Genetic damage in wood dust-exposed workers

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Abstract

Exposure to wood dust is common in carpentry workshops. Wood dust is known to be a human carcinogen, with a very high relative risk of adenocarcinoma of the nasal cavities and paranasal sinuses. The goal of this investigation was to conduct genotoxicity monitoring of carpenters involved in wooden furniture industry in order to test possible wood dust-induced genotoxic effects due to occupational exposure. The level of genetic damage was determined by comet, micronucleus and chromosomal aberration (CA) assays in peripheral blood lymphocytes (PBL) of 60 carpentry workers. In addition, the micronucleus test in buccal epithelial cells was carried out in the same subjects. Total antioxidant enzyme activities were measured by the indices: superoxide dismutase, glutathione peroxidase and catalase. A group of 60 non-exposed subjects matched by age, smoking and alcohol consumption habits were chosen as controls. The effect of age, smoking, alcohol consumption and duration of exposure was also analysed in the subjects of the present study. The results showed a statistically significant increase in mean DNA damage by comet assay, micronuclei frequency in buccal cells as well as PBL and frequency of CA in the exposed workers when compared to controls (P < 0.05). Analysis of the data showed that all the confounding factors had a significant effect on DNA damage and micronucleus frequency in buccal epithelial cells and PBL. Smoking and alcohol consumption did not have any significant effect by chromosomal aberration test. Antioxidant enzyme levels significantly decreased in the exposed subjects. Our findings indicate enhanced levels of genotoxicity in carpenters. Hence, these workers may have an increased cancer risk. © The Author 2008. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved.

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APA

Rekhadevi, P. V., Mahboob, M., Rahman, M. F., & Grover, P. (2009). Genetic damage in wood dust-exposed workers. Mutagenesis, 24(1), 59–65. https://doi.org/10.1093/mutage/gen053

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