NYC-WTC_000195164

NYC 9/11 Public Portal Document

. ASBESTOS REPROTEXT ® System Page 9 of 27

Previous in vivo exposure to asbestos has been associated with increases in stable chromosome aberrations in human lymphocytes, as visualized by fluorescent in situ hybridization with whole-chromosome probes ("chromosome painting") (Ramsey et al, 1995). F. Cell transformation by asbestos depends on fiber length; long thin fibers are more effective than short thick fibers (Harbison, 1998). G. Asbestos (as chrysotile or crocidolite) inhibited proliferation of human bronchial epithelial cells in culture; chrysotile was up to 300 times more potent. Chrysotile, but not crocidolite, induced micronuclei (a measure of chromosome breaks) in these cells. Structural aberrations were increased only after the longest incubation time (24 hours) (Kodama et al, 1993). H. Induction of mutations in oncogenes is thought to be part of the mechanism of carcinogenesis for some cancers. 1. Lung tumor specimens from lung cancer patients had a high frequency of a specific kind of ras oncogene mutation: 57 percent of the adenocarcinoma samples had K-ras mutations. N-ras and H-ras mutations were not present. The K-ras mutations were increased 4.9-fold in samples from heavy smokers, and 2.2-fold samples from persons with occupational asbestos exposure (Husgafvel-Pursiainen et al, 1993). 2. Although the latter increase was not statistically significant, it does indicate that asbestos may be involved in inducing K-ras mutations (Husgafvel-Pursiainen et al, 1993), and may favor the growth of cells containing the K-ras mutation (Vainio et al, 1993). 3. Asbestos can also induce expression of c-fos and c-jun oncogenes in rat pleural mesothelial cells; crocidolite was more active than chrysotile for this effect, as it is for induction of mesothelioma (Heintz et al, 1993). 4. Asbestos also induces c-jun mRNA in hamster tracheal epithelial cells, progenitors for bronchogenic carcinoma; this induction can respond to either asbestos or hydrogen peroxide, and confers the ability of cells to grow in soft agar (an endpoint of in vitro malignant transformation) (Timblin et al, 1995). I. There is a possibility that asbestos may carry mutagens into the cell because some substances can be strongly adsorbed to the fibers (Dunn, 1989). The possible genetic effects of asbestos in humans in vivo are not well understood.

7.0 REPRODUCTIVE EFFECTS A. Several studies have reported reproductive effects from occupational asbestos exposure. Among Russian railroad builders, 42 percent had abnormalities of the sex organs, but these workers were exposed to several other toxic substances in addition to asbestos, such as carbon monoxide, nitrogen dioxide, acrolein, and formaldehyde (Kogan et al, 1977). B. Russian workers exposed to asbestos cement dust had female reproductive system disorders (Kosolapova & Ulenkova, 1984). Another Russian study reported effects of asbestos on the genitals (Lebedeva, 1971). C. Asbestos is believed to cross the mammalian placental barrier (HSDB, 2001; Lemesch, 1980). 1. Uncoated chrysotile asbestos fibers were found in lung, liver, and/or placenta digests of 5 stillborn infants, indicating transplacental transfer (Haque et al, 1992). Asbestos can cross the placenta to the fetuses in rats following maternal

http://www.tomescps.eom/DATA/RE/RE356.HTM?Top=Yes 1/4/2002

CITY_21MC100_011105152

NYC-WTC_000195172