Xi Chen1, Chengli Que2, Yuan Yao3, Yiqun Han4, Hanxiyue Zhang5, Xiaoying Li6, Xinchen Lu7, Wu Chen8, Xinyan Hu9, Yusheng Wu10, Teng Wang11, Lina Zhang12, Mei Zheng13, Xinghua Qiu14, Tong Zhu15. 1. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China; GRiC, Shenzhen Institute of Building Research Co., Ltd., Xiong'an 071700, China. Electronic address: chenxi_1111@yeah.net. 2. Peking University First Hospital, Peking University, Beijing 100034, China. Electronic address: quechengli@bjmu.edu.cn. 3. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: yuanyao@pku.edu.cn. 4. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China; Department of Epidemiology and Biostatistics, MRC Centre for Environmental and Health, Imperial College London, SW7 2AZ, UK. Electronic address: yiqun.han@imperial.ac.uk. 5. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: zhanghanxiyue@pku.edu.cn. 6. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: xiaoying0303@pku.edu.cn. 7. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: luxc@pku.edu.cn. 8. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: cwvivian511@163.com. 9. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: 1101549797@qq.com. 10. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: yusheng@pku.edu.cn. 11. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: t.w@pku.edu.cn. 12. Beijing Xicheng District Shichahai Community Health Center, Beijing 100000, China. Electronic address: 10027698@qq.com. 13. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: mzheng@pku.edu.cn. 14. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: xhqiu@pku.edu.cn. 15. BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Peking University, Beijing 100871, China. Electronic address: tzhu@pku.edu.cn.
Abstract
BACKGROUND: The underlying mechanism on the susceptibility of chronic obstructive pulmonary disease (COPD) patients to air pollution has yet to be clarified. OBJECTIVES: Based on the COPD in Beijing (COPDB) study, we examined whether lung dysfunction contributed to pollutant-associated systemic inflammation in COPD patients. METHODS: Proinflammatory biomarkers including interleukin-8 (IL-8) and tumor necrosis factor α (TNFα) were measured in serum samples collected from 53 COPD and 82 healthy participants. Concentrations of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5), carbonaceous components in PM2.5, and PM size distribution were continuously monitored. Linear mixed effects models were used to examine the associations of biomarker differences with particle exposure, between COPD and healthy participants, and across subgroups with different levels of lung dysfunction. RESULTS: COPD patients showed higher differences in IL-8 and TNFα levels associated with exposure to measured pollutants, comparing to healthy controls. In advanced analysis, particle-associated differences in IL-8 and TNFα levels were higher in participants with poorer lung ventilation and diffusion capacity, and higher ratio of residual volume. For example, an interquartile range increase in average PM2.5 concentration 2 weeks before visits was associated with a 15.7% difference in IL-8 level in participants with the lowest ratio of measured value to predicted value of forced expiratory volume in 1 s (FEV1%pred) (65.2%), and the association decreased monotonically with increasing FEV1%pred. Associations between differences in TNFα level and average ultrafine particle concentration 1 week before visits increased gradually with increasing ratio of measured value to predicted value of residual volume/total lung capacity. CONCLUSIONS: COPD patients, especially those with poorer lung function, are more susceptible to systemic inflammation associated with fine particle exposure.
BACKGROUND: The underlying mechanism on the susceptibility of chronic obstructive pulmonary disease (COPD) patients to air pollution has yet to be clarified. OBJECTIVES: Based on the COPD in Beijing (COPDB) study, we examined whether lung dysfunction contributed to pollutant-associated systemic inflammation in COPDpatients. METHODS: Proinflammatory biomarkers including interleukin-8 (IL-8) and tumor necrosis factor α (TNFα) were measured in serum samples collected from 53 COPD and 82 healthy participants. Concentrations of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5), carbonaceous components in PM2.5, and PM size distribution were continuously monitored. Linear mixed effects models were used to examine the associations of biomarker differences with particle exposure, between COPD and healthy participants, and across subgroups with different levels of lung dysfunction. RESULTS:COPDpatients showed higher differences in IL-8 and TNFα levels associated with exposure to measured pollutants, comparing to healthy controls. In advanced analysis, particle-associated differences in IL-8 and TNFα levels were higher in participants with poorer lung ventilation and diffusion capacity, and higher ratio of residual volume. For example, an interquartile range increase in average PM2.5 concentration 2 weeks before visits was associated with a 15.7% difference in IL-8 level in participants with the lowest ratio of measured value to predicted value of forced expiratory volume in 1 s (FEV1%pred) (65.2%), and the association decreased monotonically with increasing FEV1%pred. Associations between differences in TNFα level and average ultrafine particle concentration 1 week before visits increased gradually with increasing ratio of measured value to predicted value of residual volume/total lung capacity. CONCLUSIONS:COPDpatients, especially those with poorer lung function, are more susceptible to systemic inflammation associated with fine particle exposure.