Effect of ambient air quality on exacerbation of COPD in patients and its potential mechanism
Received 12 October 2018
Accepted for publication 26 March 2019
Published 10 July 2019 Volume 2019:14 Pages 1517—1526
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Chunxue Bai
Peng Yan,1 Pengfei Liu,2 Rong Lin,3 Kun Xiao,2 Sheling Xie,2 Kaifei Wang,2 Yuhan Zhang,2 Xanxue He,2 Shifeng Zhao,1 Xingang Zhang,1 Martin Liu,4 Lixin Xie1
1Pulmonary and Critical Care Medicine, The General Hospital of PLA, Beijing 100853, People’s Republic of China; 2Medical School of Chinese PLA, Beijing 100853, People’s Republic of China; 3Department of Respiratory Disease, The Sanya People’s Hospital, Sanya 572000, People’s Republic of China; 4Pulmonary, Critical Care, Sleep and Allergy, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-5910, USA
Background: Chronic obstructive pulmonary disease (COPD) is a disease of continuous progress and environmental factors may affect the progress. COPD patients’ activity tolerance and quality of life are associated with air quality. COPD exacerbation from the perspective of geographical air quality has not been reported.
Objectives: To explore environmental effect of two different geographical places on COPD exacerbation and the effect of cigarette smoke extract and carbon particles on bronchial epithelial cell viability.
Methods: Total 139 COPD patients, who lived in Beijing during summer and temporarily migrated to Sanya city in winter, have been enrolled. Respiratory symptoms and lung function data were collected when they were living in Beijing or Sanya, respectively. Effect of cigarette smoke extract plus ultrafine carbon particles on airway epithelial cells were studied.
Measurements and main results: Air pollution as measured by air quality index (AQI) in Beijing summer (113.1±14.2) was significantly worse than that in Sanya winter (49.4±8.9, p<0.001). The COPD Assessment Test (CAT) score was significantly higher in Beijing (26.4±7.1) than that in Sanya (20.0±8.0, p=0.019). Modified Medical Research Council dyspnea scale was also significantly higher in Beijing (2.9±0.9) than that in Sanya (1.9±0.8, p<0.001). FEV1 was significantly improved when the patients were in Sanya (48.88±24.78%) compared to that in Beijing (41.79±20.06%, p<0.01). Compared with Beijing and Sanya, the relative risk (RR) of hospitalization and acute exacerbation were 1.64 and 3.36, respectively. In vitro study demonstrated that apoptosis of BEAS2B cells in response to cigarette smoke extract plus ultrafine carbon particles (25.50±2.10%) was significantly higher than that of control culture (2.30±1.05%, p<0.01).
Conclusion: These findings suggested that ambient air pollution cause COPD exacerbation, and that air pollutants particle matters induce apoptosis of airway epithelial cells.
Keywords: chronic obstructive pulmonary disease, temporary migration, air pollution, lung function, apoptosis of airway epithelial cells