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An effort was made to determine whether long term exposure to environmental toxicants could induce genetic damage, manifested by DNA repair deficiencies and carcinogenesis, using a host cell reactivation (HCR) assay with ultraviolet (UV) damaged plasmids to measure DNA damage among benzene (71432) exposed workers. The cohort was composed of 12 exposed workers and eight nonexposed comparisons from a benzene manufacturing facility in Texas. Whole blood samples were collected from the subjects and lymphocyte cultures were established. Xeroderma pigmentosum (XP) and Gaucher cell cultures were used as positive and negative controls, respectively, for the HCR assay. XP, Gaucher, and lymphocyte cell lines were transfected with pCMVcat plasmids that were damaged with 175 or 350 joules/square meter (J/m2) of UV light. After transfection, cell extracts were prepared for the chloramphenicol-acetyltransferase (CAT) assay, which would measure plasmid repair efficiency. All data were subjected to statistical analysis. XP cell lines exhibited lower repair activity while Gaucher cells showed normal repair rates; XP heterozygous cell lines had intermediate repair, falling between the homozygous XP cells and Gaucher cells in level of repair activity. Plasmids 175J/m2 and 350J/m2 were repaired with a mean frequency of 71% and 62% in exposed workers, respectively, compared to 66% and 58% in comparison workers. No statistical difference was noted in the repair capacity between exposed and comparison workers. The authors conclude that the absence of significant differences may result from very low exposures to benzene (less than 0.3 parts per million), small population sample studied, or lack of benzene genotoxicity at such low levels, and note that such results were consistent with a parallel hprt genetic mutation assay.
Environmental Health Perspectives, 104(3):529-534, 1996. (26 references)
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