Air pollution links to stroke risk in two population cohorts
In UK Biobank, every 5 µg/m³ increment in PM2.5 carried an incident ischemic stroke hazard ratio of 1.29, reaching 1.44 alongside high genetic susceptibility.
Neuroepidemiology
In two population-based human cohorts, researchers evaluated how ambient air pollution relates to stroke risk alongside systemic inflammation and genetic susceptibility. In the 2015 cross-sectional wave of the China Health and Retirement Longitudinal Study (n = 21,095), higher exposure to PM10 (OR 1.31, 95% CI 1.08–1.59) and PM2.5 (OR 1.26, 95% CI 1.04–1.53) was associated with higher odds of prevalent stroke. Investigators also detected significant positive multiplicative interactions between high-sensitivity C-reactive protein and several pollutants. In the prospective UK Biobank cohort (n = 368,644), each 5 µg/m³ increment in PM2.5 was associated with a higher hazard of incident ischemic stroke (HR 1.29, 95% CI 1.15–1.45). Participants with both high PM2.5 exposure and high polygenic risk scores exhibited the highest hazard ratio (HR 1.44, 95% CI 1.32–1.57).
Why it matters
Stroke is a major contributor to age-related cognitive decline, physical disability, and mortality. These findings suggest that baseline inflammatory burden and genetic predisposition can modulate cardiovascular vulnerability to environmental toxins across the lifespan.
Caveats
The two cohorts differed in design, calendar period, exposure assessment, and stroke ascertainment, preventing direct quantitative comparisons between them. Additionally, the CHARLS data are cross-sectional, and the UK Biobank analysis did not formally evaluate statistical interaction for polygenic risk.
The paper
Neuroepidemiology · 29 Sep 2026