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www.thelancet.com/oncology Published online June 22, 2011 DOI:10.1016/S1470-2045(11)70147-4
1
Carcinogenicity of radiofrequency electromagnetic fi elds
In May, 2011, 30 scientists from
14 countries met at the International
Agency for Research on Cancer
(IARC) in Lyon, France, to assess the
carcinogenicity of radiofrequency
electromagnetic fi elds (RF-EMF).
These assessments will be published as
Volume 102 of the IARC Monographs.1
Human exposures to RF-EMF
(frequency range 30 kHz–300 GHz) can
occur from use of personal devices (eg,
mobile telephones, cordless phones,
Bluetooth, and amateur radios),
from occupational sources (eg, high-
frequency dielectric and induction
heaters, and high-powered pulsed
radars), and from environmental
sources such as mobile-phone base
stations, broadcast antennas, and
medical applications. For workers,
most exposure to RF-EMF comes from
near-fi eld sources, whereas the general
population receives the highest
exposure from transmitters close to
the body, such as handheld devices like
mobile telephones. Exposure to high-
power sources at work might involve
higher cumulative RF energy deposited
into the body than exposure to mobile
phones, but the local energy deposited
in the brain is generally less. Typical
exposures to the brain from rooftop
or tower-mounted mobile-phone base
stations and from TV and radio stations
are several orders of magnitude
lower than those from global system
for mobile communications (GSM)
handsets. The average exposure
from use of digital enhanced cordless
telecommunications (DECT) phones
is around fi ve times lower than that
measured for GSM phones, and
third-generation (3G) phones em
it, on average, about 100 times less
RF energy than GSM phones, when
signals are strong. Similarly, the
average output power of Bluetooth
wireless hands-free kits is estimated to
be around 100 times lower than that
of mobile phones.
EMFs generated by RF sources
couple with the body, resulting in
induced electric and magnetic fi elds
and associated currents inside tissues.
The most important factors that
determine the induced fi elds are
the distance of the source from the
body and the output power level.
Additionally, the effi ciency of coupling
and resulting fi eld distribution inside
the body strongly depend on the
frequency, polarisation, and direction
of wave incidence on the body, and
anatomical features of the exposed
person, including height, body-
mass index, posture, and dielectric
properties of the tissues. Induced
elds within the body are highly non-
uniform, varying over several orders of
magnitude, with local hotspots.
Holding a mobile phone to the ear
to make a voice call can result in high
specifi c RF energy absorption-rate
(SAR) values in the brain, depending
on the design and position of the
phone and its antenna in relation to
the head, how the phone is held, the
anatomy of the head, and the quality
of the link between the base station
and phone. When used by children,
the average RF energy deposition
is two times higher in the brain and
up to ten times higher in the bone
marrow of the skull, compared with
mobile phone use by adults.2 Use
of hands-free kits lowers exposure
to the brain to below 10% of the
exposure from use at the ear, but it
might increase exposure to other
parts of the body.3
Epidemiological evidence for an
association between RF-EMF and
cancer comes from cohort, case-
control, and time-trend studies. The
populations in these studies were
exposed to RF-EMF in occupational
settings, from sources in the general
environment, and from use of wireless
(mobile and cordless) telephones,
which is the most extensively studied
exposure source. One cohort study4
and fi ve case-control studies5–9 were
judged by the Working Group to
off er potentially useful information
regarding associations between use of
wireless phones and glioma.
The cohort study4 included 257 cases
of glioma among 420 095 subscribers
to two Danish mobile phone companies
between 1982 and 1995. Glioma
incidence was near the national average
for the subscribers. In this study,
reliance on subscription to a mobile
phone provider, as a surrogate for
mobile phone use, could have resulted
in considerable misclassifi cation in
exposure assessment. Three early
case-control studies5–7 encompassed
a period when mobile phone use was
low, users typically had low cumulative
exposures, time since fi rst use of a
mobile phone was short, and eff ect
estimates were generally imprecise;
the Working Group considered these
studies less informative. Time-trend
analyses did not show an increased
rate of brain tumours after the increase
in mobile phone use. However, these
studies have substantial limitations
because most of the analyses examined
trends until the early 2000s only. Such
analyses are uninformative if excess
risk only manifests more than a decade
after phone use begins, or if phone
use only aff ects a small proportion of
cases—eg, the most heavily exposed, or
a subset of brain tumours.
The INTERPHONE study,8 a
multicentre case-control study, is
the largest investigation so far of
mobile phone use and brain tumours,
including glioma, acoustic neuroma,
and meningioma. The pooled analysis
included 2708 glioma cases and
2972 controls (participation rates 64%
and 53%, respectively). Comparing those
who ever used mobile phones with
those who never did yielded an odds
ratio (OR) of 0·81 (95% CI 0·70–0·94). In
terms of cumulative call time, ORs were
uniformly below or close to unity for all
deciles of exposure except the highest
decile (>1640 h of use), for which the OR
for glioma was 1·40 (95% CI 1·03–1·89).
There was suggestion of an increased
risk for ipsilateral exposure (on the same
Published Online
June 22, 2011
DOI:10.1016/S1470-
2045(11)70147-4
For more on the IARC
Monographs see
http://monographs.iarc.fr/
Upcoming meetings
Oct 11–18, 2011
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and some heterocyclic polycyclic
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June 5–12, 2012
Diesel and gasoline engine
exhausts and some nitroarenes
Monograph Working Group
Members
J Samet—Chair (USA);
B Armstrong, M Sim (Australia);
E Degrave [not present during
evaluations], L Verschaeve
(Belgium); J Siemiatycki,
J McNamee (Canada);
D Leszczynski, J Juutilainen
(Finland); R de Seze, J-F Doré
(France); M Blettner,
C Dasenbrock (Germany);
J Miyakoshi, T Shirai (Japan);
S Szmigielski ([unable to
attend] Poland); N Kim
(Republic of Korea); I Belyaev
(Slovak Republic); E Cardis
(Spain); L Hardell (Sweden);
M Mevissen, M Röösli
(Switzerland); S Mann (United
Kingdom); C Blackman, P Inskip
[not present during fi nal
evaluation], D McCormick,
R Melnick, C Portier,
D Richardson, Vijayalaxmi (USA)
Invited specialists
A Ahlbom ([withdrew] Sweden);
N Kuster (Switzerland)
Representatives
L Bontoux, K Bromen (European
Commission DG SANCO,
Belgium); H Dekhil (Agence
Nationale de Contrôle Sanitaire
et Environnementale des
Produits, Tunisia); C Galland,
O Merckel (ANSES, France)
News
2
www.thelancet.com/oncology Published online June 22, 2011 DOI:10.1016/S1470-2045(11)70147-4
side of the head as the tumour) and for
tumours in the temporal lobe, where
RF exposure is highest. Associations
between glioma and cumulative specifi c
energy absorbed at the tumour location
were examined in a subset of 553 cases
that had estimated RF doses.10 The OR
for glioma increased with increasing
RF dose for exposures 7 years or more
before diagnosis, whereas there was
no association with estimated dose
for exposures less than 7 years before
diagnosis.
A Swedish research group did a
pooled analysis of two very similar
studies of associations between mobile
and cordless phone use and glioma,
acoustic neuroma, and meningioma.9
The analysis included 1148 glioma
cases (ascertained 1997–2003) and
2438 controls, obtained through cancer
and population registries, respectively.
Self-administered mailed question-
naires were followed by telephone
interviews to obtain information
on the exposures and covariates of
interest, including use of mobile and
cordless phones (response rates 85%
and 84%, respectively). Participants
who had used a mobile phone for more
than 1 year had an OR for glioma of 1·3
(95% CI 1·1–1·6). The OR increased with
increasing time since fi rst use and with
total call time, reaching 3·2 (2·0–5·1)
for more than 2000 h of use. Ipsilateral
use of the mobile phone was associated
with higher risk. Similar fi ndings were
reported for use of cordless phones.
Although both the INTERPHONE
study and the Swedish pooled analysis
are susceptible to bias—due to recall
error and selection for participation—
the Working Group concluded that
the fi ndings could not be dismissed
as refl ecting bias alone, and that a
causal interpretation between mobile
phone RF-EMF exposure and glioma
is possible. A similar conclusion was
drawn from these two studies for
acoustic neuroma, although the case
numbers were substantially smaller
than for glioma. Additionally, a study
from Japan11 found some evidence of
an increased risk for acoustic neuroma
associated with ipsilateral mobile
phone use.
For meningioma, parotid-gland
tumours, leukaemia, lymphoma, and
other tumour types, the Working
Group found the available evidence
insuffi cient to reach a conclusion on
the potential association with mobile
phone use. Epidemiological studies of
individuals with potential occupational
exposure to RF-EMF have investigated
brain tumours, leukaemia, lymphoma,
and other types of malignancy
including uveal melanoma, and
cancers of the testis, breast, lung,
and skin. The Working Group noted
that the studies had methodological
limitations and the results were
inconsistent. In reviewing studies that
addressed the possible association
between environmental exposure
to RF-EMF and cancer, the Working
Group found the available evidence
insuffi cient for any conclusion.
The Working Group concluded
that there is “limited evidence in
humans” for the carcinogenicity of RF-
EMF, based on positive associations
between glioma and acoustic neuroma
and exposure to RF-EMF from wireless
phones. A few members of the
Working Group considered the current
evidence in humans “inadequate”. In
their opinion there was inconsistency
between the two case-control studies
and a lack of an exposure-response
relationship in the INTERPHONE study
results; no increase in rates of glioma
or acoustic neuroma was seen in the
Danish cohort study,4 and up to now,
reported time trends in incidence rates
of glioma have not shown a parallel to
temporal trends in mobile phone use.
The Working Group reviewed more
than 40 studies that assessed the
carcinogenicity of RF-EMF in rodents,
including seven 2-year cancer bioassays.
Exposures included 2450 MHz RF-EMF
and various RF-EMF that simulated
emissions from mobile phones. None
of the chronic bioassays showed an
increased incidence of any tumour type
in tissues or organs of animals exposed
to RF-EMF for 2 years. An increased
total number of malignant tumours
was found in RF-EMF-exposed animals
in one of the seven chronic bioassays.
Increased cancer incidence in exposed
animals was noted in two of 12 studies
with tumour-prone animals12,13 and
in one of 18 studies using initiation-
promotion protocols.14 Four of six
co-carcinogenesis studies showed
increased cancer incidence after
exposure to RF-EMF in combination
with a known carcinogen; however, the
predictive value of this type of study for
human cancer is unknown. Overall, the
Working Group concluded that there
is “limited evidence” in experimental
animals for the carcinogenicity of
RF-EMF.
The Working Group also reviewed
many studies with endpoints relevant
to mechanisms of carcinogenesis,
including genotoxicity, eff ects on
immune function, gene and protein
expression, cell signalling, oxidative
stress, and apoptosis. Studies of
the possible eff ects of RF-EMF on
the blood-brain barrier and on a
variety of eff ects in the brain were
also considered. Although there was
evidence of an eff ect of RF-EMF on
some of these endpoints, the Working
Group reached the overall conclusion
that these results provided only weak
mechanistic evidence relevant to RF-
EMF-induced cancer in humans.
In view of the limited evidence in
humans and in experimental animals,
the Working Group classifi ed RF-
EMF as “possibly carcinogenic to
humans” (Group 2B). This evaluation
was supported by a large majority of
Working Group members.
Robert Baan, Yann Grosse,
Béatrice Lauby-Secretan,
Fatiha El Ghissassi, Véronique Bouvard,
Lamia Benbrahim-Tallaa, Neela Guha,
Farhad Islami, Laurent Galichet,
Kurt Straif, on behalf of the WHO
International Agency for Research on
Cancer Monograph Working Group
International Agency for Research on
Cancer, Lyon, France
We declare that we have no confl icts of interest.
Observers
J Elder (Mobile Manufacturers
Forum); C Marrant (Léon Bérard
Centre, France); R Nuttall
(Canadian Cancer Society,
Canada); J Rowley (GSM
Association, UK); M Swicord
(CTIA Wireless Association, USA)
IARC Secretariat
R Baan, L Benbrahim-Tallaa,
V Bouvard, G Byrnes, R Carel,
I Deltour, F El Ghissassi,
L Galichet, Y Grosse, N Guha,
A Harbo Poulsen, F Islami,
A Kesminiene, B Lauby-Secretan,
M Moissonnier, R Saracci, J Schüz,
K Straif, E van Deventer
Confl icts of interest
MS’s spouse owns shares
(worth €1350) in Telstra, a
telecommunications company in
Australia. BA has received travel
and accommodation expenses
for presentations on mobile
phone use and brain tumours,
from various Australian
organisations and government
groups. EC has received travel
and accommodation expenses
for presentations organised by
France Telecom. RdS has received
research support from Fondation
Santé et Radiofréquences, and
was a paid advisor (<€1000) for
the plaintiff ’s lawyer on a lawsuit
involving radiofrequency
exposure. NK is director and
board member of the non-profi t
IT’IS foundation that performs
exposure assessments for
industry and governments, and
is president of the board and
shareholder of Near-Field
Technology AG, which controls
two companies that develop
near-fi eld measurement
instruments, simulation
software, and medical test
equipment. All other Working
Group members, specialists,
representatives, and secretariat
declared no confl icts of interest.
News
www.thelancet.com/oncology Published online June 22, 2011 DOI:10.1016/S1470-2045(11)70147-4
3
1 IARC. IARC monographs on the evaluation of
carcinogenic risks to humans, vol 102.
Non-ionizing radiation, part II: radiofrequency
electromagnetic fi elds. Lyon: International
Agency for Research on Cancer (in press).
2 Christ A, Gosselin MC, Christopoulou M,
Kühn S, Kuster N. Age-dependent
tissue-specifi c exposure of cell phone users.
Phys Med Biol 2010; 55: 1767–83.
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Assessment of the radio-frequency
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4 Schüz J, Jacobsen R, Olsen JH, Boice JD Jr,
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7 Auvinen A, Hietanen M, Luukkonen R,
Koskela RS. Brain tumors and salivary gland
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Epidemiology 2002; 13: 356–59.
8 INTERPHONE Study Group. Brain tumour risk
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9 Hardell L, Carlberg M, Hansson Mild K. Pooled
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10 Cardis E, Armstrong BK, Bowman JD, et al. Risk
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11 Sato Y, Akiba S, Kubo O, Yamaguchi N.
A case-case study of mobile phone use and
acoustic neuroma risk in Japan.
Bioelectromagnetics 2011; 32: 85–93.
12 Repacholi MH, Basten A, Gebski V, Noonan D,
Finnie J, Harris AW. Lymphomas in E mu-Pim1
transgenic mice exposed to pulsed 900 MHZ
electromagnetic fi elds. Radiat Res 1997;
147: 631–40.
13 Szmigielski S, Szudzinski A, Pietraszek A,
Bielec M, Janiak M, Wrembel JK. Accelerated
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benzopyrene-induced skin cancer in mice
exposed to 2450-MHz microwave radiation.
Bioelectromagnetics 1982; 3: 179–91.
14 Hruby R, Neubauer G, Kuster N, Frauscher M.
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... RF radiation from devices that emit non-ionizing RF radiation in the frequency range 30 kHz-300 GHz, is a Group 2B, i.e. a 'possible', human carcinogen. 33,34 Later studies have corroborated these findings and have thus strengthened the evidence. 35,36 For children this risk may be accentuated because of a cumulative effect during a long lifetime use. ...
... In May 2011 IARC evaluated the carcinogenic potential from RF-EMF. The expert group classified RF-EMF in the frequency range 30 kHz-300 GHz as "possibly carcinogenic to humans", Group 2B (Baan et al., 2011;IARC, 2013). ...
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... A study conducted by [12,13] , stated that there were no relationship between locations or regions of the brain exposed to radiations and brain tumor . It has also been concluded that there is a risk of acoustic neuroma as well as aglioma [14][15][16], and it increases with the increase in the cell phone use duration. Mobile or cell phones now a days became an important part of current telecommunications in every individual life. ...
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... Some of these studies analysed the influence of the use of mobile telephones on cognitive function and behavioural problems in adolescents (Thomas et al., 2010;Divan et al., 2012), and others analysed the blood, heart, and autonomous nervous system (Havas, 2013) or the relationship between the use of mobile telephones and the risk of brain tumours and acoustic neuroma (Hardell et al., 2006;Coureau et al., 2014;INTERPHONE Study Group, 2011). Concerned about the increase of malignant brain cancers associated with the growing use of mobile telephones, the International Agency for Research on Cancer (IARC), a body dependent on the World Health Organization (WHO), has classified radio frequency electromagnetic fields (RF EMF) as possibly carcinogenic to humans (group 2 B) (Baan et al., 2011). ...
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... This widespread use of devices emitting electromagnetic waves is causing increasing exposure to electromagnetic fields, and this is recognized as "electro-smog" or "electro-pollution" [165]. Radio frequencies classified in group 2B are regarded as possibly carcinogenic for humans [166]. Currently, the legally recommended maximum specific absorption rates of cell phones are limited to 2.0 W/kg [167]. ...
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In this study, the radiation emission from mobile phones when used with wireless and wired hands-free kits (HFK) was evaluated to determine the necessity for a dedicated compliance procedure and the extent to which the use of wired and wireless HFK can reduce human exposure. The specific absorption rates (SAR) from wireless HFK were determined experimentally. Wired HFK were evaluated dosimetrically while connected to mobile phones (GSM900/1800, UMTS1950) under maximized current coupling onto the HFK cable and various wire routing configurations. In addition, experimentally validated simulations of a wired HFK and a mobile phone operating on anatomical whole-body models were performed. The maximum spatial peak SAR in the head when using wired HFK was more than five times lower than ICNIRP limits. The SAR in the head depends on the output power of the mobile phone, the coupling between the antenna and cable, external attenuation and potential cable specific attenuation. In general, a wired HFK considerably reduces the exposure of the entire head region compared to mobile phones operated at the head, even under unlikely worst-case coupling scenarios. However, wired HFK may cause a localized increase of the exposure in the region of the ear inside the head under worst-case conditions. Wireless HFK exhibit a low but constant exposure.
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A relative paucity of data exist on the possible health effects of using cellular telephones. To test the hypothesis that using handheld cellular telephones is related to the risk of primary brain cancer. Case-control study conducted in 5 US academic medical centers between 1994 and 1998 using a structured questionnaire. A total of 469 men and women aged 18 to 80 years with primary brain cancer and 422 matched controls without brain cancer. Risk of brain cancer compared by use of handheld cellular telephones, in hours per month and years of use. The median monthly hours of use were 2.5 for cases and 2.2 for controls. Compared with patients who never used handheld cellular telephones, the multivariate odds ratio (OR) associated with regular past or current use was 0.85 (95% confidence interval [CI], 0.6-1.2). The OR for infrequent users (<0. 72 h/mo) was 1.0 (95% CI, 0.5-2.0) and for frequent users (>10.1 h/mo) was 0.7 (95% CI, 0.3-1.4). The mean duration of use was 2.8 years for cases and 2.7 years for controls; no association with brain cancer was observed according to duration of use (P =.54). In cases, cerebral tumors occurred more frequently on the same side of the head where cellular telephones had been used (26 vs 15 cases; P =.06), but in the cases with temporal lobe cancer a greater proportion of tumors occurred in the contralateral than ipsilateral side (9 vs 5 cases; P =.33). The OR was less than 1.0 for all histologic categories of brain cancer except for uncommon neuroepitheliomatous cancers (OR, 2.1; 95% CI, 0.9-4.7). Our data suggest that use of handheld cellular telephones is not associated with risk of brain cancer, but further studies are needed to account for longer induction periods, especially for slow-growing tumors with neuronal features.
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Concern has arisen that the use of hand-held cellular telephones might cause brain tumors. If such a risk does exist, the matter would be of considerable public health importance, given the rapid increase worldwide in the use of these devices. We examined the use of cellular telephones in a case-control study of intracranial tumors of the nervous system conducted between 1994 and 1998. We enrolled 782 patients through hospitals in Phoenix, Arizona; Boston; and Pittsburgh; 489 had histologically confirmed glioma, 197 had meningioma, and 96 had acoustic neuroma. The 799 controls were patients admitted to the same hospitals as the patients with brain tumors for a variety of nonmalignant conditions. As compared with never, or very rarely, having used a cellular telephone, the relative risks associated with a cumulative use of a cellular telephone for more than 100 hours were 0.9 for glioma (95 percent confidence interval, 0.5 to 1.6), 0.7 for meningioma (95 percent confidence interval, 0.3 to 1.7), 1.4 for acoustic neuroma (95 percent confidence interval, 0.6 to 3.5), and 1.0 for all types of tumors combined (95 percent confidence interval, 0.6 to 1.5). There was no evidence that the risks were higher among persons who used cellular telephones for 60 or more minutes per day or regularly for five or more years. Tumors did not occur disproportionately often on the side of head on which the telephone was typically used. These data do not support the hypothesis that the recent use of hand-held cellular telephones causes brain tumors, but they are not sufficient to evaluate the risks among long-term, heavy users and for potentially long induction periods.