Exposure to fine particulate matter and the temporal dynamics of episodic memory and depressive symptoms in older women

Abstract

TPS 732: Neurological effects in adults, Exhibition Hall, Ground floor, August 27, 2019, 3:00 PM - 4:30 PM Background/Aim: Older adults with higher PM2.5 (particulate matter with aerodynamic diameter <2.5 μm) exposures have earlier declines in episodic memory (EM), occurring in the preclinical stage of dementias. Emerging data also suggest PM2.5 exposure may increase depressive symptoms. Although late-life depressive symptoms are associated with EM, the inter-relationship between PM2.5, depressive symptoms, and EM is unexamined. Methods: Older women (n = 2,202; aged 67-83 in 1999) enrolled in the Women’s Health Initiative Study of Cognitive Aging completed up to eight annual assessments of depressive symptoms (15-item Geriatric Depression Scale) and EM (California Verbal Learning Test; scaled on T-score metric). A nationwide spatiotemporal model (1999-2010) estimated 3-year average ambient PM2.5 exposure at residential locations preceding each assessment. Univariate and bivariate latent-change score structural equation models (SEM) examined how exposures affect the temporal dynamics and bidirectional relation of annual changes in depressive symptoms and EM. Results: In univariate SEMs, one inter-quartile (4.04 μg/m3) greater PM2.5 exposure was associated with accelerated declines (p<.05) in verbal learning (List A trials 1-3: β=-1.477) and free-recall memory (short-delay: β=-1.426; long-delay: β=-1.106), but not with change in depressive symptoms (β=.119; p=.709). In bivariate SEM, elevated PM2.5 exposures also accelerated the declines in EM measures (β=-1.443 to -.985; p<.05), which subsequently increased depressive symptoms (β=-.078 to -.053; p<.05), resulting in significant indirect PM2.5 effects on changes in depressive symptoms (β=.077 to .095; p<.05). In contrast, there was no appreciable association between PM2.5 and change in depressive symptoms and no association between depressive symptoms with subsequent EM decline. Findings remained after adjusting for multiple demographic, lifestyle, and clinical factors. Conclusions: Findings suggest that PM2.5 neurotoxicity may damage brain areas implicated in EM, followed by manifestation of depressive symptoms. Our data did not support depressive symptoms as the neuropsychological mediator of accelerated brain aging associated with PM2.5 exposure.