Epidemiology of environmental and occupational cancer

Our plain-English summary of Epidemiology of environmental and occupational cancer, by P. Boffetta (Oncogene, 2004).

The study

• Author: P. Boffetta
• Journal: Oncogene
• Published: 2004;23(38):6392-403
• Type of article: Review
• Cited by: 86 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Environmental carcinogens, in a strict sense, include outdoor and indoor air pollutants, as well as soil and drinking water contaminants. An increased risk of mesothelioma has consistently been detected among individuals experiencing residential exposure to asbestos, while results for lung cancer are less consistent. Several good-quality studies have investigated lung cancer risk from outdoor air pollution based on measurement of specific agents. Their results tend to show an increased risk in the categories at highest exposure, with relative risks in the range 1.5. A causal association has been established between exposure to environmental tobacco smoke and lung cancer, with a relative risk in the order of 1.2. Radon is another carcinogen present in indoor air, with a relative risk in the order of 1.06 for exposure at 100 Bq/m3. In several Asian populations, an increased risk of lung cancer results among women from indoor pollution from cooking and heating. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high arsenic contamination; results for other drinking water contaminants, including chlorination by-products, are inconclusive. A total of 29 occupational agents are established human carcinogens, and another 30 agents are suspected carcinogens. In addition, at least 12 exposure circumstances entail exposure to carcinogens. Exposure is still widespread for many important occupational carcinogens, such as asbestos, coal tar, arsenic and silica, in particular in developing countries. Although estimates of the global burden of occupational and environmental cancer result in figures in the order of 2% and less than 1%, respectively, these cancers concentrate in subgroups of the population; furthermore, exposure is involuntary and can, to a large extent, be avoided.

In plain English

This article was a review, not a new study. The author summarized published evidence on cancer from environmental exposures, including residential asbestos, and from workplace carcinogens. In earlier residential asbestos studies from several countries, compiled in a table, the author reported mesothelioma risk greatly increased in all but one. Lung cancer results were less consistent: raised in South African and Chinese studies but not in European or North American ones. For workplace exposure, the author wrote that all forms of asbestos (chrysotile and amphiboles, including crocidolite, amosite and tremolite) cause mesothelioma and lung cancer, though chrysotile's potency might be lower, especially for mesothelioma. Lung cancer risk was smaller in studies of miners and friction product makers, intermediate in asbestos cement and product makers, and highest in asbestos textile workers. The author concluded that environmental cancer likely accounts for about 0.5 to 1% of cancers in most populations, and more in some, such as near an important source of asbestos exposure. The author noted that exposure was hard to measure and smoking hard to control for.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: narrative review of published epidemiological evidence on environmental and occupational cancer
• Who was studied: Published studies, not new participants. For residential asbestos, Table 1 lists 15 studies from South Africa, Canada, the USA, Austria, Italy, Spain, Switzerland, the UK, China, New Caledonia and Australia. For occupational asbestos, the reviewed studies were of miners, manufacturers and applicators.
• Exposure: Residential and household asbestos exposure was one focus. This included living near asbestos mines, plants or other sources, contaminated building materials, and dust brought home on workers' clothes. Occupational asbestos exposure was another, covering mining, asbestos-cement, textile and friction materials manufacture, and application. The review also covered outdoor and indoor air pollution, environmental tobacco smoke, radon, arsenic and chlorination by-products in drinking water, and other occupational carcinogens.
• Main results:
  • Across the residential (environmental) asbestos studies the author compiled, mesothelioma risk was greatly increased in all but one study.
  • For lung cancer after residential asbestos exposure, results were less consistent. Risk was increased in studies from South Africa and China, but not in studies from Europe and North America.
  • The author stated that all forms of asbestos cause mesothelioma and lung cancer in humans. Chrysotile's potency might be lower than that of other types, particularly for mesothelioma.
  • In the occupational studies reviewed, lung cancer risk was smaller among miners and friction product manufacturers and intermediate among asbestos cement and asbestos product manufacturers. It was highest among asbestos textile workers.
  • Citing an earlier analysis (Liddell, 2001), the author reported that the relative risk from asbestos seemed higher in nonsmokers than in smokers. This suggests less than multiplicative interaction between asbestos and smoking.
  • A pooled analysis by other researchers (Darby et al., 2001), cited in the review, gave a lung cancer relative risk of 1.06 (95% CI 1.01 to 1.10). This was for residential radon exposure at 100 Bq/m3 compared with unexposed people.
  • IARC had classified 29 agents, groups of agents and mixtures, plus 12 exposure circumstances, as carcinogenic. Asbestos was among those listed.
  • Estimates cited by the author put the global burden of occupational cancer at about 2 to 4% of cancers.
• The authors' conclusion: The author concluded that environmental cancer is likely responsible for a relatively small share of cancers in most populations (about 0.5 to 1%). The author added that this share is likely higher in populations with special exposures, such as arsenic in drinking water or living near an important source of asbestos exposure.
• Limitations the authors state:
  • Nonoccupational asbestos exposure is hard to assess because levels are generally low. Its duration, frequency and fiber type are seldom known precisely.
  • The residential asbestos studies, especially ecological ones, may include people who also had occupational or household asbestos exposure.
  • Imperfect control for smoking and other lung carcinogens may explain the inconsistent lung cancer results in the residential asbestos studies.
  • In occupational asbestos studies, the role of confounders, especially tobacco smoking, can hardly be evaluated.

Topics

Medical terms in this study, explained in our Lexicon: Epidemiology, Mesothelioma, Lung Cancer, Relative Risk.

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• Asbestos spraying, an occupational and environmental hazard — R. Barnes (1976)
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• Contribution of environmental factors to cancer risk — P. Boffetta, F. Nyberg (2003)

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