Association and biological pathways between lifetime occupational exposure to workplace hazards and incident chronic obstructive pulmonary disease and cardiovascular disease in middle-aged and older adults
File(s) manuscript_all.pdf (2.05 MB)
Accepted version
Author(s)
Yang, Yang
Qichen, Liu
Filippidis, Filippos
Peng, Lu
Yuming, Guo
Type
Journal Article
Abstract
The long-term impact of lifetime occupational exposure (LOE) on chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) risk remains unclear.
This study examined associations between LOE and the risks of COPD and CVD in middle-aged and older adults. A prospective cohort study was conducted using UK Biobank data, including demographic, lifestyle, and genetic information. Cox proportional hazard models assessed associations of one-hazard (OLOE) and total- hazards LOE (TLOE) with cardiopulmonary outcomes. Mediation analyses explored the role of biomarkers and metabolites. Over a median 12.5-year follow-up, 2.4% (2,426/103,176) developed COPD and 20.6% (18,035/87,419) developed CVD. All OLOEs, except pesticide, were associated with elevated risks for both diseases. Higher TLOE was linked to increased COPD (HR: 1.21, 95% CI: 1.15–1.26) and CVD (HR: 1.05, 95% CI: 1.03–1.06) risks per exposure level increase. Clear dose-response relationships were observed. Inflammatory markers, such as white blood cell count, neutrophil count, and C-reactive protein, partially mediated these associations. Moreover, TLOE was significantly associated with the onset of a single cardiopulmonary disease and its progression to comorbidity. Our findings underscored the potential long-term cardiopulmonary burden of occupational hazards and supported the need for workplace hazard reduction to promote healthy aging.
Environmental Implication
This study reveals that lifetime occupational exposures to workplace hazards significantly increase long-term risks of COPD and CVD in aging populations, revealing an underrecognized environmental health challenge as populations age and working lives extend. By identifying inflammatory and metabolic pathways mediating
these associations, our findings provide biological targets for early detection and preventive interventions in occupational settings. The demonstration that occupational exposures facilitate disease progression from single conditions to multimorbidity underscores the need for comprehensive workplace hazard elimination strategies throughout workers' careers rather than focusing solely on acute exposure prevention, and highlight the importance of integrating occupational health surveillance with chronic disease prevention programs to promote healthy aging and reduce the growing burden of cardiopulmonary multimorbidity.
This study examined associations between LOE and the risks of COPD and CVD in middle-aged and older adults. A prospective cohort study was conducted using UK Biobank data, including demographic, lifestyle, and genetic information. Cox proportional hazard models assessed associations of one-hazard (OLOE) and total- hazards LOE (TLOE) with cardiopulmonary outcomes. Mediation analyses explored the role of biomarkers and metabolites. Over a median 12.5-year follow-up, 2.4% (2,426/103,176) developed COPD and 20.6% (18,035/87,419) developed CVD. All OLOEs, except pesticide, were associated with elevated risks for both diseases. Higher TLOE was linked to increased COPD (HR: 1.21, 95% CI: 1.15–1.26) and CVD (HR: 1.05, 95% CI: 1.03–1.06) risks per exposure level increase. Clear dose-response relationships were observed. Inflammatory markers, such as white blood cell count, neutrophil count, and C-reactive protein, partially mediated these associations. Moreover, TLOE was significantly associated with the onset of a single cardiopulmonary disease and its progression to comorbidity. Our findings underscored the potential long-term cardiopulmonary burden of occupational hazards and supported the need for workplace hazard reduction to promote healthy aging.
Environmental Implication
This study reveals that lifetime occupational exposures to workplace hazards significantly increase long-term risks of COPD and CVD in aging populations, revealing an underrecognized environmental health challenge as populations age and working lives extend. By identifying inflammatory and metabolic pathways mediating
these associations, our findings provide biological targets for early detection and preventive interventions in occupational settings. The demonstration that occupational exposures facilitate disease progression from single conditions to multimorbidity underscores the need for comprehensive workplace hazard elimination strategies throughout workers' careers rather than focusing solely on acute exposure prevention, and highlight the importance of integrating occupational health surveillance with chronic disease prevention programs to promote healthy aging and reduce the growing burden of cardiopulmonary multimorbidity.
Date Issued
2026-02-15
Date Acceptance
2026-01-16
Citation
Journal of Hazardous Materials, 2026, 504
ISSN
0304-3894
Publisher
Elsevier
Journal / Book Title
Journal of Hazardous Materials
Volume
504
Copyright Statement
Copyright © 2026 Copyright Owner. This is the author’s accepted manuscript made available under a CC-BY licence in accordance with Imperial’s Research Publications Open Access policy (www.imperial.ac.uk/oa-policy)
License URL
Publication Status
Published
Article Number
141188
Date Publish Online
2026-01-21
