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Monitoring Low Benzene Exposure: Comparative Evaluation of Urinary Biomarkers, Influence of Cigarette Smoking, and Genetic Polymorphisms

¹ Department of Occupational and Environmental Health, University of Milan and Fondazione Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Milan, Italy; ² School of Public Health, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey; ³ Cancer Biomarkers and Prevention Group, Biocentre and ⁴ Medical Research Council, Institute for Environmental and Health, University of Leicester, Leicester, United Kingdom; and ⁵ Environmental Epidemiology and Biostatistics, Department of Cancer Etiology and Epidemiology, National Cancer Research Institute, Genoa, Italy

Requests for reprints: Silvia Fustinoni, Department of Occupational and Environmental Health, University of Milan and Instituti Clinici di Perfezionamento, Via S. Barnaba, 8, 20122 Milan, Italy. Phone: 39-2-503-20116; Fax: 39-2-503-20110. E-mail: silvia.fustinoni{at}unimi.it

Benzene is a human carcinogen and an ubiquitous environmental pollutant. Identification of specific and sensitive biological markers is critical for the definition of exposure to low benzene level and the evaluation of the health risk posed by this exposure. This investigation compared urinary trans,trans-muconic acid (t,t-MA), S-phenylmercapturic acid, and benzene (U-benzene) as biomarkers to assess benzene exposure and evaluated the influence of smoking and the genetic polymorphisms CYP2E1 (RsaI and DraI) and NADPH quinone oxidoreductase-1 on these indices. Gas station attendants, urban policemen, bus drivers, and two groups of controls were studied (415 subjects). Median benzene exposure was 61, 22, 21, 9 and 6 µg/m³, respectively, with higher levels in workers than in controls. U-benzene, but not t,t-MA and S-phenylmercapturic acid, showed an exposure-related increase. All the biomarkers were strongly influenced by cigarette smoking, with values up to 8-fold higher in smokers compared with nonsmokers. Significant correlations of the biomarkers with each other and with urinary cotinine were found. A possible influence of genetic polymorphism of CYP2E1 (RsaI and/or DraI) on t,t-MA and U-benzene in subjects with a variant allele was found. Multiple linear regression analysis correlated the urinary markers with exposure, smoking status, and CYP2E1 (RsaI; R² up to 0.55 for U-benzene). In conclusion, in the range of investigated benzene levels (<478 µg/m³ or <0.15 ppm), smoking may be regarded as the major source of benzene intake; among the study indices, U-benzene is the marker of choice for biomonitoring low-level occupational and environmental benzene exposure.

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