PRESS RELEASE N° 208
31 May 2011
IARC CLASSIFIES RADIOFREQUENCY ELECTROMAGNETIC FIELDS AS
POSSIBLY CARCINOGENIC TO HUMANS
Lyon, France, May 31, 2011 The WHO/International Agency for Research on Cancer (IARC) has classified radiofrequency electromagnetic fields as possibly carcinogenic to humans (Group 2B), based on an increased risk for glioma, a malignant type of brain cancer1, associated with wireless phone use.
Over the last few years, there has been mounting concern about the possibility of adverse health effects resulting from exposure to radiofrequency elecromagnetic fields, such as those emitted by wireless communication devices. The number of mobile phone subscriptions is estimated at 5 billion globally
From May 24–31 2011, a Working Group of 31 scientists from 14 countries has been meeting at IARC in Lyon, France, to assess the potential carcinogenic hazards from exposure to radiofrequency electromagnetic fields. These assessments will be published as Volume 102 of the IARC Monographs, which will be the fifth volume in this series to focus on physical agents, after Volume 55 (Solar Radiation), Volume 75 and Volume 78 on ionizing radiation (Xrays, gammarays, neutrons, radionuclides), and Volume 80 on nonionizing radiation (extremely lowfrequency electromagnetic fields).
The IARC Monograph Working Group discussed the possibility that these exposures might induce longterm health effects, in particular an increased risk for cancer. This has relevance for public health, particularly for users of mobile phones, as the number of users is large and growing, particularly among young adults and children.
The IARC Monograph Working Group discussed and evaluated the available literature on the following exposure categories involving radiofrequency electromagnetic fields:
occupational exposures to radar and to microwaves;
environmental exposures associated with transmission of signals for radio, television
and wireless telecommunication; and
personal exposures associated with the use of wireless telephones.
International experts shared the complex task of tackling the exposure data, the studies of cancer in humans,
the studies of cancer in experimental animals, and the mechanistic and other relevant data
The evidence was reviewed critically, and overall evaluated as being limited2 among users of wireless telephones for
glioma and acoustic neuroma, and inadequate3 to draw conclusions for other types of cancers. The evidence from the
occupational and environmental exposures mentioned above was similarly judged inadequate. The Working Group did
not quantitate the risk; however, one study of past cell phone use (up to the year 2004), showed a 40% increased risk
for gliomas in the highest category of heavy users (reported average: 30 minutes per day over a 10year period).
Dr Jonathan Samet (University of Southern California, USA), overall Chairman of the Working Group, indicated that
"the evidence, while still accumulating, is strong enough to support a conclusion and the 2B classification. The conclusion means that there could be some risk, and therefore we need to keep a close watch for a link between
cell phones and cancer risk."
"Given the potential consequences for public health of this classification and findings," said IARC Director
Christopher Wild, "it is important that additional research be conducted into the longterm, heavy use of mobile phones. Pending the availability of such information, it is important to take pragmatic measures to reduce exposure such as handsfree devices or texting. "
The Working Group considered hundreds of scientific articles; the complete list will be published in the Monograph.
It is noteworthy to mention that several recent inpress scientific articles4 resulting from the Interphone study were made available to the working group shortly before it was due to convene, reflecting their acceptance for publication at that time, and were included in the evaluation.
A concise report summarizing the main conclusions of the IARC Working Group and the evaluations of the carcinogenic
hazard fromradiofrequency electromagnetic fields (including the use of mobile telephones) will be published in
The Lancet Oncology in its July 1 issue, and in a few days online.
1 237 913 new cases of brain cancers (all types combined) occurred around the world in 2008 (gliomas represent 2/3 of these).
Source: Globocan 2008
For more information, please contact
Dr Kurt Straif, IARC Monographs Section, at +33 472 738 511, or email@example.com;
Dr Robert Baan, IARC Monographs Section, at +33 472 738 659, or firstname.lastname@example.org; or
Nicolas Gaudin, IARC Communications Group, at email@example.com (+33 472 738 478)
Link to the audio file posted shortly after the briefing:
The International Agency for Research on Cancer (IARC) is part of the World Health Organization. Its mission is to
coordinate and conduct research on the causes of human cancer, the mechanisms of carcinogenesis, and to develop
scientific strategies for cancer control. The Agency is involved in both epidemiological and laboratory research and
disseminates scientific information through publicaions, meetings, courses, and fellowships.
ABOUT THE IARC MONOGRAPHS
What are the IARC Monographs?
The IARC Monographs identify environmental factors that can increase the risk of human cancer. These include
chemicals, complex mixtures, occupational exposures, physical and biological agents, and lifestyle factors. National
health agencies use this information as scientific support for their actions to prevent exposure to potential carcinoens.
Interdisciplinary working groups of expert scientists review the published studies and evaluate the weight of the
evidence tha an agent can increase the risk of cancer. The principles, procedures, and scientific criteria that guide the
evaluations are described in the Preamble to the IARC Monographs.
Since 1971, more than 900 agents have been evaluated, of which approximately 400 have been identified as
carcinogenic or potentially carcinogenic to humans.
Group 1: The agent is carcinogenic to humans.
This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent may be
placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficent
evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent acts
through a relvant mechanism of carcinogenicity.
This category includes agents for which, at one extreme, the degree of evidence of carcinogenicity in humans is
almost sufficient, as well as those for which, at the other extreme, there are no human data but for which there is
evidence of carcinogenicity in experimental animals. Agents are assigned to either Group 2A (probably carcinogenic
to humans) or Group 2B (possibly carcinogenic to humans) on the basis of epidemiological and experimental evidence
of carcinogenicity and mechanistic and other relevant data. The terms probably carcinogenic and possibly carcinogenic
have no quantitative significance and are used simply as descriptorsof different levels of evidence of human
carcinogenicity, with probably carcinogenic signifying a higher level of evidence than possibly carcinogenic.
Group 2A: The agent is probably carcinogenic to humans.
This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of
carcinogenicity inexperimental animals. In some cases, an agent may be classified in this category when there
is inadequate evidence of carcinogenicity in humans and sufficient evidnce of carcinogenicity in experimental
animals and strong evidence that the carcinogenesis is mediated by a mechanism that alsooperates in humans.
Exceptionally, an agent may be classified in this category solely on the basis of limited evidence of carcinogenicity
in humans. An agent may be assigned to this category if it clearly belongs, based on mechanistic considerations, to a
class of agents for which one or more members have been classified in Group 1 or Group 2A.
Group 2B: The agent is possibly carcinogenic to humans.
This category is used for agents for which there is limited evidence of carcinogenicity in humans and less than
sufficient evidnce of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence
of carcinogenicity in humans but there is sufficient evidence of carcinoenicity in experimental animals. In some
instances, an agent for which there is inadequate evidence of carcinogenicity in humans and less than sufficient
evidence of carcinogenicty in experimental animals together with supporting evidence from mechanistic and other
relevant data may be placed in this grop. An agent may be classified in this category solely on the basis of strong
evidence from mechanistic and other relevant data.
Group 3: The agent is not classifiable as to its carcinogenicity to humans.
This category is used most commonly for agents for which the evidence of carcinogenicity is inadequate in humans
and inadequateor limited in experimental animals.
Exceptionally, agents for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental
animals may be placed n this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans.
Agents that do not fall into any other group are also placed in this category.
An evaluation in Group 3 is not a determination of noncarcinogenicity or overall safety. It often means that further research is needed, especially when exposures are widespread or the cancer data are consistent with differing interpretations.
Group 4: The agent is probably not carcinogenic to humans.
This category is used for agents for which there is evidence suggesting lack of carcinogenicity in humans and in
experimental aimals. In some instances, agents for which there is inadequate evidence of carcinogenicity in humans
but evidence suggesting lack of carcinogenicity in xperimental animals, consistently and strongly supported by a
broad range of mechanistic and other relevant data, may be classified in this group.
Definitions of evidence, as used in IARC Monographs for studies in humans
The evidence relevant to carcinogenicity from studies in humans is classified into one of the following categories:
Sufficient evidence of carcinogenicity: The Working Group considers that a causal relationship has been established between exposure to the agent and human cancer. That is, a positive relationship has been observed between the exposure and cancer in studies in which chance, bias and confounding could be ruled out with reasonable confidence.
A statement that there is sufficient evidence is followed by a separate sentence that identifies the target organ(s) or tissue(s) where an increased risk of cancer was observed in humans. Identification of a specific target organ or tissue does not preclude the possibility that the agent may cause cancer at othersites.
Limited evidence of carcinogenicity: A positive association has been observed between exposure to the agent and cancer for which a causal interpretation is consideed by the Working Group to be credible, but chance, bias or confounding could not be ruled out with reasonable confidence.
Inadequate evidence of carcinogenicity: The available studies are of insufficient quality, consistency or statistical power to permit a conclusion regarding the presence or absence of a causal association between expoure and cancer, or no data on cancer in humans are available.
Evidence suggesting lack of carcinogenicity: There are several adequate studies covering the full range of levels of exposure that humans are known to encounter, which are mutually consistent in not showing a positive association between exposure to the agent and any studied cancer at an observed level of exposure. The results from these studies alone or combined should have narrow confidence intervals with an upper limit close to the nullvalue (e.g. a relative risk of 1.0). Bias and confounding should be ruled out with reasonable confidence, and the studies should have an adequate length of follow up. A conclusion of evidence suggesting lack of carcinogenicity is inevitably limited to the cancer sites, conditions and levels of exposure, and length of observation covered by the available studies. In addition, the possibility of a very small risk at the levels of exposure studied can never be excluded.
In some instances, the above categories may be used to classify the degree of evidence related to carcinogenicity in specific organs or tissues.
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