Source-Specific Air Pollution and Loss of Independence in Older Adults Across the US.

Importance: Air pollution is a recognized risk factor associated with chronic diseases, including respiratory and cardiovascular conditions, which can lead to physical and cognitive impairments in later life. Although these losses of function, individually or in combination, reduce individuals' likelihood of living independently, little is known about the association of air pollution with this critical outcome. Objective: To investigate associations between air pollution and loss of independence in later life. Design, Setting, and Participants: This cohort study was conducted as part of the Environmental Predictors Of Cognitive Health and Aging study and used 1998 to 2016 data from the Health and Retirement Study. Participants included respondents from this nationally representative, population-based cohort who were older than 50 years and had not previously reported a loss of independence. Analyses were performed from August 31 to October 15, 2023. Exposures: Mean 10-year pollutant concentrations (particulate matter less than 2.5 µm in diameter [PM2.5] or ranging from 2.5 µm to 10 µm in diameter [PM10-2.5], nitrogen dioxide [NO2], and ozone [O3]) were estimated at respondent addresses using spatiotemporal models along with PM2.5 levels from 9 emission sources. Main Outcomes and Measures: Loss of independence was defined as newly receiving care for at least 1 activity of daily living or instrumental activity of daily living due to health and memory problems or moving to a nursing home. Associations were estimated with generalized estimating equation regression adjusting for potential confounders. Results: Among 25 314 respondents older than 50 years (mean [SD] baseline age, 61.1 [9.4] years; 11 208 male [44.3%]), 9985 individuals (39.4%) experienced lost independence during a mean (SD) follow-up of 10.2 (5.5) years. Higher exposure levels of mean concentration were associated with increased risks of lost independence for total PM2.5 levels (risk ratio [RR] per 1-IQR of 10-year mean, 1.05; 95% CI, 1.01-1.10), PM2.5 levels from road traffic (RR per 1-IQR of 10-year mean, 1.09; 95% CI, 1.03-1.16) and nonroad traffic (RR per 1-IQR of 10-year mean, 1.13; 95% CI, 1.03-1.24), and NO2 levels (RR per 1-IQR of 10-year mean, 1.05; 95% CI, 1.01-1.08). Compared with other sources, traffic-generated pollutants were most consistently and robustly associated with loss of independence; only road traffic-related PM2.5 levels remained associated with increased risk after adjustment for PM2.5 from other sources (RR per 1-IQR increase in 10-year mean concentration, 1.10; 95% CI, 1.00-1.21). Other pollutant-outcome associations were null, except for O3 levels, which were associated with lower risks of lost independence (RR per 1-IQR increase in 10-year mean concentration, 0.94; 95% CI, 0.92-0.97). Conclusions and Relevance: This study found that long-term exposure to air pollution was associated with the need for help for lost independence in later life, with especially large and consistent increases in risk for pollution generated by traffic-related sources. These findings suggest that controlling air pollution could be associated with diversion or delay of the need for care and prolonged ability to live independently.

School Bus Rebate Program and Student Educational Performance Test Scores.

Importance: Students who ride older school buses are often exposed to high levels of exhaust during their commutes, which may adversely affect health and school attendance. As a result, the US Environmental Protection Agency (EPA) has awarded millions of dollars to school districts to replace older, highly polluting school buses with newer, cleaner buses. Objective: To leverage the EPA's randomized allocation of funding under the 2012-2016 School Bus Rebate Programs to estimate the association between replacing old, highly polluting buses and changes in district-average standardized test scores. Design, Setting, and Participants: This study examined changes in reading and language arts (RLA) and math test scores among US school district applicants to the EPA's 2012-2016 national School Bus Rebate Programs 1 year before and after each lottery by selection status. Data analysis was conducted from January 15 to July 30, 2023. Exposure: Selection to receive EPA funding to replace older school buses with newer, cleaner alternatives. Main Outcomes and Measures: School district changes in RLA and math test scores among students in grades 3 through 8 before and after the EPA funding lotteries by selection status were measured using an intention-to-treat approach. Results: This study included 1941 school district applicants to the 2012-2106 EPA School Bus Rebate Programs. These districts had a mean (SD) of 14.6 (33.7) schools per district, 8755 (23 776) students per district, and 41.3% (20.2%) of students with free lunch eligibility. Among the applicants, 209 districts (11%) were selected for the clean bus funding. District-average student test scores did not improve among selected districts overall. In secondary analyses, however, districts replacing the oldest, highest polluting buses (ie, pre-1990) experienced significantly greater improvements in district-average test scores in the year after the lottery for RLA and math (SD improvement in test scores, 0.062 [95% CI, 0.050-0.074] and 0.025 [95% CI, 0.011-0.039], respectively) compared with districts without replacements. Conclusions and Relevance: In this study, the EPA funding was not associated with student test scores overall, but in secondary analyses, the replacement of the oldest school buses was associated with improved educational performance. These findings support prioritizing clean bus replacement of the oldest buses as an actionable way for improving students' educational performance.

Coarse Particulate Matter and Markers of Inflammation and Coagulation in the Multi-Ethnic Study of Atherosclerosis (MESA) Population: A Repeat Measures Analysis.

BACKGROUND: In contrast to fine particles, less is known of the inflammatory and coagulation impacts of coarse particulate matter (PM10-2.5, particulate matter with aerodynamic diameter ≤10µm and>2.5µm). Toxicological research suggests that these pathways might be important processes by which PM10-2.5 impacts health, but there are relatively few epidemiological studies due to a lack of a national PM10-2.5 monitoring network. OBJECTIVES: We used new spatiotemporal exposure models to examine associations of both 1-y and 1-month average PM10-2.5 concentrations with markers of inflammation and coagulation. METHODS: We leveraged data from 7,071 Multi-Ethnic Study of Atherosclerosis and ancillary study participants 45-84 y of age who had repeated plasma measures of inflammatory and coagulation biomarkers. We estimated PM10-2.5 at participant addresses 1 y and 1 month before each of up to four exams (2000-2012) using spatiotemporal models that incorporated satellite, regulatory monitoring, and local geographic data and accounted for spatial correlation. We used random effects models to estimate associations with interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, and D-dimer, controlling for potential confounders. RESULTS: Increases in PM10-2.5 were not associated with greater levels of inflammation or coagulation. A 10-µg/m3 increase in annual average PM10-2.5 was associated with a 2.5% decrease in CRP [95% confidence interval (CI): -5.5, 0.6]. We saw no association between annual average PM10-2.5 and the other markers (IL-6: -0.7%, 95% CI: -2.6, 1.2; fibrinogen: -0.3%, 95% CI: -0.9, 0.3; D-dimer: -0.2%, 95% CI: -2.6, 2.4). Associations consistently showed that a 10-µg/m3 increase in 1-month average PM10-2.5 was associated with reduced inflammation and coagulation, though none were distinguishable from no association (IL-6: -1.2%, 95% CI: -3.0 , 0.5; CRP: -2.5%, 95% CI: -5.3, 0.4; fibrinogen: -0.4%, 95% CI: -1.0, 0.1; D-dimer: -2.0%, 95% CI: -4.3, 0.3). DISCUSSION: We found no evidence that PM10-2.5 is associated with higher inflammation or coagulation levels. More research is needed to determine whether the inflammation and coagulation pathways are as important in explaining observed PM10-2.5 health impacts in humans as they have been shown to be in toxicology studies or whether PM10-2.5 might impact human health through alternative biological mechanisms. https://doi.org/10.1289/EHP12972.

Representativeness of the US EPA PM monitoring site locations to the US population: implications for air pollution prediction modeling.

Air pollution prediction modeling establishes relationships between measurements and geographical and meteorological characteristics to infer concentrations at locations without measurements. Since air pollution monitors are limited in number, predictions may be generated for locations different than those used to train the model. The epidemiologic impacts of this potential mismatch hinge on whether the population resides in areas well-represented by monitoring sites. Here we quantify the fraction of the population with geographical characteristics not reflected by the 2000, 2010, and 2020 EPA PM2.5 and PM10 regulatory sites. We evaluated this measure nationwide, regionally, and by race. Nationally, the networks were very representative of the population experience; however, there was less overlap regionally and in regions stratified by race. This suggests that sub-national exposure modeling should carefully consider the representativeness of monitors for their populations. It also highlights that exposure models often borrow information from distal places to predict full population exposure.

Traffic-related air pollution and dementia incidence in the Adult Changes in Thought Study.

BACKGROUND: While epidemiologic evidence links higher levels of exposure to fine particulate matter (PM2.5) to decreased cognitive function, fewer studies have investigated links with traffic-related air pollution (TRAP), and none have examined ultrafine particles (UFP, ≤100 nm) and late-life dementia incidence. OBJECTIVE: To evaluate associations between TRAP exposures (UFP, black carbon [BC], and nitrogen dioxide [NO2]) and late-life dementia incidence. METHODS: We ascertained dementia incidence in the Seattle-based Adult Changes in Thought (ACT) prospective cohort study (beginning in 1994) and assessed ten-year average TRAP exposures for each participant based on prediction models derived from an extensive mobile monitoring campaign. We applied Cox proportional hazards models to investigate TRAP exposure and dementia incidence using age as the time axis and further adjusting for sex, self-reported race, calendar year, education, socioeconomic status, PM2.5, and APOE genotype. We ran sensitivity analyses where we did not adjust for PM2.5 and other sensitivity and secondary analyses where we adjusted for multiple pollutants, applied alternative exposure models (including total and size-specific UFP), modified the adjustment covariates, used calendar year as the time axis, assessed different exposure periods, dementia subtypes, and others. RESULTS: We identified 1,041 incident all-cause dementia cases in 4,283 participants over 37,102 person-years of follow-up. We did not find evidence of a greater hazard of late-life dementia incidence with elevated levels of long-term TRAP exposures. The estimated hazard ratio of all-cause dementia was 0.98 (95 % CI: 0.92-1.05) for every 2000 pt/cm3 increment in UFP, 0.95 (0.89-1.01) for every 100 ng/m3 increment in BC, and 0.96 (0.91-1.02) for every 2 ppb increment in NO2. These findings were consistent across sensitivity and secondary analyses. DISCUSSION: We did not find evidence of a greater hazard of late-life dementia risk with elevated long-term TRAP exposures in this population-based prospective cohort study.

Residential greenspace and major depression among older adults living in urban and suburban areas with different climates across the United States.

BACKGROUND AND AIM: Residential greenspace could alleviate depression - a leading cause of disability. Fewer studies of depression and greenspace have considered major depression, and, to our knowledge, none have considered how climate, which determines vegetation abundance and type, may change the impacts of greenspace. Our aim was to investigate whether residential greenspace is associated with major depression among older adults and explore effect modification by climate. METHODS: We used biennial interviews between 2008 and 2016 from the Health and Retirement Study. We calculated greenness within walking distance of home addresses as the maximum NDVI for the year of each participant interview averaged within a 1 km buffer. Reflecting clinical criteria, a score of ≥5 on the CIDI-SF indicated major depression in the preceding 12-months. We characterized climate using Köppen-Geiger classifications. To estimate prevalence ratios, we used Poisson regression. Our models adjusted for sociodemographic characteristics, geography, annual sunshine, and bluespace. RESULTS: The 21,611 eligible participants were 65 ± 10 years old on average, 55% female, 81% White, 12% Black, 10% Hispanic/Latino, and 31% had at least a 4-year college degree. The 12-month prevalence of a major depression was 8%. In adjusted models, more residential greenspace was associated with a lower prevalence of major depression (prevalence ratio per IQR, 0.91; 95% CI, 0.84 to 0.98). There was evidence of effect modification by climate (P forinteraction, 0.062). We observed stronger associations in tropical (prevalence ratio per IQR 0.69; 95% CI, 0.47 to 1.01) and cold (prevalence ratio per IQR, 0.83; 95% CI, 0.74 to 0.93) climates compared to arid (prevalence ratio per IQR 0.99; 95% CI, 0.90 to 1.09) and temperate (prevalence ratio per IQR 0.98; 95% CI, 0.86 to 1.11) climates. CONCLUSIONS: Residential greenspace may help reduce major depression. However, climate may influence how people benefit from greenspace.

Reduction of Outdoor and Indoor PM2.5 Source Contributions via Portable Air Filtration Systems in a Senior Residential Facility in Detroit, Michigan.

Background: The Reducing Air Pollution in Detroit Intervention Study (RAPIDS) was designed to evaluate cardiovascular health benefits and personal fine particulate matter (particulate matter < 2.5 µm in diameter, PM2.5) exposure reductions via portable air filtration units (PAFs) among older adults in Detroit, Michigan. This double-blind randomized crossover intervention study has shown that, compared to sham, air filtration for 3 days decreased 3-day average brachial systolic blood pressure by 3.2 mmHg. The results also showed that commercially available HEPA-type and true HEPA PAFs mitigated median indoor PM2.5 concentrations by 58% and 65%, respectively. However, to our knowledge, no health intervention study in which a significant positive health effect was observed has also evaluated how outdoor and indoor PM2.5 sources impacted the subjects. With that in mind, detailed characterization of outdoor and indoor PM2.5 samples collected during this study and a source apportionment analysis of those samples using a positive matrix factorization model were completed. The aims of this most recent work were to characterize the indoor and outdoor sources of the PM2.5 this community was exposed to and to assess how effectively commercially available HEPA-type and true HEPA PAFs were able to reduce indoor and outdoor PM2.5 source contributions. Methods: Approximately 24 h daily indoor and outdoor PM2.5 samples were collected on Teflon and Quartz filters from the apartments of 40 study subjects during each 3-day intervention period. These filters were analyzed for mass, carbon, and trace elements. Environmental Protection Agency Positive Matrix Factorization (PMF) 5.0 was utilized to determine major emission sources that contributed to the outdoor and indoor PM2.5 levels during this study. Results: The major sources of outdoor PM2.5 were secondary aerosols (28%), traffic/urban dust (24%), iron/steel industries (15%), sewage/municipal incineration (10%), and oil combustion/refinery (6%). The major sources of indoor PM2.5 were organic compounds (45%), traffic + sewage/municipal incineration (14%), secondary aerosols (13%), smoking (7%), and urban dust (2%). Infiltration of outdoor PM2.5 for sham, HEPA-type, and true HEPA air filtration was 79 ± 24%, 61 ± 32%, and 51 ± 34%, respectively. Conclusions: The results from our study showed that intervention with PAFs was able to significantly decrease indoor PM2.5 derived from outdoor and indoor PM2.5 sources. The PAFs were also able to significantly reduce the infiltration of outdoor PM2.5. The results of this study provide insights into what types of major PM2.5 sources this community is exposed to and what degree of air quality and systolic blood pressure improvements are possible through the use of commercially available PAFs in a real-world setting.

Hypertension and Stroke as Mediators of Air Pollution Exposure and Incident Dementia.

Importance: Fine particulate matter air pollution (PM2.5) has been consistently associated with cardiovascular disease, which, in turn, is associated with an increased risk of dementia. As such, vascular dysfunction might be a mechanism by which PM2.5 mediates dementia risk, yet few prior epidemiological studies have examined this potential mechanism. Objective: To investigate whether hypertension and stroke serve as mediators and modifiers of the association of PM2.5 with incident dementia. Design, Setting, and Participants: As part of the Environmental Predictors of Cognitive Health and Aging (EPOCH) Project, this cohort study used biennial survey data collected between 1998 and 2016 from respondents of the Health and Retirement Study (HRS), a nationally representative, population-based, cohort in the US. Eligible participants were those over 50 years of age who were free of dementia at baseline and had complete exposure, mediator, outcome, and demographic data from the HRS. Data analysis was conducted from August to November 2022. Exposures: Exposure to PM2.5, calculated for the 10 years preceding each person's baseline examination according to residential histories and spatiotemporal models. Main Outcomes and Measures: Incident dementia was identified using a validated algorithm based on cognitive testing and informant reports. The 4-way decomposition causal mediation analysis method was used to quantify the degree to which hypertension and stroke mediated or modified the association of PM2.5 with incident dementia after adjustment for individual-level and area-level covariates. Results: Among 27 857 participants (mean [SD] age at baseline, 61 [10] years; 15 747 female participants [56.5%]; 19 249 non-Hispanic White participants [69.1%]), 4105 (14.7%) developed dementia during the follow-up period (mean [SD], 10.2 [5.6] years). Among participants with dementia, 2204 (53.7%) had a history of hypertension at baseline and 386 (9.4%) received a diagnosis of hypertension during the follow up. A total of 378 participants (9.2%) had a history of stroke at baseline and 673 (16.4%) developed stroke over the follow-up period. The IQR of baseline PM2.5 concentrations was 10.9 to 14.9 µg/m3. In fully adjusted models, higher levels of PM2.5 (per IQR) were not associated with increased risk of incident dementia (HR, 1.04; 95% CI, 0.98 to 1.11). Although there were positive associations of prevalent stroke (HR, 1.67; 95% CI, 1.48 to 1.88) and hypertension (HR, 1.15; 95% CI, 1.08 to 1.23) with incident dementia compared with those free of stroke and hypertension during follow-up, there was no statistically significant association of PM2.5 with stroke (odds ratio per IQR increment in PM2.5, 1.08; 95%CI, 0.91 to 1.29) and no evidence of an association of PM2.5 with hypertension (odds ratio per IQR increment in PM2.5, 0.99; 95%CI, 0.92 to 1.07). Concordantly, there was no evidence that hypertension or stroke acted as mediators or modifiers of the association of PM2.5 with incident dementia. Although the nonmediated interaction between PM2.5 and hypertension accounted for 39.2% of the total excess association (95% CI, -138.5% to 216.9%), the findings were not statistically significant. Conclusions and Relevance: These findings suggest that although hypertension may enhance the susceptibility of individuals to air pollution, hypertension and stroke do not significantly mediate or modify the association of PM2.5 with dementia, indicating the need to investigate other pathways and potential mediators of risk.

Associations between long-term aircraft noise exposure, cardiovascular disease, and mortality in US cohorts of female nurses.

There is limited research examining aircraft noise and cardiovascular disease (CVD) risk. The objective of this study was to investigate associations of aircraft noise with CVD among two US cohorts, the Nurses' Health Study (NHS) and Nurses' Health Study II (NHSII). Methods: Between 1994 and 2014, we followed 57,306 NHS and 60,058 NHSII participants surrounding 90 airports. Aircraft noise was modeled above 44 A-weighted decibels (dB(A)) and linked to geocoded addresses. Based on exposure distributions, we dichotomized exposures at 50 dB(A) and tested sensitivity of this cut-point by analyzing aircraft noise as categories (<45, 45-49, 50-54, ≥55) and continuously. We fit cohort-specific Cox proportional hazards models to estimate relationships between time-varying day-night average sound level (DNL) and CVD incidence and CVD and all-cause mortality, adjusting for fixed and time-varying individual- and area-level covariates. Results were pooled using random effects meta-analysis. Results: Over 20 years of follow-up, there were 4529 CVD cases and 14,930 deaths. Approximately 7% (n = 317) of CVD cases were exposed to DNL ≥50 dB(A). In pooled analyses comparing ≥50 with <50 dB(A), the adjusted hazard ratio for CVD incidence was 1.00 (95% confidence interval: 0.89, 1.12). The corresponding adjusted hazard ratio for all-cause mortality was 1.02 (95% confidence interval: 0.96, 1.09). Patterns were similar for CVD mortality in NHS yet underpowered. Conclusions: Among participants in the NHS and NHSII prospective cohorts who generally experience low exposure to aircraft noise, we did not find adverse associations of aircraft noise with CVD incidence, CVD mortality, or all-cause mortality.

Comparison of Particulate Air Pollution From Different Emission Sources and Incident Dementia in the US.

Importance: Emerging evidence indicates that exposure to fine particulate matter (PM2.5) air pollution may increase dementia risk in older adults. Although this evidence suggests opportunities for intervention, little is known about the relative importance of PM2.5 from different emission sources. Objective: To examine associations of long-term exposure of total and source-specific PM2.5 with incident dementia in older adults. Design, Setting, and Participants: The Environmental Predictors of Cognitive Health and Aging study used biennial survey data from January 1, 1998, to December 31, 2016, for participants in the Health and Retirement Study, which is a nationally representative, population-based cohort study in the US. The present cohort study included all participants older than 50 years who were without dementia at baseline and had available exposure, outcome, and demographic data between 1998 and 2016 (N = 27 857). Analyses were performed from January 31 to May 1, 2022. Exposures: The 10-year mean total PM2.5 and PM2.5 from 9 emission sources at participant residences for each month during follow-up using spatiotemporal and chemical transport models. Main Outcomes and Measures: The main outcome was incident dementia as classified by a validated algorithm incorporating respondent-based cognitive testing and proxy respondent reports. Adjusted hazard ratios (HRs) were estimated for incident dementia per IQR of residential PM2.5 concentrations using time-varying, weighted Cox proportional hazards regression models with adjustment for the individual- and area-level risk factors. Results: Among 27 857 participants (mean [SD] age, 61 [10] years; 15 747 [56.5%] female), 4105 (15%) developed dementia during a mean (SD) follow-up of 10.2 [5.6] years. Higher concentrations of total PM2.5 were associated with greater rates of incident dementia (HR, 1.08 per IQR; 95% CI, 1.01-1.17). In single pollutant models, PM2.5 from all sources, except dust, were associated with increased rates of dementia, with the strongest associations for agriculture, traffic, coal combustion, and wildfires. After control for PM2.5 from all other sources and copollutants, only PM2.5 from agriculture (HR, 1.13; 95% CI, 1.01-1.27) and wildfires (HR, 1.05; 95% CI, 1.02-1.08) were robustly associated with greater rates of dementia. Conclusion and Relevance: In this cohort study, higher residential PM2.5 levels, especially from agriculture and wildfires, were associated with higher rates of incident dementia, providing further evidence supporting PM2.5 reduction as a population-based approach to promote healthy cognitive aging. These findings also indicate that intervening on key emission sources might have value, although more research is needed to confirm these findings.

In-utero exposure to multiple air pollutants and childhood undernutrition in India.

BACKGROUND: Several studies have been conducted to understand the impact of socioeconomic and maternal factors on child undernutrition. However, the past literature has not directly examined the joint impacts of fuel use and ambient pollution and have primarily focused on PM2.5. OBJECTIVE: This study explored the individual and community-level associations of both indoor (cooking fuel type) and ambient air pollution (PM2.5, NO2 and SO2) during maternal gestation on child undernutrition. METHODS: This study analysed stunting, being underweight, and anaemia of children aged 0-59 months (n = 259,627) using the National Family Health Survey. In-utero exposures to ambient PM2.5, NO2, and SO2 were measured using satellite data and self-reported fuel type was a marker of indoor pollution exposure. The study used univariate and bivariate Moran's I, spatial lag model and multivariable logistic regression models after adjusting for other covariates to understand the effect of pollution on in-utero exposure and child health status at the individual and community-levels. RESULTS: Higher concentration of indoor and ambient air pollution was found in the Northern and parts of Central regions of India. Estimates of spatial modelling show that each 1 µg/m-3 increase in maternal exposure to ambient PM2.5 across the clusters of India was associated with a 0.11, 9 and 19 percentage points increase in the prevalence of stunting, underweight and anaemia, respectively. The results of multi-pollutant model show that a higher ambient PM2.5 exposure during pregnancy was linked to higher odds of stunting (AOR:1.38; 95% CI:1.32-1.44), underweight (AOR:1.59; 95% CI:1.51-1.67) and anaemia (AOR:1.61; 95% CI:1.52-1.69) in children. Weaker but similar associations were observed for NO2, but not with SO2. Indoor pollution exposure during in-utero periods was also significantly associated with childhood undernutrition and this association was modified by ambient PM2.5 levels, where exposure to both indoor and ambient air pollution had even greater odds of being undernourished. IMPACT STATEMENT: Our research on multi-pollutant models has revealed the initial proof of the individual impacts of indoor and outdoor pollution (PM2.5, NO2, and SO2) exposure during fetal development on children's nutrition.

Health benefits from cleaner vehicles and increased active transportation in Seattle, Washington.

BACKGROUND: Climate mitigation policies that focus on the transportation sector yield near-term health co-benefits that could motivate policy action. OBJECTIVE: We quantified CO2 emission reductions as well as the air pollution and health benefits of urban transportation policies promoting electric vehicles (EV) and walking and bicycling in Seattle, Washington. METHODS: We compared a business-as-usual scenario projected to 2035 with intervention scenarios in which 35% of gasoline vehicles were switched to EV, and 50% of car trips less than 8 kilometers were replaced by walking or bicycling. We modeled changes in primary traffic-generated oxides of nitrogen (NOx) and fine particulate matter (PM2.5) as well as walking and bicycling activity, CO2 emissions from traffic, and fatal traffic injuries due to the transportation policy scenarios. We estimated the impacts of these changes on annual cases of asthma and premature mortality in the Seattle population. RESULTS: Increasing the use of EV, walking, and bicycling is estimated to reduce CO2 emissions by 744 tons/year (30%) and lower annual average concentrations of primary traffic-generated NOx and PM2.5 by 0.32 ppb (13%) and 0.08 µg/m3 (19%), respectively. In Seattle, the lower air pollutant concentrations, greater active transportation, and lower fatal traffic injuries would prevent 13 (95% CI: -1, 28), 49 (95% CI: 19, 71), and 5 (95% CI: 0, 14) premature deaths per year, respectively and 20 (95% CI: 8, 27) cases of asthma per year. SIGNIFICANCE: Moving towards cleaner vehicles and active transportation can reduce CO2 emissions, improve air quality, and population health. The resulting public health benefits provide important motivation for urban climate action plans. IMPACT STATEMENT: Using key components of the health impact assessment framework, we quantify the environmental and health benefits of urban transportation policy scenarios that promote electric vehicle use and replace short car trips with walking and bicycling as compared with a business as usual scenario in 2035. Our findings demonstrate that transportation scenarios promoting cleaner vehicles and active transportation can reduce CO2 emissions, improve air quality, and increase physical activity levels, resulting in significant public health benefits.

Exposure to Primary Air Pollutants Generated by Highway Traffic and Daily Mortality Risk in Near-Road Communities: A Case-Crossover Study.

Most epidemiologic studies fail to capture the impact of spatiotemporal fluctuations in traffic on exposure to traffic-related air pollutants in the near-road population. Using a case-crossover design and the Research LINE source (R-LINE) dispersion model with spatiotemporally resolved highway traffic data, we quantified associations between primary pollutants generated by highway traffic-particulate matter with an aerodynamic diameter less than or equal to 2.5 µm (PM2.5), oxides of nitrogen (NOx), and black carbon (BC)-and daily nonaccidental, respiratory, cardiovascular, and cerebrovascular mortality among persons who had resided within 1 km (0.6 mile) of major highways in the Puget Sound area of Washington State between 2009 and 2013. We estimated these associations using conditional logistic regression, adjusting for time-varying covariates. Although highly resolved modeled concentrations of PM2.5, NOx, and BC from highway traffic in the hours before death were used, we found no evidence of an association between mortality and the preceding 24-hour average PM2.5 exposure (odds ratio = 0.99, 95% confidence interval: 0.96, 1.02) or exposure during shorter averaging periods. This work did not support the hypothesis that mortality risk was meaningfully higher with greater exposures to PM2.5, NOx, and BC from highways in near-road populations, though we did incorporate a novel approach to estimate exposure to traffic-generated air pollution based on detailed traffic congestion data.

Long-Term Exposures to Urban Noise and Blood Pressure Levels and Control Among Older Adults.

[Figure: see text].

Exposure to Air Pollution in Relation to Risk of Dementia and Related Outcomes: An Updated Systematic Review of the Epidemiological Literature.

BACKGROUND: Dementia is a devastating neurologic condition that is common in older adults. We previously reviewed the epidemiological evidence examining the hypothesis that long-term exposure to air pollution affects dementia risk. Since then, the evidence base has expanded rapidly. OBJECTIVES: With this update, we collectively review new and previously identified epidemiological studies on air pollution and late-life cognitive health, highlighting new developments and critically discussing the merits of the evidence. METHODS: Using a registered protocol (PROSPERO 2020 CRD42020152943), we updated our literature review to capture studies published through 31 December 2020, extracted data, and conducted a bias assessment. RESULTS: We identified 66 papers (49 new) for inclusion in this review. Cognitive level remained the most commonly considered outcome, and particulate matter (PM) remained the most commonly considered air pollutant. Since our prior review, exposure estimation methods in this research have improved, and more papers have looked at cognitive change, neuroimaging, and incident cognitive impairment/dementia, though methodological concerns remain common. Many studies continue to rely on administrative records to ascertain dementia, have high potential for selection bias, and adjust for putative mediating factors in primary models. A subset of 35 studies met strict quality criteria. Although high-quality studies of fine particulate matter with aerodynamic diameter ≤2.5µm (PM2.5) and cognitive decline generally supported an adverse association, other findings related to PM2.5 and findings related to particulate matter with aerodynamic diameter ≤10µm (PM10, NO2, and NOx) were inconclusive, and too few papers reported findings with ozone to comment on the likely direction of association. Notably, only a few findings on dementia were included for consideration on the basis of quality criteria. DISCUSSION: Strong conclusions remain elusive, although the weight of the evidence suggests an adverse association between PM2.5 and cognitive decline. However, we note a continued need to confront methodological challenges in this line of research. https://doi.org/10.1289/EHP8716.

Fine Particulate Matter and Dementia Incidence in the Adult Changes in Thought Study.

BACKGROUND: Air pollution may be associated with elevated dementia risk. Prior research has limitations that may affect reliability, and no studies have evaluated this question in a population-based cohort of men and women in the United States. OBJECTIVES: We evaluated the association between time-varying, 10-y average fine particulate matter (PM2.5) exposure and hazard of all-cause dementia. An additional goal was to understand how to adequately control for age and calendar-time-related confounding through choice of the time axis and covariate adjustment. METHODS: Using the Adult Changes in Thought (ACT) population-based prospective cohort study in Seattle, we linked spatiotemporal model-based PM2.5 exposures to participant addresses from 1978 to 2018. Dementia diagnoses were made using high-quality, standardized, consensus-based protocols at biennial follow-ups. We conducted multivariable Cox proportional hazards regression to evaluate the association between time-varying, 10-y average PM2.5 exposure and time to event in a model with age as the time axis, stratified by apolipoprotein E (APOE) genotype, and adjusted for sex, education, race, neighborhood median household income, and calendar time. Alternative models used calendar time as the time axis. RESULTS: We report 1,136 cases of incident dementia among 4,166 individuals with nonmissing APOE status. Mean [mean ± standard deviation (SD)] 10-y average PM2.5 was 10.1 (±2.9) µg/m3. Each 1-µg/m3 increase in the moving average of 10-y PM2.5 was associated with a 16% greater hazard of all-cause dementia [1.16 (95% confidence interval: 1.03, 1.31)]. Results using calendar time as the time axis were similar. DISCUSSION: In this prospective cohort study with extensive exposure data and consensus-based outcome ascertainment, elevated long-term exposure to PM2.5 was associated with increased hazard of all-cause dementia. We found that optimal control of age and time confounding could be achieved through use of either age or calendar time as the time axis in our study. Our results strengthen evidence on the neurodegenerative effects of PM2.5. https://doi.org/10.1289/EHP9018.

Household use of polluting cooking fuels and late-life cognitive function: A harmonized analysis of India, Mexico, and China.

INTRODUCTION: Exposure to high levels of air pollution is associated with poor health, including worse cognitive function. Whereas many studies of cognition have assessed outdoor air pollution, we evaluate how exposure to air pollution from combustion of polluting household fuels relates with cognitive function using harmonized data from India, Mexico, and China. MATERIALS & METHODS: We analyze adults age 50+ in three nationally representative studies of aging with common data collection methods: the 2017-2019 Longitudinal Aging Study in India (n = 50,532), 2015 Mexican Health and Aging Study (n = 12,883), and 2013 China Health and Retirement Longitudinal Study (n = 12,913). Use of polluting fuels was assessed by self-report of wood, coal, kerosene, crop residue, or dung for cooking. Cognitive function was measured by performance across several cognitive domains and summarized into a total cognition score. We used linear regression, by country, to test how polluting cooking fuel use relates with cognition adjusting for key demographic and socioeconomic factors. RESULTS: Approximately 47%, 12%, and 48% of respondents in India, Mexico, and China, respectively, relied primarily on polluting cooking fuel, which was more common in rural areas. Using polluting cooking fuels was consistently associated with poorer cognitive function in all countries, independent of demographic and socioeconomic characteristics. Adjusted differences in cognitive function between individuals using polluting and clean cooking fuel were equivalent to differences observed between individuals who were 3 years of age apart in Mexico and China and 6 years of age apart in India. Across countries, associations between polluting cooking fuel use and poorer cognition were larger for women. CONCLUSIONS: Results suggest that household air pollution from the use of polluting cooking fuel may play an important role in shaping cognitive outcomes of older adults in countries where reliance on polluting fuels for domestic energy needs still prevails. As these countries continue to age, public health efforts should seek to reduce reliance on these fuels.

Fine Particulate Matter and Markers of Alzheimer's Disease Neuropathology at Autopsy in a Community-Based Cohort.

BACKGROUND: Evidence links fine particulate matter (PM2.5) to Alzheimer's disease (AD), but no community-based prospective cohort studies in older adults have evaluated the association between long-term exposure to PM2.5 and markers of AD neuropathology at autopsy. OBJECTIVE: Using a well-established autopsy cohort and new spatiotemporal predictions of air pollution, we evaluated associations of 10-year PM2.5 exposure prior to death with Braak stage, Consortium to Establish a Registry for AD (CERAD) score, and combined AD neuropathologic change (ABC score). METHODS: We used autopsy specimens (N = 832) from the Adult Changes in Thought (ACT) study, with enrollment ongoing since 1994. We assigned long-term exposure at residential address based on two-week average concentrations from a newly developed spatiotemporal model. To account for potential selection bias, we conducted inverse probability weighting. Adjusting for covariates with tiered models, we performed ordinal regression for Braak and CERAD and logistic regression for dichotomized ABC score. RESULTS: 10-year average (SD) PM2.5 from death across the autopsy cohort was 8.2 (1.9) µg/m3. Average age (SD) at death was 89 (7) years. Each 1µg/m3 increase in 10-year average PM2.5 prior to death was associated with a suggestive increase in the odds of worse neuropathology as indicated by CERAD score (OR: 1.35 (0.90, 1.90)) but a suggestive decreased odds of neuropathology as defined by the ABC score (OR: 0.79 (0.49, 1.19)). There was no association with Braak stage (OR: 0.99 (0.64, 1.47)). CONCLUSION: We report inconclusive associations between PM2.5 and AD neuropathology at autopsy among a cohort where 94% of individuals experienced 10-year exposures below the current EPA standard. Prior studies of AD risk factors and AD neuropathology are similarly inconclusive, suggesting alternative mechanistic pathways for disease or residual confounding.

Long-term community noise exposure in relation to dementia, cognition, and cognitive decline in older adults.

INTRODUCTION: Exposure to noise might influence risk of Alzheimer's disease (AD) dementia. METHODS: Participants of the Chicago Health and Aging Project (≥65 years) underwent triennial cognitive assessments. For the 5 years preceding each assessment, we estimated 5227 participants' residential level of noise from the community using a spatial prediction model, and estimated associations of noise level with prevalent mild cognitive impairment (MCI) and AD, cognitive performance, and rate of cognitive decline. RESULTS: Among these participants, an increment of 10 A-weighted decibels (dBA) in noise corresponded to 36% and 29% higher odds of prevalent MCI (odds ratio [OR] = 1.36; 95% confidence interval [CI], 1.15 to 1.62) and AD (OR = 1.29, 95% CI, 1.08 to 1.55). Noise level was associated with worse global cognitive performance, principally in perceptual speed (-0.09 standard deviation per 10 dBA, 95% CI: -0.16 to -0.03), but not consistently associated with cognitive decline. DISCUSSION: These results join emerging evidence suggesting that noise may influence late-life cognition and risk of dementia.