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Pneumotoxic effects of exposure to welding fumes: cross-week evaluation of Clara cell protein and manganese, in blood of shipyard workers

机译:暴露于焊接烟雾中的气毒性效应:船厂工人血液中Clara细胞蛋白和锰的跨周评估

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Welders exposed to fumes containing manganese (Mn) develop inflammatory changes in the lower airways. However, the assessment of pneumotoxic effects of welding fumes is limited because of the lack of adequate biomarkers of early toxic effects. Bronchiolar epithelial Clara cell secretory protein (CC16) has a potential role in pulmonary inflammation, and the fall in CC16 serum level is a useful biomarker of the dysfunction of the respiratory system. In the present study, a feasibility of CC 16 as an early biomarker of Mn-induced pneumotoxicity has been evaluated. Cross-week determination of Mn concentrations in plasma and urine as well as determination of CC16 and hyalu-ronic acid (HA), a marker of pulmonary inflammation, were performed in welders exposed to welding fumes and in unexposed shipyard workers. In addition, pulmonary function tests (FVC, FEV-1 FEF-50) were done in both groups, and airborne Mn levels in working environment were determined. The results demonstrate the increased prevalence of Mn levels in blood exceeding 8 mug/dm~3 in a group exposed to welding fumes. Furthermore, increased prevalence of respiratory dysfunction in subjects with Mn levels exceeding 8 ug/dm~3 was observed. On the basis of our data, the threshold limit for Mn concentration in blood is about 8 mug/dm~3. Serum CC16 concentrations were markedly decreased in welders in whom significant reductions of FEF-50 (less than 60% of predicted value) were observed. In addition, within the range exceeding the threshold value (> 8 ug/dm~3) we found close negative correlation between Mn and CC 16 concentrations. Thus, the present study demonstrates that CC16 is a good peripheral biomarker of early pneumotoxic effect produced by welding fumes.
机译:暴露于含锰烟雾的焊工在下呼吸道发炎。然而,由于缺乏足够的早期毒性作用的生物标志物,对焊接烟雾的肺毒性作用的评估是有限的。支气管上皮克拉拉细胞分泌蛋白(CC16)在肺部炎症中具有潜在作用,而CC16血清水平的下降是呼吸系统功能障碍的有用生物标志物。在本研究中,已经评估了CC 16作为Mn引起的肺毒性的早期生物标记的可行性。在暴露于焊接烟雾中的焊工和未暴露的造船厂工人中,进行跨星期的血浆和尿液中Mn浓度测定以及CC16和透明质酸(HA)(肺部炎症的标志物)的测定。此外,两组均进行了肺功能测试(FVC,FEV-1 FEF-50),并确定了工作环境中的空气中锰含量。结果表明,在暴露于焊接烟雾的一组中,血液中锰含量的流行率超过8个大杯/ dm〜3。此外,观察到锰水平超过8 ug / dm〜3的受试者呼吸功能障碍的患病率增加。根据我们的数据,血液中锰浓度的阈值极限约为8个大杯/ dm〜3。焊工的血清CC16浓度显着降低,其中FEF-50显着降低(不到预测值的60%)。此外,在超过阈值(> 8 ug / dm〜3)的范围内,我们发现Mn和CC 16浓度之间存在密切的负相关。因此,本研究表明CC16是焊接烟雾产生的早期肺毒性作用的良好外周生物标志物。

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