To investigate whether occupational exposure to lead is genotoxic, we evaluated data from 103 lead-exposed workers and 78 matched controls. These data correspond to three different sampling periods, and we measured genetic damage as increases in the frequency of binucleated cells with micronuclei (BNMN) in peripheral blood lymphocytes. The levels of exposure were determined according to the lead levels in blood. Clearly significant increases in BNMN were observed in the exposed groups when compared to the control group. In addition, for the overall population (n = 181), we observed a clear relationship between lead levels in blood and BNMN (r = 0.497; p < 0.001). When we examined four exposure levels--very low exposure (< 1.20 microM/L), low exposure (1.20-1.91 microM/L), high exposure (1.92-2.88 microM/L), and very high exposure (> 2.88 microM/L)--we found significant differences in the genetic damage induction. We conclude that exposure to levels of lead higher than 1.20 microM/L may pose an increase in genetic risk. In addition, our data show that blood lead level is a good indicator of genetic damage induction.

We examined sister chromatid exchanges (SCEs) and micronuclei (MN; cytokinesis-block method) in cultured peripheral lymphocytes from 52 female workers of two shoe factories and from 36 unexposed age- and sex-matched referents. The factory workers showed an elevated level of urinary hippuric acid, a biomarker of toluene exposure, and workplace air contained high concentrations of various organic solvents such as toluene, gasoline, acetone, and (in one of the plants only) ethylacetate and methylenediphenyl diisocyanate. The shoe factory workers showed a statistically significant higher frequency of micronucleated binucleate lymphocytes in comparison with the referents. This finding agreed with three preliminary MN determinations (each comprising 27-32 shoe workers and 16-20 controls) performed in one of the plants 2-5 years earlier. The shoe factory workers also had a lower average level of blood hemoglobin than the referents. In contrast, no difference was found between the groups in SCE analysis. Smokers showed significantly higher mean frequencies of SCEs per cell and high frequency cells (HFC) than nonsmokers. Aging was associated with increased MN rates and reduced cell proliferation. Polymorphism of the glutathione S-transferase M1 gene (GSTM1) did not affect the individual level of SCEs; but in smoking shoe workers an effect of the occupational exposure on the frequency of micronucleated cells could be seen only in GSTM1 null subjects. The low prevalence of the glutathione S-transferase T1 (GSTT1) null genotype precluded the evaluation of the influence of GSTT1 polymorphism. Our results show that the shoe factory workers have experienced genotoxic exposure, which is manifest as an increase in the frequency of MN, but not of SCEs, in peripheral lymphocytes. The exposures responsible for the MN induction could not be identified with certainty, but exposure to benzene in gasoline and methylenediphenyl diisocyanate may explain some of the findings.

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