Asbestos cancer

Dixon JR, Lowe DB, Richards DE, et al. 1970. The role of trace metals in chemical carcinogenesis Asbestos cancers. Cancer Res 30 1068-1074. 

Bevan DR, Ulman MR. 1991. Examination of factors that may influence disposition of benzo[a]pyrene in vivo Vehicles and asbestos. Cancer Lett 57 173-179. 

Holtz G, Bresnick E. 1988. Ascorbic acid inhibits the squamous metaplasia that results from treatment of tracheal explants with asbestos or benzo[a]pyrene-coated asbestos. Cancer Lett 42 23-28. 

Kannio A, Ridanpaa M, Koskinen H, et al. 1996. A molecular and epidemiological study on bladder cancer P53 mutations, tobacco smoking, and occupational exposure to asbestos. Cancer Epidemiol Biomarkers Prev 5 33-39. 

Nelson HH, Wiencke JK, Gunn L, et al. 1998. Chromosome 3p 14 alterations in lung cancer Evidence the FHIT exon deletion is a target of tobacco carcinogens and asbestos. Cancer Res 58 1804-1807. 

Varga C, Horvath G, Timbrell V. 1996a. In vivo studies on genotoxicity and cogenotoxicity of ingested UICC anthophyllite asbestos. Cancer Lett 105 181-185. 

Wagner JC. 1972. Current opinions on the asbestos cancer problem. Ann Occup Hyg 15 61-64. 

Gilson, J. C. (1976). Asbestos cancers as an example of the problem of comparative risks. lARC Sci Puhl 13, 107-116. 

J. LaDou, The Asbestos Cancer Epidemic, Environ. Health Perspect. 112 (2003) 285-290. 

A further consensus developed within the scientific community regarding the relative carcinogenicity of the different types of asbestos fibers. There is strong evidence that the genotoxic and carcinogenic potentials of asbestos fibers are not identical in particular mesothelial cancer is mostiy, if not exclusively, associated with amphibole fibers (43). 

The replacement of asbestos fibers by other fibrous materials has raised similar health issues in relation to substitute materials. However, since lung cancer has a latency period of approximately 25 years, and since the fiber exposure levels in contemporary industries is far lower than those which prevailed half a century ago, the epidemiological data on most substitutes is insufficient. A possible exception is slag fibers for which several studies on worker populations are available over extended periods (44) some results show a substantial increase in lung cancer occurrence. Consequentiy, the toxicity of asbestos substitute fibers remains a subject of active investigation. 

Carcinogens Cancer-producing agents Skin Respiratory Bladder/urinary tract Liver Nasal Bone marrow Coal tar pitch dust crude anthracene dust mineral oil mist arsenic. Asbestos polycyclic aromatic hydrocarbons nickel ore arsenic bis-(chloromethyl) ether mustard gas. p-naphthylamine benzidine 4-am i nodi pheny lam ine. Vinyl chloride monomer. Mustard gas nickel ore. Benzene. 

Marsh, J. P., and Mossman, B. L (1991) Role of asbestos and active oxygen species in. ictiva-rion. and expression of ornirhinc decarboxylase in hamster tracheal epithelial cells. Cancer Ra. 51(1), 167-173. 

Bronchogenic carcinoma A lung cancer associated with asbestos exposure. 

Fibers in this category are composed of naturally occurring materials. A good example is asbestos. The most common type is chrysotile, representing more than 95% of world asbestos production. Chemically it is magnesium silicate (Mg6(OH)4 Si205). Today, use of this fiber is limited because long exposure to it may cause bronchial cancer. 

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). 

Phagocyte-derived ROMs have been implicated in the pathogenesis of a number of pulmonary diseases, including emphysema, acute respiratory distress syndrome, and various environmental diseases such as asbestos-related fibrosis and cancer (Mossman and Marsh, 1985). The relatively high oxygen tension in pulmonary tissue renders the lung prone to oxidative stress (Edwards and Lloyd, 1988). 

Goodlick, L.A. and Kane, A.B. (1986). Role of reactive oxygen metabolites in crocidolite asbestos toxicity to mouse macrophages. Cancer Res. 46, 5558-5566. 

Levine, D.S. (1985). Does asbestos exposure cause gastrointestinal cancer Digest. Dis. Sci. 30, 1189-1198. 

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