The Excess Risk of Cancer after Asbestos Exposure

Asbestos exposure has been known to cause cell transformation and chromosomal mutations.  One group of workers that has been extensively studied is factory employees in London.  One interesting study is called, "Mortality from all cancers of asbestos factory workers in east London 1933–80" by G Berry, M L Newhouse, J C Wagner - Occup Environ Med 2000;57:782-785.  Here is an excerpt: "Abstract – Objective - To give the observed and expected deaths due to cancer at all separate sites in asbestos workers in east London, and to analyse these for overall effect and exposure-response trend.  METHODS - The mortality experience of a cohort of over 5000 men and women followed up for over 30 years since first exposure to asbestos has been extracted. RESULTS - There was a large excess of deaths due to cancer (537 observed, 222 expected). Most of these were due to cancer of the lung (232 observed, 77 expected) and pleural (52) and peritoneal (48) mesothelioma. The exposure-response trend for all these three causes was highly significant. There was also an excess of cancer of the colon (27 observed, 15 expected) which was significantly related to exposure. There were significant excesses of cancer of the ovary, of the liver, and of the oesophagus but with no consistent relation to exposure.

CONCLUSIONS - The excess risk of cancer after exposure to asbestos was mainly due to cancer of the lung and mesothelioma. An exposure related excess of cancer of the colon was also detected but the possibility that some of these deaths may have been peritoneal mesotheliomas could not be excluded. There was no consistent evidence of exposure related excesses at any other site."

Another interesting study is called, "Role of Phagocytosis in Syrian Hamster Cell Transformation and Cytogenetic Effects Induced by Asbestos and Short and Long Glass Fibers" by Thomas W. Hesterberg, Charles J. Butterick, Mitsuo Oshimura, Arnold R. Brody and J. Carl Barrett - Environmental Carcinogenesis Group, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 - Cancer Research 46, 5795-5802, November 1, 1986.  Here is an excerpt: "We have shown previously that asbestos and other mineral dusts, including glass fibers, induce cell transformation and chromosomal mutations in Syrian hamster embryo cells in culture. In the present study, we observed that both asbestos and glass fibers were phagocytized by these cells and accumulated in the perinuclear region of the cytoplasm. In order to understand the mechanism of fiber length-dependent cellular effects, we examined the phagocytosis and intracellular distribution of glass fibers of differing lengths in cells at various times after treatment. Glass fiber length was decreased by milling with a mortar and pestle. Cells treated with an equal dose of milled glass fibers (on a weight per surface area basis) were exposed to 7-fold more fibers since milling of glass fibers resulted in a 7-fold decrease in length with little change in diameter.

However, cells exposed to milled glass fibers phagocytized a similar number of fibers as cells exposed to an equal mass of unmilled glass fibers, indicating that milled fibers were less readily phagocytized. In cells treated with either unmilled or milled glass fibers, the length of the intracellular fibers was more than 2-fold greater than the length of the fibers on the surface, suggesting that cells selectively internalized longer fibers. Fiber length, however, did not appear to affect the migration of intracellular fibers to the perinuclear region of the cytoplasm. Even though cells treated with milled glass fibers contained a similar number of fibers as those treated with unmilled glass fibers, the resulting cytotoxicity, transformation frequency, and frequency of micronuclei were greatly reduced in the cultures treated with milled glass fibers. Thus, fiber length appears to affect the phagocytosis of fibers as well as the ability of intracellular fibers to induce cytogenetic damage and the resultant transformation."

Another interesting study is called, "Airway function in lifetime-nonsmoking older asbestos workers" by R. Bégin, A. Cantin, Y. Berthiaume, R. Boileau, S. Péloquin, S. Massé - The American Journal of Medicine, Volume 75, Issue 4, Pages 631-638.  Here is an excerpt: "Abstract - Previous studies of lung function in asbestos workers have documented airflow limitation in many of the workers, but the specific influence of asbestos exposure could not be clearly differentiated from the effects of the cigarette smoking habit. In this study, airway function was evaluated in lifetime-nonsmoking, long-term workers of the mines and mills of Québec. The 17 asbestos workers in this study had worked for an average of 28 years in the mines and mills of the local asbestos industry and did not have any other respiratory industrial dust exposure. They did not have a history of previous pulmonary disease and did not meet the usual diagnostic criteria for chronic bronchitis, emphysema, or asthma. Seven of the workers met the diagnostic criteria for asbestosis and 10 workers did not. The latter group of workers did not differ from a matched control group except in terms of a higher isoflow volume (p < 0.05). The workers with asbestosis, however, had a restrictive pattern of lung function, increased isoflow volume, and Increased upstream resistance at low lung volumes (p < 0.01). Lung biopsy in three of the patients with the disease demonstrated peribronchiolar alveolitls and fibrosis with obliteration and narrowing of the small airways.

These data on lifetime-nonsmoking, long-term asbestos workers provide further evidence of small airway obstruction associated with asbestos exposure and independent of the smoking habit. This airflow limitation was observed predominantly in workers with a restrictive pattern of lung function associated with peribronchiolar alveolltis. The lifetime-nonsmoking asbestos workers without restrictive patterns of lung function had minimal dysfunction of the peripheral airways."

If you found any of these excerpts, please read them in their entirety.  We all owe a debt of gratitude to these researchers.