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Original research
Occupational exposure to inhaled pollutants and risk of airflow obstruction: a large UK population-based UK Biobank cohort
  1. Steven S Sadhra1,
  2. Nuredin Mohammed2,
  3. Om P Kurmi3,
  4. David Fishwick4,
  5. Sara De Matteis5,
  6. Sally Hutchings6,
  7. Debbie Jarvis7,
  8. Jon G Ayres2,
  9. Lesley Rushton8
  1. 1 Occupational and Environmental Medicine, University of Birmingham, Birmingham, UK
  2. 2 Institute of Occupational and Environmental Medicine, University of Birmingham, Birmingham, West Midlands, UK
  3. 3 Population Health Research Institute, Department of Medicine, McMaster University, Hamilton, Ontario, Canada
  4. 4 Centre for Workplace Health, HSE Centre for Science and Research, Buxton, UK
  5. 5 Department of Respiratory Epidemiology, Occupational Medicine and Public Health, National Heart & Lung Institute, Imperial College London, London, UK
  6. 6 School of Health Sciences, University of Manchester, Manchester, Greater Manchester, UK
  7. 7 Faculty of Medicine, National Heart and Lung Institute, Imperial College London, London, UK
  8. 8 Epidemiology and Public Health, Imperial College London, London, UK
  1. Correspondence to Dr Steven S Sadhra, Occupational and Environmental Medicine, University of Birmingham, Birmingham B15 2TT, UK; s.sadhra{at}bham.ac.uk

Abstract

Background Although around 10% to 15% of COPD burden can be attributed to workplace exposures, little is known about the role of different airborne occupational pollutants (AOP). The main aim of the study was to assess the effect size of the relationship between various AOP, their level and duration of exposure with airflow obstruction (AFO).

Methods A cross-sectional analysis was conducted in 228 614 participants from the UK Biobank study who were assigned occupational exposure using a job exposure matrix blinded to health outcome. Adjusted prevalence ratios (PRs) and 95% CI for the risk of AFO for ever and years of exposure to AOPs were estimated using robust Poisson model. Sensitivity analyses were conducted for never-smokers, non-asthmatic and bi-pollutant model.

Results Of 228 614 participants, 77 027 (33.7%) were exposed to at least one AOP form. 35.5% of the AFO cases were exposed to vapours, gases, dusts or fumes (VGDF) and 28.3% to dusts. High exposure to vapours increased the risk of occupational AFO by 26%. Exposure to dusts (adjusted PR=1.05; 95% CI 1.01 to 1.08), biological dusts (1.05; 1.01 to 1.10) and VGDF (1.04; 1.01 to 1.07) showed a significantly increased risk of AFO, however, statistically not significant following multiple testing. There was no significant increase in risk of AFO by duration (years) of exposure in current job. The results were null when restricted to never-smokers and when a bi-pollutant model was used. However, when data was analysed based on the level of exposure (low, medium and high) compared with no exposure, directionally there was increase in risk for those with high exposure to vapours, gases, fumes, mists and VGDF but statistically significant only for vapours.

Conclusion High exposure (in current job) to airborne occupational pollutants was suggestive of higher risk of AFO. Future studies should investigate the relationship between lifetime occupational exposures and COPD.

  • COPD epidemiology
  • occupational lung disease
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Footnotes

  • NM and OPK contributed equally.

  • Contributors SSS and OPK designed the analysis plan. NIM performed the data analysis. SSS, OPK and DF interpreted the finding and drafted the initial version of the manuscript. SDM, LR, SH, DJ and JGA commented on drafts, data interpretation and its presentation. All approved the final version for submission.

  • Funding This research was supported by contract OH1511 from the Health and Safety Executive (HSE).

  • Disclaimer The content of this paper contains the views of the authors, and not necessarily those of the funders Health and Safety Executive (HSE).

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval UK Biobank has received ethics approval from the National Health Service National Research Ethics Service (Ref 11/NW/0382).

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

  • 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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