Long-Term Exposure to Ozone Increases Neurological Disability after Stroke: Findings from a Nationwide Longitudinal Study in China

SIMPLE SUMMARY: In China, ozone is a major air pollutant that has been linked to stroke incidence and mortality. However, how long-term exposure to ozone affects the life quality among stroke survivors is unknown. This study presents a longitudinal analysis of nationwide data of Chinese adults, and shows that exposure to ozone can increase the risk of post-stroke disability. Taking ambient O(3) under control can delay the progression of neurological disability among stroke survivors. ABSTRACT: Exposure to ozone (O(3)) is associated with stroke incidence and mortality. However, whether long-term exposure to O(3) is associated with post-stroke neurological disability remains unknown. This study investigated the relationship based on the longitudinal analysis of China National Stroke Screening Survey (CNSSS), which included 65,778 records of stroke patients. All of the analyzed patients were followed-up at least twice. Stroke disability was assessed using the modified Rankin scale (mRS). Long-term exposure was assessed by the peak-season or annual mean of maximum 8-h O(3) concentrations for 365 days before the mRS measurement. We used fixed-effect models to evaluate the associations between O(3) and mRS score, with adjustment for multiple confounders, and found a 10 µg/m(3) increase in peak-season O(3) concentration was associated with a 0.0186 (95% confidence interval [CI] 0.0115–0.0256) increment in the mRS score. The association was robust in various subpopulations. For secondary outcomes, for each 10 µg/m(3) increment in peak-season O(3), the odds ratio of an increased mRS score (vs. unchanged or decreased mRS score) increased by 23% (95% CI 9–37%). A nonlinear analysis showed a sublinear association between O(3) exposure and risk for post-stroke disability. A saturation effect was observed at an O(3) concentration of more than ~120 μg/m(3). Our study adds to evidence that long-term exposure to O(3) increases the risk of neurological disability after stroke.