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Diverse Mesothelioma Causes
Some of the earlist and most convincing evidence of chemical carciogenesis in human (like mesothelioma),
has come from observations made regarding workplace exposures. Percivals Pott's eighteenth century observations of scrotal skin cancers in chymney sweeps exposed to chimney soot is commonly cited as the earliest such occupational health description. Prior to the mid-twentieth century, occupational exposures to materials later shown to be carcinogenic were often substantial. By virtue of such relatively high dose exposures, coupled with the ability to document workplace conditions for individual workers thought industrial records, both cohort and case control epidemiologic studies have been able to establish clear evidence of carcinogenesis in occupational settings. Prominent examples include lung cancer and
mesothelioma in asbestos workers, hepatic angiosarcomas in vinyl chloride polymerization workers, and myeloid leukemias in workers exposed to benzene used as a solvent in rubber industry.
In the case of asbestos exposure, lung cancer risk is greatly increased through synergy with cigarette smoking. The large number of workers exposed in the past to asbestos in various trades (insulation workers, shipyard workers, automotive and construction workers), has made asbestos carcinogenicity a relatively prominent public health issue, intensified by concern lower dose exposures in the general public from deteriorating asbestos insulation in buildings. It seems likely that only about 3% to 4% of all humans cancer are attributable to occupational exposures, despite higher estimates in the past.
Exposures to chemical carcinogens in the environment have been the subject of much concern and investigation in recent years. Exposure levels in the general environment however, are generally much lower than those observed in the past worksite exposures; hence, documentation of carcinogenicity in human epidemiologic studies has not been clearly established. Examples include various carcinogenic materials in air pollution, halogenated hydrocarbons in drinking water, chemicals such as polychlorinated biphenyls and dibenzodioxins from chemical plant emissions or inadequate waste chemical disposal, and pesticide residues in various food products. These general environmental exposures are not likely to be substantial contributors to the overall human cancer burden, despite the alarming circumstances in which they often occur.
Occasionally, the exposures can be extensive (for example the industrial accident at Seveso, Italy, in which dioxin emissions occurred. And it can’t be assumed, even at very low doses, that no carcinogenic effect will occur. Given the man-made and hence man-controllable, nature of such exposures, their continuous monitoring and control is essential, to the extent that is technically practical. The mechanisms to control occupational and environmental exposures have been established, especially over the past two decades, by means of laws passed in the United States to regulate toxic substances and to safeguard worker’s health.
Source : Clinical Oncology, Arthur Holleb, Diane J. Fink
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