The role of cardiovascular disease as a mediator in mitigating the impact of ambient PM2.5 on dementia risk.

Abstract

Background: Previous research suggested that stricter ambient particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM_2.5) standards would reduce the risk of dementia, but immediate reductions in PM_2.5 levels are not always feasible. Limited studies have quantified the extent to which cardiovascular disease (CVD) interventions could mitigate the effect of not achieving stricter PM_2.5 standards on dementia risk.

Methods: This study included 283,813 participants in the UK Biobank cohort aged ≥60 years without dementia diagnosis or CVD hospitalization at baseline (2015). We applied the longitudinal targeted maximum likelihood estimation to estimate the total effect of no PM_2.5 intervention compared with hypothetical PM_2.5 interventions on the 5-year risk of dementia. We also estimated the controlled direct effect by setting all participants free from CVD hospitalization in both scenarios.

Results: Compared with the hypothetical intervention of reducing PM_2.5 exposure by 10% if it is above the standard of 10 µg/m³, the total effect of no PM_2.5 intervention increased the 5-year dementia risk by 3.77 (95% confidence interval [CI] = 1.47, 4.39) cases per 1000 participants. By setting all participants free from CVD hospitalization, the controlled direct effect was an increase of 2.82 (95% CI = 0.74, 3.30) cases per 1000 participants. The proportion of the total effect that could be mitigated by preventing CVD hospitalization was 25.27% (95% CI = 17.49%, 49.42%) among all eligible participants.

Conclusion: Part of the effect of not achieving stricter ambient PM_2.5 standards on dementia risk could be mitigated by preventing CVD hospitalization in the UK Biobank cohort. This finding indicates the potential of promoting cardiovascular health to reduce dementia burden.