Workplace Pollution and Risk of Incident Coronary Artery Disease

Our plain-English summary of Workplace Pollution and Risk of Incident Coronary Artery Disease, by H. Gao, K.U. Jarr, Y. Kojima, et al (medRxiv, 2026).

The study

• Authors: H. Gao, K.U. Jarr, Y. Kojima, T. Xiong, J.B. Kim, P. Cheng, L. Trasande, A. Peters, G. Pasterkamp, C. Giannarelli, N.J. Leeper
• Journal: medRxiv
• Published: 2026
• Read it: PubMed · Publisher · Free full text

Abstract

Importance: Genetic factors only explain ~50% of an individual's lifetime CAD risk. Workplace pollution exposure likely represents a significant, under-recognized, and modifiable contributor. Clarifying its independent effect - distinct from residential air pollution - could inform targeted prevention, clinical risk assessment, and policy strategies.

Objective: To quantify the independent association between workplace pollution exposure and incident CAD, rigorously adjusting for canonical risk factors, genetic risk, socioeconomic deprivation index, and residential air pollution.

Design Setting And Participants: A prospective cohort analysis of 103,599 adults in the UK Biobank with complete baseline employment history and specialized workplace environment surveys. Participants with prior CAD, or missing genetic information, canonical risk factor data, or residential air pollution measurements, were excluded.

Exposure: Cumulative, self-reported duration of exposure to workplace pollutants (including dust, smoke, exhaust, chemicals, asbestos, paints, and pesticides), summarized as a percentile measure.

Main Outcomes And Measures: Incident CAD. Associations were estimated using Cox proportional hazards models adjusted for demographics, comorbidities, CAD polygenic risk score, and residential air pollution metrics, accounting for competing death events.

Results: The cohort (median age 64 years; 43% male) had high baseline prevalence of smoking (41%) and co-morbidities (hypertension 27%, hyperlipidemia 16%, diabetes 4.3%). Common exposures included smoke (56%), dust (39%), and chemicals (27%). Over a median 7.5-year follow-up, 4,327 CAD cases occurred. Compared to the low exposure group, high workplace pollution exposures showed a stronger unadjusted association with CAD (hazard ratio [HR], 1.51; 95% CI, 1.40-1.63) relative to residential air pollution (unadjusted HR, 1.23; 95% CI, 1.14-1.33). Importantly, in multivariable models, workplace pollution remained independently associated with higher CAD incidence (adjusted HR, 1.21; 95% CI, 1.03-1.41), robust to all adjustment. Significant specific drivers included paints, thinners or glues, diesel exhaust, fumes, asbestos, and dust.

Conclusions And Relevance: Workplace pollution is confirmed as a robust, independent risk factor for incident CAD. Its association is demonstrably stronger than residential air pollution and persists despite comprehensive adjustment for genetic predisposition and traditional cardiovascular risk factors. These findings underscore the need to strengthen worker protections, integrate occupational history into clinical risk assessment, and prioritize mechanistic research into non-lipid pollution pathways.

In plain English

This preprint, posted without peer review, reported a prospective cohort study of 103,599 UK Biobank participants (median age 64; 43% male; 98% White). All had completed a work environment questionnaire and had no prior coronary artery disease (CAD). For each job, participants reported whether their workplace had dust, chemical or other fumes, cigarette smoke, materials containing asbestos, paints, thinners or glues, pesticides, or diesel exhaust. In total, 9.5% reported asbestos, for a median of 19 years among those exposed. Over a median follow-up of 7.5 years, 4,327 participants developed CAD. The authors adjusted for risk factors including smoking, genetic risk, deprivation and home-area air pollution. After adjustment, overall workplace pollution was associated with higher CAD incidence, with a hazard ratio of 1.21 (95% CI 1.03-1.41) for a rise from the lowest to the highest exposure level on a percentile scale. For asbestos alone, the adjusted hazard ratio was 1.20 (95% CI 1.02-1.43). The authors concluded that workplace pollution is an independent risk factor for CAD. They noted that exposure was self-reported and open to recall bias, and that the findings could not be repeated in another cohort.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Prospective cohort study using UK Biobank data, analyzed with cause-specific Cox proportional hazards models treating death as a competing event
• Who was studied: 103,599 UK Biobank participants in the UK, analyzed out of 120,075 who completed the work environment questionnaire. Those with prior CAD or missing genetic, risk factor, deprivation or residential air pollution data were excluded. Median age 64 years; 43% male; 41% ever smokers; 98% White. Follow-up ran to September 2025.
• Exposure: Self-reported workplace exposure across employment periods to seven components: dust; chemical or other fumes; cigarette smoke; materials containing asbestos; paints, thinners or glues; pesticides; diesel exhaust. Cumulative years of exposure were converted to percentile scores from 0 to 1, and the composite measure was the highest percentile across the seven components. No asbestos fiber type was specified.
• Main results:
  • 9.5% of the cohort reported workplace asbestos exposure, with a median duration of 19 years among those exposed
  • Over a median follow-up of 7.5 years, 4,327 incident CAD events occurred in the cohort of 103,599
  • Unadjusted: the high workplace pollution group (N = 51,785; 2,598 events) had a hazard ratio of 1.51 (95% CI, 1.40-1.63) compared with the low workplace and residential air pollution reference group (N = 25,768; 870 events)
  • Unadjusted: the high residential air pollution group (N = 51,795; 2,136 events) had a hazard ratio of 1.23 (95% CI, 1.14-1.33)
  • Fully adjusted: composite workplace pollution had a hazard ratio of 1.21 (95% CI, 1.03-1.41), reported per one-unit increase on the percentile scale, which represents a change from the lowest (0%) to the highest (100%) exposure level
  • Fully adjusted: residential air pollution had a borderline significant hazard ratio of 1.14 (95% CI, 1.00-1.29)
  • Individual components, adjusted: statistically significant hazard ratios were found for asbestos (1.20; 95% CI 1.02-1.43), paints/thinners/glues (1.26; 1.10-1.46), diesel exhaust (1.24; 1.07-1.43), chemical or other fumes (1.22; 1.08-1.39) and dust (1.14; 1.02-1.28). Pesticides and cigarette smoke were not listed as significant.
• The authors' conclusion: The authors concluded that workplace pollution exposure is an independent risk factor for incident CAD, persisting after adjustment for genetic and traditional risk factors, and that the association was stronger than for residential air pollution
• Limitations the authors state:
  • Workplace exposure was self-reported and may be affected by recall bias and reporting variability
  • The findings could not be replicated in an independent cohort
  • Generalizability may be limited

Topics

Medical terms in this study, explained in our Lexicon: Hazard Ratio, Occupational History.

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