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Background: The effect of ambient air pollution on global variations and trends in asthma prevalence is unclear. Objectives: Our goal was to investigate community-level associations between asthma prevalence data from the International Study of Asthma and Allergies in Childhood (ISAAC) and satellite-based estimates of particulate matter with aerodynamic diameter < 2.5 microm (PM2.5) and nitrogen dioxide (NO2), and modelled estimates of ozone. Methods: We assigned satellite-based estimates of PM2.5 and NO2 at a spatial resolution of 0.1deg × 0.1deg and modeled estimates of ozone at a resolution of 1deg × 1deg to 183 ISAAC centers. We used center-level prevalence of severe asthma as the outcome and multilevel models to adjust for gross national income (GNI) and center- and country-level sex, climate, and population density. We examined associations (adjusting for GNI) between air pollution and asthma prevalence over time in centers with data from ISAAC Phase One (mid-1900s) and Phase Three (2001-2003). Results: For the 13- to 14-year age group (128 centers in 28 countries), the estimated average within-country change in center-level asthma prevalence per 100 children per 10% increase in center-level PM2.5 and NO2 was -0.043 [95% confidence interval (CI): -0.139, 0.053] and 0.017 (95% CI: -0.030, 0.064) respectively. For ozone the estimated change in prevalence per parts per billion by volume was -0.116 (95% CI: -0.234, 0.001). Equivalent results for the 6- to 7-year age group (83 centers in 20 countries), though slightly different, were not significantly positive. For the 13- to 14-year age group, change in center-level asthma prevalence over time per 100 children per 10% increase in PM2.5 from Phase One to Phase Three was -0.139 (95% CI: -0.347, 0.068). The corresponding association with ozone (per ppbV) was -0.171 (95% CI: -0.275, -0.067). Conclusion: In contrast to reports from within-community studies of individuals exposed to traffic pollution, we did not find evidence of a positive association between ambient air pollution and asthma prevalence as measured at the community level.

Air pollution is a major risk factor for global health, with 3 million deaths annually being attributed to fine particulate matter ambient pollution (PM2.5).The primary source of information for estimating population exposures to air pollution has been measurements from ground monitoring networks but, although coverage is increasing, regions remain in which monitoring is limited. The data integration model for air quality supplements ground monitoring data with information from other sources, such as satellite retrievals of aerosol optical depth and chemical transport models. Set within a Bayesian hierarchical modelling framework, the model allows spatially varying relationships between ground measurements and other factors that estimate air quality. The model is used to estimate exposures, together with associated measures of uncertainty, on a high resolution grid covering the entire world from which it is estimated that 92% of the world's population reside in areas exceeding the World Health Organization's air quality guidelines.

Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels. We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM2·5) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure–response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure–response functions spanning the global range of exposure. Ambient PM2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000–422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015. Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction. Bill & Melinda Gates Foundation and Health Effects Institute.

We investigate socioeconomic disparities in air quality at public schools in the contiguous US using high resolution estimates of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) concentrations. We find that schools with higher proportions of people of color (POC) and students eligible for the federal free or reduced lunch program, a proxy for poverty level, are associated with higher pollutant concentrations. For example, we find that the median annual NO2 concentration for White students, nationally, was 7.7 ppbv, compared to 9.2 ppbv for Black and African American students. Statewide and regional disparities in pollutant concentrations across racial, ethnic, and poverty groups are consistent with nationwide results, where elevated NO2 concentrations were associated with schools with higher proportions of POC and higher levels of poverty. Similar, though smaller, differences were found in PM2.5 across racial and ethnic groups in most states. Racial, ethnic, and economic segregation across the rural‐urban divide is likely an important factor in pollution disparities at US public schools. We identify distinct regional patterns of disparities, highlighting differences between California, New York, and Florida. Finally, we highlight that disparities exist not only across urban and non‐urban lines but also within urban environments. Plain Language Summary We find that, nationally, US public schools with higher proportions of impoverished and racially/ethnically marginalized students are associated with higher average concentrations of two types of air pollutants, particulate matter and nitrogen dioxide (NO2), relative to schools with lower proportions of marginalized students. Disparities in pollutant concentrations are also more pronounced in some regions of the US where marginalized students are concentrated in urban areas and non‐marginalized students are concentrated in rural areas, such as the state of New York. We find that larger relative disparities exist for NO2 compared to particulate matter, but qualitative results are similar. Key Points US public school students from ethnically/racially marginalized groups are likely exposed to higher air pollutant concentrations US public schools with higher poverty levels are associated with higher air pollutant concentrations At public schools within urban areas, we still find some disparities in pollutant concentrations across racial/ethnic groups

Emissions of fine particulate matter (PM2.5) from human activities have been linked to substantial disease burdens, but evidence regarding how reducing PM2.5 at its sources would improve public health is sparse. We followed a population-based cohort of 2.7 million adults across Canada from 2007 through 2016. For each participant, we estimated annual mean concentrations of PM2.5 and the fractional contributions to PM2.5 from the five leading anthropogenic sources at their residential address using satellite observations in combination with a global atmospheric chemistry transport model. For each source, we estimated the causal effects of six hypothetical interventions on 10-y nonaccidental mortality risk using the parametric g-formula, a structural causal model. We conducted stratified analyses by age, sex, and income. This cohort would have experienced tangible health gains had contributions to PM2.5 from any of the five sources been reduced. Compared with no intervention, a 10% annual reduction in PM2.5 contributions from transportation and power generation, Canada’s largest and fifth-largest anthropogenic sources, would have prevented approximately 175 (95%CI: 123–226) and 90 (95%CI: 63–117) deaths per million by 2016, respectively. A more intensive 50% reduction per year in PM2.5 contributions from the two sources would have averted 360 and 185 deaths per million, respectively, by 2016. The potential health benefits were greater among men, older adults, and low-income earners. In Canada, where PM2.5 levels are among the lowest worldwide, reducing PM2.5 contributions from anthropogenic sources by as little as 10% annually would yield meaningful health gains.

Recent studies have identified inequality in the distribution of air pollution attributable health impacts, but to our knowledge this has not been examined in Canadian cities. We evaluated the extent and sources of inequality in air pollution attributable mortality at the census tract (CT) level in seven of Canada's largest cities. We first regressed fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) attributable mortality against the neighborhood (CT) level prevalence of age 65 and older, low income, low educational attainment, and identification as an Indigenous (First Nations, Métis, Inuit) or Black person, accounting for spatial autocorrelation. We next examined the distribution of baseline mortality rates, PM 2.5 and NO 2 concentrations, and attributable mortality by neighborhood (CT) level prevalence of these characteristics, calculating the concentration index, Atkinson index, and Gini coefficient. Finally, we conducted a counterfactual analysis of the impact of reducing baseline mortality rates and air pollution concentrations on inequality in air pollution attributable mortality. Regression results indicated that CTs with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality. Concentration index, Atkinson index, and Gini coefficient values revealed different degrees of inequality among the cities. Counterfactual analysis indicated that inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities. Reducing inequality in air pollution attributable mortality requires reducing disparities in both baseline mortality and air pollution exposure. Is air pollution attributable mortality equally distributed within cities? What population characteristics drive inequalities? Does the degree of inequality differ between cities? To what extent are inequalities in air pollution attributable mortality driven by exposure inequalities versus baseline mortality inequalities? In this study of seven Canadian cities, we found that neighborhoods with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality. However, there were different degrees of inequality among the cities. Inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities. Census tracts with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality The magnitude of inequality differed among seven Canadian cities Inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities

Air pollution is a major risk factor for global health, with both ambient and household air pollution contributing substantial components of the overall global disease burden. One of the key drivers of adverse health effects is fine particulate matter ambient pollution (PM\\(_{2.5}\\)) to which an estimated 3 million deaths can be attributed annually. The primary source of information for estimating exposures has been measurements from ground monitoring networks but, although coverage is increasing, there remain regions in which monitoring is limited. Ground monitoring data therefore needs to be supplemented with information from other sources, such as satellite retrievals of aerosol optical depth and chemical transport models. A hierarchical modelling approach for integrating data from multiple sources is proposed allowing spatially-varying relationships between ground measurements and other factors that estimate air quality. Set within a Bayesian framework, the resulting Data Integration Model for Air Quality (DIMAQ) is used to estimate exposures, together with associated measures of uncertainty, on a high resolution grid covering the entire world. Bayesian analysis on this scale can be computationally challenging and here approximate Bayesian inference is performed using Integrated Nested Laplace Approximations. Model selection and assessment is performed by cross-validation with the final model offering substantial increases in predictive accuracy, particularly in regions where there is sparse ground monitoring, when compared to current approaches: root mean square error (RMSE) reduced from 17.1 to 10.7, and population weighted RMSE from 23.1 to 12.1 \\(\\mu\\)gm\\(^{-3}\\). Based on summaries of the posterior distributions for each grid cell, it is estimated that 92% of the world's population reside in areas exceeding the World Health Organization's Air Quality Guidelines.

Subcortical brain structures are integral to motion, consciousness, emotions, and learning. We identified common genetic variation related to the volumes of nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen, and thalamus, using genome-wide association analyses in over 40,000 individuals from CHARGE, ENIGMA and the UK-Biobank. We show that variability in subcortical volumes is heritable, and identify 25 significantly associated loci (20 novel). Annotation of these loci utilizing gene expression, methylation, and neuropathological data identified 62 candidate genes implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease.