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.
JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.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 piM/L), low exposure (1.20-1.91 pM/L), high exposure (1.92-2.88 pM/L), and very high exposure (> 2.88 pM/L)-we found significant differences in the genetic damage induction. We conclude that exposure to levels of lead higher than 1.20 pM/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. This investigation was supported in part by the Bulgarian government (HZ-13/92) and by a contract with Elhim-Izkra Ltd. (N97/21.03.1996). We thank N. Bandev, director of the starter battery plant, for his financial support. We are grateful to the Spanish Ministry of Education and Culture, which granted a visiting research position to A. Vaglenov (DGES, SAB 1995-0689). We are indebted to G. Umbert and A. Corral for their expert technical assistance. The secretarial help of M. McCarthy is very much appreciated.
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