Workplace Pollution and Risk of Incident Coronary Artery Disease

ImportanceGenetic factors only explain [~]50% of an individuals 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. ObjectiveTo 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 ParticipantsA 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. ExposureCumulative, 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 MeasuresIncident 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. ResultsThe 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 RelevanceWorkplace 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.