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Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000–2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM_2.5), nitrogen dioxide (NO₂), and ozone (O₃) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases (N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases (N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM_2.5 (3.2 µg/m³), NO₂ (11.6 ppb), and warm-season O₃ (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM_2.5 and NO₂ were approximately linear. Our study suggests that exposures to PM_2.5 and NO₂ are associated with incidence of dementia and AD.

Growing evidence suggests that fine particulate matter (PM _2.5 ) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. Here, we conducted a nationwide population-based cohort study (2000 to 2017) by integrating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM _2.5 major chemical composition, including black carbon (BC), organic matter (OM), nitrate (NO ₃ ⁻ ), sulfate (SO ₄ ²⁻ ), ammonium (NH ₄ ⁺ ), and soil dust (DUST). To investigate the impact of long-term exposure to PM _2.5 constituents on incident all-cause dementia and Alzheimer’s disease (AD), hazard ratios for dementia and AD were estimated using Cox proportional hazards models, and penalized splines were used to evaluate potential nonlinear concentration–response (C-R) relationships. Results using two exposure datasets consistently indicated higher rates of incident dementia and AD for an increased exposure to PM _2.5 and its major constituents. An interquartile range increase in PM _2.5 mass was associated with a 6 to 7% increase in dementia incidence and a 9% increase in AD incidence. For different PM _2.5 constituents, associations remained significant for BC, OM, SO ₄ ²⁻ , and NH ₄ ⁺ for both end points (even after adjustments of other constituents), among which BC and SO ₄ ²⁻ showed the strongest associations. All constituents had largely linear C-R relationships in the low exposure range, but most tailed off at higher exposure concentrations. Our findings suggest that long-term exposure to PM _2.5 is significantly associated with higher rates of incident dementia and AD and that SO ₄ ²⁻ , BC, and OM related to traffic and fossil fuel combustion might drive the observed associations.

Background: Studies examining the nonfatal health outcomes of exposure to air pollution have been limited by the number of pollutants studied and focus on short-term exposures. Methods: We examined the relationship between long-term exposure to fine particulate matter with an aerodynamic diameter <2.5 micrometers (PM _2.5 ), NO ₂ , and tropospheric ozone and hospital admissions for 4 cardiovascular and respiratory outcomes (myocardial infarction, ischemic stroke, atrial fibrillation and flutter, and pneumonia) among the Medicare population of the United States. We used a doubly robust method for our statistical analysis, which relies on both inverse probability weighting and adjustment in the outcome model to account for confounding. The results from this regression are on an additive scale. We further looked at this relationship at lower pollutant concentrations, which are consistent with typical exposure levels in the United States, and among potentially susceptible subgroups. Results: Long-term exposure to fine PM _2.5 was associated with an increased risk of all outcomes with the highest effect seen for stroke with a 0.0091% (95% CI, 0.0086–0.0097) increase in the risk of stroke for each 1-µg/m ³ increase in annual levels. This translated to 2536 (95% CI, 2383–2691) cases of hospital admissions with ischemic stroke per year, which can be attributed to each 1-unit increase in fine particulate matter levels among the study population. NO ₂ was associated with an increase in the risk of admission with stroke by 0.00059% (95% CI, 0.00039–0.00075) and atrial fibrillation by 0.00129% (95% CI, 0.00114–0.00148) per ppb and tropospheric ozone was associated with an increase in the risk of admission with pneumonia by 0.00413% (95% CI, 0.00376–0.00447) per parts per billion. At lower concentrations, all pollutants were consistently associated with an increased risk for all our studied outcomes. Conclusions: Long-term exposure to air pollutants poses a significant risk to cardiovascular and respiratory health among the elderly population in the United States, with the greatest increase in the association per unit of exposure occurring at lower concentrations.