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Background: Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect., Methods: We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000-2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM 2.5 , PM 10 , and NO 2 . We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for a priori confounders., Results: Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer's disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes., Conclusions: The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Evidence suggests exposure to air pollution increases the risk of dementia. Cognitively stimulating activities and social interactions, made available through the social environment, may slow cognitive decline. We examined whether the social environment buffers the adverse effect of air pollution on dementia in a cohort of older adults., Methods: This study draws from the Ginkgo Evaluation of Memory Study. Participants aged 75 years and older were enrolled between 2000 and 2002 and evaluated for dementia semi-annually through 2008. Long-term exposure to particulate matter and nitrogen dioxide was assigned from spatial and spatiotemporal models. Census tract-level measures of the social environment and individual measures of social activity were used as measures of the social environment. We generated Cox proportional hazard models with census tract as a random effect and adjusted for demographic and study visit characteristics. Relative excess risk due to interaction was estimated as a qualitative measure of additive interaction., Results: This study included 2,564 individuals. We observed associations between increased risk of dementia and fine particulate matter (µg/m 3 ), coarse particulate matter (µg/m 3 ), and nitrogen dioxide (ppb); HRs per 5 unit increase were 1.55 (1.01, 2.18), 1.31 (1.07, 1.60), and 1.18 (1.02, 1.37), respectively. We found no evidence of additive interaction between air pollution and the neighborhood social environment., Conclusions: We found no consistent evidence to suggest a synergistic effect between exposure to air pollution and measures of the social environment. Given the many qualities of the social environment that may reduce dementia pathology, further examination is encouraged., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2023 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Background: Anti-Müllerian hormone (AMH) concentrations are a marker of ovarian reserve and are indicative of a woman's reproductive lifespan. Exposure to tobacco smoke has been associated with lower AMH concentrations; however, less is known about the association between ambient air pollution and ovarian reserve., Methods: For 883 premenopausal Sister Study participants recruited between 2003 and 2009 in the United States, adult residential annual average concentrations of PM 2.5 , PM 10 , and NO 2 were estimated using validated universal kriging models incorporating land-use regression. We estimated the distance in meters to the nearest major road for both adult enrollment and childhood residences. Serum AMH was measured using an ultrasensitive ELISA assay. Samples with AMH concentrations below the detection limit were analyzed using a picoAMH ELISA assay. Multivariable-adjusted linear regression was used to estimate the percent change in AMH in relation to ambient residential air pollution, categorized in quartiles and per interquartile range increase, and distance to a major roadway., Results: Overall, we observed little to no evidence of associations between AMH and air pollution concentrations or proximity to roadways. Women in the highest quartile of NO 2 exposure, a traffic-related pollutant, had higher estimated AMH concentrations (Q4 vs. Q1, 42.9%; 95% CI = -3.4, 111.4) compared with the lowest quartile. However, lower mean AMH concentrations were observed for women living closer to a major roadway (<50 m to nearest roadway vs. ≥200 m = -32.9%; 95% CI = -56.1, 2.6)., Conclusions: We saw little consistent evidence to support an association between outdoor air pollution and diminished ovarian reserve in US women ages 35-54., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Background: Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows., Objective: To assess associations between prenatal fine particulate matter exposure and asthma at age 4., Methods: This study included mother-child dyads from two pregnancy cohorts-CANDLE and TIDES-within the ECHO-PATHWAYS consortium (births in 2007-2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM 2.5 ) exposures during the pseudoglandular (5-16 weeks gestation), canalicular (16-24 weeks gestation), saccular (24-36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors., Results: Children (n=1469) were on average 4.3 (standard deviation 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m 3 higher PM 2.5 exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma (95% CI: 1.06-1.58). A similar association was observed with current asthma (RR 1.27, 95% CI: 1.04-1.54), but not current wheeze (RR 1.11, 95% CI: 0.92-1.33). Effect estimates for associations during other developmental windows had confidence intervals that included the null., Conclusions: Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM 2.5 ., Competing Interests: Conflict of interest: The authors declare that they have no relevant conflicts of interest.

Emerging evidence from animal and human studies indicates that exposure to traffic-related air pollution may adversely affect fertility., Methods: Among 7,342 female pregnancy planners from the United States and 1,448 from Canada, we examined the association between residential proximity to major roads and fecundability, the per-cycle probability of conception. From 2013 to 2019, women 21-45 years old who were trying to conceive without fertility treatment completed an online baseline questionnaire and follow-up questionnaires every 8 weeks for up to 12 months or until pregnancy. We geocoded residential addresses reported at baseline and during follow-up, and calculated distance to nearest major roads and length of major roads within buffers of 50, 100, 300, and 400 meters around the residence as proxies for traffic-related air pollution. We used proportional probabilities regression models to estimate fecundability ratios (FRs) and 95% confidence intervals (CIs), adjusting for individual- and neighborhood-level characteristics., Results: In the United States, the FR comparing women who lived <50 meters with those who lived ≥400 meters from the closest major road was 0.88 (95% CI = 0.80, 0.98). The association among Canadian women was similar in magnitude, but less precise (FR = 0.93; 95% CI = 0.74, 1.16). Likewise, length of major roads within buffers of 50 and 100 meters was associated with lower fecundability in both countries; associations were attenuated within larger buffers., Conclusions: These results are consistent with the hypothesis that traffic-related air pollution or other near-road exposures may adversely affect fecundability., Competing Interests: PRESTO has received in-kind donations from FertilityFriend.com, Kindara.com, Sandstone Diagnostics, and Swiss Precision Diagnostics for primary data collection. L.A.W. serves as a consultant to AbbVie, Inc. for her work on uterine fibroids. The other authors have no conflicts to report. The results reported herein correspond to specific aim 2 of grant R01-ES028923 to investigators Wise and Hatch from the National Institute of Environmental Health Sciences (NIEHS). This work was also supported by grant P30-ES007033 from the NIEHS, grant R01-HD086742 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), grant R21-HD072326 from the NICHD, grant R01-HD060680 from the NICHD, and grant R21-HD050264 from the NICHD. The authors received funding to support open access publishing.Sponsorships or competing interests that may be relevant to content are disclosed at the end of the article., (Copyright © 2020 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Background: Ambient air pollution is classified as a human carcinogen by the International Agency for Research on Cancer (IARC). However, epidemiologic studies supporting this classification have focused on lung cancer mortality rather than incidence, and spatial and temporal resolutions of exposure estimates have varied considerably across studies., Methods: We evaluated the association of outdoor air pollution and lung cancer incidence among never-smoking participants of the Women's Health Initiative (WHI) study, a large, US-based cohort of postmenopausal women (N = 65,419; 265 cases). We used geospatial models to estimate exposures to fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) based on residential addresses at baseline and throughout follow-up. We also characterized exposures to traffic-related air pollution by proximity to major roadways. We estimated hazard ratios (HRs) for the risk of lung cancer in association with these exposure metrics using Cox proportional hazards regression models., Results: No compelling associations of PM 2.5 and NO 2 exposures with lung cancer risk were observed. An increased risk of lung cancer was observed when comparing those individuals with residences <50 versus ≥200 meters from a primary limited access highway (HR = 5.23; 95% confidence interval = 1.94, 14.13)., Conclusions: Our results do not exclude lung cancer risk estimates observed in association with PM 2.5 and NO 2 exposures identified in previous studies. Our results suggest that residential proximity to major roadways may be a proxy for carcinogenic exposures not correlated with PM 2.5 or NO 2 levels. New studies of air pollution and lung cancer incidence should characterize additional aspects of proximity to major roadways., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2019 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of Environmental Epidemiology. All rights reserved.)

Background: Limited research suggests ambient air pollution impairs fecundity but groups most susceptible have not been identified. We studied whether long-term ambient air pollution exposure prior to an in vitro fertilization (IVF) cycle was associated with successful livebirth, and whether associations were modified by underlying infertility diagnosis., Methods: Data on women initiating their 1 st autologous IVF cycle in 2012-13 were obtained from four U.S. clinics. Outcomes included pregnancy, pregnancy loss, and livebirth. Annual average exposure to fine particulate matter (PM 2.5 ), PM 10 , and nitrogen dioxide (NO 2 ) prior to IVF start were estimated at residential address using a validated national spatial model incorporating land-use regression and universal kriging. We also assessed residential distance to major roadway. We calculated risk ratios (RR) using modified Poisson regression and evaluated effect modification (EM) by infertility diagnosis on additive and multiplicative scales., Results: Among 7,463 eligible participants, 36% had a livebirth. There was a non-significant indication of an association between PM 2.5 or NO 2 and decreased livebirth and increased pregnancy loss. Near roadway residence was associated with decreased livebirth (RR: 0.96, 95% CI: 0.82, 0.99. There was evidence for EM between high exposure to air pollutants and a diagnosis of diminished ovarian reserve (DOR) or male infertility and decreased livebirth., Conclusions: Despite suggestive but uncertain findings for the overall effect of air pollution on fecundity, we found a suggestive indication that there may be synergistic effects of air pollution and DOR or male infertility diagnosis on livebirth. This suggests two possible targets for future research and intervention., Competing Interests: Conflict of interest statement: No relevant conflicts of interest

Background: Differences in traffic-related air pollution (TRAP) composition may cause heterogeneity in associations between air pollution exposure and cardiovascular health outcomes. Clustering multi-pollutant measurements allows investigation of effect modification by TRAP profiles., Methods: We measured TRAP components with fixed-site and on-road instruments for two two-week periods in Baltimore, Maryland. We created representative TRAP profiles for cold and warm seasons using predictive k -means clustering. We predicted cluster membership for 1005 participants in the Multi-Ethnic Study of Atherosclerosis and Air Pollution with follow-up between 2000 and 2012. We estimated cluster-specific relationships between coronary artery calcification (CAC) progression and long-term exposure to fine particulate matter (PM 2.5 ) and oxides of nitrogen (NO X )., Results: We identified two clusters in the cold season, notable for higher ratios of gases and ultrafine particles, respectively. A 5 μg/m 3 difference in PM 2.5 was associated with 17.0 (95% Confidence Interval [CI]: 7.2, 26.7) and 42.6 (95% CI: 25.7, 59.4) Agatston units/year CAC progression among participants in clusters 1 and 2, respectively (effect modification p =0.006). A 40ppb difference in NO X was associated with 22.2 (95% CI: 7.7, 36.7) and 41.9 (95% CI: 23.7, 60.2) Agatston units/year CAC progression in clusters 1 and 2, respectively ( p =0.08). Similar trends occurred using clusters identified from warm season measurements. Clusters correlated highly with baseline pollution level., Conclusions: Clustering TRAP measurements identified spatial differences in composition. We found evidence of greater CAC progression rates per unit PM 2.5 exposures among people living in areas characterized by high ratios of ultrafine particle counts relative to NO X concentrations., Competing Interests: Conflict of Interest: None declared.