炉工人的血CC16水平与肺功能变化之间的关联:从2014年到2023年的队列研究
Jiajun Wei1, Yong Wang1, Hongyue Kong1
1MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention, Xinjiannan Road 56, Taiyuan City, Shanxi Province 030001, China.
Ecotoxicology and environmental safety
|September 6, 2024
概括
多环芳 (PAHs) 暴露会降低细胞分泌蛋白 (CC16) 水平,这是一个肺部健康标志物. 焦炭炉工人的较低CC16预测未来的肺功能下降,特别是在高PAH暴露和吸烟的情况下.
科学领域:
- 环境健康 环境健康
- 职业医疗 职业医疗 职业医学
- 肺部毒理学 肺部毒理学
背景情况:
- 俱乐部细胞分泌蛋白 (CC16) 是肺上皮质健康和透性的生物标志物.
- 多环芳 (PAH) 对CC16水平和长期肺功能的影响的流行病学证据有限.
- 炉工人面临着大量的PAH暴露,对呼吸系统健康构成风险.
研究的目的:
- 为了研究PAH暴露对炉工人的血CC16水平的影响.
- 检查9年间基线CC16水平与长期肺功能变化之间的关联.
- 探索PAH暴露和吸烟对CC16-肺功能关系的改变作用.
主要方法:
- 对307名焦炭炉工人的纵向研究,基线测量于2014年,随访9年.
- 测量尿中PAH代谢物和血CC16水平.
- 使用贝叶斯核机器回归 (BKMR) 分析混合PAHs效应和限制立方线 (RCS) 模型用于剂量效应关联.
主要成果:
- 氧化的代谢物与血CC16水平和强迫生命能力 (FVC) 呈现负相关性.
- 在随访时,较低的基线CC16水平与减少的FVC,FEV1和增加的小气道功能障碍风险显著相关.
- 高水平的PAH暴露和吸烟加剧了CC16和肺功能下降之间的负面关联.
结论:
- 职业接触PAHs有助于减少炉工人的血CC16水平.
- 低基线CC16是随着时间的推移加速肺功能下降的预测指标.
- 针对PAH暴露和戒烟的干预措施对于保护暴露工人的肺部健康至关重要.
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