Premium
Assessment of abnormal DNA repair responses and genotoxic effects in lead exposed workers
Author(s) -
Karakaya Ali Esat,
Ozcagli Eren,
Ertas Nusret,
Sardas Semra
Publication year - 2005
Publication title -
american journal of industrial medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.7
H-Index - 104
eISSN - 1097-0274
pISSN - 0271-3586
DOI - 10.1002/ajim.20145
Subject(s) - dna damage , medicine , dna repair , genotoxicity , toxicology , lead exposure , occupational exposure , comet assay , toxicity , dna , pharmacology , environmental health , genetics , biology , cats
Background One of the main sources of occupational exposure to lead (Pb) in Turkey is in workers of battery industries. Genotoxic studies in human populations exposed to this metal have had conflicting results. Methods Genotoxic effects of Pb were studied in blood cell samples from workers of battery manufactures exposed to Pb compounds by chromosomal aberration (CA) assay and X‐ray induced challenge (XRC) assay to assess DNA damage and interference with DNA repair processes after an in vitro exposure of X‐ray (1 Gy). The battery manufacturers (n = 23) and 23 people who were not occupationally exposed to lead compounds were selected as a control group and classified into categories according to their blood lead levels. Results The CA frequencies in the exposed and control group were not significantly different ( P > 0.05) by conventional CA (CCA) assay, however, the XRC assay demonstrated significantly elevated CAs ( P < 0.05). Statistically non‐significant but reduced DNA repair responses have also been observed in lead exposed workers. Conclusion The results of this study showed significant increases in the CAs by XRC assay in Pb exposed workers compared to CCA assay. Our data suggests that Pb exposure may cause reduction in DNA repair capacity and these individuals will be more prone to DNA damage. Therefore, preventive measures should be improved against genotoxic risk in workplaces. Am. J. Ind. Med. 47:358–363, 2005. © 2005 Wiley‐Liss, Inc.