Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.
Institute for Risk Assessment Sciences, Division of Environmental Epidemiology, Utrecht University, Utrecht, The Netherlands.
Environ Mol Mutagen. 2021 Oct;62(8):458-470. doi: 10.1002/em.22455. Epub 2021 Aug 16.
Urinary mutagenicity reflects systemic exposure to complex mixtures of genotoxic/carcinogenic agents and is linked to tumor development. Coal combustion emissions (CCE) and diesel engine exhaust (DEE) are associated with cancers of the lung and other sites, but their influence on urinary mutagenicity is unclear. We investigated associations between exposure to CCE or DEE and urinary mutagenicity. In two separate cross-sectional studies of nonsmokers, organic extracts of urine were evaluated for mutagenicity levels using strain YG1041 in the Salmonella (Ames) mutagenicity assay. First, we compared levels among 10 female bituminous (smoky) coal users from Laibin, Xuanwei, China, and 10 female anthracite (smokeless) coal users. We estimated exposure-response relationships using indoor air concentrations of two carcinogens in CCE relevant to lung cancer, 5-methylchrysene (5MC), and benzo[a]pyrene (B[a]P). Second, we compared levels among 20 highly exposed male diesel factory workers and 15 unexposed male controls; we evaluated exposure-response relationships using elemental carbon (EC) as a DEE-surrogate. Age-adjusted linear regression was used to estimate associations. Laibin smoky coal users had significantly higher average urinary mutagenicity levels compared to smokeless coal users (28.4 ± 14.0 SD vs. 0.9 ± 2.8 SD rev/ml-eq, p = 2 × 10 ) and a significant exposure-response relationship with 5MC (p = 7 × 10 ). DEE-exposed workers had significantly higher urinary mutagenicity levels compared to unexposed controls (13.0 ± 10.1 SD vs. 5.6 ± 4.4 SD rev/ml-eq, p = .02) and a significant exposure-response relationship with EC (p-trend = 2 × 10 ). Exposure to CCE and DEE is associated with urinary mutagenicity, suggesting systemic exposure to mutagens, potentially contributing to cancer risk and development at various sites.
尿液致突变性反映了对遗传毒性/致癌性混合剂的全身暴露情况,与肿瘤的发展有关。煤燃烧排放物(CCE)和柴油发动机废气(DEE)与肺癌和其他部位的癌症有关,但它们对尿液致突变性的影响尚不清楚。我们研究了暴露于 CCE 或 DEE 与尿液致突变性之间的关联。在两项针对非吸烟者的独立横断面研究中,使用沙门氏菌(Ames)致突变性测定中的 YG1041 菌株评估尿液有机提取物的致突变性水平。首先,我们比较了来自中国来宾和宣威的 10 名女性烟煤(多烟)使用者和 10 名女性无烟煤(无烟)使用者之间的水平。我们使用与肺癌相关的 CCE 中两种致癌物(5-甲基胆蒽(5MC)和苯并[a]芘(B[a]P)的室内空气浓度来估计暴露-反应关系。其次,我们比较了 20 名高暴露柴油厂工人和 15 名未暴露男性对照组之间的水平;我们使用元素碳(EC)作为 DEE 的替代物来评估暴露-反应关系。使用年龄调整的线性回归来估计关联。来宾烟煤使用者的尿液致突变性水平明显高于无烟煤使用者(28.4 ± 14.0 SD 与 0.9 ± 2.8 SD rev/ml-eq,p = 2×10),与 5MC 呈显著的暴露-反应关系(p = 7×10)。暴露于 DEE 的工人的尿液致突变性水平明显高于未暴露的对照组(13.0 ± 10.1 SD 与 5.6 ± 4.4 SD rev/ml-eq,p = 0.02),与 EC 呈显著的暴露-反应关系(p 趋势= 2×10)。暴露于 CCE 和 DEE 与尿液致突变性有关,这表明全身暴露于致突变剂,可能导致不同部位的癌症风险和发展。