PAH-DNA adducts in a Chinese population: relationship to PAH exposure, smoking and polymorphisms of metabolic and DNA repair genes
PAH-DNA adducts in a Chinese population: relationship to PAH exposure, smoking and polymorphisms of metabolic and DNA repair genes
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DOI：
10.1080/13547500701671895
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发表时间：
2008-01-01
期刊：
影响因子：
2.6
通讯作者：
Qu, Qingshan
中科院分区：
文献类型：
--
作者：
Hu, Yu;Li, Gang;Qu, Qingshan
本研究在中国人群中进行，以评估PAH-DNA加合物作为PAH暴露的生物标志物的有用性和敏感性，并检查吸烟和响应基因多态性对PAH暴露诱导的DNA加合物形成的潜在影响。检测的基因多态性包括GSTM 1、GSTT 1、CYP 1A 1、微粒体环氧化物水解酶（mEH）和切除修复交叉互补组2（ERCC 2）。共招募了194名具有广泛PAH暴露的受试者，包括116名职业暴露工人，49名大城市居民和29名郊区园丁。在整个受试者组中，观察到PAH暴露与白细胞中DNA加合物之间存在显著的风险-反应关系（p < 0.0001）。多环芳烃最低职业暴露（< 0.1 μ g BaPm（-3））亚组的多环芳烃-DNA加合物水平显著高于城市居民和郊区园丁。然而，没有显着差异，居民和园丁之间检测，平均苯并（a）芘浓度为0.028和0.011 μ g m（-3），分别。除ERCC 2 Lys 751 Gln基因型外，其他基因多态性对PAH诱导的加合物形成无显著影响。携带野生型ERCC 2的受试者中PAH-DNA加合物水平显著高于携带杂合子或纯合子变异等位基因的受试者（p < 0.01）。吸烟、年龄和性别在本研究中对PAH诱导的DNA加合物形成没有实质性影响。这项研究表明，多环芳烃-DNA加合物可以作为一个可靠的生物标志物的多环芳烃暴露在职业环境中，但可能不够敏感，用于人群与环境暴露的多环芳烃。
The present study was conducted in a Chinese population to evaluate the usefulness and sensitivity of PAH-DNA adduct as a biomarker of PAH exposure, and to examine the potential effects of smoking and polymorphisms of responsive genes on DNA adduct formation induced by PAH exposure. The polymorphisms of genes examined include GSTM1, GSTT1, CYP1A1, microsomal epoxide hydrolase (mEH) and excision repair cross-complementary group 2 (ERCC2). A total of 194 subjects with a broad range of PAH exposures were recruited, including 116 occupationally exposed workers, 49 metropolitan residents and 29 suburban gardeners. A significant exposure-response relationship was observed between PAH exposure and DNA adducts in leukocytes across the entire group of subjects (p < 0.0001). The levels of PAH-DNA adducts in the subgroup with lowest occupational exposure to PAHs (< 0.1 mu g BaP m(-3)) was significantly higher than that in metropolitan residents and suburban gardeners. However, no significant difference was detected between residents and gardeners, with mean BaP concentrations of 0.028 and 0.011 mu g m(-3), respectively. The polymorphisms of genes examined failed to show significant effects on PAH-induced adduct formation except ERCC2 Lys751Gln genotypes. A significantly higher level of PAH-DNA adduct was found in subjects with wild-type ERCC2 than those who have either heterozygous or homozygous variant alleles (p < 0.01). Smoking, age and gender did not substantially contribute to PAH-induced DNA adduct formation in this study. The study suggests that PAH-DNA adducts may serve as a reliable biomarker of PAH exposure in occupational settings but may not be sensitive enough to be used in populations with environmental exposures to PAHs.