Journal Article

Environmental air pollution and DNA adducts in Copenhagen bus drivers—Effect of <i>GSTM1</i> and <i>NAT2</i> genotypes on adduct levels

Per Sabro Nielsen, Nettie de Pater, Henrik Okkels and Herman Autrup

in Carcinogenesis

Volume 17, issue 5, pages 1021-1027
Published in print May 1996 | ISSN: 0143-3334
e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.5.1021
Environmental air pollution and DNA adducts in Copenhagen bus drivers—Effect of GSTM1 and NAT2 genotypes on adduct levels

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The lymphocyte bulky PAH-DNA adduct levels have been studied in persons occupationally exposed to ambient air pollution. The exposure group consisted of 90 healthy, nonsmoking bus drivers from the Copenhagen area, divided into three exposure groups according to driving area, and 60 rural controls (smokers and non-smokers). PAH-DNA adducts were determined by 32P-postlabelling with the butanol enrichment procedure. The bus drivers answered a comprehensive questionnaire on passive smoking, residential area, diet and other potential confounding variables. A significantly higher adduct level was observed in bus drivers working in central Copenhagen (1.214 fmol/μg DNA, n = 49) compared with both those driving in the dormitory (median: 0.507 fmol/μg DNA, P = 0.046, n = 16) and suburban (median: 0.585 fmol/μg DNA, P = 0.041, n = 25) areas. All three groups had higher adduct levels than rural controls (0.074 fmol/μg DNA, n = 60, P < 0.001). No significant influence on adduct levels was demonstrated from potential confounders, including smoking and diet The effect of the metabolizing enzymes, GSTM1 and NAT2, on adduct levels was investigated. No statistically significant effects were observed on adduct levels from GSTM1 or NAT2, either individually or combined, but a non-significant trend was seen for individuals with GSTMl*0/0 (null), since they had higher adduct levels in all exposure groups. This study demonstrated that lymphocyte PAH-DNA adduct levels were related to levels of exposure to urban air pollution and indicated that these adducts might be helpful as a means of classifying better different exposure groups for epidemiological studies. Furthermore, it demonstrated the ability of 32P-postlabelling to discern small differences in low exposure to ambient air pollution and suggested a possible effect of GSTM1*0/0 on DNA adduct levels.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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