Accelerated decline in episodic memory was associated with long-term PM2.5 exposure. - GreenMedInfo Summary
Exposure to fine particulate matter and temporal dynamics of episodic memory and depressive symptoms in older women.
Environ Int. 2019 Dec 24 ;135:105196. Epub 2019 Dec 24. PMID: 31881430
Andrew J Petkus
BACKGROUND: Emerging data suggests PM(particulate matter with aerodynamic diameter<2.5 μm) may be associated with both earlier declines in episodic memory (EM) and increased depressive symptoms in older adults. Although late-life depressive symptoms are associated with EM, no longitudinal studies have examined the inter-relationship among PM, depressive symptoms and EM.
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). A nationwide spatiotemporal model (1999-2010) was used to estimate ambient PMexposure at residential locations. Univariate and bivariate structural equation models (SEMs) for latent-change scores were used to examine how 3-year average PMpreceding each assessment affects the temporal dynamics and bidirectional relations of annual changes in depressive symptoms and EM.
RESULTS: In univariate SEMs, one inter-quartile (4.04 μg/m) increment of 3-year PMwas significantly (p < 0.05) associated with accelerated declines in verbal learning (List A trials 1-3: β = -1.48) and free-recall memory (short-delay: β = -1.43; long-delay: β = -1.11), but not with change in depressive symptoms (β = 0.12; p = 0.71). In bivariate SEMs, significant associationswere observed between PMand accelerated declines in EM measures (β = -1.44 to -0.99; p < 0.05) and between EM performance and changes in depressive symptoms (β = -0.08 to -0.05; p < 0.05), with significant indirect PMeffects on changes in depressive symptoms (β = 0.08-0.10; p < 0.05). These findings were robust with adjustment for multiple demographic, lifestyle, and clinical factors, and remained after excluding subjects with dementia or mild cognitive impairment. No associations were found between PMand change in depressive symptoms or depressive symptoms and subsequent EM decline.
CONCLUSIONS: Findings suggest that PMneurotoxicity 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 PMexposure.
