/enquiries
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Scientific Committee on Health, Environmental and Emerging
Risks
SCHEER
Statement on emerging health and environmental
issues (2018)
The SCHEER adopted this statement by written procedure on 20 December 2018.
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SCHEER Statement on Emerging Issues (2018)
____________________________________________________________________________________
ABSTRACT
The purpose of this SCHEER statement is to draw the EU Commission Services’
attention to emerging issues in the non-food area that SCHEER members have
identified as having the potential to impact human health and /or on the
environment in the future. The Secretariat will use this list when discussing potential
new mandates with relevant Commission services.
Keywords:
SCHEER, emerging issues, emerging risks, newly identified health risks,
health, environment, impacts
Opinion to be cited as:
SCHEER (Scientific Committee on Health, Environmental and Emerging Risks)
Statement on emerging health and environmental issues (2018), 20 December
2018.
ACKNOWLEDGMENTS
Members of the Working Group are acknowledged for their valuable contribution to
this Opinion. The members of the Working Group are:
The SCHEER members:
Roberto Bertollini
Teresa Borges
Wim de Jong
Pim de Voogt
Raquel Duarte-Davidson
Peter Hoet
Rodica Mariana Ion
Renate Krätke
Demosthenes Panagiotakos
Ana Proykova
Theodoros Samaras
Marian Scott (Rapporteur)
Remy Slama
Emanuela Testai
Theo Vermeire (Chair)
Marco Vighi
Sergey Zacharov
All declarations by Working Group members are available at the following webpage:
https://ec.europa.eu/health/scientific_committees/experts/declarations/scheer_en
__________________________________________________________________
2
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SCHEER Statement on Emerging Issues (2018)
____________________________________________________________________________________
About the Scientific Committees (2016-2021)
Two independent non-food Scientific Committees provide the Commission with the
scientific advice it needs when preparing policy and proposals relating to consumer
safety, public health and the environment. The Committees also draw the
Commission's attention to the new or emerging problems which may pose an actual
or potential threat.
The Scientific Committee on Consumer Safety (SCCS) and the Scientific Committee
on Health, Environmental and Emerging Risks (SCHEER) review and evaluate
relevant scientific data and assess potential risks. Each committee includes top
independent scientists from all over the world who are committed to working in the
public interest.
In the formulation of its policies and proposals, the Commission also relies on other
Union bodies, such as the European Food Safety Authority (EFSA), the European
Medicines Agency (EMA), the European Centre for Disease prevention and Control
(ECDC) and the European Chemicals Agency (ECHA).
SCHEER
This Committee, on request of Commission services, provides Opinions on questions
concerning health, environmental and emerging risks. The Committee addresses
questions on:
- health and environmental risks related to pollutants in the environmental media
and other biological and physical factors in relation to air quality, water, waste and
soils.
- complex or multidisciplinary issues requiring a comprehensive assessment of risks
to consumer safety or public health, for example antimicrobial resistance,
nanotechnologies, medical devices and physical hazards such as noise and
electromagnetic fields.
SCHEER members
Roberto Bertollini, Teresa Borges, Wim de Jong, Pim de Voogt, Raquel Duarte-
Davidson, Peter Hoet, Rodica Mariana Ion, Renate Kraetke, Demosthenes
Panagiotakos, Ana Proykova, Theo Samaras, Marian Scott , Remy Slama, Emanuela
Testai, Theo Vermeire, Marco Vighi, Sergey Zacharov
Contact:
European Commission
DG Health and Food Safety
Directorate C: Public Health, Country Knowledge, Crisis management
Unit C2
–
Country Knowledge and Scientific Committees
Office: HTC 03/073 L-2920 Luxembourg
[email protected]
© European Union, 2017
ISSN
2467-4559
doi:10.2875/840266
ISBN
978-92-76-00231-4
EW-CA-19-003-EN-N
__________________________________________________________________
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SCHEER Statement on Emerging Issues (2018)
____________________________________________________________________________________
The Opinions of the Scientific Committees present the views of the independent
scientists who are members of the committees. They do not necessarily reflect the
views of the European Commission. The Opinions are published by the European
Commission in their original language only.
http://ec.europa.eu/health/scientific_committees/policy/index_en.htm
__________________________________________________________________
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SCHEER Statement on Emerging Issues (2018)
____________________________________________________________________________________
TABLE OF CONTENTS
ABSTRACT
..........................................................................................................
2
ACKNOWLEDGMENTS
.........................................................................................
2
1.
2.
3.
4.
INTRODUCTION
..........................................................................................
6
FORMAT FOR DESCRIBING AN EMERGING ISSUE
.......................................
6
NEXT STEPS
................................................................................................
8
ISSUES
.......................................................................................................
9
4.1. Personal communication and listening devices
..........................................
9
4.2
4.3
4.4
4.5
4.6
Virtual reality
...........................................................................................
11
E-cigarette and chronic diseases
..............................................................
12
Potential effects on wildlife of increases in electromagnetic radiation
.....
14
Chemicals in recycled materials, an issue in a circular economy
..............
16
Pharmaceuticals
(human
and
veterinary)
and
illicit
drugs
in
wastewater and surface waters
...............................................................
18
4.7
4.8
Substance Mobility: a new criterion in chemicals regulation
....................
20
Drinking water treatment interactions with compounds and potential
health effects
...........................................................................................
22
4.9
Per- and polyfluorinated organic substances............................................ 24
4.10 New RNA pesticides and gene editing to reduce/eradicate pest
populations
..............................................................................................
26
4.11 Do-it-Yourself Synthetic Biology, biohacking
...........................................
28
4.12 Micro and nano-plastic in the environment
..............................................
30
4.13 Nanoparticles released from Building Materials and construction waste
to the Environment
...................................................................................
32
4.14 Environmental factors and the Human Microbiome
..................................
34
5.
6.
CONCLUSIONS
..........................................................................................
36
REFERENCES
.............................................................................................
37
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1.
INTRODUCTION
The primary purpose of this position statement is to draw the attention of the EU
Commission Services to emerging issues in the non-food area that have been
identified by the SCHEER members as having the potential to significantly impact
human health and /or on the environment in the future.
Identifying emerging issues early on may greatly help for ensure a high level of
public safety and environmental protection. However, the data available to correctly
identify emerging issues and their impacts is inevitably likely to be very limited. It is
therefore important that each issue that is identified is regularly reviewed. The
SCHEER aims, therefore, to regularly review any relevant new developments and to
produce an updated position statement twice during the Scientific Committee term
(this term is from 2016-2021). The Committee can also submit an urgent issue to
the Commission at any time. In considering emerging issues, the SCHEER would like
to work closely with other EU scientific advisory committees whose mandates also
include looking at emerging issues.
The SCHEER recognised the need to establish a very flexible framework to aid the
correct identification of emerging issues and their potential impacts (see document
‘Emerging Issues and the Role of the SCHEER, Position Paper’).
SCHEER members have been asked during plenary meetings, in dedicated
'brainstorming sessions', to identify emerging/relevant issues that they think should
be flagged for the Commssion Services.
The criteria used to identify an emerging issue were as follows:
Novelty of the stressor or process
Scale of possible impacts on man and /or the environment
Severity of impacts for particular organisms (priority for life threatening)
Urgency i.e. the temporal nature of the likely changes (priority for rapid
increases)
Not investigated in depth recently by a reputable scientific body
Anticipated to be increasingly important over time
To aid this, a standardised format has been used and issues have been placed in
particular categories. It is acknowledged that further consideration of some of the
issues that have been identified should be led by other scientific committees.
2.
FORMAT FOR DESCRIBING AN EMERGING ISSUE
A common format was proposed to describe emerging issues. This was in the format
of a table in which the committee members have been asked to fill in the following:
The topic proposed
The author (name of SCHEER submitter)
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Sources (one or more selected items from the ones mentioned under point 1
between 1-12)
Causative factors (one or more selected items from the ones mentioned
under point 2 between a and h)
Preliminary ranking of the hazard ((*,1, 2 or 3 where *=uncertain and 3 is
high for uniqueness, soundness, severity, spatial scale, urgency, and
interactions, respectively)
Preliminary estimation of importance (*,1, 2 or 3 where *=uncertain and 3 is
high)
Description / background
1) Sources
Risks associated with:
1) Buildings and infrastructure
2) Energy and electronic communications
3) Disease evolution e.g. due to pathogen changes
4) Industrial and related activities
5) Waste processing and utilisation
6) Use of natural resources
7) Transport and storage
8) Human behaviour (socio-economic, lifestyle, perception)
9) Medical developments (technology, pharmaceuticals)
10) Environmental change
11) Product use/misuse
12) Agriculture and food
13) New materials
2) Causes / Contributing factors:
a) Technical advances opening up the prospect of new products and/or processes
and/or raising concerns about waste treatment safety
b) A consequence of changes in the natural environment
c) Changes resulting from alterations in price, supply of materials and commodities
d) Changes due to alterations in legislation or public welfare measures
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e) Other socio-cultural or demographic elements
f) Outcomes of research
g) Large scale illegal activities
h) Public/political concern
3.
NEXT STEPS
The list will be used by the Secretariat when discussing potential new mandates with
relevant Commission services.
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4.
ISSUES
4.1.
Topic
Initiator(s)
Personal communication and listening devices
Personal communication and listening devices
Theodoros Samaras
Sources
Causative factors
(see section 2 of
this document)
Hazard
(Rank features as
1,2,3 or *)
-uniqueness
-soundness
-severity
-scale
-urgency
-interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors)
8, 11
a, c, e
1
1
*
3
1
2
It has already been established that driving while using a portable device
presents a quantifiable risk for traffic accidents. In addition, texting has
been linked in the past to orthopaedic problems of hand and arm joints,
as well as to more serious musculoskeletal injuries. More information:
Fares
et al.
(2017).
The use of personal digital devices adds to the exposure to screen light
(this has been dealt with in previous Opinions about artificial light and
LED exposure). Moreover, it exacerbates the problems resulting from
environmental noise (also assessed in the past), especially by using high
volume levels on earphones.
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including
reliability of data,
a key reference if
possible any other
reasons for
concern.
1
There are mainly two issues associated with personal communication and
listening devices, which mostly concern young people since they
constitute the main users of such devices and start to use them at an
ever earlier age.
The first one has to do with pedestrian safety. Distraction due to texting,
listening to music or using multimedia apps can compromise cognitive
and audiovisual awareness and may pose a risk for the safety of
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pedestrians (e.g. at street crossings).
The second issue has to do with nearsightedness (myopia). The increased
use of personal digital devices has been mentioned as a risk factor for
this trend (especially in the under-40 age group). For more information:
References
1. Schwebel D.C.
et al.
(2012).
2. Schabrun S.M.
et al.
(2014).
3. Holden B.A.
et al.
(2016).
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4.2
Topic
Initiator(s)
Virtual reality
Virtual reality
Ana Proykova
Sources
Causative factors
(see section 2 of
this document)
8, 11
a,e,f
Virtual reality (VR) and augmented reality (AR) are gaining momentum
as promising new technologies. They can potentially expand the field of
human knowledge by changing how people learn, work, play and
entertain themselves. High-tech VR and AR headsets are popping up
everywhere
–
from the expensive ones from Samsung, Google and
Facebook, to the generic cardboard headsets for the lower-end market.
Health risks: anxiety, nausea, eye strain, radiation exposure.
VR can have neurological effects because of its eerily realistic simulated
motion. Virtual Reality (VR) sickness can cause intense discomfort,
shorten the duration of a VR experience, and create an aversion to
further use of VR.
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors)
Preliminary
Estimation of
importance (*, 1, 2
or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
3
*
*
3
3
*
Parallel with Army Aviation - Simulator sickness
Environmental Social Stress
3
Considering the broad usage of Virtual Reality (from games to hospital
treatment of anxiety)
The hazard and risks are under investigation.
References
1.
2.
3.
4.
5.
Fernandes A.S., Feiner S.K. (2016).
Pallavicini F.
et al.
(2013).
Veling W.
et al..
(2016).
Jáuregui-Renaud K. (2015).
Cobb S.V.G., Nichols S.C., Wilson, J.R. (1995).
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4.3
Topic
Initiator(s)
Sources
E-cigarette and chronic diseases
E-cigarettes and chronic diseases
Demosthenes Panagiotakos
9
E-cigarettes, in their modern form, were introduced in the early 2000s as
a means for smoking cessation. The e-cigarette liquid contains several
chemicals, like nicotine, propylene glycol, glycerin, flavourings and
others. Current research suggests that the e-cigarette aerosol contains
substances that could be considered as harmful, including flavouring
chemicals, metals (like lead), and other cancer-causing chemicals. There
is no consistent evidence regarding the effectiveness of e-cigarettes in
helping people to quit smoking. Moreover, there is a tendency in people
to start vaping (e-cigarettes), instead of smoking. Compared with
“regular” cigarettes,
e-cigarettes may be less harmful in terms of
smoking-related chronic diseases, but regarding their use compared to
no smoking, the health effects are not well understood or appreciated.
Moreover, taking into account that e-cigarette use is increasingly
prevalent and fashionable, especially among adolescents and younger
people, it can be regarded as an emerging public health issue.
Causative factors
(see section 2 of
this document)
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors.
2
1
*
3
3 (due to the increasing frequency of use)
3 (due to the interactions with other lifestyle determinants and
psychological stressors)
The e-cigarette has been described as a possible form of harm reduction.
To date, there has been no consistent evidence that e-cigarette can
significantly reduce smoking in the population, and there have not been
enough studies done on the effect of (active or passive) e-cigarette
exposure compared to non-smoking on human health. Moreover,
cigarette smoking, in general, is known to interact with a variety of
unfavourable lifestyle behaviours, like unhealthy dietary habits and
physical inactivity, as well as the presence of chronic stress, leading to
increased risk for cardiovascular disease, COPD and types of cancer.
Taking into account that the aforementioned synergistic factors are now
increasing at alarming rates and the fact that data about the effects of e-
cigarette on human health are not well understood yet, the study of e-
cigarette on human health is considered more important as ever before,
in terms of public health prevention.
3
Preliminary
Estimation of
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importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
E-cigarettes have been patented since the 1960s, however, they have
been available as a product from the early 2000s. The use of e-cigarettes
has risen exponentially over the past 10 years; however, it is difficult to
estimate its use at population level. E-cigarettes are now available in
Europe and in the majority of countries in the Western world, but with
significant differences in use between countries. It is notable that the use
of the e-cigarette tends to be a habit by a considerable proportion of
young adults and adolescents in many European countries. The health
risks of e-cigarettes are uncertain. There are studies suggesting that e-
cigarettes may cause, similar to tobacco cigarettes, harm to the
cardiovascular and lung system. Although some of the identified harmful
components in e-cigarettes were measured in lower quantities than those
in cigarettes, recent studies unveiled that the toxic effects of e-cigarettes
should not be understated. There is an overlap between tobacco laws and
medical drug policies and e-cigarette legislation in many countries. A
European Directive of 2016 set standards for liquids, vaporizers,
ingredients and child-proof liquid containers while the US FDA extended
its regulatory power to include e-cigarettes. In some countries, new
legislations are underway to regulate e-cigarette use.
References
Filippidis F.T., Laverty A.A., Vardavas C.I. (2016).
Ioakeimidis N., Vlachopoulos C., Tousoulis D. (2016).
Makadia L.D., Roper P.J., Andrews J.O., Tingen M.S. (2017).
Cai H., Wang C. (2017).
Chun L.F., Moazed F., Calfee C.S., Matthay M.A., Gotts J.E.
(2017).
6. Benowitz N.L., Burbank A.D. (2016).
7. Rahman M.A., Hann N., Wilson A., Mnatzaganian G., Worrall-
Carter L. (2015).
8.
European Commission (2014). MEMO, 26 February 2014.
1.
2.
3.
4.
5.
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4.4
Potential effects on wildlife of increases in electromagnetic
radiation
Potential effects on wildlife of increases in electromagnetic
radiation
Marian Scott
2
e
“On
the horizon, a new generation of even shorter high frequency 5G
wavelengths is being proposed to power the Internet of Things (IoT). The
IoT promises us convenient and easy lifestyles with a massive 5G
interconnected telecommunications network. However, the expansion of
broadband with shorter wavelength radiofrequency radiation highlights
the concern that health and safety issues remain unknown. Controversy
continues with regard to harm from current 2G, 3G and 4G wireless
technologies. 5G technologies are far less studied for human or
environmental effects”
(Russell, 2018).
Topic
Initiator(s)
Sources
Causative factors
(see section
2section 2 of this
document)
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors.
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
2
1
*
3
3
3 (due to the interactions with other ecosystems and species)
This concern is more related to the change to 5G rather than a
completely new concern. The effects of electromagnetic radiation have
been generally well studied, however low frequency electromagnetic
radiation is less well studied, hence the justification for introducing this
an emerging issue.
3
5G networks will soon be rolled out for mobile phone and smart device
users. How exposure to electromagnetic fields could affect humans
remains a controversial area, and studies have not yielded clear evidence
of the impact on mammals, birds or insects. The lack of clear evidence to
inform the development of exposure guidelines to 5G technology leaves
open the possibility of unintended biological consequences.
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References
1.
https://www.rsm.govt.nz/projects-auctions/current-
projects/preparing-for-5g-in-new-zealand/folder-potential-health-
effects-of-5g-technology/submissions-relating-to-health-
concerns.pdf
2.
Aertsa S., Wiart J., Martens L., Joseph W. (2017).
3.
Pall M.L. (2018).
4.
Di Ciaula A. (2018).
5.
Russell C.L. (2018).
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4.5
Chemicals in recycled materials, an issue in a circular
economy
Chemicals in recycled materials, an issue in a circular economy
Theo Vermeire
Topic
Initiator(s)
Sources
Causative factors
(see section 2 of
this document)
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging
issues.
Potential
interactions
with
other stressors)
Many potential sources
a, c, g, h
1
3
*
3
3
3
In view of EU-wide strategies toward a circular economy, the issue of
hazardous substances in recycled products is getting more and more
attention. Risks can arise for the environment, consumers, workers.
Over the last decade interest in the circular economy and therefore in
recycling has increased considerably. One of the problems of recycling is
that the materials may contain substances that pose a risk to man and
the environment. So the possible advantages of recycling, such as more
energy-efficient and CO
2
-efficient production, should be weighed against
the potential effects of these substances. Examples of hazardous
substances incorporated into potentially recyclable material: the flame
retardant hexabromocyclododecane (HBCDD) in extruded polystyrene,
the plasticiser DEHP, cadmium and lead in polyvinyl chloride (PVC),
heavy metals and PAHs in rubber crump from tyres.
3
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including
reliability of data,
a key reference if
possible any other
reasons for
Examples are:
Lead, phthalates, cadmium, organotins, POPs, BDEs, HBCDD, e-waste,
hazardous chemicals in rubber crump and toys.
References
1. EFSA
CEF
Panel
(EFSA
Panel
on
Food
Contact
Materials,
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concern.
2.
3.
4.
5.
Flavourings and Processing Aids) (2015).
Grant K., Goldizen F.C., Sly P.D., Brune M.-N., Neira M., van den
Berg M., Norman R.E. (2013).
Janssen M.P.M.
et al.
(2016).
KEMI (2012).
Verschoor A.J., Bodar C.W.M., Baumann R.A. (2018).
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4.6
Pharmaceuticals (human and veterinary) and illicit drugs in
wastewater and surface waters
Pharmaceuticals (human and veterinary) and illicit drugs in
wastewater and surface waters
Pim de Voogt, Marco Vighi
Topic
Initiator(s)
Sources
5
Urban waste water. Wastes from pharmaceutical industries and from
illegal drugs manufacturing. Animal farm emissions. Agricultural soils
treated with WWTP sludge or animal manure. Aquaculture.
Causative factors
(see section 2 of
this document)
Hazard
(Rank features as
1,2,3 or *)
Pharmaceuticals and illicit drugs loads in wastewater increase as a result
of increased use of legal, illicit and counterfeit drugs, aging of the
population and also due to fly tipping of waste from illegal drug
manufacturing sites (Emke
et al.
2018). As a result wastewater treatment
facilities may become jeopardised. Exposure of aquatic environments
(receiving surface waters) because WWTPs don´t (completely) remove
residuals (Wang
et al.
2016; Bijlsma
et al.
2012).
The occurrence of pharmaceuticals in wastewater and surface waters has
been object of systematic research since the 1990s (Zuccato
et al.,
2006). Therefore, it might seem as if the issue should not be considered
as an emerging risk. However, knowledge on the hazards for aquatic
communities is still far from being complete and, in many cases, the
possible effects on the aquatic ecosystems are completely unknown.
Pharmaceuticals and illicit drugs are, by definition, biologically active
compounds. The type of biological effect is highly specific and, in most
cases, unwanted for natural populations.
At the concentrations likely to occur in surface waters, the possibility of
effects that may be studied with tools capable to measure traditional
endpoints (e.g. acute or chronic toxicity) or more specific effects (e.g.
endocrine disrupting effects) is, in most cases, highly improbable.
Nevertheless, other types of direct or indirect effects on the functioning of
ecosystems determined by the specific biological activity, are possible and
largely unknown.
A couple of examples of the most known cases are:
Occurrence and spread of antibiotic resistance (AMR). Determined by
the presence of antibiotics in surface water, this may represent a
change in ecosystem functioning and a risk for human health (see, for
example, Xi
et al.,
2009).
Behavioural changes due to antidepressants. Psychoactive drugs alter
the behaviour of aquatic vertebrates, for example reducing the
capability to escape from predators, with dramatic changes in
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ecosystem functioning (see, for example, Brooks, 2014).
Other possible effects are fully unknown and difficult to predict.
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors)
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including
reliability of data,
a key reference if
possible any other
reasons for
concern.
1
*
*
3
3
*
Interactions among different
synergisms or antagonisms.
pharmaceuticals
with
possibilities
of
3
References
Bijlsma L., Emke E., Hernández F., de Voogt P. (2012)
Brooks B. (2014).
Emke E., Vughs D., Kolkman A., de Voogt P (2018).
Wang J., Wang S. (2016).
Xi C., Zhang Y., Marrs C.F., Ye W., Simon C., Foxman B., Nriagu J.
(2009).
6.
Zuccato E., Castiglioni S., Fanelli R., Reitano G., Bagnati R.,
Chiabrando C., Pomati F., Rossetti C., Calamari D. (2006).
7.
http://score-cost.eu/emcdda-wastewater-analysis-and-drugs/
1.
2.
3.
4.
5.
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4.7
Topic
Initiator(s)
Substance Mobility: a new criterion in chemicals regulation
Substance Mobility: a new criterion in chemicals regulation
Pim de Voogt
Sources
Causative factors
(see section 2 of
this document)
5, 8, 9, 11
d,e
Changes in public welfare measures / demographic changes
Our society is using increasingly more chemical substances, and
among the new emerging pollutants we are finding an increasing
number of polar organic compounds. Although the concentration level
of total organic contaminants decreases by about 2 orders of
magnitude going from WWTP effluents to groundwater used for
drinking water production to tapwater. The most polar contaminants
in the WWTP effluents remain in the water throughout its passage to
groundwater and also withstand traditional drinking water treatment
processes.
As a result, persistent mobile organic chemicals (PMOCs) may reach
drinking water. Examples include trifluoromethanesulfonic acid and its
halogenated homologues; 1-naphthalenesulfonic acid; 1,3-di-o-
tolylguanidine
and
GenX
(2,3,3,3-Tetrafluoro-2-(heptafluoro-
propoxy)propanoic acid; aka FRD-903 or HFPO-DA)
.
Hazard
(Rank features as
1,2,3 or *)
PMOC may be of an equivalent level of concern as PBT substances. If
emissions of PMOC or very persistent very mobile substances are
ongoing and removal during water treatment is incomplete, their
environmental concentrations will increase over time as these
substances circulate and enrich in the water cycle.
3
3
3
3
3
2
European legislation on chemical substances (REACH) primarily
focuses on substances that do not easily break down and are
therefore Persistent (P), accumulate in organisms (Bioaccumulation,
B) and have an effect on organisms (Toxicity, T). This PBT legislation
pays insufficient attention to the drinking water function of our
surface waters and groundwater. After all, there are substances that
do not accumulate very much but that are very difficult to remove
from water. Due to their great affinity for water such substances are
Mobile (M). If substances have PMT properties then they can present
an exposure risk for humans via drinking water.
- uniqueness
- soundness
- severity
- scale
- urgency
-interactions
Parallels with
past emerging
issues. Potential
interactions with
other stressors)
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Potential Interactions: Exposure to (mixtures of) chemicals
Preliminary
Estimation of
importance (*, 1,
2 or 3 where
*=uncertain and 3
is high)
Background
including
reliability of data,
a key reference if
possible any other
reasons for
concern.
3
-Topic is highly relevant for REACH legislation
-German UBA has issued a revised proposal for implementing criteria
and an assessment procedure to identify Persistent, Mobile and Toxic
(PMT) and very Persistent, very Mobile (vPvM) substances registered
under REACH.
Whether an organic compound does or does not possess an affinity
for water is mainly determined by the polarity of that substance. Polar
substances and those that have a permanent charge (ions, such as
salts) have an extremely high affinity for water. That high affinity
means that polar and charged substances dissolve easily in water and
are poorly retained in soils through which the water passes, in
riverbanks or by sorptive water treatment processes. Such substances
are difficult to remove from water during purification. In other words,
the substances move easily with the (moving) water, are transported
along with it and can easily reach drinking water: the substance is
Mobile (M).
Drinking water companies are certainly increasingly confronted with
new expenditures necessary to cope with polar substances.
References
1. Reemtsma T., Berger U., Arp H.P.H., Gallard H., Knepper T.P.,
Neumann M., Quintana J.B., de Voogt P. (2016).
2. Sjerps R.M.A., Vughs D. van Leerdam J.A., ter Laak T.L., van
Wezel A.P. (2016).
3. http://www.ufz.de/promote/
4.
https://www.umweltbundesamt.de/en/publikationen/protectin
g-the-sources-of-our-drinking-water-from
5. Zahn D., Frömel T., Knepper T.P. (2016).
6. Montes R., Aguire J., Vidal X., Rodil R., Cela R., Quintana J.B.
(2017).
7. Versteegh J.F.M., de Voogt P. (2017).
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4.8
Drinking water treatment interactions with compounds and
potential health effects
Drinking
water
treatment
interactions
compounds and potential health effects
Marian Scott
5,6,10
a,b
New and modified drinking water treatments are being used to deal with
removal of chemical (natural and anthropogenic) contaminants in the
source waters. It is anticipated that in the light of climate change, there
may be further interactions between such natural contaminants, leading
to new (or increased) concentrations of by-products with potential for
human health concerns.
with
Topic
Initiator(s)
Sources
Causative factors
(see section 2 of
this document)
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors.
2
1
2
3
1
*
Many disinfection methods are being used in the production of drinking
water. Among these, the advanced oxidation processes serve the dual
purposes of disinfection and removal of chemical contaminants present in
source water.
Studies have shown that water containing natural organic matter, when
treated with UV for disinfection, generated multiple disinfection
byproducts (DBPs). [Bond
et al.
Water Res 45 (2011) 4341-54;
Richardson
et al.
Mutat. Res. 636 (2007) 178-242; Ceretti
et al.
J Public
Health Res. 2016 Dec 9; 5(3), 769], including Nitrogen-containing
mutagenic DBPs [Vughs
et al.
Environ Sci Pollut Res 25 (2018) 3951-64].
Climate change is expected to increase surface run off in river
catchments, leading to increased amounts and loads, as well as possible
changes in characteristics, of natural organic matter in the source waters
[Soh
et al.,
The Environmentalist 28 (2007) 158-165].
used for
producing drinking water. This means that there is an increased
probability that DBPs are being formed in the treatment processes
required for disinfection and purification.
Climate change effects may result in the need to modify water treatment
processes resulting in potentially new interactions, and lead to the
development of new treatment methods which could result in the
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formation of novel disinfection products with health effects including
mutagenicity.
Preliminary
Estimation of
importance (*, 1, 2
or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
2
There are a variety of papers and studies being published concerning
interactions between water treatment chemicals, organic material and
residues in drinking water, exacerbated by climate change and with
potential health effects (including neurological disorders). Aluminium has
been implicated in the past, but the treatment interactions with chemical
contaminants and the possible effects of climate change mean that this
topic is gaining renewed interest. Examples of some of the studies are
given below.
References
1. Lalas S., Athanasiadis V., Dourtoglou V.G. (2018).
2. Glassmeyer S.T., Furlong E.T., Kolpin D.W., Batt A.L., Benson R.,
Boone J.S., Conerly O., Donohue M.J., King D.N., Kostich M.S.,
Mash H.E., Pfaller S.L., Schenck K.M., Simmons J.E., Varughese
E.A., Vesper S.J., Villegas E.N., Wilson V.S. (2017).
3. Benson R., Conerly, O.D. Sander W., Batt A.L., Boone J.S.,
Furlong E.T., Glassmeyer S.T., Kolping D.W. Mash H.E., Schenck
K.M., Simmonsi J.E. (2017).
4. Kessing, L.V., Gerds T. A. Nygård Knudsen N.,
et al.
(2017).
5. Post G.B., Gleason J.A., Cooper K.R. (2017).
6. Bond T., Huang J., Templeton M.R., Graham N. (2011).
7. Richardson S.D., Plewa M.J., Wagner E.D., Schoeny R., Demarini
D.M. (2007).
8. Ceretti E., Moretti M., Zerbini I., Villarini M., Zani C., Monarca S.,
Feretti D. (2016).
9. Vughs D., Baken K.A., Kolkman A., Martijn A.J., de Voogt P.
(2018).
10. Soh Y., Roddick F., Van Leeuwen J. (2007).
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4.9
Topic
Per- and polyfluorinated organic substances
Per- and polyfluorinated alkyl substances (PFAS)
Initiator(s)
Pim de Voogt
Sources
Causative factors
see section 2
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors)
4, 11, 13
c, d, h
Because of the persistence of PFAS, these compounds constitute potential
risks for humans and the environment.
3
3
3
3
3
*
Parallels: POPs
Very few PFAS have been regulated (PFOS Stockholm convention; PFOS
in products (EC); TDIs for PFOS and PFOA (EFSA). A new Opinion on
PFOS and PFOA in food, by the EFSA Contam panel, has been finalised in
Mar 2018. A Scientific Opinion by EFSA on the risk to human health
related to the presence of Perfluoroalkylated substances in food, other
than Perfluorooctane sulfonate and Perfluorooctanoic acid, is in the
process of completion. PFOA is under review by the Stockholm POP
convention.
Possible interactions: dietary exposure to (mixtures of) chemicals.
Preliminary
Estimation of
prioritisation (*, 1,
2 or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
2-3
As a result of new information becoming available on the toxicity of PFAS,
the revision of current guideline values (e.g. TDIs, drinking water
guidelines) is urgent and for some members of the PFAS group it is
underway. For others essential data are still missing. Hence the
prioritisation is high.
For several members of the PFAS group PBT properties have been
demonstrated. Others appear to be persistent and mobile (PM) and cross
natural or technological barriers, thus posing risks to public health
because of human exposure. Replacements by industry for the major
part appear to rely on fluorine chemistry (e.g. GenX) which inherently
leads to similarities in persistence. Many more emerging PFAS have been
recently found to occur in surface waters (see e.g. Gebbink
et al.,
2017).
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References
1. Scientific Panel on Contaminants in the Food Chain, Minutes of the
85
th
Plenary meeting held on 4-6 July 2017, Parma (Italy).
https://www.efsa.europa.eu/sites/default/files/event/170704-
m.pdf;
http://registerofquestions.efsa.europa.eu/roqFrontend/questionLo
ader?question=EFSA-Q-2015-00526;
http://registerofquestions.efsa.europa.eu/roqFrontend/questionDo
cumentsLoader?question=EFSA-Q-2017-00549
2. Gebbink W.A., van Asseldonk L., van Leeuwen S.P.J. (2017)..
3. Blum A., Balan S.A., Scheringer M., Trier X., Goldenman G.,
Cousins I., Diamond M., Fletcher T., Higgins C., Lindeman A.E.,
Peaslee G., de Voogt P., Wang Z., Weber R. (2015).
4. Ritscher A.
et al.
(2018).
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4.10
New RNA pesticides and gene editing to reduce/eradicate
pest populations
Topic
New RNA pesticides and gene editing to reduce/eradicate pest
populations
Marian Scott
6,8,10,12
a,f,h
With increasing concerns about the negative impact of the use of
chemical pesticides (see recent debates concerning glyphosates and
neonicotinoids), on both the environment and humans, there are new
developments in the use of gene technology (in the broadest sense) to
manage pest populations).
Initiator(s)
Sources
Causative factors
(see section 2 of
this document)
Hazard
(Rank features as
1, 2, 3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors)
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
2
1
2
3
3
3
Effects of various pesticides including examples such as neonicotinoids
and glyphosate have been much contested, and any form of gene editing
is likely to be met with concerns particularly given the social and political
debates concerning GMO.
3
Laboratory tests have shown that topical application of RNA could be a
new way of controlling plant pests, including viruses and insects, by
silencing genes that affect survival and reproduction. It is thought this
method could be more publicly acceptable than other forms of genetic
modification because its effects will not be passed on to offspring.
However, the impact of widespread use of the method as a pesticide on
non-target species is not yet known.
New gene editing technologies could also be used to control animal
populations, including invasive species, within the coming decade. For
instance, applications of CRISPR-enabled gene drive technology are
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foreseen for several applications, such as the elimination or suppression
of insect vectors and transmitting (plant) diseases. At a cost of more
than £3 million a year, New Zealand aims to rid itself of rats, possums
and stoats by 2050. These methods raise both ethical and ecological
questions, from repercussions on wider ecosystems to the potential for
gene traits to spread and wipe-out species in unintended areas.
References
1.
2.
3.
4.
Lundgren J.G., Duan J.J. (2013).
Albright
et al.
(2017).
Medina R.F. (2018).
Royal Society Te Apārangi Gene Editing Panel. (2017).
https://royalsociety.org.nz/assets/Uploads/Gene-editing-in-pest-
control-technical-paper.pdf
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4.11
Do-it-Yourself Synthetic Biology, biohacking
Topic
Do-it-Yourself Synthetic Biology, biohacking
Initiator(s)
Theo Vermeire
Sources
Causative factors
see section 2
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors)
3, 9, 11
a, c, g
2
2
3
3
2
1
As SynBio advances, its methods, equipment and technologies will be
cheaper, simpler and easier to use. The number and complexity of
products, new pathways to risk-assessment endpoints, large range of
types of products, new actors, including DIY bioengineers (also known as
biohackers) and complex alignment of potential future products with
agency authorities are likely to change rapidly as biotechnology
advances. SynBio will likely foster citizen science, i.e. attracting DIY
biologists into a field traditionally reserved for highly trained
professionals. The nature of the citizen science community raises
concerns that its practitioners will not abide by risk assessment and
biosafety practices required by law of the professional SynBio
community. The issue is not whether SynBio can be safely practiced; it is
a question of whether DIY biologists will practice it safely. Accidental use
or misuse of SynBio kits by consumers was identified as a cause of
concern in the SCENIHR Opinion on SynBio. There is evidence that this
may lead to actual risks, e.g. when a kit is contaminated by pathogenic
species or malware is incorporated in DNA-samples.
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
3
References
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including reliability
of data, a key
reference if
possible any other
reasons for
concern.
1. SCHER (Scientific Committee on Health and Environmental Risks),
SCENIHR (Scientific Committee on Emerging and Newly Identified
Health Risks), SCCS (Scientific Committee on Consumer Safety),
Synthetic Biology II - Risk assessment methodologies and safety
aspects, Opinion, December, 2014.
2. Epstein M., Vermeire T. (2016).
3. National Academies of Sciences, Engineering, and Medicine
(2017).
4. Schmidt M. (2008).
5.
http://www.dw.com/en/biohacking-genetic-engineering-from-
your-garage/a-42030559?maca=en-rss-en-all-1573-rdf
6.
https://groups.google.com/forum/#!topic/diybio/PXeoidiWPYA
7.
https://www.wired.com/story/malware-dna-hack/
8.
https://www.youtube.com/watch?v=F9HScPlBFhM
9.
https://www.lgl.bayern.de/presse/detailansicht.htm?tid=680089
10.
https://www.scientificamerican.com/article/mail-order-crispr-kits-
allow-absolutely-anyone-to-hack-dna/?sf188033786=1
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4.12
Micro and nano-plastic in the environment
Topic
Initiator(s)
Micro and nano-plastic in the environment
Marco Vighi, Qasim Chaudhry (SCCS)
Sources
Causative factors
(see section 2 of
this document)
Hazard
(Rank features as
1,2,3 or *)
5
Urban and industrial waste water. Agricultural soils treated with WWTP
sludge. Macroplastic debris. Tyre debris.
a
The increasing environmental pollution by plastic materials has recently
come to the attention of authorities around the world. For example, WHO
has recently launched a health review after microplastics were found in
90% of bottled water (www.bbc.co.uk/news/science-environment-
43389031). The UK has banned the use of plastic microbeads in cosmetic
products (https://chemicalwatch.com/62944/uk-microbeads-ban-enters-
into-force).
The production, use and disposal of plastic materials is now ubiquitous.
The largest area of plastic use is for packaging materials and a wide
range of other objects.
Plastic polymers have not been considered substances of health concern
because they are generally inert in nature, and are unlikely to be
absorbed in the body due to large molecular sizes. They are nevertheless
highly persistent in the environment where they may end up via a variety
of disposal/emission routes. Gradual degradation of plastic materials over
time is known to result in microplastics - which in theory could also
further degrade to nano-plastics. Some forms of microplastics are also
used in cosmetic products which makes their direct emission into the
aquatic environment possible.
The effects of MPs on living organisms may be direct, mainly physical
(damages to respiratory systems or digestive tracts) or behavioural
(changes in food intake), or indirect, determined by the uptake of
chemicals adsorbed on the plastic. The actual relevance of these effects
is dependent on the realistic exposure in soil and water environments,
which is still largely unknown.
-
-
-
-
-
-
uniqueness
soundness
severity
scale
urgency
interactions
3
*
*
3
3
*
This is a relatively new topic and after decades of ignorance has recently
come under the focus of attention of researchers, authorities and the
Parallels with past
emerging issues.
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Potential
interactions with
other stressors)
Preliminary
Estimation of
importance (*, 1, 2
or 3 where
*=uncertain and 3
is high)
general public.
Possible interactions between MPs and potentially toxic chemicals.
*
Considering the amount of the emissions, the issue could be of high
importance. However the available information on actual exposure in the
different environmental compartments as well as on the effects on living
organisms is still highly controversial. The sampling methods for
microplastic as well the analytical methods are not standardised and
different procedures, providing different results, are used in monitoring
studies. Therefore, measured data in the aquatic environment reported in
the literature are often difficult to compare. As for the effect assessment,
microplastic (arbitrarily defined as bigger than 1 m) should not cross cell
membranes and, if ingested, should remain in the digestive system,
producing only physical effects. On the contrary, nanoplastics can
probably enter the cells and, possibly, interact with cell metabolism.
However, to date, these are just hypotheses. There is some evidence in
the literature of the cellular uptake of nanoplastic but the threshold below
which this may occur is unknown, as well as the type of biological effects.
These uncertainties point to the need for a better assessment of hazard
and risk. It is opinion of the SCHEER that the standardisation of methods
for assessing exposure, as well as the development of methods for
assessing the different behaviour in living organisms of micro and nano
plastics, represent urgent priorities.
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
The occurrence of micro and macro plastic in the environment is
recognised as one of the most serious environmental problems at the
global level. In particular, microplastics (MPs) in the marine environment
have been extensively studied for a long time (GESAMP, 2015), while, in
freshwater, the problem is much less known (Breuninger
et al.,
2017).
References
1. GESAMP (2015). Joint Group of Experts on the Scientific Aspects
of Marine Environmental Protection).
2.
Breuninger E., Bänsch-Baltruschat B., Brennholt N., Hatzky S.,
Kochleus C., Reifferscheid G., Koschorreck J. (2017).
3. Wright S.L., Kelly F.J. (2017).
4. Andrady A.L. (2017).
5. Galloway T.S., Cole M., Lewis C. (2017).
6.
www.efsa.europa.eu/en/press/news/160623
7.
www.independent.co.uk/environment/microplastics-microbeads-
health-risks-investigations-uk-government-ban-possibility-
a7416271.html
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4.13
Nanoparticles
released from Building
construction waste to the Environment
Topic
Initiator(s)
Sources
Causative factors
(see section 2 of
this document)
Materials
and
Nanoparticles released from Building Materials and construction
waste to the Environment
Rodica-Mariana Ion
1,4,5
a,
Sources:
Nanomaterials are found in construction products, primarily in
surface coatings, concrete, window glass, insulation and steel. Not all of
them contain nanoparticles. However, some nanomaterials may be
hazardous due to the presence of very small particles and the similarities
observed between some nanomaterials and asbestos fibres. The involved
materials have potential impact on both human health and on the
environment. The most used are: TiO
2
, SiO
2
, ZnO, Ag, CuO, and CaCO
3
.
Also, there are some nanomaterials in cement such as: SiO
2
, Al
2
O
3
,
Fe
2
O
3
, ZrO
2
, carbon nanotubes (CNTs) and carbon nanofibers (CNFs).
Titanium dioxide particles or antimicrobial silver nanoparticles or even
carbon nanotubes (CNTs) provide concrete with self-cleaning properties,
or antimicrobials or give it with improved strength and potentially
electrical conductivity.
Causative factors:
various nanomaterials used in the building industry
and their potential release from paint waste, during the renovation and
demolition processes, during recycling, landfilling and incineration
technologies. The release of NPs may occur when the coatings are not
adequately fixed to the stone or when they are not sufficiently effective
to prevent stone degradation and crumbling. Those NPs that end up in
the water systems can adversely affect aquatic and marine life and in the
soil, essential microbial interactions may be interfered with, affecting
functional diversity.
Hazard
(Rank features as
1,2,3 or *)
-uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors
3
*
*
3
3
*
Several building materials exist from the older building technologies still
exist and are used because of their proximity, availability and
geographical location. Such material includes mud bricks (adobe), stones,
cobs and wood to mention a few. These the traditional building materials
are stereotypically binary: earth related material and wood related.
There is currently lack of regulations requiring labeling or other listings of
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these materials containing nanomaterials The possible release of
nanomaterials into the environment by this route must therefore be
taken into consideration, as follows:
[i] identify the sources and the flows of released nanomaterials in
construction waste,
[ii] identify the potential exposure pathways of released nanomaterials
for humans and other organisms,
[iii] identify the release of released nanomaterials to technical
compartments and the environment and
[iv] identify the hazard they represent for organisms. After gathering all
these elements, a characterisation of risk is plausible.
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
3
References
Christine G., Benjamín O.O.M. (2018).
Shandilya N.,
et al.
(2015).
Hincapié I., Caballero-Guzmán A., Nowack B. (2015).,
Mitrano D.M., Mehrabi K., Dasilva Y.A.R. Nowack B. (2017).
Dulger M., Sakallioglu T., Temizel I., Demirel B., Copty N.K.,.
Onay T.T., Uyguner-Demirel C.S., Karanfil T. (2016).
6. Sakallioglu T., Bakirdoven M., Temizel I., Demirel B., Copty N.K.,
Onay T.T., Uyguner Demirel C.S., Karanfil T. (2016).
7. van Broekhuizen P., van Broekhuizen F., Cornelissen R., Reijnders
L. (2011)..
8. Hanus M.J., Harris A.T. (2013).
1.
2.
3.
4.
5.
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4.14
Environmental factors and the Human Microbiome
Topic
Initiator(s)
Sources
Causative factors
(see Section 2 of
this document)
b and f
Microbiome
refers to “the entire habitat, including the microorganisms
(bacteria, archaea, lower and higher eukaryotes and viruses), their
genome (i.e., genes), and surrounding environmental conditions”
(Marchesi and Ravel 2015). A key aspect of the human microbiome is the
variation in its composition and function observed among populations,
over the human life span, and between body sites such as the gut, skin,
or respiratory microbiome. Research is showing that the human
microbiome has a modulating role between environmental factors and the
health status (Fallani 2016; Gibson
et al.
2016; Yassour
et al.
2016; Chu
et al.
2017). On the other hand, microbial changes in the human
microbiome are being linked to an array of neurological, gastrointestinal,
metabolic, oncologic, hepatic, respiratory and auto immune disorders
(Lynch and Pedersen 2016). In this sense, it seems sensible to have a
better understanding on the relation between human exposure to
environmental stressors, changes occurring in the human microbiome
and onset of certain health conditions. Additionally, there is sufficient
scientific knowledge on toxicity and risk assessment of a great number of
environmental chemicals, generated during the last decades under
several regulatory frameworks (WHO, IPCS, EPA, EFSA, ECHA) that can
contribute substantially to gaining a better understanding of the
underlying critical factors.
Environmental factors and the Human Microbiome
Teresa Borges
Hazard
(Rank features as
1,2,3 or *)
- uniqueness
- soundness
- severity
- scale
- urgency
- interactions
Parallels with past
emerging issues.
Potential
interactions with
other stressors
2
2
*
2
2
3
The structure and function of the human microbiome in both disease and
healthy states have been benefiting from improvements in high-
throughput and accuracy of DNA sequencing of the genomes of microbial
communities that are associated with human samples, complemented by
OMICS analysis (transcriptomes, proteomes, metabolomes and
immunomes) and by mechanistic experiments in model systems. Also, as
a result of international projects dedicated to the Human Microbioma, gut
microbioma has been subjected to intensive research and quality criteria
and standardisations have been developed i.e. reference microbiota
strains, in housing protocols, human sampling protocols. Presently, gut
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microbes can be transplanted effectively and under experimental
controlled conditions into germ-free mice to recapitulate their associated
phenotypes (Blanton
et al.,
2016). Also, Schwarzer
et al.
(2016) showed
in mice that strains of
Lactobacillus plantarum
in the gut microbiota
sustained growth hormone activity via signalling pathways in the liver,
thus overcoming growth hormone resistance. This evidence strengthens
the correlation between the changes in children's gut microbiota
composition and children's growth factors, therefore showing that
beneficial gut microbes can potentially be exploited to resolve
undernutrition syndromes in children. It is expected that in the near
future, metrics and biomarkers will be identified to set more effective
measures and health therapies (Dietert and Silbergeld 2015).
Preliminary
Estimation of
importance (*,1,2
or 3 where
*=uncertain and 3
is high)
Background
including reliability
of data, a key
reference if
possible any other
reasons for
concern.
2
References
1. Gilbert J.A., Blaser M.J., Caporaso J.G., Jansson J.K., Lynch S.V.,
Knight R. (2018).
2. Schwarzer M.,
et al
(2016).
3. Blanton L.V.
et al.
(2016).
4. Collado M.C.
et al.
(2016)
5. Fallani 2016; Gibson
et al.
2016; Yassour
et al.
2016; Chu et al.
2017.
6. Lynch S.V., Pederson O. (2016)
7. Dietert R.R. and Silbergeld E.K. (2015).
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5.
CONCLUSIONS
The SCHEER identified 14 emerging issues to bring to the attention of the
Commission services. The overall prioritisation scores (*, 1,2,3 where *=uncertain
and 3 is high) are as follows:
4.1
4.2
4.3
4.4
4.5
4.6
Personal communication and listening devices
Virtual reality
E-cigarette and chronic diseases
Potential effects on wildlife of increases in electromagnetic radiation
Chemicals in recycled materials, an issue in a circular economy
Pharmaceuticals (human and veterinary) and illicit drugs in wastewater and
surface waters
Substance Mobility: a new criterion in chemicals regulation
Drinking water treatment interactions with compounds and potential health
effects
Per- and polyfluorinated organic substances
New RNA pesticides and gene editing to reduce/eradicate pest populations
Do-it-Yourself Synthetic Biology, biohacking
Micro and nano-plastic in the environment
Nanoparticles released from Building Materials and construction waste to the
Environment
Environmental factors and the Human Microbiome
1
3
3
3
3
3
4.7
4.8
3
2
4.9
4.10
4.11
4.12
4.13
2-3
3
3
*
3
4.14
2
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6.
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