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 (PM2.5), 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 PM2.5 (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 PM2.5 and NO2 were approximately linear. Our study suggests that exposures to PM2.5 and NO2 are associated with incidence of dementia and AD.

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Background Evidence suggests a link between air pollution and dementia. Cardiovascular disease (CVD) may be a potential determinant of dementia. This motivated us to quantify the contribution of CVD to the association between air pollution and dementia. Methods A cohort of Canadian-born residents of Ontario, who participated in the 1996–2003 Canadian Community Health Surveys, was followed through 2013 or until dementia diagnosis. Exposure to nitrogen dioxide (NO2) and fine particulate matter (PM2.5) was estimated with a 3-year average and 5-year lag before dementia diagnosis. Incident CVD was evaluated as a mediator. We used multi-level Cox proportional and Aalen additive hazard regression models, adjusting for individual- and neighbourhood-level risk factors to estimate associations with NO2 and PM2.5. We estimated the total, direct and indirect effects of air pollution on dementia through cardiovascular disease. Results This study included 34 391 older adults. At baseline, the mean age of this cohort was 59 years. The risk of dementia was moderately higher among those more exposed to NO2 (hazard ratio (HR) 1.10, 95% confidence interval (CI) 0.99–1.19; and 100 additional cases per 100 000 [standard error (SE) <100x10-5]) and PM2.5 [(HR 1.29, 95% CI 0.99–1.64; 200 additional cases per 100 000] [SE 100x10-5]) after adjusting for covariates; however, these estimates are imprecise. A greater proportion of the relationship between PM2.5 and dementia was mediated through CVD than NO2 for both scales. Conclusions These results suggest some of the association between air pollution and dementia is mediated through CVD, indicating that improving cardiovascular health may prevent dementia in areas with higher exposure to air pollution.

Background. Exposure to high air temperature in late pregnancy is increasingly recognized as a risk factor for preterm birth (PTB). However, the combined effects of heatwaves with air pollution and green space are still unexplored. In the context of climate change, investigating the interaction between environmental factors and identifying communities at higher risk is important to better understand the etiological mechanisms and design targeted interventions towards certain women during pregnancy. Objectives. To examine the combined effects of heatwaves, air pollution and green space exposure on the risk of PTB. Methods. California birth certificate records for singleton births (2005–2013) were obtained. Residential zip code-specific daily temperature during the last week of gestation was used to create 12 definitions of heatwave with varying temperature thresholds and durations. We fit multi-level Cox proportional hazard models with time to PTB as the outcome and gestational week as the temporal unit. Relative risk due to interaction (RERI) was applied to estimate the additive interactive effect of air pollution and green space on the effect of heatwaves on PTB. Results. In total, 1 967 300 births were included in this study. For PM2.5, PM10 and O3, we found positive additive interactions (RERIs >0) between heatwaves and higher air pollution levels. Combined effects of heatwaves and green space indicated negative interactions (RERIs <0) for less intense heatwaves (i.e. shorter duration or relatively low temperature), whereas there were potential positive interactions (RERIs >0) for more intense heatwaves. Conclusion. This study found synergistic harmful effects for heatwaves with air pollution, and potential positive interactions with lack of green space on PTB. Implementing interventions, such as heat warning systems and behavioral changes, targeted toward pregnant women at risk for high air pollution and low green space exposures may optimize the benefits of reducing acute exposure to extreme heat before delivery.

Extreme heat and ozone are co-occurring exposures that independently and synergistically increase the risk of respiratory disease. To our knowledge, no joint warning systems consider both risks; understanding their interactive effect can warrant use of comprehensive warning systems to reduce their burden. We examined heterogeneity in joint effects (on the additive scale) between heat and ozone at small geographical scales. A within-community matched design with a Bayesian hierarchical model was applied to study this association at the zip code level. Spatially varying relative risks due to interaction (RERI) were quantified to consider joint effects. Determinants of the spatial variability of effects were assessed using a random effects metaregression to consider the role of demographic/neighborhood characteristics that are known effect modifiers. A total of 817,354 unscheduled respiratory hospitalizations occurred in California from 2004 to 2013 in the May to September period. RERIs revealed no additive interaction when considering overall joint effects. However, when considering the zip code level, certain areas observed strong joint effects. A lower median income, higher percentage of unemployed residents, and exposure to other air pollutants within a zip code drove stronger joint effects; a higher percentage of commuters who walk/bicycle, a marker for neighborhood wealth, showed decreased effects. Results indicate the importance of going beyond average measures to consider spatial variation in the health burden of these exposures and predictors of joint effects. This information can be used to inform early warning systems that consider both heat and ozone to protect populations from these deleterious effects in identified areas.

Introduction:Growing evidence implicates air pollution as a risk factor for dementia, but prior work is limited by challenges in diagnostic accuracy and assessing exposures in the decades prior to disease development. We evaluated the impact of long-term fine particulate matter (PM 2.5 ) exposures on incident dementia (all-cause, Alzheimer's disease [AD], and vascular dementia [VaD]) in older adults.Methods: A panel of neurologists adjudicated dementia cases based on extensive neuropsychological testing and magnetic resonance imaging. We applied validated finescale air pollutant models to reconstructed residential histories to assess exposures.Results: An interquartile range increase in 20-year PM 2.5 was associated with a 20% higher risk of dementia (95% confidence interval [CI]: 5%, 37%) and an increased risk of mixed VaD/AD but not AD alone.Discussion: Our findings suggest that air pollutant exposures over decades contribute to dementia and that effects of current exposures may be experienced years into the future.