环境空气污染暴露,介导生物标志物和COPD风险:一个队列研究和元分析
Tinggui Wang1,2,3, Mengdan Liang1,3, Xiaoying Ye1,3
1Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou, China.
空气污染,包括细颗粒物 (PM2.5) 和氧化 (NOx),显著降低肺功能,增加COPD风险. 像脂质和炎症标志物这样的生物标志物会调解这种有害关系,
科学领域:
- 环境健康
- 呼吸系统医学
- 毒理学
背景情况:
- 对空气污染对肺功能和生物标志物的系统影响的理解有限.
- 需要对空气污染,COPD和肺功能相关性进行全面评估.
- 探索与空气污染相关的呼吸道疾病中的生物标志物.
研究的目的:
- 评估各种空气污染物对肺功能和COPD发病率的影响.
- 研究生物标志物在空气污染与呼吸系统健康之间的关系中的作用.
- 通过元分析对先前的研究结果进行综合.
主要方法:
- 对451,566名英国生物银行参与者的前性分析.
- 土地利用回归模型用于估计对PM2.5,PM10,PM2.5吸收率,NO2和NOx的暴露.
- 肺功能 (FEV1,FVC,PEF) 和COPD风险的线性回归和考克斯回归;生物标志物的分析和中介分析.
主要成果:
- 增加PM2. 5吸收率,NOx和NO2与肺功能减弱和COPD风险增加相关.
- 在种族分层分析中发现了显著的相互作用,白人群体更容易受到影响.
- 分析证实了空气污染与COPD的联系;介导分析确定了脂质代谢物,炎症细胞和细胞因子作为关键中间体.
结论:
- 空气污染与肺功能下降和COPD风险增加有关,
- 脂质,炎症和血液生物标志物介导空气污染对呼吸系统的不良影响.
- 迫切需要控制空气污染以减少呼吸道损害并制定有针对性的干预措施.
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