Polycyclic aromatic hydrocarbons are associated with increased risk of chronic obstructive pulmonary disease during haze events in China.
Although exposure to particulate matter with a diameter of <2.5μm (PM2.5) is associated with chronic obstructive pulmonary disease (COPD), the major components of PM2.5in COPD pathogenesis are controversial. Here we employed the human lung epithelial cell line BEAS-2B to elucidate the association between COPD and the organic and water-soluble components of PM2.5. We found that the PM2.5organic extract was a potential major risk factor for pulmonary epithelial barrier dysfunction through the depletion of proteins from the zonula occludens. This extract induced severe oxidative stress that increased DNA damage and the production of proinflammatory cytokines by BEAS-2B cells as well as decreased α1-antitrypsin expression, suggesting a mechanism that increases the risk of COPD. These effects were mainly mediated by polycyclic aromatic hydrocarbons (PAHs) through the aryl hydrocarbon receptor pathway. PAHs with high benzo(a)pyrene (BaP)-equivalent concentrations, but not major PAH components, have an increased risk of causing COPD, suggesting that BaP-equivalent concentrations represent a PM2.5-induced COPD risk metric, which may contribute to provide a rationale for the remediation of air pollution.
Key Laboratory of Nano-Bio Interface, Division of Nanobiomedicine, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Suzhou 215123, China.
Lingyan
L
Yang
Research Center for Environmental Changes, Academia Sinica, Taipei 11529, Taiwan.
Wen-Cheng
WC
Wang
Research Center for Environmental Changes, Academia Sinica, Taipei 11529, Taiwan.
Shih-Chun Candice
SC
Lung
Key Laboratory of Nano-Bio Interface, Division of Nanobiomedicine, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Suzhou 215123, China.
Zhelin
Z
Sun
School of Environmental Science and Engineering, Suzhou University of Science and Technology, Suzhou 215009, China.
Chongjun
C
Chen
Institute of Biomedical Engineering & Nanomedicine, National Health Research Institutes, Miaoli 35053, Taiwan.
Jen-Kun
JK
Chen
Suzhou Environmental Monitor Center, Suzhou 215004, China.
Qiang
Q
Zou
Department of Food and Beverage Management, Taipei College of Maritime Technology, Taipei 11174, Taiwan.
Yu-Hsin
YH
Lin
Department of Biotechnology, National Formosa University, Yunlin 63208, Taiwan. Electronic address: vicchlin@nfu.edu.tw.
Chia-Hua
CH
Lin
D000393:Air Pollutants / Q000009:adverse effects*; D002460:Cell Line; D002681:China / Q000453:epidemiology; D004847:Epithelial Cells / Q000187:drug effects*; D006801:Humans; D010316:Particle Size; D052638:Particulate Matter / Q000009:adverse effects; D011084:Polycyclic Aromatic Hydrocarbons / Q000009:adverse effects*; D029424:Pulmonary Disease, Chronic Obstructive / Q000453:epidemiology*
D000393:Air Pollutants; D052638:Particulate Matter; D011084:Polycyclic Aromatic Hydrocarbons
Aryl hydrocarbon receptor; COPD; Oxidative stress; PM(2.5); Polycyclic aromatic hydrocarbons