Liu Ai-Lin, Lu Wen-Qing, Wang Zeng-Zhen, Chen Wei-Hong, Lu Wen-Hong, Yuan Jing, Nan Pei-Hong, Sun Jian-Ya, Zou Ya-Lin, Zhou Li-Hong, Zhang Chi, Wu Tang-Chun
Department of Occupational and Environmental Health and Ministry of Education Key Lab for Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Environ Health Perspect. 2006 May;114(5):673-7. doi: 10.1289/ehp.8562.
To investigate associations among occupational exposure to coke oven emissions (COEs), oxidative stress, cytogenotoxic effects, change in the metabolizing enzyme glutathione S-transferase (GST), and internal levels of polycyclic aromatic hydrocarbons (PAHs) in coke oven workers, we recruited 47 male coke oven workers and 31 male control subjects from a coke oven plant in northern China. We measured the levels of 1-hydroxypyrene (1-OHP) and 8-hydroxy-2 -deoxyguanosine (8-OHdG) in urine, micronucleated binucleated cells (BNMNs) in peripheral blood lymphocyte, and GST in serum. Our results showed that the group exposed to COEs had significantly increased levels of 1-OHP [median 5.7; interquartile range (IQR), 1.4-12.0 micromol/mol creatinine] compared with the control group (3; 0.5-6.4 micromol/mol creatinine). In addition, the median levels (IQR) of 8-OHdG, BNMNs, and GST were markedly increased in the exposed [1.9 (1.4-15.4) micromol/mol creatinine; 6 (2-8) per thousand ; 22.1 (14.9-31.2) U/L, respectively] compared with controls [1.3 (1.0-4.0) micromol/mol creatinine, 2 (0-4) per thousand; and 13.1 (9.5-16.7) U/L, respectively]. These results appeared to be modified by smoking. However, multivariate logistic regression analysis revealed that exposure to COEs had the highest odds ratio among variables analyzed and that smoking was not a significant confounder of the levels of studied biomarkers. Overall, the present findings suggest that COE exposure led to increased internal PAH burden, genetic damage, oxidative stress, and GST activity. The consequences of the changes in these biomarkers, such as risk of cancer, warrant further investigations.
为了研究焦炉工人职业暴露于焦炉排放物(COEs)、氧化应激、细胞遗传毒性效应、代谢酶谷胱甘肽S-转移酶(GST)变化以及体内多环芳烃(PAHs)水平之间的关联,我们从中国北方一家焦化厂招募了47名男性焦炉工人和31名男性对照受试者。我们测量了尿中1-羟基芘(1-OHP)和8-羟基-2'-脱氧鸟苷(8-OHdG)的水平、外周血淋巴细胞中的微核双核细胞(BNMNs)以及血清中的GST。我们的结果显示,与对照组(3;0.5 - 6.4 μmol/mol肌酐)相比,暴露于COEs的组1-OHP水平显著升高[中位数5.7;四分位数间距(IQR),1.4 - 12.0 μmol/mol肌酐]。此外,与对照组[分别为1.3(1.0 - 4.0)μmol/mol肌酐、2(0 - 4)‰和13.1(9.5 - 16.7)U/L]相比,暴露组中8-OHdG、BNMNs和GST的中位数水平(IQR)显著升高[分别为1.9(1.4 - 15.4)μmol/mol肌酐、6(2 - 8)‰和22.1(14.9 - 31.2)U/L]。这些结果似乎受吸烟影响。然而,多因素逻辑回归分析显示,在分析的变量中,暴露于COEs的比值比最高,且吸烟并非所研究生物标志物水平的显著混杂因素。总体而言,目前的研究结果表明,暴露于COEs会导致体内PAH负担增加、遗传损伤、氧化应激和GST活性增加。这些生物标志物变化的后果,如癌症风险,值得进一步研究。