Zhang Jun-hong, Zhang Jun, Sun Jian-ya, Tian Lin, Niu Qiao
Taiyuan Center for Disease Control and Prevention, Taiyuan 030001, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2008 Jan;26(1):16-9.
To explore the relationship between the expression of heat shock protein 90, 60 and 27 (HSP90, HSP60 and HSP27) and genetic damage in peripheral blood of workers exposed to coke oven emissions.
288 coke oven workers in a steel factory were divided into the high-dose group and the low-dose group on the basis of environment monitoring result and work place. There were 172 men in high-dose group (workers who worked at the oven top and oven side) and 116 men in low-dose group (workers who worked at the oven bottom and others who were engaged to aided work). 38 workers unexposed occupationally to carcinogenic substances were selected as the control group, who were employed in medical therapy unit nearby 2 kilometers from the steel factory. Their general information, history of personal and occupational exposure, and the work environment were investigated. Blood samples were collected immediately after a shift at the end of a working day from 288 coke oven workers and 38 control workers. Levels of HSP90, HSP60 and HSP27 in peripheral blood lymphocytes were measured by Western blot, and the degree of DNA damage was detected by the comet assay.
Levels of HSP90 in peripheral blood lymphocytes in three groups were 0.24 +/- 0.32, 0.12 +/- 0.30 and 0.06 +/- 0.33 respectively. They increased significantly compared with that of the control. But levels of HSP60 and HSP27 were not significantly different among those groups. Compared with the control group, there was significant difference in tail length, olive tail moment et al of SCGE (G +/- s(G)) of occupational exposure workers. High-dose group > low-dose group > control group (P < 0.05). The degree of DNA damage increased with the rise of exposure BaP dose (Spearman r = -0.345, P < 0.01).
Levels of HSP90 in peripheral blood lymphocytes and the degree of DNA damage increase with the rise of exposure polycyclic aromatic hydrocarbons (PAHs) dose.
探讨焦炉逸散物暴露工人外周血中热休克蛋白90、60及27（HSP90、HSP60及HSP27）表达与遗传损伤的关系。
某钢铁厂288名焦炉工人根据环境监测结果及工作岗位分为高剂量组和低剂量组。高剂量组172名男性（炉顶和炉侧作业工人），低剂量组116名男性（炉底作业工人及其他辅助作业工人）。选取38名未职业接触致癌物的工人作为对照组，其就职于距钢铁厂2公里外的医疗单位。调查其一般资料、个人及职业暴露史和工作环境。在工作日结束轮班后，立即采集288名焦炉工人及38名对照工人的血样。采用蛋白质免疫印迹法检测外周血淋巴细胞中HSP90、HSP60及HSP27水平，采用彗星试验检测DNA损伤程度。
三组外周血淋巴细胞中HSP90水平分别为0.24±0.32、0.12±0.30及0.06±0.33。与对照组相比均显著升高。但三组间HSP60及HSP27水平差异无统计学意义。职业暴露工人的单细胞凝胶电泳（SCGE）（G±s（G））尾长、橄榄尾矩等与对照组相比差异有统计学意义。高剂量组>低剂量组>对照组（P<0.05）。DNA损伤程度随苯并[a]芘暴露剂量升高而增加（Spearman r=-0.345，P<0.01）。
外周血淋巴细胞中HSP90水平及DNA损伤程度随多环芳烃（PAHs）暴露剂量升高而增加。
