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News Published online June 22, 2011 DOI:10.1016/S1470-2045(11)70147-4
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
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June 22, 2011
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Monograph Working Group
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)
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)
2 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
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
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.
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 Published online June 22, 2011 DOI:10.1016/S1470-2045(11)70147-4
1 IARC. IARC monographs on the evaluation of
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Non-ionizing radiation, part II: radiofrequency
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2 Christ A, Gosselin MC, Christopoulou M,
Kühn S, Kuster N. Age-dependent
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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). ...
Exposure to extremely low-frequency electromagnetic fields (ELF-EMF) was in 2002 classified as a possible human carcinogen, Group 2B, by the International Agency for Research on Cancer at WHO based on an increased risk for childhood leukemia. In case-control studies on brain and head tumours during 1997-2003 and 2007-2009 we assessed life-time occupations in addition to exposure to different agents. The INTEROCC ELF-EMF Job-Exposure Matrix was used for associating occupations with ELF-EMF exposure (μT) with acoustic neuroma. Cumulative exposure (μT-years), average exposure (μT) and maximum exposed job (μT) were calculated. No increased risk for acoustic neuroma was found in any category. For cumulative exposure in the highest exposure category 8.52+ μT years odds ratio (OR) = 1.2, 95 % confidence interval (CI) = 0.8-2.0, p linear trend = 0.37 was calculated. No statistically significant risks were found in the time windows 1-14 years, and 15+ years, respectively. In conclusion occupational ELF-EMF was not associated with an increased risk for acoustic neuroma.
... 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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Aim: With increase in use of cell phone and exposure to radiation emission from Wi-Fi,cell damage in all the body systems is found.It is necessary to find ways and means to prevent that cell damage that may affect normal functioning of the organs etc. The objective of this study was to assess the damage to brain caused by exposure to cell phones connected with Wi-Fi and prevention of that damage with Vitamin E. Methods: Thirty male Wistar Albino rats were used in the study,rats were divided in different groups, they were exposed to cell phones and Wi-Fi for 8 weeks. The rats were treated with Vit. E 50 IU/kg of bodyweight for 4 weeks.Results: Histopathological examination of the rat brain revealed that, exposure of rats to cell phones and Wi-Fi caused significant damage to the neurons in different areas of rat brain .The rats treated with Vit. E showed less damage in comparison to untreated rat groups.Conclusion: In the brain of rats, treated with Vit. E intact neuronal architecture was found along with less inflammation.
... 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). ...
The main objective of this work was to evaluate human exposure to electromagnetic fields in a city of about one hundred thousand inhabitants, both inside and outside dwellings, using exposure quotients. To this end, a personal exposure meter was used, collecting data in different frequency bands, including radio and television broadcasting, mobile telephony, cordless telephones, and wireless communication networks. The indoor measurements were made with the exposure meter in a static position. Those outdoor were made by walking around the building with the exposure meter held by the operator. The median electric field was 0.200 V/m outdoors and 0.102 V/m indoors. The median of the ICNIRP exposure quotients for multiple-frequency sources was 25 10-6 outside and 16 10-6 inside. The proximity of the operator's body caused the readings of the electric field in the FM band to be overestimated by a factor of 1.35, and in the mobile telephony bands by factors from 0.76 to 1.02. The standard deviation of the measurements repeated inside a dwelling over five days was of the order of the exposure meter's standard uncertainty of calibration, but the spatial dispersion at the scale of a dwelling and of the city was much greater. The two main contributors to the exposure were FM radio followed by the "downlink" mobile telephony bands. Inside the dwellings, the DECT and WIFI bands contributed less. Exposure quotients are dimensionless parameters that characterize exposure, and reflect the relative weight of each service to that exposure.
... 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]. ...
Male infertility currently has an increasing incidence globally while affecting 13–18% of males in their lifetime. Well-defined etiologies of male infertility are broad, with numerous underlying lifestyle and environmental risk factors established. Importantly, a significant proportion of male infertility remains idiopathic or unexplained. Lifestyle activities and environmental contaminant exposures contribute as significant risk factors for male infertility. There has been a significant increase in synthetic chemical production since the 1940s, increasingly contaminating the environment and negatively affecting ecosystems, including human health. These chemicals include various solvents, plastics, pesticides, and heavy metal contamination, which enter the water and food chain, negatively affecting human health with consequences for the next generation. Furthermore, there has been a significant increase in nonionizing radiation through cell phone use and Wi-Fi, which have rapidly contaminated the environment with negative effects on male fertility. Many of the environmental and lifestyle exposures to various environmental contaminants mediate increased oxidative stress in the male reproductive tract, with associated increased DNA damage and epigenetic modification. These mechanisms are associated with infertility and poor fertilization capacity of the oocyte, increased risk of pregnancy complications, and recurrent pregnancy loss, as well as have negative impact on the health and development of the offspring. This chapter reviews current information on chemicals associated with male fertility as well as potential mechanisms. This includes metals (arsenic, cadmium, lead, mercury, chromium, copper), endocrine-disrupting chemicals and xenoestrogens, pesticides, synthetic and occupation chemicals (benzene, carbon disulfide, glycol ether, methoxychlor, phthalates, bisphenol A), ionizing radiation (ultraviolet and gamma rays) and nonionizing radiation (cell phones and Wi-Fi), tobacco, and air pollution. The current evidence for male infertility association, as well as any known mechanisms, is presented for the environmental factors known to negatively affect male infertility.
... Согласно заключению Международного агентства по изучению рака (IARC), имеются ограниченные доказательства (limited evidence) канцерогенного действия ЭМИ, хотя в IARC есть мнение меньшинства о недостаточности имеющихся доказательств [12,13]. «Limited evidence» означает, что причинно-следственная связь возможна, но другая интерпретация данных (случайность, уклон, мешающие факторы) не исключена. ...
Full-text available
... L'exposition aux ondes électromagnétiques issues des téléphones mobiles a été considérée par l'Organisation Mondiale de la Santé (OMS) comme un facteur cancérogène possible après une utilisation intensive et prolongée (Guha et al. 2011;Morgan et al. 2015) Une étude in-vivo montre également une corrélation possible entre l'exposition à des radiations radio-fréquence et l'apparition de tumeurs (Wyde et al. 2018). ...
Le glioblastome est un cancer du cerveau très agressif dont les thérapies actuelles n’augmentent que très peu la durée de vie. Dans cette thèse, nous étudions un nouveau traitement par effet magnéto-mécanique de particules (TEMMP). Un champ magnétique rotatif à faible fréquence (20 Hz) est appliqué pour faire vibrer des particules magnétiques en contact avec les cellules cancéreuses. Les particules développées sont produites par une approche top-down en salle blanche. Les disques de permalloy utilisés présentent une configuration en vortex avec une faible rémanence et une bonne dispersion en suspension. Des particules multicouches de Co/Pt avec une anisotropie perpendiculaire et des vortex de permalloy en forme d’ellipses sont aussi étudiés. L’efficacité du TEMMP est évaluée in-vitro sur des cellules de glioblastome et les différents paramètres sont optimisés. Une forte diminution du nombre de cellules après traitement est alors observée et le comportement des cellules restantes est affecté. Le TEMMP est ensuite adapté pour une étude in-vivo dans un modèle orthotopique de glioblastome chez la souris nude. L’injection des particules en intra-tumoral est mise au point. Les tissus sont peu affectés par le TEMMP comparé à une injection de particules, et une faible augmentation de la survie est observée. Pour mimer les propriétés mécaniques du cerveau de manière plus pertinente, un modèle in-vitro 3D est alors développé et validé. Conçu avec des sphéroïdes de cellules pris dans un gel d’agarose, ce modèle apporte des pistes d’optimisation.
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Effects [of exposure to 5G] include increased cancer risk, cellular stress, increase in harm- ful free radicals, genetic damages, structural and functional changes of the reproductive systems, learning and memory deficits, neu- rological disorders, and negative impacts on general well-being in humans. Living organisms at all levels, the scientists added, are affected by exposure to electro- magnetic fields produced by smartphone devices and transmission towers. Damage is not limited to humans as there is growing evidence of harmful effects in both plant and animal life.
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Due to the rapid development of mobile phone technology, we are continuously exposed to 1.7 GHz LTE radio frequency electromagnetic fields (RF-EMFs), but their biological effects have not been clarified. Here, we investigated the non-thermal cellular effects of these RF-EMFs on human cells, including human adipose tissue-derived stem cells (ASCs), Huh7 and Hep3B liver cancer stem cells (CSCs), HeLa and SH-SY5Y cancer cells, and normal fibroblast IMR-90 cells. When continuously exposed to 1.7 GHz LTE RF-EMF for 72 h at 1 and 2 SAR, cell proliferation was consistently decreased in all the human cells. The anti-proliferative effect was higher at 2 SAR than 1 SAR and was less severe in ASCs. The exposure to RF-EMF for 72 h at 1 and 2 SAR did not induce DNA double strand breaks or apoptotic cell death, but did trigger a slight delay in the G1 to S cell cycle transition. Cell senescence was also clearly observed in ASC and Huh7 cells exposed to RF-EMF at 2 SAR for 72 h. Intracellular ROS increased in these cells and the treatment with an ROS scavenger recapitulated the anti-proliferative effect of RF-EMF. These observations strongly suggest that 1.7 GHz LTE RF-EMF decrease proliferation and increase senescence by increasing intracellular ROS in human cells.
Whether radiofrequency (RF) fields are carcinogenic is controversial; epidemiological data have been inconclusive and animal tests limited. The aim of the present study was to determine whether long-term exposure to pulse-modulated RF fields similar to those used in digital mobile telecommunications would increase the incidence of lymphoma in E mu-Pim1 transgenic mice, which are moderately predisposed to develop lymphoma spontaneously. One hundred female E mu-Pim1 mice were sham-exposed and 101 were exposed for two 30-min periods per day for up to 18 months to plane-wave fields of 900 MHz with a pulse repetition frequency of 217 Hz and a pulse width of 0.6 ms. Incident power densities were 2.6-13 W/m2 and specific absorption rates were 0.008-4.2 W/kg, averaging 0.13-1.4 W/kg. Lymphoma risk was found to be significantly higher in the exposed mice than in the controls (OR = 2.4. P = 0.006, 95% CI = 1.3-4.5). Follicular lymphomas were the major contributor to the increased tumor incidence. Thus long-term intermittent exposure to RF fields can enhance the probability that mice carrying a lymphomagenic oncogene will develop lymphomas. We suggest that such genetically cancer-prone mice provide an experimental system for more detailed assessment of dose-response relationships for risk of cancer after RF-field exposure.
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The objective of this study was to examine the associations of brain tumours with radio frequency (RF) fields from mobile phones. Patients with brain tumour from the Australian, Canadian, French, Israeli and New Zealand components of the Interphone Study, whose tumours were localised by neuroradiologists, were analysed. Controls were matched on age, sex and region and allocated the 'tumour location' of their matched case. Analyses included 553 glioma and 676 meningioma cases and 1762 and 1911 controls, respectively. RF dose was estimated as total cumulative specific energy (TCSE; J/kg) absorbed at the tumour's estimated centre taking into account multiple RF exposure determinants. ORs with ever having been a regular mobile phone user were 0.93 (95% CI 0.73 to 1.18) for glioma and 0.80 (95% CI 0.66 to 0.96) for meningioma. ORs for glioma were below 1 in the first four quintiles of TCSE but above 1 in the highest quintile, 1.35 (95% CI 0.96 to 1.90). The OR increased with increasing TCSE 7+ years before diagnosis (p-trend 0.01; OR 1.91, 95% CI 1.05 to 3.47 in the highest quintile). A complementary analysis in which 44 glioma and 135 meningioma cases in the most exposed area of the brain were compared with gliomas and meningiomas located elsewhere in the brain showed increased ORs for tumours in the most exposed part of the brain in those with 10+ years of mobile phone use (OR 2.80, 95% CI 1.13 to 6.94 for glioma). Patterns for meningioma were similar, but ORs were lower, many below 1.0. There were suggestions of an increased risk of glioma in long-term mobile phone users with high RF exposure and of similar, but apparently much smaller, increases in meningioma risk. The uncertainty of these results requires that they be replicated before a causal interpretation can be made.
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We studied the association between use of mobile and cordless phones and malignant brain tumours. Pooled analysis was performed of two case-control studies on patients with malignant brain tumours diagnosed during 1997-2003 and matched controls alive at the time of study inclusion and one case-control study on deceased patients and controls diagnosed during the same time period. Cases and controls or relatives to deceased subjects were interviewed using a structured questionnaire. Replies were obtained for 1,251 (85%) cases and 2,438 (84%) controls. The risk increased with latency period and cumulative use in hours for both mobile and cordless phones. Highest risk was found for the most common type of glioma, astrocytoma, yielding in the >10 year latency group for mobile phone use odds ratio (OR) = 2.7, 95% confidence interval (CI) = 1.9-3.7 and cordless phone use OR = 1.8, 95% CI = 1.2-2.9. In a separate analysis, these phone types were independent risk factors for glioma. The risk for astrocytoma was highest in the group with first use of a wireless phone before the age of 20; mobile phone use OR = 4.9, 95% CI = 2.2-11, cordless phone use OR = 3.9, 95% CI = 1.7-8.7. In conclusion, 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.
Results of case-control studies of mobile phone use and acoustic neuroma have been inconsistent. We conducted a case-case study of mobile phone use and acoustic neuroma using a self-administered postal questionnaire. A total of 1589 cases identified in 22 hospitals throughout Japan were invited to participate, and 787 cases (51%) actually participated. Associations between laterality of mobile phone use prior to the reference dates (1 and 5 years before diagnosis) and tumor location were analyzed. The overall risk ratio was 1.08 (95% confidence interval (CI), 0.93-1.28) for regular mobile phone use until 1 year before diagnosis and 1.14 (95% CI, 0.96-1.40) for regular mobile phone use until 5 years before diagnosis. A significantly increased risk was identified for mobile phone use for >20 min/day on average, with risk ratios of 2.74 at 1 year before diagnosis, and 3.08 at 5 years before diagnosis. Cases with ipsilateral combination of tumor location and more frequently used ear were found to have tumors with smaller diameters, suggesting an effect of detection bias. Furthermore, analysis of the distribution of left and right tumors suggested an effect of tumor-side-related recall bias for recall of mobile phone use at 5 years before diagnosis. The increased risk identified for mobile phone users with average call duration >20 min/day should be interpreted with caution, taking into account the possibilities of detection and recall biases. However, we could not conclude that the increased risk was entirely explicable by these biases, leaving open the possibility that mobile phone use increased the risk of acoustic neuroma.
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The peak spatial specific absorption rate (SAR) assessed with the standardized specific anthropometric mannequin head phantom has been shown to yield a conservative exposure estimate for both adults and children using mobile phones. There are, however, questions remaining concerning the impact of age-dependent dielectric tissue properties and age-dependent proportions of the skull, face and ear on the global and local absorption, in particular in the brain tissues. In this study, we compare the absorption in various parts of the cortex for different magnetic resonance imaging-based head phantoms of adults and children exposed to different models of mobile phones. The results show that the locally induced fields in children can be significantly higher (>3 dB) in subregions of the brain (cortex, hippocampus and hypothalamus) and the eye due to the closer proximity of the phone to these tissues. The increase is even larger for bone marrow (>10 dB) as a result of its significantly high conductivity. Tissues such as the pineal gland show no increase since their distances to the phone are not a function of age. This study, however, confirms previous findings saying that there are no age-dependent changes of the peak spatial SAR when averaged over the entire head.
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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.
C3H/HeA mice with high incidence of spontaneous breast cancer and Balb/c mice treated with 3,4-benzopyrene (BP) (by painting of the skin resulting in the development of skin cancer) were irradiated with 2,450-MHz microwaves (MW) in an anechoic chamber at 5 or 15 mW/cm2 (2 h daily, 6 sessions per week). C3H/HeA mice were irradiated from the 6th week of life, up to the 12th month of life. Balb/c mice treated with BP were irradiated either prior to (over 1 or 3 months) or simultaneously with BP treatment (over 5 months). The appearance of palpable tumors in C3H/HeA mice and of skin cancer in BP-treated Balb/c mice was checked every 2 weeks for 12 months. Two additional groups of mice were exposed to chronic stress caused by confinement or to sham-irradiation in an anechoic chamber; these served as controls. Irradiation with MWs at either 5 or 15 mW/cm2 for 3 months resulted in a significant lowering of natural antineoplastic resistance (mean number of lung neoplastic colonies was 2.8 ± 1.6 (SD) in controls, 6.1 ± 1.8 in mice exposed at 5 mW/cm2 and 10.8 ± 2.1 in those irradiated at 15 mW/cm2) and acceleration of development of BP-induced skin cancer (285 days in controls, 230 days for 5 mW/cm2 and 160 days for 15 mW/cm2). Microwave-exposed C3H/HeA mice developed breast tumors earlier than controls (322 days in controls, 261 days for 5 mW/cm2 and 219 days for 15 mW/cm2). A similar acceleration was observed in the development of BP-induced skin cancer in mice exposed simultaneously to BP and MWs (285 days in controls, 220 day for 5 mW/cm2 and 121 days for 15 mW/cm2). The acceleration of cancer development in all tested systems and lowering of natural antineoplastic resistance was similar in mice exposed to MW at 5 mW/cm2 or to chronic stress caused by confinement but differed significantly from the data obtained on animals exposed at 15 mW/cm2, where local thermal effects (“hot” spots) were possible.
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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.