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  • Title: Susceptibility of individuals with chronic obstructive pulmonary disease to respiratory inflammation associated with short-term exposure to ambient air pollution: A panel study in Beijing.
    Author: Yao Y, Chen X, Chen W, Wang Q, Fan Y, Han Y, Wang T, Wang J, Qiu X, Zheng M, Que C, Zhu T.
    Journal: Sci Total Environ; 2021 Apr 20; 766():142639. PubMed ID: 33069482.
    Abstract:
    BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. There is no clear evidence of whether COPD patients are more susceptible to respiratory inflammation associated with short-term exposure to air pollutants than those without COPD. OBJECTIVES: This study directly compared air pollutant-associated respiratory inflammation between COPD patients and healthy controls. METHODS: This study is based on the COPDB panel study (COPD in Beijing). Fractional exhaled nitric oxide (FeNO) was repeatedly measured in 53 COPD patients and 82 healthy controls at up to four clinical visits. Concentrations of carbon monoxide (CO), nitrogen monoxide, nitrogen dioxide (NO2), sulfur dioxide (SO2), fine particulate matter (PM2.5), black carbon (BC), ultrafine particles (UFPs), and accumulated-mode particles (Acc) were monitored continuously at a fixed-site monitoring station. Linear mixed-effects models were used to compare the associations between ln-transformed FeNO and average 1-23 h concentrations of air pollutants before the clinical visits. RESULTS: FeNO was positively associated with interquartile range (IQR) increases in average concentrations of CO, NO2, SO2, BC, UFPs, and Acc in all participants, with the strongest associations in different time-windows (range from 6.6% for average 1 h NO2 exposure to 32.1% for average 7 h SO2 exposure). Associations between FeNO and average 13-23 h PM2.5 exposure differed significantly according to COPD status. Increases in FeNO associated with average 1-2 h NO exposure were significant in COPD patients (range 8.9-10.2%), while the associations were nonsignificant in healthy controls. Associations between FeNO and average 1-23 h CO and SO2 exposure tended to be higher in COPD patients than in healthy controls, although the differences were not significant. UFPs-associated respiratory inflammation was robust in both subgroups. CONCLUSIONS: COPD patients are more susceptible to respiratory inflammation following PM2.5, NO, CO, and SO2 exposure than individuals without COPD.
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