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Crocidolite exposures

The vimentin system of the foetal Syrian hamster lung epithelial cell line M3E3/C3 collapsed completely after crocidolite exposure while a concentration of vimentin could be observd at the sites of contact between silicon carbide fibres and the cell (Aufderheide et al. 1994). [Pg.230]

Mesotheliomas are the characteristic asbestos-related tumours of the pleura. Exposure of explants of human pleura to crocidolite blue asbestos in culture produces a... [Pg.249]

The initial connection between asbestos and mesothelioma was made by Wagner et al. (1960), when all but one patient in a study of mesothelioma-related deaths were found to be miners, workers, members of their families, or others living in the area of South Africa where the amphibole-asbestos crocidolite was mined. A comparable occupational exposure to crocidolite has been documented in Australia, with similar results (Armstrong et al., 1984). Mann and his associates (1966) documented three cases of mesothelioma among fifty-four patients dying of pulmonary asbestosis, and in two of the patients the mesotheliomas were peritoneal rather than pleural. [Pg.133]

Mesothelioma, a relatively rare and rapidly fatal neoplasm seen chiefly in crocidolite workers, may occur without radiological evidence of asbestosis at exposure levels lower than those required for prevention of radiolog-ically evident asbestosis. 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, although the disease may occur after a very limited exposure 20-30 years earlier. [Pg.60]

While lung cancer and mesothelioma are generally associated with chronic exposure to asbestos, there are several studies that indicate that short-term exposures are also of concern. For example, it has been noted that workers exposed to asbestos for only 1-12 months had an increased risk of developing lung cancer a number of years later. In animals, mesotheliomas developed in two rats exposed to high concentrations of amosite or crocidolite for only 1 day. These data are not extensive enough to define the dose- or time-dependency of health risks from short-term exposure to asbestos, but the data do indicate that short-term exposures should not be disregarded. [Pg.33]

Animal studies also indicate that inhalation exposure to asbestos produces mesotheliomas. Mesotheliomas have been observed in rats exposed to chrysotile, amosite, anthophyllite, crocidolite, or tremolite at concentrations ranging from 350 to 1,600 f/mL for 1-2 years (Davis and Jones 1988 Davis et al. 1985 Wagner et al. 1974, 1980a) and in baboons exposed to either 1,110-1,220 f/mL for 4 years (Goldstein and Coetzee 1990) or 1,100-1,200 17mL for up to 898 days (Webster et al. 1993). Incidences of mesothelioma ranged from 0.7 % to 42% in these studies. [Pg.72]

No studies were located regarding death in humans or animals after acute or intermediate oral exposure to asbestos. Feeding studies in rats and hamsters indicate that ingestion of high amounts (1% in the diet, equivalent to doses of 500-800 mg/kg/day) of chrysotile, amosite, crocidolite, or tremolite does not cause premature lethality, even when exposure occurs for a lifetime (NTP 1983, 1985, 1988, 1990a, 1990b, 1990c). [Pg.75]

The geometric mean asbestos body and crocidolite fiber content in 90 former workers in the Wittenoon crocodiolite industry in Western Australia were 17.5 asbestos bodies/g wet tissue and 183 TEM 17p,g dry tissue, respectively (de Klerk et al. 1996). The geometric mean intensity of exposure, duration of exposure, and cumulative exposure were 20 fimL, 395 days, and 20.9 f-5T/mL, respectively. The fiber concentration in the lung was correlated to the intensity and duration of exposure. [Pg.200]

Dopp E, Jonas L, Nebe B, et al. 2000. Dielectric changes in membrane properties and cell interiors of human mesothelial cells in vitro after crocidolite asbestos exposure. Environ Health Perspect 108(2) 153-158. [Pg.255]

Fung H, Kow YW, Van Houten B, et al. 1997a. Patterns of 8-hydroxydeoxyguanosine formation in DNA and indications of oxidative stress in rat and human pleural mesothelial cells after exposure to crocidolite asbestos. Carcinogenesis 18 825-832. [Pg.267]

Hansen J, de Klerk NH, Musk AW, et al. 1998. Environmental exposure to crocidolite and mesothelioma Exposure-response relationships. Am J Respir Crit Care Med 157 69-75. [Pg.272]

Marczynski B, Kerenyi T, Czuppon AB, et al. 1994b. Increased incidence of DNA double-strand breaks in lung and liver of rats after exposure to crocidolite asbestos fibers. Inhal Toxicol 6 395-406. [Pg.298]

Marczynski B, Kerenyi T, Marek W, et al. 1994c. Induction of DNA - damage after rats exposure to crocidolite asbestos libers. In Davis IMG, Jaurand MC, ed. Cellular and molecular effects of mineral and synthetic dusts and fibres. Berlin Springer-Verlag, 227-232. [Pg.299]

McDonald AD, Fry JS, Woolley AJ, et al. 1982. Dust exposure and mortality in an American factory using chrysotile, amosite, and crocidolite in mainly textile manufacture. Br J Ind Med 39 368-374. [Pg.300]

Miller K, Webster I, Handfleld RI, et al. 1978. Ultrastmctuie of the lung in the rat following exposure to crocidolite and asbestos and quartz. J Pathol 124 39-44. [Pg.303]

Musselman R, Miiller W, Bastes W, et al. 1994a. Biopersistence of crocidolite versus man-made vitreous fibers in rat lungs after brief exposures. In Mohr U, Dungworth DL, Mauderly JL, et al, ed. Toxic and carcinogenic effects of solid particles in the respiratory tract. Washington,DC ILSI Press, 451-454. [Pg.307]


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