NYC-WTC_000195068

NYC 9/11 Public Portal Document

- ASBESTOS MEDITEXT ® - Medical Management Page 8 of 15

seems to be related to fiber length, type, size, geometry, and insolubility in aqueous solutions (Brown et al, 1990; Churg et al, 1989; Gibbs, 1990; ILO, 1983; Lippman, 1988; McDonald et al, 1989; Mossman & Gee, 1989; Sebastien et al, 1989; Spumy et al, 1983; ACGIH, 1991). a. Asbestos fibers in order of toxicity are - crocidolite, amosite, and chrysotile. 1. In a fatality due to widely metastatic malignant mesothelioma, asbestos fibers were extracted from many tissues, including lungs, pleura, pericardium, tunica vaginalis testis, lymph nodes with tumor metastasis, small intestine, liver, spleen and kidney. All tissues examined contained asbestos fibers, with lung parenchyma containing numerous fibers (Watanabe et al, 1994). The precise mechanism of carcinogenesis by asbestos fibers is unclear. The role of pulmonary macrophages has been postulated. b. Respirable particles are generally between 0.5 and 5 microns in diameter, with a length-to-width ratio of 3:1. However, in the case of asbestos, some fibers as large as 10 microns in diameter may penetrate to the lower pulmonary regions (ATSDR, 1990). 1. An increased incidence of lung cancer has been produced by fibers longer than 5 microns (ATSDR, 1995). 2. TRACE METALS - Some authors think that trace metals may contribute to asbestos' cancer-causing abilities. Nickel, cobalt, chromium, manganese, and iron have been found in samples of amosite, crocidolite, and chrysotile (Roy-Chowdhury et al, 1973). 3. SMOKING - Generally, lung cancer occurs with heavy asbestos exposure; the incidence is increased among smokers (Gefter & Conant, 1988; Mossman & Gee, 1989; Newhouse, 1983; Robinson, 1989). However, the synergistic effect of smoking and asbestos on development of cancers of the stomach, colon-rectum, and kidney has not yet been confirmed (ATSDR, 1990). In addition, the effects of asbestos exposure on the risk of developing mesothelioma does not appear to be increased by smoking (Clayton & Clayton, 1993; ATSDR, 1995). a. Smoking may impair the lung's ability to clear asbestos fibers, and may enhance asbestos-induced fibrogenesis (Mossman & Gee, 1989). b. Rat studies showed that asbestos potentiates physical transport of adherent molecules (including hydrocarbon carcinogens) into the lung where phagocytosis of asbestos fibers incorporates hydrocarbons into pulmonary macrophages (Talcott & Antman, 1988). 4. ASBESTOSIS - While individuals with radiographic or clinical evidence of asbestosis probably have, on average, a higher risk of cancer due to heavier exposure to asbestos (Edelman, 1990); asbestosis is not required for increased cancer risk in those with asbestos exposure. Cancer risk is increased even in the absence of overt asbestosis (Finkelstein, 1997; Hillerdal & Henderson, 1997; Egilman & Reinert, 1996). C. RISK FACTORS 1. EVIDENCE OF CAUSATION includes the following - a. DOSE-RESPONSE - The chance of developing tumors is dose-related to asbestos exposure, but there is no "critical level" where the risk of cancer is zero (ATSDR, 1990). No known threshold for asbestos induced lung cancer has been established (ATSDR, 1995). b. Although mesothelial tumors may have a long latency period of up to 68 years, these may occur with exposure of less than one year duration (ATSDR, 1990; Mowe et al, 1984; Newhouse, 1983). 1. A multiplicative relative risk of 1.9 for mesothelioma was estimated for each

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NYC-WTC_000195076