Amja Manullang1, Chi-Li Chung2,3, Yueh-Lun Lee4, Tzu-Hsuen Yuan5, Huan Minh Tran6,7, Firdian Makrufardi1,8, Kian Fan Chung9, Kang-Yun Lee10,11, Jer-Hwa Chang This email address is being protected from spambots. You need JavaScript enabled to view it.2,12, Hsiao-Chi Chuang This email address is being protected from spambots. You need JavaScript enabled to view it.2,9,10,13,14 1 International Ph.D. Program in Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
2 School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan
3 Division of Thoracic Medicine, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
4 Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
5 Department of Health and Welfare, College of City Management, University of Taipei, Taipei, Taiwan
6 Ph.D. Program in Global Health and Health Security, College of Public Health, Taipei Medical University, Taipei, Taiwan
7 Faculty of Public Health, Da Nang University of Medical Technology and Pharmacy, Da Nang, Viet Nam
8 Department of Child Health, Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada – Dr. Sardjito Hospital, Yogyakarta, Indonesia
9 National Heart and Lung Institute, Imperial College London, London, UK
10 Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan
11 Division of Pulmonary Medicine, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
12 Division of Pulmonary Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
13 Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
14 Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan
Received:
February 15, 2023
Copyright The Author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are cited.
Revised:
May 16, 2023
Accepted:
May 21, 2023
Download Citation:
||https://doi.org/10.4209/aaqr.230035
Manullang, A., Chung, C.L., Lee, Y.L., Yuan, T.H., Tran, H.M., Makrufardi, F., Chung, K.F., Lee, K.Y., Chang, J.H., Chuang, H.C. (2023). COPD with Eosinophilic Inflammation is Susceptible to Particulate Air Pollution Exposure. Aerosol Air Qual. Res. https://doi.org/10.4209/aaqr.230035
Cite this article:
Chronic obstructive pulmonary disease (COPD) has been linked to air pollution exposure. Air pollution has been associated with eosinophilic inflammation of respiratory disease. The objective of this study was to determine associations between air pollution and eosinophilic inflammation in COPD. A cross-sectional study was conducted on 291 COPD patients recruited from hospitals in Taipei between January 2014 and 2021, including 147 patients with eosinophil blood count ≥ 2% and 144 patients < 2%. Land use regression (LUR) model was used to estimate exposure levels to particulate matter with an aerodynamic diameter of < 10 µm (PM10), PM2.5 (< 10 µm), nitrogen oxides (NOx) and nitrogen dioxides (NO2). We investigated associations of air pollution with COPD outcomes by performing a linear regression approach. A two-pollutant approach was applied to examine the associations of PM10 or PM2.5 with NOx or NO2 in COPD with eosinophilic inflammation. An increase of 1 µg m-3 in PM10 was associated with a 0.62% (95% CI: -1.10%, -0.13%) decrease in the forced vital capacity (FVC) in COPD. An increase of 1 µg m-3 in PM2.5 was associated with a 0.38% (95% CI: -0.71%, -0.05%) decrease in the FVC. A 1 µg m-3 increase in PM10 was associated with a 0.92% (95% CI: -1.68%, -0.16%) decrease in the FVC in COPD patients with eosinophilic inflammation. A 1 µg/m3 increase in PM2.5 was associated with an increase of 0.26 points (95% CI: -1.68%, -0.16%) in the COPD Assessment Test (CAT) and a 0.03-times year-1 (95% CI: 0.01, 0.05) increase in the acute exacerbation (AE) of COPD eosinophilic inflammation. Associations of PM10 and PM2.5 with lung function decline in COPD eosinophilic inflammation were confirmed by the two-pollutant model. Exposure to particulate air pollution increased the risk of deleterious health outcomes in COPD with eosinophilic inflammation. COPD with eosinophilic inflammation may represent a susceptible group to particulate air pollution exposure.HIGHLIGHTS
ABSTRACT
Keywords:
Acute exacerbation, Air pollution, Lung function, PM10, PM2.5
