Mortality Rates From Cardiovascular Diseases And Mesothelioma

Mesothelioma is a form of cancer that is caused by exposure to asbestos. One of the main risk factors for developing this disease is exposure in the work place. Because it has affected so many people, Mesothelioma has been the focus of intense research. One interesting study is called, The prevention of asbestos-induced hemolysis by Rashmibala Desaia, Paul Hexta and Roy Richardsa - Department of Biochemistry, University College, P.O. Box 78, Cardiff CF1 1XL, Wales, U.K. - Life Sciences - Volume 16, Issue 12, 15 June 1975, Pages 1931-1938. Here is an excerpt: Abstract - The hemolytic potency of different types of asbestos dusts and silica (min-u-sil) is described. Dust-induced hemolysis can be prevented to varying degrees by protection with erythrocyte membranes, tissue culture medium (containing 20% serum) and by pulmonary surfactant. It is suggested that the binding of relatively non-soluble serum or surfactant materials to asbestos dusts (particularly chrysotile) is important to prevent hemolysis. The relevance of the present study to the initiation of cellular damage by inhaled asbestos is discussed.

A second study is called, Asbestos-associated diseases in a cohort of cigarette-filter workers by JA Talcott, WA Thurber, AF Kantor, EA Gaensler, JF Danahy, KH Antman, and FP Li - Volume 321:1220-1223 November 2, 1989 Number 18 - The New England Journal of Medicine - Here is an excerpt: Abstract - To estimate the effects on health of occupational exposure to crocidolite, a highly toxic form of asbestos, we studied a cohort of 33 men who worked in 1953 in a Massachusetts factory that manufactured cigarette filters containing crocidolite fibers from 1951 to 1957. Twenty-eight of the men have died, as compared with 8.3 deaths expected. This increased mortality was attributable to asbestos-associated diseases. Fifteen deaths were caused by cancer, as compared with 1.8 expected (relative risk, 8.2; 95 percent confidence interval, 4.6 to 13.4), including eight from lung cancer, five from malignant mesothelioma, and two from other types of cancer. There were seven deaths from nonmalignant respiratory disease, as compared with 0.5 expected (relative risk, 14.7; 95 percent confidence interval, 5.9 to 30.3), of which five were due primarily to asbestosis. In contrast, the mortality rates from cardiovascular diseases and all other causes were not increased. Four of the five living workers have pulmonary asbestosis; three of them have recently diagnosed cancers, including two additional lung cancers. We conclude that the extremely high morbidity and mortality in these workers were caused by intense exposure to crocidolite asbestos fibers.

A third study is called, Inhaled asbestos fibers induce expression in the rat lung by Mishra A, Liu JY, Brody AR, Morris GF - Department of Pathology, Tulane University Medical Center, New Orleans, Louisiana 70112, USA. Am J Respir Cell Mol Biol. 1997 Apr;16(4):479-85. Here is an excerpt: Abstract - Humans and rodents exposed to an aerosol of asbestos fibers develop lung injury that can lead to a fibroproliferative response culminating in excessive scarring and impaired lung function. To define the early events that precede asbestos-induced fibrotic lung disease, rats were exposed to an aerosol of chrysotile asbestos fibers for 5 h. At various times after exposure, the lungs of the asbestos-exposed animals were evaluated immunohistochemically for expression of the p53 tumor suppressor protein, a growth regulatory protein. p53 became detectable by immunostaining at the predicted sites of fiber deposition (the bronchiolar-alveolar duct bifurcations) by 24 h after exposure. The number of cells positive for p53 immunostaining increased to a maximal level at 8 days after exposure, decreased by 14 days and returned to a low basal level at the 30-day time point. Control groups of rats that were unexposed or exposed to an aerosol of iron beads were negative for p53 immunostaining throughout the 30-day assessment period. Simultaneous detection of the proliferating cell nuclear antigen (PCNA) at the sites of fiber deposition in the asbestos-exposed animals agrees with our previous finding that p53 binds and regulates the PCNA promoter.

If you found any of these studies interesting, please read them in their entirety. We all owe a great deal of thanks to the people who are researching these important issues.

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