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硬质合金粉尘接触工人肺损伤生物标志物影响因素的路径分析

Pathway analysis of influencing factors to the biomarkers of lung injury in workers exposured to hard metal dust
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摘要 目的 长期反复吸入硬质合金粉尘能够引起肺部健康损害,应用路径分析探索职业接触、年龄、工龄、性别、吸烟等因素对肺损伤生物标志物的影响,为接触工人的健康状况评估和健康监护提供依据。方法 通过整群抽样选择硬质合金生产和加工企业的工人作为研究对象,根据是否接触硬质合金粉尘将其分为接触组(735人)和对照组(449人)。通过作业场所短时定点采样测定空气中钨及其化合物、钴及其化合物浓度,计算工人接触钨、钴8 h时间加权平均浓度(TWA)。对研究对象进行肺活量(VC)和第1秒用力呼气容积(FEV_(1.0))检查;采集研究对象全血样品,检测全血中钨、钴元素及血清中人Ⅱ型肺泡细胞表面抗原(krebs.von den lungen-6,KL-6)和转化生长因子-β_(1)(transforming growth factor-β_(1),TGF-β_(1))水平。应用路径分析,探讨职业接触硬质合金粉尘、作业场所空气中钨和钴8 h时间加权平均浓度、年龄、性别、工龄、吸烟与生物标志物VC%、FEV_(1.0)%、血钨、血钴、KL-6、TGF-β_(1)之间的因果关系。结果 接触组血清KL-6和TGF-β_(1)水平[(1.65±1.40)ng/ml,(17.73±5.60)ng/ml]显著高于对照组[(1.38±1.20)ng/ml,(16.23±4.80)ng/ml](P<0.05)。接触组全血钨、钴的检出率分别为9.3%、45.4%,均高于对照组(2.5%、12.7%)(P<0.05)。接触硬质合金粉尘、作业场所空气中钴浓度与血清KL-6、TGF-β_(1)和血钴均有正向因果关系(P<0.05)。结论 接触硬质合金粉尘和作业场所空气中钴浓度是影响接触工人肺损伤生物标志物的重要因素,KL-6、TGF-β_(1)、血钴可作为硬质合金粉尘接触工人生物监测的敏感指标。 Objective Long-term repeated inhalation of hard metal dust can cause lung damage.Path analysis was used to assess the relationship between biomarkers related to respiratory injury and potential causes,including occupational exposure,age,working age,gender and smoking.The study results could provide supports for health assessment and monitoring.Methods The workers in the hard alloy production and processing enterprises were selected as the subjects by cluster sampling,and were divided into exposure group(735 workers)and control group(449 workers)according to whether they were exposed with hard metal dust or not.The concentration of tungsten and its compounds,cobalt and its compounds in the air was measured by short-time fixed point sampling in the workplace,then the time-weighted average concentration(TWA)of workers exposed to tungsten and cobalt for 8 h was calculated.The subjects were tested for vital capacity(VC)and forced expiratory volume in 1 second(FEV_(1.0)).The whole blood samples of the subjects were collected to detect tungsten and cobalt elements.Human typeⅡalveolar-cell surface resistance(krebs.von den lungen-6,KL-6)and transforming growth factor-β_(1)(TGF-β_(1))were measured in serum.Path analysis was used to investigate the relationship between the causes(occupational exposure to hard metal dust,concentrations of tungsten and cobalt for 8 h in workplace air,age,gender,working age and smoking)and effects(VC%,FEV_(1.0)%,blood tungsten,blood cobalt,KL-6 and TGF-β_(1)).Results The levels of KL-6 and TGF-β_(1) in serum increased significantly in exposed workers[(1.65±1.40)ng/ml,(17.73±5.60)ng/ml]when compared with the control group[(1.38±1.20)ng/ml,(16.23±4.80)ng/ml](P<0.05).The detection rates of tungsten and cobalt in whole blood were higher in exposed workers(9.3%and 45.4%)than in control workers(2.5%and 12.7%)(P<0.05).Exposure to hard metal dust and level of cobalt in workplace air can increase the level of KL-6、TGF-β_(1) in serum and cobalt in whole blood(P<0.05).Conclusion Exposure to hard metal dust and cobalt concentration in workplace air are key factors affecting biomarkers of lung injury in exposed workers.KL-6,TGF-β_(1),cobalt in whole blood might be used as sensitive indicators for biological monitoring in hard metal dust exposed workers.
作者 张雪艳 何卫红 彭仁和 贾宁 曲颖 王忠旭 ZHANG Xueyan;HE Weihong;PENG Renhe;JIA Ning;QU Ying;WANG Zhongxu(National Institute for Occupational Health and Poison Control,Chinese Center for Disease Control and Prevention,Beijing 100050,China;不详)
出处 《中国工业医学杂志》 CAS 2023年第3期195-199,211,共6页 Chinese Journal of Industrial Medicine
基金 国家公益性行业科研专项——新增法定职业病防治关键技术研究(编号:201402021)。
关键词 Ⅱ型肺泡细胞表面抗原(KL-6) 转化生长因子-β_(1)(TGF-β_(1)) 硬质合金 tungsten cobalt krebs.von den lungen-6(KL-6) transforming growth factor-β_(1)(TGF-β_(1)) hard metal
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  • 1张忠义,刚葆琪.钴及其化合物的生物学作用[J].工业卫生与职业病,1995,21(2):121-125. 被引量:3
  • 2贾如宝.钨(W)对人体健康的双向影响[J].金属世界,1995(4):27-27. 被引量:4
  • 3蔡后荣,曹敏,孟凡青,魏静义,侯杰.巨细胞间质性肺炎一例及文献复习[J].中华结核和呼吸杂志,2006,29(5):313-316. 被引量:11
  • 4黄燕军,潘志霞,李姝,宋慧.钴、锡、锶单独或钴锌协同作用对大鼠肝脏脂质过氧化的影响[J].现代预防医学,2006,33(11):2036-2037. 被引量:3
  • 5Philip R, Carl JJ, Jacqueline P, et al. A perpetual cascade of cytokines postirradiation leads to pulmonary fibrosis[J]. Int J Radiation Oncol Biol Phys, 1995, 33(1): 99-109.
  • 6Fuchs O. Role of cytokine signaling pathways of the transforming growth factor-beta family in the regulation of hematopoiesis[J]. Cas Lek Cesk, 2002, 22 (Suppl): 141: 18-22.
  • 7司徒镇强.细胞培养[M].西安:世界图书出版社,2000.186.
  • 8Michele M, Jean-louse L, Sylvie D, et al. TGFβ1 and radiation fibrosis: a master switch and a specific therapeutic target?[J]. Int J Radiation Oncol Biol Phys, 2000, 47(2): 277-290.
  • 9Rik D, Xin-Hua F. TGFβ receptor signaling [J]. Biochimica et Biophysica Acta, 1997, 1333: 105-150.
  • 10Petridou S, Maltseva O, Spanakis S, et al. TGF-β receptor expression and Smad2 localization are cell density dependent in fibroblasts [J]. IOVS, 2000, 41(1): 89-95.

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