Exposure to epichlorohydrin and dimethylformamide, glutathione S-transferases and sister chromatid exchange frequencies in peripheral lymphocytes

Citation
Tj. Cheng et al., Exposure to epichlorohydrin and dimethylformamide, glutathione S-transferases and sister chromatid exchange frequencies in peripheral lymphocytes, ARCH TOXIC, 73(4-5), 1999, pp. 282-287
Citations number
34
Categorie Soggetti
Pharmacology & Toxicology
Journal title
ARCHIVES OF TOXICOLOGY
ISSN journal
03405761 → ACNP
Volume
73
Issue
4-5
Year of publication
1999
Pages
282 - 287
Database
ISI
SICI code
0340-5761(199906/07)73:4-5<282:ETEADG>2.0.ZU;2-C
Abstract
Workers in epoxy resin, synthetic leather, and printed circuit board manufa cturing plants are exposed to epichlorohydrin (ECH), or dimethylformamide ( DMF), or both. ECH, an alkylating agent, has been shown to cause malignancy in animals, but its genotoxicity in humans is unclear. DMF is a well-known hepatotoxic chemical, although evidence of its genotoxicity in humans is a lso limited. In this study, we examined the effects of exposure to ECH and DMF on sister chromatid exchange (SCE) in plant workers, in order to examin e the genotoxicity of these two agents. Because the genotoxicity of certain agents can be modulated by metabolic traits, we also investigated influenc e of the glutathione S-transferase (GST) mu (GST M1) and GST theta (GST T1) genes on the genotoxicity of ECH and DMF. A total of 85 male plant workers were included in this study. The subjects were divided into five exposure groups, based on their job titles and the airborne ECH and DMF concentratio ns in their areas of work. A questionnaire was administered to obtain detai led occupational, smoking, alcohol consumption, and medication histories. S tandardized cytogenetic methods were used to determine the frequency of sis ter chromatid exchange (SCE) in peripheral blood lymphocytes. GST M1 and GS T T1 genotypes were identified using polymerase chain reaction (PCR). In an alysis, smoking was significantly associated with increased SCE frequency ( P < 0.01). Workers with high ECH exposure also had significantly higher SCE frequencies than those with low or no ECH exposure (P < 0.05). However, DM F exposure was not associated with SCE frequency. The GST M1 null genotype was also found to be associated with an increased SCE frequency (P = 0.06). We conclude that ECH exposure may be associated with genetic toxicity and that DMF does not appear to be genotoxic.