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ASBESTOS HAZARDTEXT ® - Hazard Management Page 1 of 2

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ASBESTOS HAZARDTEXT ® - Hazard Management

6.0 RANGE OF TOXICITY

6.1 MINIMUM LETHAL EXPOSURE

A. Using the presence of persistent, high-pitched rales in the basal portions of the lungs as criterion for the diagnosis of asbestosis, it was determined from a population of asbestos textile workers that less than 100 fiber-years of exposure (2 fibers/cc over a 50-year working period or 4 fibers/cc over a 25-year period) would cause the development of asbestosis in no more than 1 percent of the workers (ACGIH, 1991). B. Occasionally, asbestosis may develop fully in 7 to 9 years after exposure. Mesothelioma can occur after a short, intensive exposure; cases in children under 19 years of age indicate that the latent time period for development may be shorter than first estimated. Usually, however, asbestosis, pneumoconiosis, and mesothelioma develop 20 to 40 years after exposure (Hathaway et al, 1996).

6.2 MAXIMUM TOLERATED EXPOSURE

A. The major route of exposure is inhalation of airborne fibers (ATSDR, 1990). 1. Weil et al (1979) indicated via statistical analysis that low level exposures or occupational exposure for under 2 years were not associated with increased mortality. 2. Development of asbestosis probably depends on a combination of asbestos dust concentration, fiber morphology, and length of exposure (Hathaway et al, 1996). 3. Cigarette smoking is strongly implicated as a cocarcinogen among asbestos workers. Asbestos workers who smoke have approximately 15 times the risk of developing lung cancer compared to non-smoking asbestos workers (ACGIH, 1991; Hathaway et al, 1996; lARC, 19??). B. Oral exposure to asbestos may be experienced through drinking water, beer and other alcoholic beverages, and foods. This may be due to contamination, use of asbestos filters, or asbestos piping (ATSDR, 1990; Howe et al, 1989; McRae, 1988; Polissar et al, 1985). 1. Such exposures have not generally been considered dangerous, although because of the long latent period to onset of asbestosis, several groups have been investigated (Anon, 1978; Howe et al, 1989; McRae, 1988). 2. Minor oral exposure occurs from ingestion of contaminated drinking water or after mucociliary clearance from the lungs, but the role, if any, of ingested asbestos as an etiologic agent is not known (ATSDR, 1990). 3. The US EPA proposed maximum contaminant level for asbestos in drinking water is 7 million fibers (larger than 10 microns in length) per liter (ATSDR, 1990). 4. Gastrointestinal tumors potentially caused by asbestos have only been statistically significantly increased in persons with occupational exposure (Anon, 1978). A possible synergistic effect of smoking and asbestos for cancers of the stomach, colon-rectum, and

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