Susceptibility of Individuals with COPD to Air Pollution Exposure: A Case-Control Panel Study in Beijing, China

Abstract

Introduction Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide, characterized by chronic inflammation, and is one of the main diseases contribute to mortality attributable to PM2.5. Exposure to air pollution is one of the high-risk factors contributing to occurrence and development of COPD, it is important to reveal the biological mechanism of inflammation associated with exposure to air pollution in COPD patients and to know if subjects with COPD are more susceptible to air pollution than health one.Methodology With a case-control panel study (COPD), we recruited 44 stable COPD patients and 58 healthy control from Beijing Xicheng District Shichahai Community Health Center. Each subject has undergone 4 times repeated clinical visits from 2016 to 2017. Biomarkers, including breath volatile organic carbons, lung function, fractional exhaled nitric oxide(FeNO), fasting blood and cholesterol, inflammatory cytokines and cells, heart rate and blood oxygen were repeatedly collected from each subject in four visits. Gaseous air pollutants along with detailed chemical components and size distribution of particulate matter were continuously measured before and during each visits, 24 hours personal exposure to PM2.5 of each subjects prior to clinical visit was measured with a personal PM2.5 sampler. Linear mixed-effect model was fitted to estimate the association.Results Preliminary results shows increases in the levels of FeNO and heart rate, and decreases in the capabilities of pulmonary ventilation following air pollution exposure were more serious in the COPD patients, and adjusted by the forced expiratory volume. The association these effects with the exposure to CO, SO2, black carbon, organic carbon, and ultrafine particles were most robust.Conclusions After exposure to air pollution, the COPD patients had higher acute responses and worse capability of inflammatory regulation.