4.1 Article

Genotoxic effects of asbestos in humans

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.mrfmmm.2004.06.027

Keywords

asbestos; occupational exposure; oxidative DNA damage; DNA repair; chromosome aberrations

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Risks of carcinogenic and non-carcinogenic effects from asbestos continue owing to the persistence of the fibres in building materials and other products. For this reason, epidemiological and mechanistic research on the toxic effects of asbestos and mineral fibres is still needed. The present molecular epidemiological study was conducted in a former asbestos cement plant in Slovakia. Altogether 82 subjects were investigated, 61 exposed subjects (24 smokers and 37 nor-smokers), and 21 factory controls (8 smokers and 13 non-smokers). Workers were exposed to asbestos for between 5 and 40 years. Though the exposure to asbestos during past 40 years was relatively high, at the time of sampling the concentrations of asbestos in the production hall exceeded the Slovak occupational limit (0.001 fibre/cm(3)) by a factor of only 3-5. The office area levels were below this limit. Biomarkers of exposure, effect and individual susceptibility were measured, including DNA damage (strand breaks [SBs], base oxidation and alkylation, using the comet assay); cytogenctic parameters; and individual DNA repair capacity (incision at 8-oxoguanine measured using a modified comet assay). Oxidised pyrimidines were significantly higher in exposed men compared with non-exposed (P = 0.04). There was also a positive association between S Bs (P = 0.04) and age, and alkylation damage to DNA(P= 0.04) and age. Moreover, oxidised pyrimidines (P= 0.01) and alkylated bases (P = 0.001) strongly correlated with years of occupational exposure. Micronucleus frequency did not differ between exposed and control subjects. Repair capacity overall did not show any effect of exposure, though female controls had higher incision rates than did female exposed subjects. However, exposed asbestos workers had significantly higher numbers of chromosomal aberrations (P = 0.01) compared with control group. This finding is consistent with the known association of chromosome aberrations with cancer-risk. (C) 2004 Published by Elsevier B.V.

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