PM2.5 and dementia – APOE-ε4 and odor identification ability as moderators

Abstract

BACKGROUND AND AIM: There is growing evidence that long term exposure to air pollution increases the risk of dementia. However, more research regarding possible moderators and mediators are needed in order to identify vulnerable populations, and to better understand the complicated pathways between air pollution and dementia. The aim of this study was to investigate 1) the associations between PM2.5 exposure and dementia incidence, and 2) the possible mediating or moderating role of APOE-ε4 and odor identification ability, two known risk factors of dementia. METHODS: Data was drawn from the Betula project, a longitudinal study on aging, memory, and dementia in Sweden. DNA was extracted via blood samples to allow for genotyping of the APOE gene. Odor identification ability was assessed using the Scandinavian Odor Identification Test (SOIT). Variation in within-city annual mean PM2.5 concentrations were obtained from a dispersion-model and matched at the participants’ residential address. Proportional hazard regression was used to calculate hazard ratios. RESULTS: Of 1846 participants, 348 developed dementia during the follow up period. Each 1 µg/m3 increase in annual mean PM2.5-concentration was associated with a hazard ratio of 1,24 for dementia (95% CI: 1,02–1,51). Both APOE status and odor identification ability acted as moderators, as in subsequent analyses, significant associations persisted only for APOE-ε4 carriers, and low performers on the SOIT. CONCLUSIONS: Locally emitted PM2.5 was associated with an increased risk of dementia in this moderately polluted setting. APOE-ε4 carriers, and those with below average odor identification ability were particularly vulnerable. KEYWORDS: Air pollution, Alzheimer’s disease, vascular dementia, apolipoprotein E, olfaction.