Abstract

Air pollutants are found associated with various health effects in chronic obstructive pulmonary patients. Given the complicate chemical components of air pollutants, it is not clear which components are the main risk factors for these health effects. Based on the COPD in Beijing (COPDB) study and exposome concept, we examined comprehensively the air pollution components to screen out high-risk factors for systemic inflammation of COPD patients. Concentrations of PM with aerodynamic diameter≤2.5μm (PM2.5), ultrafine and accumulated-mode particles (UFPs and Acc), PM2.5-contained carbonaceous components/elements/water soluble ions, gaseous pollutants, temperature, and relative humidity (RH) were continuously monitored around participants. Urinary polycyclic aromatic hydrocarbons (PAHs) and cotinine, and serum tumor necrosis factor α (TNFα) were measured from 53 COPD and 82 non-COPD participants. Lifestyle variables were recorded using follow-up questionnaire. Linear mixed effects (LME) models were used to assess the associations of TNFα differences with exposure to air pollutants, meteorological variations, and lifestyle. In COPD patients, the associations of TNFα differences with exposure to ozone, Cd, UFPs, Acc, 2-hydroxydibenzofuran, temperature and RH parameters, and several elements in PM2.5 were significant in certain time-windows. For example, per interquartile range (IQR) increase in average ozone concentration 14 d before visits was associated with 17.3% (95% confidence interval: 6.8%, 27.7%) TNFα difference. Associations between ozone, Cd, UFPs, Acc, the maximum value of RH, and 2-hydroxydibenzofuran exposure and TNFα differences remained robust in two-pollutant models, and contributed to 19.0%, 10.5%, 2.2%, 1.6%, 2.1%, and 1.5% TNFα differences, respectively. Among the high-risk factors for COPD patients, the responses to UFPs, Acc, and 2-hydroxydibenzofuran were not robust in non-COPD participants. Ozone, Cd, UFPs, Acc, PAHs exposure and RH variation were high-risk factors of systemic inflammation for COPD patients, and the profile of high-risk factors were different from those in general population.

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