NYC-WTC_000195164

NYC 9/11 Public Portal Document

• ASBESTOS REPROTEXT ® System Page 10 of 27

intravenous injection (Cunningham &Pontemet, 1974). 2. Asbestos fibers were found in tissues of stillborn infants at higher frequencies and concentrations than for normal deliveries. Maximum concentrations were seen in lungs, then in liver and placenta. Although placentas from stillbirths averaged 164,500 fibers/g (n = 4), no asbestos fibers were seen in the placentas from normal births. Presence of asbestos fibers was strongly correlated with working status of the mothers (Haque et al, 1996). D. When administered in the drinking water, asbestos had no effect on embryo survival and was not teratogenic in rats (Schneider & Mauere, 1977). It has been reported to affect embryonic development in mice (Valerio et al, 1980). Chrysotile asbestos was not teratogenic in mice at an oral dose of 143 mcg (Shepards, 2001). E. No effects on sperm were seen in Swiss albino mice given chrysotile asbestos in the drinking water at a dose of 20 mg/kg/day (Rita & Reddy, 1986). F. Blastocyst exposure to asbestos did not result in decreased postimplantation survival (Shepards, 2001).

8.0 PREDISPOSING CONDITIONS A. MEDICAL: Immunocompromised persons, or those with pre-existing lung disease, might be at increased risk from asbestos exposure. B. CHEMICAL: Because asbestos can strongly adsorb other substances, persons also exposed to other carcinogens might be at increased risk. C. SMOKING increases the risk of asbestos-related lung cancer approximately 15 times (Hathaway et al, 1991). D. GENETIC: 1. Asbestos insulators with the NAT2 slow-acetylator phenotype were more than twice as likely to develop both malignant and non-malignant pulmonary diseases, compared with the NAT2 fast-acetylator phenotypes, and their risk for malignant mesothelioma was approximately four-fold higher. 2. Individuals who had both the NAT2 slow-acetylator phenotype and who were null for the GSTMl gene had a five-fold increased risk for malignant and nonmalignant pulmonary diseases, versus those who were NAT2 fast-acetylators and present for the GSTMl gene. In the latter group (slow-acetylators and null for GSTMl), their risk for malignant mesothelioma was 8-fold increased over the same comparison group (Hirvonen et al, 1996).

9.0 BIOMONITORING A. An effective method for biological monitoring is the detection of so-called ferruginous bodies in the sputum (Greenberg et al, 1976). Analysis of sputum for asbestos bodies is a fairly insensitive means of assessing exposure, but a positive sputum sample is indicative of high lung burden for asbestos (Teschler et al, 1996). Persons who work with asbestos should have periodic sputum analysis, chest X-rays, and pulmonary function tests.

11.0 SUMMARY AND CONCLUSIONS A. The greatest risks with occupational exposure to asbestos are mesothelioma and carcinoma of the lung, and asbestosis. While there are some reports that occupational exposure to asbestos may be associated with abnormalities of the sex organs, these

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