低水平焦炉逸散物对接触人群尿中8-羟基脱氧鸟苷影响分析

Impact of low-level coke oven emissions on urinary 8-hydroxy-2'-deoxyguanosine in exposed workers

目的探讨低水平焦炉逸散物（COE）接触与焦炉作业工人尿中8-羟基脱氧鸟苷（8-OHd G）的剂量-效应关系。方法采用横断面调查方法,以某焦化厂263名焦炉作业工人为接触组,以某氧气厂113名非焦炉作业工人为对照组。检测2组人群工作场所空气中COE短时间接触浓度（CSTEL）。分别采用高效液相色谱法和超高效液相色谱-质谱法测定研究对象尿中1-羟基芘（1-OHP）和8-OHd G水平。结果对照组和接触组工作场所空气中COE的CSTEL分别为0.020~0.070（0.042±0.018）、0.100~0.320（0.208±0.069）mg/m3;接触组人群工作场所空气中COE的CSTEL高于对照组（P〈0.01）;对照组和接触组炉底、炉侧、炉顶亚组工作场所空气中COE的CSTEL分别为0.020~0.070（0.042±0.018）、0.100~0.160（0.132±0.023）、0.180~0.300（0.223±0.040）、0.190~0.320（0.269±0.049）mg/m3,呈从低到高趋势（P〈0.01）。接触组人群尿中1-OHP和8-OHd G水平均高于对照组[0.466（0.160,1.420）vs 0.026（0.011,0.110）μmol/mol肌酐,237.990（128.727,458.055）vs 160.000（94.578,274.256）μg/mol肌酐,P〈0.01]。研究对象尿中1-OHP水平从低到高依次为对照组〈接触组炉底亚组〈接触组炉侧亚组〈接触组炉顶亚组（P〈0.05）。多重线性回归分析结果显示,在排除性别、年龄、工龄、吸烟、饮酒和体质量超重等混杂因素的影响后,尿中1-OHP水平和8-OHd G水平均与COE接触有关联（P〈0.05）;接触组人群COE接触水平与尿中1-OHP水平呈剂量-效应关系（P〈0.01）,尿中1-OHP水平与8-OHd G水平呈剂量-效应关系（P〈0.01）。结论低水平COE接触仍可导致焦炉作业工人DNA氧化损伤,其COE接触水平与DNA氧化损伤标志物尿中8-OHd G水平呈剂量-效应关系。

Objective To investigate the dose-effect relationship between urinary 8-hydroxy-2 ＇-deoxyguanosine（ 8-OHd G） in workers exposed to the low-level coke oven emissions（ COE）. Methods By using cross-sectional survey method,263 coke oven workers in a coke oven plant were recruited as COE-exposed group,and 113 workers without COE exposure in an oxygen making plant as control group. The concentration on short term exposure limit（ CSTEL） of COE at their workplaces was detected. Urinary 1-hydroxypyrene（ 1-OHP） levels were measured by high performance liquid chromatography. Urinary 8-OHd G levels were detected by ultra-high performance liquid chromatography-mass spectrometer. Results The CSTELof COE at workplaces in control group and COE-exposed group were 0. 020-0. 070（ 0. 042 ± 0. 018） and 0. 100-0. 320（ 0. 208 ± 0. 069） mg/m3 respectively. CSTELin COE-exposed group was higher than that of the controls（ P〈0. 01）. The levels of COE CSTELwere 0. 020-0. 070（ 0. 042 ± 0. 018）,0. 100-0. 160（ 0. 132 ±0. 023）,0. 180-0. 300（ 0. 223 ± 0. 040）,and 0. 190-0. 320（ 0. 269 ± 0. 049） mg / m3 in control group,bottom-oven,side-oven,and top-oven subgroup of COE-exposed group,respectively,with an increasing trend（ P〈0. 01）. Levels of urinary 1-OHP and 8-OHd G in COE-exposed group were both higher than those in controls [0. 466（ 0. 160,1. 420） vs0. 026（ 0. 011,0. 110） μmol / mol creatinine,237. 990（ 128. 727,458. 055） vs 160. 000（ 94. 578,274. 256） μg / mol creatinine,respectively; P〈0. 01 for all]. The lowest level of urinary 1-OHP was found in control group,and followed by the sequence of bottom-oven,side-oven,and top-oven subgroup among COE-exposed population,respectively（ P〈0. 05）. Multiple linear regression indicated that both levels of urinary 1-OHP and urinary 8-OHd G were correlated to COE exposure（ P〈0. 05）,after controlling the confounding effects from gender,age,working years,smoking status,alcohol drinking status,and overweight body mass. There were dose-effect relationship between COE exposure and urinary 1-OHP levels（ P〈0. 01） and significant dose-effect relationship between urinary 1-OHP and urinary 8-OHd G levels（ P〈0. 01）in COE-exposed population. Conclusion Low level exposure to COE may induce oxidative DNA damage in coke oven workers,showing a good dose-effect relationship between COE levels and urinary 8-OHd G level.