- LAST REVIEWED: 15 June 2015
- LAST MODIFIED: 23 August 2017
- DOI: 10.1093/obo/9780199756797-0104
- LAST REVIEWED: 15 June 2015
- LAST MODIFIED: 23 August 2017
- DOI: 10.1093/obo/9780199756797-0104
The recognition and diagnosis of occupational cancers dates back to medieval times. Knowledge of the biological mechanisms that cause cancers has increased but remains incomplete as does recognition of multiple factors and mixtures that may operate in the etiology of many such cancers and at different stages in, or after, tumor development. Genetic, biological, physical, and chemical factors as well as those in work and wider environments may be involved singly or together. Toxicology, occupational hygiene, and occupational epidemiology as well as sentinel clinical case studies have all been used to identify occupational cancers. Legal recognition of many occupational carcinogens and occupational cancers—and related compensation—has proved exceptionally slow and challenging while debates about safe levels, if any, for carcinogen exposure continue. Tens of thousands of commercial substances are used globally. Few have been fully assessed for toxicity, including carcinogenicity. Many new substances also appear each year and very few have complete toxicity assessments. Additionally, co-carcinogens and promoters may exist in occupational settings and complex interactions may occur in work and wider environments. Hence, in cases in which work contributes to cancer development, cancers may be described as either work caused directly or work related. Epigenetics has become important too for recognizing carcinogens in addition to genotoxic assessments. Recognition and recording may therefore be challenging. Cancers such as mesothelioma, numerically due almost exclusively to asbestos exposure, and liver angiosarcoma, due to vinyl chloride monomer exposure, are often very specifically occupational and more easily recognized; however, most cancers are not so readily identifiable and could have a wide range of causes, including occupation. Criteria for both listing and reporting occupational carcinogens may vary from country to country and even from agency to agency. Opinions vary regarding the value of experimental evidence and bioassays versus epidemiological studies, and some consider too many false negative studies have been produced. Estimating attributable fractions (AFs) of cancers due to or related to occupation for both technical and policy reasons is also problematic. Such estimates can produce a somewhat sterile debate on numbers and, at times, can divert preventative action away from action on known and suspect carcinogens. Controversies exist around known and proven, probable and possible carcinogens, the extent of population exposures, weighting environment versus lifestyle, and the threshold levels for exposure. Debates are ongoing about whether there are safe levels for carcinogens. A further complication existed in occupational cancer studies with early assumptions that multi-causality and interactions between various factors did not occur in some work-related cancers. Agreement is now growing among international agencies and many national regulatory agencies that greater regulation and enforcement is needed in taking precautionary measures because of the high human and economic costs of work-related cancers. Many control strategies are widely accepted, including removing workplace carcinogens, substituting less hazardous materials, and, when this cannot be done, rigorously isolating or controlling substances coupled with providing information that warns of the hazard. The challenges in taking these steps may be considerable, as evidenced by the increased use of asbestos in some countries. The best medical treatment for occupational cancers is, of course, the same as for any other group of cancers, with perhaps an exception in the case of mesothelioma.
General Overviews and Key Debates on Causes and Prevention
In the decade from 2000 to 2010, interest grew in work-related cancers among international agencies and regulators, which has led to more research and greater numbers of publications on the subject. This article includes classic and comprehensive texts and illustrative or significant specialist papers that detail research and provide clinical and public health policy material on established carcinogens that are still widely used globally. Research in this field in the Scandinavian countries and the United States has been very strong and Scandinavia has also had some of the best data sets and exposure matrices available for the longest time. Materials that treat debates about either methods available to identify such cancers or lists of such cancers have been included together with examples. The major debate in the field has centered on the contribution to cancer rates made by “lifestyle” and work and wider environments, and these are linked to assessing animal and human evidence. Epstein and Schwarz 1991 considers that environmental factors, including work, play a significant part in cancer etiology and mortality. Ames, et al. 1987 does not think that such factors play a role. The analysis in Tomatis, et al. 1997 indicates the importance of prioritizing animal research on workplace and wider environmental carcinogens in the event that the epidemiology is weak. Doll and Peto 1981 provides the most influential early epidemiological analysis supporting lifestyle factors as the principal causes of cancer mortality. Clapp, et al. 2006 reviews research undertaken since the 1980s and the authors reassess and revise upward the contribution made by occupation to cancer morbidity and mortality. O’Neill, et al. 2007 does the same.
Ames, Bruce N., Renae Magaw, and L. S. Gold. 1987. Ranking possible carcinogenic hazards. Science 236.4799 (17 April): 271–280.
Lab-based researchers who developed non-animal carcinogenicity assays in the laboratory and who contested the Epstein analysis. Considers that animal cancer tests could not predict absolute cancer risk in humans. Argues that natural carcinogens exist in food and drink at higher levels than those such as pesticides in work and wider environments: The latter presents minimal risks.
Clapp, Richard W., Genevieve K. Howe, and Molly Jacobs. 2006. Environmental and occupational causes of cancer re-visited. Journal of Public Health Policy 27.1: 61–76.
This article is based on a large review of the recent scientific literature and provides a detailed reassessment of the Doll-Peto estimates with the emphasis placed less on cancer attributable fractions and more on the carcinogens. The European registration and evaluation of chemicals (REACH) legislation is viewed as a major workplace cancer prevention tool.
Doll, R., and Richard Peto. 1981. The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today. Journal of the National Cancer Institute 66.6: 1191–1308.
The classic epidemiological paper still setting the parameters for debate. The authors dispute earlier higher estimates of occupational cancer and calculate the proportion of cancer deaths attributable to occupation at around 4 percent of all recorded cancer deaths although they argue that this still merited action. They highlight “lifestyle,” particularly smoking, as the major cause of cancers in the United States.
Epstein, Samuel S., and Joel B. Schwarz. 1991. Fallacies of lifestyle cancer theories. Nature 289:127–130.
The major challengers of the estimates made by Doll and Peto from the late 1970s and 1980s. Epstein and Schwartz give greater weight to toxicological and clinical research and challenge the relatively low estimates given by Doll and Peto to work and wider environmental factors.
O’Neill, Rory, Simon Pickvance, and Andrew Watterson. 2007. Burying the evidence: How Great Britain is prolonging the occupational cancer epidemic. International Journal of Occupational and Environmental Health 13.4: 428–436.
Explores past occupational cancer policy especially in Great Britain, Germany, and the European Union (EU). Identifies neglect of older workers, women, multiple exposures, many jobs, latency periods, exposure years, control standards, occupational cancer costs, and failures of governments and enforcement agencies to address old and new carcinogens. Proposes greater emphasis on prevention and social justice using existing knowledge.
Tomatis, L., J. Huff, I. Hertz-Picciotto, et al. 1997. Avoided and avoidable risks of cancer. Carcinogenesis 18.1: 97–105.
Authors affirm that estimating attributable risks from carcinogens is based on “unverified assumptions” in which evidence, some strong and some weak, is treated equally. Effective primary cancer prevention should reduce carcinogen numbers or exposures. Experimental evidence with mechanisms of action and suggestive epidemiology linking cancers and exposures is likely to produce a larger and better list of human carcinogens and target organs.
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