Noncommunicable Diseases and Mental Health
Lyon, France, June 12, 2012 ‐‐ After a week-long meeting of international experts, the International Agency for Research on Cancer (IARC), which is part of the World Health Organization (WHO), today classified diesel engine exhaust as carcinogenic to humans (Group 1), based on sufficient evidence that exposure is associated with an increased risk for lung cancer.
In 1988, IARC classified diesel exhaust as probably carcinogenic to humans (Group 2A). An Advisory Group which reviews and recommends future priorities for the IARC Monographs Program had recommended diesel exhaust as a high priority for re-evaluation since 1998.
There has been mounting concern about the cancer-causing potential of diesel exhaust, particularly based on findings in epidemiological studies of workers exposed in various settings. This was re-emphasized by the publication in March 2012 of the results of a large US National Cancer Institute/National Institute for Occupational Safety and Health study of occupational exposure to such emissions in underground miners, which showed an increased risk of death from lung cancer in exposed workers (1).
The scientific evidence was reviewed thoroughly by the Working Group and overall it was concluded that there was sufficient evidence in humans for the carcinogenicity of diesel exhaust. The Working Group found that diesel exhaust is a cause of lung cancer (sufficient evidence) and also noted a positive association (limited evidence) with an increased risk of bladder cancer (Group 1).
The Working Group concluded that gasoline exhaust was possibly carcinogenic to humans (Group 2B), a finding unchanged from the previous evaluation in 1989.
Large populations are exposed to diesel exhaust in everyday life, whether through their occupation or through the ambient air. People are exposed not only to motor vehicle exhausts but also to exhausts from other diesel engines, including from other modes of transport (e.g. diesel trains and ships) and from power generators.
Given the Working Group’s rigorous, independent assessment of the science, governments and other decision-makers have a valuable evidence-base on which to consider environmental standards for diesel exhaust emissions and to continue to work with the engine and fuel manufacturers towards those goals.
Increasing environmental concerns over the past two decades have resulted in regulatory action in North America, Europe and elsewhere with successively tighter emission standards for both diesel and gasoline engines. There is a strong interplay between standards and technology – standards drive technology and new technology enables more stringent standards. For diesel engines, this required changes in the fuel such as marked decreases in sulfur content, changes in engine design to burn diesel fuel more efficiently and reductions in emissions through exhaust control technology.
However, while the amount of particulates and chemicals are reduced with these changes, it is not yet clear how the quantitative and qualitative changes may translate into altered health effects; research into this question is needed. In addition, existing fuels and vehicles without these modifications will take many years to be replaced, particularly in less developed countries, where regulatory measures are currently also less stringent. It is notable that many parts of the developing world lack regulatory standards, and data on the occurrence and impact of diesel exhaust are limited.
Dr Christopher Portier, Chairman of the IARC working Group, stated that “The scientific evidence was compelling and the Working Group’s conclusion was unanimous: diesel engine exhaust causes lung cancer in humans.” Dr Portier continued: “Given the additional health impacts from diesel particulates, exposure to this mixture of chemicals should be reduced worldwide.“(2)
Dr Kurt Straif, Head of the IARC Monographs Program, indicated that “The main studies that led to this conclusion were in highly exposed workers. However, we have learned from other carcinogens, such as radon, that initial studies showing a risk in heavily exposed occupational groups were followed by positive findings for the general population. Therefore actions to reduce exposures should encompass workers and the general population.”
Dr Christopher Wild, Director, IARC, said that “while IARC’s remit is to establish the evidence-base for regulatory decisions at national and international level, today’s conclusion sends a strong signal that public health action is warranted. This emphasis is needed globally, including among the more vulnerable populations in developing countries where new technology and protective measures may otherwise take many years to be adopted.”
The summary of the evaluation will appear in The Lancet Oncology as an online publication ahead of print on June 15, 2012.
(1) JNCI J Natl Cancer Inst (2012) doi:10.1093/jnci/djs034
JNCI J Natl Cancer Inst (2012) doi: 10.1093/jnci/djs035
(2) Dr Portier is Director of the National Center for Environmental Health and the Agency for Toxic Substances and Disease Registry at the Centers for Disease Control and Prevention (USA)
For more information, please contact:
Dr Kurt Straif, IARC Monographs Section, at +33 472 738 507, or
Link to the audio file posted shortly after the media 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 publications, meetings, courses, and fellowships.
Evaluation groups - Definitions
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 sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent acts through a relevant 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 descriptors of 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 in experimental animals. In some cases, an agent may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates 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 evidence 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 carcinogenicity in experimental animals. In some instances, an agent for which there is inadequate evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals together with supporting evidence from mechanistic and other relevant data may be placed in this group. 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 inadequate or limited in experimental animals.
Exceptionally, agents for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in 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 non‐carcinogenicity 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 animals. In some instances, agents for which there is inadequate evidence of carcinogenicity in humans but evidence suggesting lack of carcinogenicity in experimental animals, consistently and strongly supported by a broad range of mechanistic and other relevant data, may be classified in this group.
Evidence for studies in humans - Definition
As shown previously, the evidence relevant to carcinogenicity is evaluated using standard terms. For studies in humans, evidence is defined 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 other sites.
Limited evidence of carcinogenicity: A positive association has been observed between exposure to the agent and cancer for which a causal interpretation is considered 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 exposure 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 any observed level of exposure. The results from these studies alone or combined should have narrow confidence intervals with an upper limit close to the null value (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.