Department of Pulmonary and Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, No.1 Wangfujing Hutong, Beijing, 100730, China.
School of Statistics, Shandong University of Finance and Economics, Jinan, 250014, China.
Environ Health. 2020 Jan 30;19(1):12. doi: 10.1186/s12940-020-0568-1.
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.
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.
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 μm in aerodynamic diameter (PM), nitrogen dioxide (NO), sulfur dioxide (SO) 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 γ (IFNγ), monocyte displacing protein 1 (MCP-1) and soluble CD40 ligand (sCD40L).
Acute exposures to PM, NO, SO 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.
空气污染暴露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影响的研究结果并不一致，且数量较少。本研究旨在评估大气污染对中国北京 COPD 队列的肺功能参数和血清细胞因子水平的影响。
我们从 2015 年 12 月至 2017 年 9 月在北京以滚动方式招募 COPD 患者。对每位患者每 3 个月进行一次随访。每 6 个月检测一次 20 种细胞因子的血清水平。同时，我们从北京 35 个监测站获取同一时期的每小时环境污染物水平。使用参与者的地理编码居住地址来估算每日平均污染暴露。应用线性混合效应模型来探索污染物对第一年随访期间健康状况的影响。
基线时共纳入 84 例 COPD 患者。其中，75 例 COPD 患者完成了第一年的随访。我们发现，在 COPD 患者中，细颗粒物（PM）、二氧化氮（NO）、二氧化硫（SO）和一氧化碳（CO）的累积效应呈不良趋势，与用力肺活量占预计值的百分比（FVC % pred）呈负相关。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 水平降低有关，与血清白细胞介素 2（IL-2）、白细胞介素 12（IL-12）、白细胞介素 17A（IL-17A）、干扰素 γ（IFNγ）、单核细胞趋化蛋白 1（MCP-1）和可溶性 CD40 配体（sCD40L）水平升高有关。
PM、NO、SO 和 CO 的急性暴露与 COPD 患者的 FVC % pred 降低有关。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 Th1 和 Th17 细胞因子增加和 Th2 细胞因子减少。
