Background Few large studies have assessed the relationship of long-term ambient air pollution exposure with the prevalence and incidence of symptoms of chronic bronchitis and cough. Methods We leveraged Lifelines cohort data on 132 595 (baseline) and 65 009 (second assessment) participants linked to ambient air pollution estimates. Logistic regression models adjusted for sex, age, educational attainment, body mass index, smoking status, pack-years smoking and environmental tobacco smoke at home were used to assess associations of air pollution with prevalence and incidence of chronic bronchitis (winter cough and sputum almost daily for ≥3 months/year), chronic cough (winter cough almost daily for ≥3 months/year) and prevalence of cough and sputum symptoms, irrespective of duration. Results Associations were seen for all pollutants for prevalent cough or sputum symptoms. However, for prevalent and incident chronic bronchitis, statistically significant associations were seen for nitrogen dioxide (NO 2) and black carbon (BC) but not for fine particulate matter (PM 2.5). For prevalent chronic bronchitis, associations with NO 2 showed OR: 1.05 (95% CI: 1.02 to 1.08) and with BC OR: 1.06 (95% CI: 1.03 to 1.09) expressed per IQR; corresponding results for incident chronic bronchitis were NO 2 OR: 1.07 (95% CI: 1.02 to 1.13) and BC OR: 1.07 (95% CI: 1.02 to 1.13). In subgroup analyses, slightly stronger associations were observed among women, never smokers and younger individuals. Conclusion This is the largest analysis to date to examine cross-sectional and longitudinal associations between ambient air pollution and chronic bronchitis. NO 2 and BC air pollution was associated with increased odds of prevalent and incident chronic bronchitis.
Bibliographical noteFunding Information:
Competing interests JB reports grants from CIHR, grants from Canadian Respiratory Research Network (CRRN), personal fees from Canadian Thoracic Society, personal fees from CHEST, grants from Foundation of the MUHC, grants from Aerocrine, grants and personal fees from AstraZeneca, grants and personal fees from Boehringer Ingelheim, grants and personal fees from Grifols, grants and personal fees from GlaxoSmithKline, grants and personal fees from Novartis, grants and personal fees from Trudell, all outside the submitted work.
1Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University, Centre for Outcomes Research and Evaluation, Research Institute of the McGill University Health Centre, Montréal, Québec, Canada 2Swiss Tropical and Public Health Institute, Basel, Basel-Stadt, Switzerland 3University of Basel, Basel, Basel-Stadt, Switzerland 4Centre for Environmental Health and Sustainability, University of Leicester, Leicester, UK 5MRC Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK Acknowledgements The authors wish to acknowledge the services of the Lifelines Cohort Study, the contributing research centres delivering data to Lifelines and all the study participants. The Lifelines Cohort Study initiative has been made possible by subsidy from the Dutch Ministry of Health, Welfare and Sport, the Dutch Ministry of Economic Affairs, the University Medical Centre Groningen (UMCG the Netherlands), University Groningen and the Northern Provinces of the Netherlands.
Funding This work was supported by the National Institute for Health Research (NIHR) Health Protection Research Unit in Environmental Exposures and Health, a partnership between Public Health England, the Health and Safety Executive and the University of Leicester, under grant number NIHR200901 (to ALH). The views expressed are those of the author(s) and not necessarily those of the NIHR, Public Health England, the Health and Safety Executive or the Department of Health and Social Care.
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