Key PointsQuestionIs long-term exposure to air pollution associated with increased risk of late-onset depression diagnosis among older adults in the US? FindingsIn the US nationwide Medicare cohort with 1526690 late-onset depression diagnoses, statistically significant harmful associations were observed between long-term exposure to common levels of air pollution and increased risk of depression diagnosis after age 64 years, accounting for climate coexposures, neighborhood greenness, socioeconomic conditions, health care access, and urbanicity level. MeaningThis study suggests that air pollution is a potential risk factor for late-onset depression. ImportanceEmerging evidence has suggested harmful associations of air pollutants with neurodegenerative diseases among older adults. However, little is known about outcomes regarding late-life mental disorders, such as geriatric depression. ObjectiveTo investigate if long-term exposure to air pollution is associated with increased risk of late-life depression diagnosis among older adults in the US. Design, Setting, and ParticipantsThis population-based longitudinal cohort study consisted of US Medicare enrollees older than 64 years. Data were obtained from the US Centers for Medicare and Medicaid Services Chronic Conditions Warehouse. The participants were continuously enrolled in the Fee-for-Service program and both Medicare Part A and Part B. After the 5-year washout period at entry, a total of 8907422 unique individuals were covered over the study period of 2005 to 2016, who contributed to 1526690 late-onset depression diagnoses. Data analyses were performed between March 2022 and November 2022. ExposuresThe exposures consisted of residential long-term exposure to fine particulate matter (PM2.5), measured in micrograms per cubic meter; nitrogen dioxide (NO2), measured in parts per billion; and ozone (O-3), measured in parts per billion. Main Outcomes and MeasuresLate-life depression diagnoses were identified via information from all available Medicare claims (ie, hospital inpatient, skilled nursing facility, home health agency, hospital outpatient, and physician visits). Date of the first occurrence was obtained. Hazard ratios and percentage change in risk were estimated via stratified Cox proportional hazards models accounting for climate coexposures, neighborhood greenness, socioeconomic conditions, health care access, and urbanicity level. ResultsA total of 8907422 Medicare enrollees were included in this study with 56.8% being female individuals and 90.2% being White individuals. The mean (SD) age at entry (after washout period) was 73.7 (4.8) years. Each 5-unit increase in long-term mean exposure to PM2.5, NO2, and O-3 was associated with an adjusted percentage increase in depression risk of 0.91% (95% CI, 0.02%-1.81%), 0.61% (95% CI, 0.31%- 0.92%), and 2.13% (95% CI, 1.63%-2.64%), respectively, based on a tripollutant model. Effect size heterogeneity was found among subpopulations by comorbidity condition and neighborhood contextual backgrounds. Conclusions and RelevanceIn this cohort study among US Medicare enrollees, harmful associations were observed between long-term exposure to air pollution and increased risk of late-life depression diagnosis. This cohort study investigates if long-term exposure to air pollution is associated with increased risk of late-life depression diagnosis among US older adults.

BACKGROUND AND AIM: Cardiovascular health of long-term exposure to noise and air pollution has been examined worldwide while few studies have been conducted in U.S. especially in aging population. We examined the effects of community noise and traffic air pollution exposures on incidences of cardiovascular (CVD) and neurological diseases in older adults. Methods: We constructed a cohort comprising Medicare beneficiaries aged over 65 years in New York state from 2000 to 2018. Annual mean nitrogen dioxides (NO2) and noise exposures combining road traffic and aviation sources were estimated using advanced geo-statistical models and assigned to the participants according to their ZIP-code of residence. We applied Cox proportional hazards models to examine the associations of exposure to community noise and NO2 with incidences of CVD and its subtypes, depression, and Alzheimer's disease and related dementias (ADRD), adjusting for potential confounders. Results: Of 742,366 participants, 38% developed their first CVD and 7% and 9% had new ADRD and depression during 9.3 years mean follow-up. Community noise exposure (per 25 dB) was significantly associated with increased hazard ratio (HR) of ADRD (1.047, 95%CI: 1.023, 1.073) and overall CVD incidences (1.092, 95% CI: 1.079, 1.105) including its subtypes (ischemic heart disease: 1.099, 95%CI: 1.086, 1.113; heart failure: 1.079, 95%CI: 1.064, 1.095; stroke: 1.116, 95%CI: 1.095, 1.137), but not with depression, acute myocardial infraction and atrial fibrillation, after mutual adjustment for NO2 exposure. For NO2 (per 10 ppb) exposure, the associations remain significant with incidences of ADRD and CVDs (except stroke) though the estimated HRs were attenuated compared to the effects of community noise. Conclusion: Long-term exposure to community noise and traffic air pollution are associated with increased risks of CVD and ADRD in older adults, with noise effects being dominant. Keywords: Community noise; traffic air pollution; cardiovascular disease; dementia

Growing evidence suggests that fine particulate matter (PM2.5) 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 inte-grating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM2.5 major chemical composition, including black carbon (BC), organic matter (OM), nitrate (NO3-), sulfate (SO42-), ammonium (NH4+), and soil dust (DUST). To investigate the impact of long-term exposure to PM2.5 con-stituents 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 PM2.5 and its major constituents. An interquartile range increase in PM2.5 mass was associated with a 6 to 7% increase in dementia incidence and a 9% increase in AD incidence. For different PM2.5 constituents, associations remained significant for BC, OM, SO42-, and NH4+ for both end points (even after adjustments of other constituents), among which BC and SO42- 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 PM2.5 is significantly associated with higher rates of incident dementia and AD and that SO42-, BC, and OM related to traffic and fossil fuel combustion might drive the observed associations.

It is well documented that fine particles matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) are associated with a range of adverse health outcomes. However, most epidemiologic studies have focused on understanding their additive effects, despite that individuals are exposed to multiple air pollutants simultaneously that are likely correlated with each other. Therefore, we applied a novel method - Bayesian Kernel machine regression (BKMR) and conducted a population-based cohort study to assess the individual and joint effect of air pollutant mixtures (PM2.5, O3, and NO2) on all-cause mortality among the Medicare population in 15 cities with 656 different ZIP codes in the southeastern US. The results suggest a strong association between pollutant mixture and all-cause mortality, mainly driven by PM2.5. The positive association of PM2.5 with mortality appears stronger at lower percentiles of other pollutants. An interquartile range change in PM2.5 concentration was associated with a significant increase in mortality of 1.7 (95% CI: 0.5, 2.9), 1.6 (95% CI: 0.4, 2.7) and 1.4 (95% CI: 0.1, 2.6) standard deviations (SD) when O3 and NO2 were set at the 25th, 50th, and 75th percentiles, respectively. BKMR analysis did not identify statistically significant interactions among PM2.5, O3, and NO2. However, since the small sub-population might weaken the study power, additional studies (in larger sample size and other regions in the US) are in need to reinforce the current finding.

BACKGROUND:Ambient air pollution has been characterized as a leading cause of mortality worldwide and has been associated with cardiovascular and respiratory diseases. There is increasing evidence that short-term exposure to nitrogen dioxide (NO2), is related to adverse health effects and mortality. METHODS:We conducted a systematic review of short-term NO2 and daily mortality, which were indexed in PubMed and Embase up to June 2021. We calculated random-effects estimates by different continents and globally, and tested for heterogeneity and publication bias. RESULTS:We included 87 articles in our quantitative analysis. NO2 and all-cause as well as cause-specific mortality were positively associated in the main analysis. For all-cause mortality, a 10 ppb increase in NO2 was associated with a 1.58% (95%CI 1.28%-1.88%, I2 = 96.3%, Eggers' test p < 0.01, N = 57) increase in the risk of death. For cause-specific mortality, a 10 ppb increase in NO2 was associated with a 1.72% (95%CI 1.41%-2.04%, I2 = 87.4%, Eggers' test p < 0.01, N = 42) increase in cardiovascular mortality and a 2.05% (95%CI 1.52%-2.59%, I2 = 78.5%, Eggers' test p < 0.01, N = 38) increase in respiratory mortality. In the sensitivity analysis, the meta-estimates for all-cause mortality, cardiovascular and respiratory mortality were nearly identical. The heterogeneity would decline to varying degrees through regional and study-design stratification. CONCLUSIONS:This study provides evidence of an association between short-term exposure to NO2, a proxy for traffic-sourced air pollutants, and all-cause, cardiovascular and respiratory mortality.

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 (NO 2 ), and ozone (O 3 ) 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/m 3 ), NO 2 (11.6 ppb), and warm-season O 3 (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 NO 2 were approximately linear. Our study suggests that exposures to PM 2.5 and NO 2 are associated with incidence of dementia and AD.

BACKGROUND:Mounting evidence has shown that long-term exposure to fine particulate matter [PM ≤2.5μm in aerodynamic diameter (PM2.5)] and ozone (O3) can increase mortality. However, the health effects associated with long-term exposure to nitrogen dioxide (NO2) are less clear, in particular the evidence is scarce for NO2 at low levels that are below the current international guidelines. METHODS:We constructed a population-based full cohort comprising all Medicare beneficiaries (aged ≥65, N=13,590,387) in the southeastern United States from 2000 to 2016, and we then further defined the below-guideline cohort that included only those who were always exposed to low-level NO2, that is, with annual means below the current World Health Organization guidelines (i.e., ≤21 ppb). We applied previously estimated spatially and temporally resolved NO2 concentrations and assigned annual means to study participants based on their ZIP code of residence. Cox proportional hazards models were used to examine the association between long-term exposure to low-level NO2 and all-cause mortality, adjusting for potential confounders. RESULTS:About 71.1% of the Medicare beneficiaries in the southeastern United States were always exposed to low-level NO2 over the study period. We observed an association between long-term exposure to low-level NO2 and all-cause mortality, with a hazard ratio (HR)= 1.042 (95% CI: 1.040, 1.045) in single-pollutant models and a HR= 1.047 (95% CI: 1.045, 1.049) in multipollutant models (adjusting for PM2.5 and O3), per 10-ppb increase in annual NO2 concentrations. The penalized spline indicates a linear exposure-response relationship across the entire NO2 exposure range. Medicare enrollees who were White, female, and residing in urban areas were more vulnerable to long-term NO2 exposure. CONCLUSION:Using a large and representative cohort, we provide epidemiological evidence that long-term exposure to NO2, even below the national and global ambient air quality guidelines, was approximately linearly associated with a higher risk of mortality among older adults, independent of PM2.5 and O3 exposure. Improving air quality by reducing NO2 emissions, therefore, may yield significant health benefits. https://doi.org/10.1289/EHP9044.