Abstract

The role of environmental exposures in chronic obstructive pulmonary disease (COPD) remains inconclusive. We examined the association between environmental exposures (PM2·5, greenness, and urbanicity) and COPD prevalence using the UK Biobank cohort data to identify key built environment correlates of COPD. In this cross-sectional, observational study we used baseline data for UK Biobank participants. Included participants were aged 39 years and older, white, had available spirometry data, and had complete data for phenotypes and exposures. COPD was defined by spirometry with the 2017 Global Initiative for Chronic Obstructive Lung Disease criteria. Environmental exposures were PM2·5 derived from monitoring data and interpolated using land-use regression at the participants' geocoded residential addresses. Built environment metrics of residential greenness were modelled in terms of normalised difference vegetation index from remotely sensed colour infrared data within a 500 m residential catchment, and an urbanicity index derived from spatial analyses and measured with a 1 km buffer around each participant's residential address. Logistic regression models examined the associations between environmental exposures and COPD prevalence adjusting for a range of confounders. Subgroup analyses by urbanicity and effect modification by white blood cell count as an inflammatory marker were also done. We assessed 96 779 participants recruited between April 4, 2006, and Oct 1, 2010, of which 5391 participants had COPD with a prevalence of 5·6%. Each 10 μg/m3 increment in ambient PM2·5 exposure at a participant's residential location was associated with higher odds of COPD (odds ratio 1·55, 95% CI 1·14-2·10). Among the built environment metrics, urbanicity was associated with higher odds of COPD (1·05, 1·01-1·08 per interquartile increment), whereas residential greenness was protective, being associated with lower odds of COPD (0·89, 0·84-0·93 for each interquartile increment in greenness). The results remained consistent in models of COPD defined as per lower limit of normal criteria. The highest quartile of white blood cell count was associated with lower lung function and higher COPD risk with a significant interaction between PM2·5 and white blood cell count only in the model of lung function (p=0·0003). In this study of the built environment and COPD, to our knowledge the largest done in the UK, we found that exposure to ambient PM2·5 and urbanicity were associated with a higher risk of COPD. Residing in greener areas, as measured by normalised difference vegetation index, was associated with lower odds of COPD, suggesting the potential value of urban planning and design in minimising or offsetting environmental risks for the prevention and management of COPD. University of Hong Kong, UK Biobank, and UK Economic & Social Research Council.

Highlights

  • Valid spirometry data as per American Thoracic Society or European Respiratory Society guidelines were available for 275 897 participants

  • After restricting analyses to white European ancestry and excluding those with incomplete phenotypes and those not meeting the American Thoracic Society or European Respiratory Society criteria, as well as missing data for pack years of smoking, 208 722 participants remained with valid data for prevalent Chronic obstructive pulmonary disease (COPD)

  • Comparisons of the analytical sample with the full UK Biobank cohort are presented in the appendix

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Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is a global public health challenge affecting approximately 174·5 million people, accounting for 3·2 million deaths in 2015.1 It has emerged as the tenth leading cause of years of life lost and eighth in terms of years lived with disability globally.[2,3] A 2016 UK study estimated that COPD prevalence will increase from 1·79% to 2·19% in England and 2·03% to 2·20% in Scotland from 2011–30, with a projected total health cost of £2·53 billion by 2030.4Exposure to air pollution is one of the main triggers for symptoms of COPD and its exacerbation.[5,6,7,8,9] Outdoor PM2·5, in particular, poses considerable health risks, being the fifth leading risk factor for death globally.[10]. Chronic obstructive pulmonary disease (COPD) is a global public health challenge affecting approximately 174·5 million people, accounting for 3·2 million deaths in 2015.1 It has emerged as the tenth leading cause of years of life lost and eighth in terms of years lived with disability globally.[2,3] A 2016 UK study estimated that COPD prevalence will increase from 1·79% to 2·19% in England and 2·03% to 2·20% in Scotland from 2011–30, with a projected total health cost of £2·53 billion by 2030.4. The soluble components can enter the bloodstream in the form of ultrafine particulate matter via the alveolar capillaries and the insoluble components can be deposited as sediments in lungs. COPD develop­ment and its exacerbations have been attributed to airflow obstruction, inflammation, oxidative stress, immune dysfunction, altered airway epithelial structure, and the microbiome.[11,12]

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