BENZENE EXPOSURE, GLUTATHIONE-S-TRANSFERASE-THETA HOMOZYGOUS DELETION, AND SISTER-CHROMATID EXCHANGES

Citation
Xp. Xu et al., BENZENE EXPOSURE, GLUTATHIONE-S-TRANSFERASE-THETA HOMOZYGOUS DELETION, AND SISTER-CHROMATID EXCHANGES, American journal of industrial medicine, 33(2), 1998, pp. 157-163
Citations number
45
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
02713586
Volume
33
Issue
2
Year of publication
1998
Pages
157 - 163
Database
ISI
SICI code
0271-3586(1998)33:2<157:BEGHD>2.0.ZU;2-7
Abstract
Recent studies have shown a strong positive correlation between chromo somal aberrations and future cancer risk. Sister chromatid exchange (S CE) has been widely), applied in monitoring early biological effects t o assess human genetic risk of cancer at the population level. We stud ied 45 Chinese workers (23 in the painting workshop of a glass factory with occupational exposure to benzene, and 22 fitters and planers in the punching and planing machine workshops of a nearby shipyard withou t such an exposure) to examine the association between occupational ex posure to benzene and SCE frequency in peripheral blood lymphocytes. W e also sought to investigate whether the glutathione S-transferase cla ss theta gene (GSTT1) affects individual susceptibility to cytogenetic damage induced by in vivo exposure to benzene or in vitro exposure to diepoxybutane. The time-weighted average concentrations of benzene we re 0.71 ppm in the exposed group and 0.03 ppm in the non-exposed group . Controlling for age, gender and educational level, cigarette smoking was significantly associated with increased SCE frequencies (P < 0.05 ), while GSTT1 genotype was significantly associated with DEB-induced SCEs (P < 0.01). There was no relationship between benzene exposure an d baseline or DEB-induced SCEs. After stratification by smoking status , the GSTT1 deletion was a significant predictor of DEB-induced SCEs f or both smokers (P < 0.05) and nonsmokers (P < 0.01). A significant be nzene-GSTT1 interaction was found in nonsmokers (P < 0.05). Our study suggests that GSTT1 is an important determinant of heterogeneity in in dividual susceptibility to chromosomal damage associated with exposure to benzene. (C) 1998 Wiley-Liss, Inc.