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Original research
Lifetime occupational exposures and chronic obstructive pulmonary disease risk in the UK Biobank cohort
  1. Sara De Matteis1,2,
  2. Debbie Jarvis1,3,
  3. Lucy Darnton4,
  4. Dario Consonni5,
  5. Hans Kromhout6,
  6. Sally Hutchings7,
  7. Steven S Sadhra8,
  8. David Fishwick4,
  9. Roel Vermeulen6,
  10. Lesley Rushton3,9,
  11. Paul Cullinan1
  1. 1National Heart and Lung Institute, Imperial College London, London, UK
  2. 2Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy
  3. 3MRC Centre for Environment and Health, Imperial College, London, UK
  4. 4Science Division, Health and Safety Executive, Harpur Hill Buxton, UK
  5. 5Epidemiology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
  6. 6Institute for Risk Assessment Sciences, University of Utrecht, Utrecht, The Netherlands
  7. 7School of Health Sciences, University of Manchester, Manchester, UK
  8. 8Occupational and Environmental Medicine, University of Birmingham, Birmingham, UK
  9. 9Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
  1. Correspondence to Dr Sara De Matteis, National Heart & Lung Institute, Imperial College London, London SW7 2BX, UK; s.de-matteis{at}imperial.ac.uk

Abstract

Background and aim Occupational exposures are important, preventable causes of COPD. We previously found an increased risk of COPD among six occupations by analysing lifetime job histories and lung function data in the population-based UK Biobank cohort. We aimed to build on these findings and elucidate the underlying potential causal agents to focus preventive strategies.

Methods We applied the ALOHA+job exposure matrix (JEM) based on the International Standard Classification of Occupations V.1988 codes, where exposure to 12 selected agents was rated as 0 (no exposure), 1 (low) or 2 (high). COPD was spirometrically defined as FEV1/FVC less than the lower limit of normal. We calculated semiquantitative cumulative exposure estimates for each agent by multiplying the duration of exposure and squared intensity. Prevalence ratio (PR) and 95% CI for COPD were estimated using robust Poisson regression adjusted for centre, sex, age, smoking and coexposure to JEM agents. Only associations confirmed among never-smokers and never-asthmatics were considered reliable.

Results Out of 116 375 participants with complete job histories, 94 514 had acceptable/repeatable spirometry and smoking data and were included in the analysis. Pesticide exposure showed increased risk of COPD for ever exposure (PR=1.13, 95% CI 1.01 to 1.28) and high cumulative exposure (PR=1.32, 95% CI 1.12 to 1.56), with positive exposure–response trends (p trend=0.004), which were confirmed among never-smokers (p trend=0.005) and never-asthmatics (p trend=0.001).

Conclusion In a large population-based study, occupational exposure to pesticides was associated with risk of COPD. Focused preventive strategies for workers exposed to pesticides can prevent the associated COPD burden.

  • occupational lung disease
  • COPD epidemiology

Data availability statement

Data may be obtained from a third party and are not publicly available. We used UK Biobank data to analyse and report the findings. Data access policy can be obtained from https://www.ukbiobank.ac.uk/.

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Data availability statement

Data may be obtained from a third party and are not publicly available. We used UK Biobank data to analyse and report the findings. Data access policy can be obtained from https://www.ukbiobank.ac.uk/.

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Footnotes

  • Contributors SDM conceived and performed the statistical analyses, interpreted the results and wrote the article. PC, LR and DJ, as PIs of the HSE-COPD project, coordinated and supervised the analyses and contributed to the interpretation of the results. PC is the guarantor. HK and RV developed the ALOHA+JEM. DC and SH contributed to data management and statistical analyses. LD, SSS and DF are participants of the HSE-COPD project. All authors contributed to the interpretation of the results and reviewed the final manuscript.

  • Funding This work was supported by contract OH1511 from the Health and Safety Executive (HSE). This research has been conducted using the UK Biobank resource under application number 178.

  • Disclaimer This publication and the work it describes, including any opinions and/or conclusions expressed, are those of the authors and do not necessarily reflect HSE policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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