Background/Aim: Cross-sectional studies have found associations of cognitive deficits with long-term exposure to particulate matter. Few longitudinal studies have shown inconsistent associations, and their analyses with limited neuropsychological assessments could not separate learning effects from trajectories of cognitive decline in late life. Methods: We examined how fine particulate matter (PM2.5: PM with aerodynamic diameters <2.5µm) was associated with cognitive declines in a geographically-diverse US population of older women (N=7064; aged 65-80) from the Women’s Health Initiative Memory Study, with up to 9 annual global cognitive assessments (in 6.3±2.1 visits) using the Modified Mini-Mental State (3MS) Exam. Given residential histories and ambient monitoring data coupled with air quality model simulation, the Bayesian Maximum Entropy method was used to estimate long-term (3-year average) PM2.5 exposures preceding each visit. We fit longitudinal linear mixed-effects models to standardized 3MS z-scores and assessed how cognitive trajectories were influenced by PM2.5 exposures, adjusting for socio-demographic (age; residential geography; race/ethnicity; education; income; employment status), lifestyle (smoking; alcohol use), and clinical factors (body mass index; hypertension; cardiovascular diseases). Results: Two concurrent processes of cognitive aging were identifiable. The first trajectory showed 3MS scores increased with visit numbers (p<0.001), likely reflecting a systematic difference that included the learning effect. The second trajectory was defined by the age-related decrease in 3MS, incrementally with faster declines during the extended follow-up (interaction p<0.0001). For the first trajectory, we found no appreciable differences by PM2.5 exposure (interaction p=0.88). The effect of aging on 3MS was accelerated by increased PM2.5 (interaction p<0.0001); this apparent neurotoxic effect was masked when the second trajectory was ignored in the mixed-effect model. Conclusions: This longitudinal study provides further evidence that late-life exposure to PM2.5 accelerates age-related cognitive decline. Our analyses also demonstrate the importance of accounting for the underlying trajectories of cognitive aging in community-dwelling populations.