The frequency of sister chromatid exchanges SCEs., high SCE frequency cells HFCs., and genetic polymorphism of genotypes glutathione S-transferase GST.M1 and T1 were analyzed in peripheral lymphocytes of 35 workers occupation- ally exposed to chromium Cr. and 35 matched control group. Results showed that workers exposed to Cr showed 6.07 SCErcell, as compared to 4.76 SCErcell for the control group p-0.01.. Smokers showed a statistically significant higher frequency of SCE than non-smokers in both groups. The work duration of Cr workers was an important factor. Workers exposed for more than 5 years showed a significantly higher level of SCEs p-0.05.. Workers exposed to Cr for 5 or more years had higher HFC rates 51.4%.than those exposed for less than 5 years 22.9%., with an odds ratio of 4.5 times than those exposed for less than 5 years. In HFC analysis, Cr workers who smoked showed a higher level of HFC 60%.than the control group 5.7%.and also had a higher odds ratio 60.4.compared with the control group. Among non-smokers, the odds ratio was 9.0. Another objective of this study is to investigate the relationship between SCE and genetic polymorphisms of GST M1 and T1 in Cr workers. The results showed that the incidence of GSTM1 null genotype was 60% in the control group and 77.1% in Cr workers, and percentages of GSTT1 deletion were 42.9% and 62.9% in control and exposed individuals, respectively. There was a slightly increased frequency of SCE among Cr workers with GSTM1 null genotype as opposed to non-null genotype individuals. A similar result was seen among the control group; however, there were no statistically significant differences. In conclusion, the current study found the positive induction of SCE in workers who smoked orrand were exposed to Cr. However, different GST genotypes did not influence the level of cytogenetic damage between groups. Despite slight variation in numbers, they all appear to be not different. q2000 Elsevier Science B.V. All rights reserved.
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS (464): 289-296