Heterogeneous air pollutant exposure effects on episodic memory decline: Evidence from WHIMS‐ECHO study

Background Episodic memory (EM) declines vary by age and underlying neuropathology. Whether exposure to ambient air pollutants contributes to the observed heterogeneity of EM decline in older people is unclear. Method We examined the associations between exposures and EM trajectories in the US‐based Women’s Health Initiative Memory Study‐Epidemiology of Cognitive Health Outcomes (WHIMS‐ECHO) cohort (N=2042, aged 74‐92 in 2008). EM was assessed annually (2008‐18) using the immediate recall total correct (3 trials) in the telephone‐based California Verbal Learning Test. Recent 3‐year average exposures to regional PM 2.5 (particulate matter with aerodynamic diameter < 2.5μm) and NO 2 (a proxy of traffic‐related air pollutants) and the corresponding remote 3‐year averages approximately at 10 years prior to inception were derived from yearly exposures estimated by regionalized national universal kriging. Latent‐class mixed models were used to classify EM trajectories and examine the exposure effect in each identified latent class. All models adjusted for social‐demographic factors, lifestyle, cardiovascular risk and other clinical covariates. Result There were two latent EM trajectories that differed by WHIMS‐ECHO baseline age (≤80 vs. oldest‐old 80+; Figure 1) and exposure characteristics (Table 1). In women aged ≤80 (N=836), greater EM decline was associated with higher PM 2.5 in the subgroup with slow‐decline (76%; −0.18/year), but not in those with fast‐decline (24%; −1.75/year). The observed association, equivalent to 1‐2 years of aging, was stronger for recent 3‐year exposure (−0.151/year, per inter‐quartile‐range [IQR]=2.86µg/m 3 , p=0.02), as compared with remote exposure (−0.096/year, per IQR=3.28µg/m 3 , p=0.09). In the oldest‐old (aged>80; N=1206), EM decline (70% steady decline by −1.37/year; 30% no apparent decline) was not associated with recent or remote PM 2.5 exposures. In both age groups, no appreciable NO 2 effects on EM decline were observed, and neither PM 2.5 nor NO 2 exposures during recent or remote years affected the levels of EM trajectories. Adjusted models further accounting for propensity scores of exposures revealed very similar results. Conclusion The accelerated EM declines associated with late‐life exposures to ambient air pollutants vary by age‐related cognitive trajectories, exposure time‐windows and pollution sources. The observed association was most consistent with PM 2.5 exposure during recent years in older women aged ≤80 with slow EM decline.