Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China
Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China
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DOI：
10.1186/s12940-020-0568-1
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发表时间：
2020-01-30
影响因子：
6
通讯作者：
Xu, Kai-Feng
中科院分区：
文献类型：
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作者：
Gao, Nannan;Xu, Wenshuai;Xu, Kai-Feng
背景暴露于空气污染与慢性阻塞性肺疾病（COPD）有关。然而，关于空气污染对中国COPD患者肺功能和全身炎症的影响的研究结果不一致且缺乏。本研究旨在评估环境空气污染对中国北京COPD队列的肺功能参数和血清细胞因子水平的影响。方法我们于2015年12月至2017年9月在中国北京滚动招募COPD参与者。每3个月对每位参与者进行一次随访。每6个月检测一次血清20种细胞因子水平。在同一时期，每小时的环境污染物水平从北京的35个监测站获得。参与者的地理编码住宅地址被用来估计每日平均污染暴露。一个线性混合效应模型被用来探讨空气污染物对健康的影响，在第一年的后续行动。结果基线时共纳入84例COPD患者。其中，75名COPD患者完成了第一年的随访。我们发现空气动力学直径小于2.5 μ m的颗粒物（PM2.5）、二氧化氮（NO2）、二氧化硫（SO2）和一氧化碳（CO）对COPD患者的用力肺活量%预测值（FVC % pred）具有不良累积效应。进一步分析表明，在COPD患者中，空气污染暴露与血清嗜酸性粒细胞趋化因子、白细胞介素4（IL-4）和IL-13水平降低相关，与血清IL-2、IL-12、IL-17 A、干扰素γ（IFN γ）、单核细胞置换蛋白1（MCP-1）和可溶性CD 40配体（sCD 40 L）水平升高相关。结论COPD患者急性暴露于PM2. 5、NO2、SO2和CO可导致FVC % pred降低。此外，短期暴露于空气污染物会增加COPD患者的全身炎症;这可能归因于Th 1和Th 17细胞因子增加以及Th 2细胞因子减少。
Background Exposure to air pollution is associated with chronic obstructive pulmonary disease (COPD). However, findings on the effects of air pollution on lung function and systemic inflammation in Chinese COPD patients are inconsistent and scarce. This study aims to evaluate the effects of ambient air pollution on lung function parameters and serum cytokine levels in a COPD cohort in Beijing, China. Methods We enrolled COPD participants on a rolling basis from December 2015 to September 2017 in Beijing, China. Follow-ups were performed every 3 months for each participant. Serum levels of 20 cytokines were detected every 6 months. Hourly ambient pollutant levels over the same periods were obtained from 35 monitoring stations across Beijing. Geocoded residential addresses of the participants were used to estimate daily mean pollution exposures. A linear mixed-effect model was applied to explore the effects of air pollutants on health in the first-year of follow-up. Results A total of 84 COPD patients were enrolled at baseline. Of those, 75 COPD patients completed the first-year of follow-up. We found adverse cumulative effects of particulate matter less than 2.5 mu m in aerodynamic diameter (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2) and carbon monoxide (CO) on the forced vital capacity % predicted (FVC % pred) in patients with COPD. Further analyses illustrated that among COPD patients, air pollution exposure was associated with reduced levels of serum eotaxin, interleukin 4 (IL-4) and IL-13 and was correlated with increased serum IL-2, IL-12, IL-17A, interferon gamma (IFN gamma), monocyte displacing protein 1 (MCP-1) and soluble CD40 ligand (sCD40L). Conclusion Acute exposures to PM2.5, NO2, SO2 and CO were associated with a reduction in FVC % pred in COPD patients. Furthermore, short-term exposure to air pollutants increased systemic inflammation in COPD patients; this may be attributed to increased Th1 and Th17 cytokines and decreased Th2 cytokines.