RT Journal Article
SR Electronic
T1 Acute air pollution exposure alters neutrophils in never-smokers and at-risk humans
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 1901495
DO 10.1183/13993003.01495-2019
A1 Denise J. Wooding
A1 Min Hyung Ryu
A1 Hang Li
A1 Neil E. Alexis
A1 Olga Pena
A1 Chris Carlsten
A1 ,
YR 2019
UL http://erj.ersjournals.com/content/early/2019/11/26/13993003.01495-2019.abstract
AB Outdoor air pollution exposure increases COPD hospitalisations, and may contribute to COPD development. The mechanisms of harm, and the extent to which at-risk populations are more susceptible, are not fully understood. Neutrophils are recruited to the lung following diesel exhaust (DE) exposure, a model of traffic-related air pollution (TRAP), but their functional role in this response is unknown. The purpose of this controlled human exposure crossover study was to assess the effects of acute DE exposure on neutrophil function in never-smokers and at-risk populations, with support from additional in vitro studies. 18 participants, including never-smokers (N=7), ex-smokers (N=4), and mild-moderate COPD patients (N=7), were exposed to DE and filtered air (FA) for 2 h on separate occasions, and neutrophil function in blood (0 h and 24 h post) and bronchoalveolar lavage (24 h post) was assessed. Compared to FA, DE exposure reduced the proportion of circulating band cells at 0 h, which was exaggerated in COPD patients. DE increased the amount of neutrophil extracellular traps (NETs) in the lung across participants. COPD patients had increased peripheral neutrophil activation following DE. In vitro, suspended diesel exhaust particles also increased the amount of NETs measured in isolated neutrophils. We propose NET formation as a possible mechanism through which TRAP exposure affects airway pathophysiology. In addition, COPD patients may be more prone to an activated inflammatory state following exposure. This is the first controlled human TRAP exposure study directly comparing at-risk phenotypes (COPD and ex-smoker) with lower-risk (never-smokers), elucidating the human susceptibility spectrum.FootnotesThis manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.Conflict of interest: Ms. Wooding reports grants from WorkSafeBC, grants from Canadian Institutes of Health Research, during the conduct of the study.Conflict of interest: Mr. Ryu reports grants from Canadian Respiratory Research Network, grants from WorkSafeBC, from Natural Sciences and Engineering Research Council of Canada, during the conduct of the study.Conflict of interest: Dr. Li reports grants from Sun Yat-sen University International Program Fund, grants from Chinese Government Scholarship, during the conduct of the study.Conflict of interest: Dr. Alexis has nothing to disclose.Conflict of interest: Dr. Pena has nothing to disclose.Conflict of interest: Dr. Carlsten reports grants from Canadian Respiratory Research Network, Canada Research Chairs Program, during the conduct of the study.