Air pollution and stroke: A two-year analysis linking short-term particulate matter 2.5 exposure to stroke severity and etiology

BACKGROUND: Air pollution is increasingly implicated in cerebrovascular disease through mechanisms of systemic inflammation, endothelial dysfunction, and neurovascular injury. Although long-term exposure to particulate matter contributes to stroke risk, the impact of short-term fluctuations, particularly during extreme pollution events such as wildfires, on stroke severity and etiology remains poorly defined. METHODS: modeled continuously. Lagged exposures of 1-2 days were also examined. RESULTS: Among 1,184 patients, presentation on high PM2.5 days was associated with greater stroke severity, including higher initial NIHSS (10.0 vs. 8.25; p = 0.004) and greater functional decline by discharge (ΔmRS 2.6 vs. 2.15; p = 0.001). In multivariable linear regression adjusting for age, sex, race, smoking status, and stroke etiology, higher PM2.5 levels remained independently associated with increased stroke severity, with each 1 µg/m³ increase corresponding to higher NIHSS (β = 0.047, 95% CI 0.027-0.067; p < 0.001). Hemorrhagic stroke was more frequent on high PM2.5 days (p = 0.027), while overall ischemic stroke incidence did not differ. LAA stroke was more common during high PM2.5 exposure (adjusted OR 1.45; 95% CI 1.08-1.86). Lagged analyses demonstrated significant associations at two days for ischemic stroke incidence, NIHSS, and ΔmRS (all p < 0.05). Ozone was not associated with stroke outcomes. CONCLUSION: elevations, particularly during wildfire smoke episodes, were independently associated with increased stroke severity and large-artery atherosclerotic ischemic stroke, with effects persisting up to 48 hours after exposure.