Last updated: 6-Jul-2011
Occupational & Environmental Carcinogens
As many as 5% of cancer deaths are due to occupational factors and 2% to environmental pollution.[1] These figures are very general approximations, as estimating the attributable mortality of carcinogens is a complex task.[2] The only occupational exposure which has been thoroughly documented is that involving asbestos, which may by itself account for half of all occupational cancer deaths.[3]
For most carcinogens, data is derived from high-dose experiments in animals; thus policy-makers must extrapolate from animals to humans and from high-dose to low-dose conditions.[4] The assumptions involved in such risk
assessment involve a lot of uncertainty, but in practice regulations “err on the side of safety.” The precautionary principle suggests that it is best to avoid exposure to a suspicious albeit useful substance, even in the absence of unequivocal evidence, as long as there are known alternatives that are safe.
Another complication both in terms of research and motivation towards prevention is the long latency period between exposure to many carcinogens and disease development—as long as 40 to 50 years. Asbestos again provides an example. Although asbestos exposure levels in Europe and other developed regions have been dramatically reduced since 1980, the expected improvement in mesothelioma[5] rates and pleural cancer deaths will not “kick in” until 2018. The highest risk is carried by men born around 1945.[6]
It will not be possible to detail the risks of and responses to each and every carcinogen. The volume of data would overwhelm this report. The World Health Organization maintains a website with over 200 monographs detailing the effects of and interventions for harmful environmental agents; the asbestos report alone includes over 40 pages of references.[7]
Even in the absence of detailed treatments, the basic pattern of intervention is clear. Once a carcinogen has been identified, primary prevention is the best strategy, i.e., eliminating sources of carcinogen exposure, or at least reducing exposure levels. Secondary prevention depends on detecting asymptomatic illness. The newest screening tests, which involve measuring various biomarkers that are also used in molecular epidemiology, can be very expensive.[8],[9]
[1] Adami H, Day N, Trichopoulos D et al. Primary and secondary prevention in the reduction of cancer morbidity and mortality European Journal of Cancer 2001; 37: S118-S127.
Some Canadian authorities have recently suggested that these figures are underestimates. Canadian Strategy for Cancer Control. Report on Environmental and Occupational Exposures Meeting, January 14, 2003. Available at http://209.217.127.72/cscc/pdf/pprev/Env&OccupMtgReport_ an142003.pdf (accessed December 2004).
[2] Levi F. Cancer prevention: epidemiology and perspectives European Journal of Cancer 1999; 35(7): 1046-58.
[3] Doll R, Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today Journal of the National Cancer Institute 1981; 66: 1191-1308.
[4] American Cancer Society. Available at http://www.cancer.org/docroot/PED/content/PED_1_3X_ Risk_Assessment.asp?sitearea=PED (accessed December 2004).
[5] A rare type of cancer in the sac lining the chest or abdomen. Exposure to airborne asbestos increases the risk of developing malignant mesothelioma.
[6] Levi F. Cancer prevention: epidemiology and perspectives European Journal of Cancer 1999; 35(7): 1046-58.
[7] Source: http://www.inchem.org/pages/ehc.html (accessed December 2004).
[8] Hrelia P, Maffei F, Angelini S et al. A molecular epidemiological approach to health risk assessment of urban air pollution Toxicology Letters 2004; 149(1-3): 261-7.
[9] Norppa H. Cytogenetic biomarkers IARC Scientific Publications 2004; (157): 179-205.