Nielsen P S, de Pater N, Okkels H, Autrup H
Department of Environmental and Occupational Medicine, Unversity of Aarhus, Denmark.
Carcinogenesis. 1996 May;17(5):1021-7. doi: 10.1093/carcin/17.5.1021.
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/microg DNA, n = 49) compared with both those driving in the dormitory (median: 0.507 fmol/microg DNA, P = 0.046, n = 16) and suburban (median: 0.585 fmol/microg DNA, P = 0.041, n = 25) areas. All three groups had higher adduct levels than rural controls (0.074 fmol/microg 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 GSTM10/0 (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 GSTM10/0 on DNA adduct levels.
已对职业性接触环境空气污染人群的淋巴细胞中多环芳烃 - DNA加合物水平进行了研究。暴露组由来自哥本哈根地区的90名健康、不吸烟的公交车司机组成,根据驾驶区域分为三个暴露组,以及60名农村对照者(吸烟者和非吸烟者)。采用丁醇富集程序的32P后标记法测定多环芳烃 - DNA加合物。公交车司机回答了一份关于被动吸烟、居住区域、饮食和其他潜在混杂变量的综合问卷。与在宿舍驾驶的司机(中位数:0.507 fmol/μg DNA,P = 0.046,n = 16)和郊区驾驶的司机(中位数:0.585 fmol/μg DNA,P = 0.041,n = 25)相比,在哥本哈根市中心工作的公交车司机的加合物水平显著更高(1.214 fmol/μg DNA,n = 49)。所有三组的加合物水平均高于农村对照者(0.074 fmol/μg DNA,n = 60,P < 0.001)。未发现包括吸烟和饮食在内的潜在混杂因素对加合物水平有显著影响。研究了代谢酶GSTM1和NAT2对加合物水平的影响。单独或联合使用GSTM1或NAT2时,未观察到对加合物水平有统计学显著影响,但对于GSTM10/0(无效)个体存在不显著的趋势,因为他们在所有暴露组中的加合物水平都较高。这项研究表明淋巴细胞多环芳烃 - DNA加合物水平与城市空气污染暴露水平相关,并表明这些加合物可能有助于更好地对不同暴露组进行分类以用于流行病学研究。此外,它证明了32P后标记法能够识别低水平环境空气污染暴露中的微小差异,并提示GSTM10/0对DNA加合物水平可能有影响。