Air pollution, lung function and COPD: results from the population-based UK Biobank study
- Dany Doiron1,2,3,
- Kees de Hoogh2,3,
- Nicole Probst-Hensch2,3,
- Isabel Fortier1,
- Yutong Cai4,5,
- Sara De Matteis6 and
- Anna L. Hansell4,7
- 1Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada
- 2Swiss Tropical and Public Health Institute, Basel, Switzerland
- 3University of Basel, Basel, Switzerland
- 4Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
- 5Department of Analytical, Environmental and Forensic Sciences, School of Population Health and Environmental Sciences, King's College London, London, UK
- 6National Heart & Lung Institute, Imperial College London, London, UK
- 7Centre for Environmental Health and Sustainability, University of Leicester, Leicester, UK
- Dr Dany Doiron, Research Institute of the McGill University Health Centre, 2155 rue Guy, office 458, Montreal, Canada, H3H 2R9. E-mail: dany.doiron{at}mail.mcgill.ca
Abstract
Ambient air pollution increases the risk of respiratory mortality but evidence for impacts on lung function and chronic obstructive pulmonary disease (COPD) is less well established. The aim was to evaluate whether ambient air pollution is associated with lung function and COPD, and explore potential vulnerability factors.
We used UK Biobank data on 3 03 887 individuals aged 40–69 years, with complete covariate data and valid lung function measures. Cross-sectional analyses examined associations of Land Use Regression-based estimates of particulate matter (PM2.5, PM10 and PMcoarse) and nitrogen dioxide (NO2) concentrations with forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), the FEV1/FVC ratio, and COPD (FEV1/FVC <lower limit of normal). Effect modification was investigated for sex, age, obesity, smoking status, household income, asthma status, and occupations previously linked to COPD.
Higher exposures to each pollutant were significantly associated with lower lung function. A 5 µg·m−3 increase in PM2.5 concentration was associated with lower FEV1 (−83.13 mL [95%CI: −92.50, −73.75]) and FVC (−62.62 mL [95%CI: −73.91, −51.32]). COPD prevalence was associated with higher concentrations of PM2.5 (OR 1.52 [95%CI: 1.42, 1.62], per 5 µg·m−3), PM10 (OR 1.08 [95%CI: 1.00, 1.16], per 5 µg·m−3), and NO2 (OR 1.12 [95%CI: 1.10, 1.14], per 10 µg·m−3), but not with PMcoarse. Stronger lung function associations were seen for males, individuals from lower income households, and “at-risk” occupations, and higher COPD associations for obese, lower income, and non-asthmatic participants.
Ambient air pollution was associated with lower lung function and increased COPD prevalence in this large study.
Footnotes
This 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: Mr. Doiron has nothing to disclose.
Conflict of interest: Dr. de Hoogh has nothing to disclose.
Conflict of interest: Dr. Probst-Hensch has nothing to disclose.
Conflict of interest: Dr. Fortier has nothing to disclose.
Conflict of interest: Dr. Cai has nothing to disclose.
Conflict of interest: Dr. De Matteis has nothing to disclose.
Conflict of interest: Dr. Hansell has nothing to disclose.
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