Abstract

Background/Aim: Chronic obstructive pulmonary disease (COPD), characterized by chronic inflammation, is one of the leading causes of death worldwide. The biological mechanism of inflammation associated with exposure to air pollution in COPD patients are not well understood. To elucidate the association between air pollution exposure and inflammatory response in COPD patients, 135 subjects, including 53 stable COPD patients and 82 healthy controls, were recruited in a panel study in Beijing, China.Methods: Fractional exhaled nitric oxide (FeNO) and serum cytokines were repeatedly measured from each subject during 4 visits. Levels of air pollutants, including mass and number concentration of fine particulate matter, mass concentration of black carbon/organic carbon (OC)/elemental carbon/ heavy metals, gaseous pollutants, were online monitored. Linear mixed-effect models were used to estimate the different inflammatory responses to the air pollution exposure between COPD patients and healthy controls.Results: Exposures to SO2, OC and ultrafine particles (UFP) were positively associated with the levels of FeNO, which were more significant in COPD patients. Increases in levels of IL-6 associated with CO, Mn and Cu exposures in COPD patients were significantly higher than those in healthy controls. Exposures to UFP and Acc were associated with increasing levels of IL-15, which were more significant in COPD patients. Exposure to CO was associated with decreasing levels of IL-1β, IL-4, IL-10, IL-13 and IL-17A in healthy controls, which was not observed in COPD patients.Conclusions: In summary, COPD patients are susceptible to the acute respiratory inflammation associated with air pollution exposure, and their capabilities to regulate inflammation are weaker than healthy controls.Acknowledgement: The study was funded by National Program on Key Basic Research Project (2015CB553401). We thank all the volunteers, students and staff involved in COPD for their contributions.

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