Benzene exposure, glutathione s-transferase theta homozygous deletion, and sister chromatid exchanges
Xu, Xiping ; Wiencke, John K. ; Niu, Tianhua ; Wang, Min ; Watanabe, Hirokatsu ; Kelsey, Karl T. ; Christiani, David C.
American Journal of Industrial Medicine
1998
33
2
157-163
benzene ; cancer ; chromosome changes ; cytogenetic studies ; glutathione ; occupational disease
Occupational diseases
English
Bibliogr.
"Associations between glutathione-S-transferase (GST) genotype and sister chromatid exchange (SCE) induction in benzene (71432) exposed workers were examined. The cohort consisted of 23 painters, 12 males, employed at Guanghua Glass Factory, Wuhu City, Anhui, China. The controls were 22 fitters and planers, 15 males, employed in machine workshops of Wuhu shipyard. The age range of subjects in both groups was 20 to 50 years. Industrial hygiene monitoring for benzene, xylene (1330207), and toluene (108883) was performed. The subjects completed a questionnaire on demographics, work history, and smoking. The lymphocytes from peripheral blood samples were harvested and scored for SCEs before and after treatment with diepoxybutane (DEB). GST genotyping was performed using a polymerase chain reaction procedure. The cohort experienced mean time weighted average benzene, toluene, and xylene exposures of 0.71, 4.76, and 1.84 parts per million (ppm), respectively. The mean benzene, toluene, and xylene exposures of the controls amounted to 0.03, 0.00, and 0.20ppm, respectively. The mean baseline and DEB induced SCE frequencies in the cohort were 8.80 and 106.3, respectively. The corresponding values in the controls were 9.69 and 97.6. When stratified according to the presence or absence of the GST-T1 genotype there was no difference in baseline SCE frequency between the cohort and controls. The absence of the GST-T1 genotype was significantly associated with an increase in DEB induced SCE frequency in the exposed workers. Smoking was significantly related to the baseline SCE frequency. After stratifying by smoking status, the absence of the GST-T1 genotype was significantly associated with an increase in DEB induced SCE frequency in both smokers and nonsmokers. A significant interaction between benzene exposure and GST-T1 genotype was detected in nonsmokers. The authors conclude that GST-T1 genotype appears to be an important determinant for individual susceptibility to chromosomal damage induced by exposure to benzene. "
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