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Background: Climate actions targeting combustion sources can generate large ancillary health benefits via associated air-quality improvements. Therefore, understanding the health costs associated with ambient fine particulate matter (PM 2·5 ) from combustion sources can guide policy design for both air pollution and climate mitigation efforts., Methods: In this modelling study, we estimated the health costs attributable to ambient PM 2·5 from six major combustion sources across 204 countries using updated concentration-response models and an age-adjusted valuation method. We defined major combustion sources as the sum of total coal, liquid fuel and natural gas, solid biofuel, agricultural waste burning, other fires, and 50% of the anthropogenic fugitive, combustion, and industrial dust source., Findings: Global long-term exposure to ambient PM 2·5 from combustion sources imposed US$1·1 (95% uncertainty interval 0·8-1·5) trillion in health costs in 2019, accounting for 56% of the total health costs from all PM 2·5 sources. Comparing source contributions to PM 2·5 concentrations and health costs, we observed a higher share of health costs from combustion sources compared to their contribution to population-weighted PM 2·5 concentration across 134 countries, accounting for more than 87% of the global population. This disparity was primarily attributed to the non-linear relationship between PM 2·5 concentration and its associated health costs. Globally, phasing out fossil fuels can generate 23% higher relative health benefits compared to their share of PM 2·5 reductions. Specifically, the share of health costs for total coal was 36% higher than the source's contributions to corresponding PM 2·5 concentrations and the share of health costs for liquid fuel and natural gas was 12% higher. Other than fossil fuels, South Asia was expected to show 16% greater relative health benefits than the percentage reduction in PM 2·5 from the abatement of solid biofuel emissions., Interpretation: In most countries, targeting combustion sources might offer greater health benefits than non-combustion sources. This finding provides additional rationale for climate actions aimed at phasing out combustion sources, especially those related to fossil fuels and solid biofuel. Mitigation efforts designed according to source-specific health costs can more effectively avoid health costs than strategies that depend solely on the source contributions to overall PM 2·5 concentration., Funding: The Health Effects Institute, the National Natural Science Foundation of China, and NASA., Competing Interests: Declaration of interests The institution of RVM received a grant from the Clean Air Fund during the study. All other authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Ambient nitrogen dioxide ( NO 2 ) and fine particulate matter with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ) threaten public health in the US, and systemic racism has led to modern-day disparities in the distribution and associated health impacts of these pollutants., Objectives: Many studies on environmental injustices related to ambient air pollution focus only on disparities in pollutant concentrations or provide only an assessment of pollution or health disparities at a snapshot in time. In this study, we compare injustices in NO 2 - and PM 2.5 -attributable health burdens, considering NO 2 -attributable health impacts across the entire US; document changing disparities in these health burdens over time (2010-2019); and evaluate how more stringent air quality standards would reduce disparities in health impacts associated with these pollutants., Methods: Through a health impact assessment, we quantified census tract-level variations in health outcomes attributable to NO 2 and PM 2.5 using health impact functions that combine demographic data from the US Census Bureau; two spatially resolved pollutant datasets, which fuse satellite data with physical and statistical models; and epidemiologically derived relative risk estimates and incidence rates from the Global Burden of Disease study., Results: Despite overall decreases in the public health damages associated with NO 2 and PM 2.5 , racial and ethnic relative disparities in NO 2 -attributable pediatric asthma and PM 2.5 -attributable premature mortality have widened in the US during the last decade. Racial relative disparities in PM 2.5 -attributable premature mortality and NO 2 -attributable pediatric asthma have increased by 16% and 19%, respectively, between 2010 and 2019. Similarly, ethnic relative disparities in PM 2.5 -attributable premature mortality have increased by 40% and NO 2 -attributable pediatric asthma by 10%., Discussion: Enacting and attaining more stringent air quality standards for both pollutants could preferentially benefit the most marginalized and minoritized communities by greatly reducing racial and ethnic relative disparities in pollution-attributable health burdens in the US. Our methods provide a semi-observational approach to track changes in disparities in air pollution and associated health burdens across the US. https://doi.org/10.1289/EHP11900.

Ambient fine particulate matter (PM 2.5 ) is the world's leading environmental health risk factor. Quantification is needed of regional contributions to changes in global PM 2.5 exposure. Here we interpret satellite-derived PM 2.5 estimates over 1998-2019 and find a reversal of previous growth in global PM 2.5 air pollution, which is quantitatively attributed to contributions from 13 regions. Global population-weighted (PW) PM 2.5 exposure, related to both pollution levels and population size, increased from 1998 (28.3 μg/m 3 ) to a peak in 2011 (38.9 μg/m 3 ) and decreased steadily afterwards (34.7 μg/m 3 in 2019). Post-2011 change was related to exposure reduction in China and slowed exposure growth in other regions (especially South Asia, the Middle East and Africa). The post-2011 exposure reduction contributes to stagnation of growth in global PM 2.5 -attributable mortality and increasing health benefits per µg/m 3 marginal reduction in exposure, implying increasing urgency and benefits of PM 2.5 mitigation with aging population and cleaner air., (© 2023. Springer Nature Limited.)

Background: Autism Spectrum Disorder (ASD) risk is highly heritable, with potential additional non-genetic factors, such as prenatal exposure to ambient particulate matter with aerodynamic diameter < 2.5 µm (PM 2.5 ) and maternal immune activation (MIA) conditions. Because these exposures may share common biological effect pathways, we hypothesized that synergistic associations of prenatal air pollution and MIA-related conditions would increase ASD risk in children., Objectives: This study examined interactions between MIA-related conditions and prenatal PM 2.5 or major PM 2.5 components on ASD risk., Methods: In a population-based pregnancy cohort of children born between 2001 and 2014 in Southern California, 318,751 mother-child pairs were followed through electronic medical records (EMR); 4,559 children were diagnosed with ASD before age 5. Four broad categories of MIA-related conditions were classified, including infection, hypertension, maternal asthma, and autoimmune conditions. Average exposures to PM 2.5 and four PM 2.5 components, black carbon (BC), organic matter (OM), nitrate (NO 3 - ), were estimated at maternal residential addresses during pregnancy. We estimated the ASD risk associated with MIA-related conditions, air pollution, and their interactions, using Cox regression models to adjust for covariates.4 2- ), were estimated at maternal residential addresses during pregnancy. We estimated the ASD risk associated with MIA-related conditions, air pollution, and their interactions, using Cox regression models to adjust for covariates., Results: ASD risk was associated with MIA-related conditions [infection (hazard ratio 1.11; 95% confidence interval 1.05-1.18), hypertension (1.30; 1.19-1.42), maternal asthma (1.22; 1.08-1.38), autoimmune disease (1.19; 1.09-1.30)], with higher pregnancy PM 2.5 [1.07; 1.03-1.12 per interquartile (3.73 μg/m 3 ) increase] and with all four PM 2.5 components. However, there were no interactions of each category of MIA-related conditions with PM 2.5 or its components on either multiplicative or additive scales., Conclusions: MIA-related conditions and pregnancy PM 2.5 were independently associations with ASD risk. There were no statistically significant interactions of MIA conditions and prenatal PM 2.5 exposure with ASD risk., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Fine particulate matter (PM 2.5 ) exposure is a leading mortality risk factor in India and the surrounding region of South Asia. This study evaluates the contribution of emission sectors and fuels to PM 2.5 mass for 29 states in India and 6 surrounding countries (Pakistan, Bangladesh, Nepal, Bhutan, Sri Lanka, and Myanmar) by combining source-specific emission estimates, stretched grid simulations from a chemical transport model, high resolution hybrid PM 2.5 , and disease-specific mortality estimates. We find that 1.02 (95% Confidence Interval (CI): 0.78-1.26) million deaths in South Asia attributable to ambient PM 2.5 in 2019 were primarily from three leading sectors: residential combustion (28%), industry (15%), and power generation (12%). Solid biofuel is the leading combustible fuel contributing to the PM 2.5 -attributable mortality (31%), followed by coal (17%), and oil and gas (14%). State-level analyses reveal higher residential combustion contributions (35%-39%) in states (Delhi, Uttar-Pradesh, Haryana) with high ambient PM 2.5 (>95 μg/m 3 ). The combined mortality burden associated with residential combustion (ambient) and household air pollution (HAP) in India is 0.72 million (95% CI:0.54-0.89) (68% attributable to HAP, 32% attributable to residential combustion). Our results illustrate the potential to reduce PM 2.5 mass and improve population health by reducing emissions from traditional energy sources across multiple sectors in South Asia.

Low haemoglobin (Hb) concentrations and anaemia in children have adverse effects on development and functioning, some of which may have consequences in later life. Exposure to ambient air pollution is reported to be associated with anaemia, but there is little evidence specific to low- and middle-income countries (LMICs), where childhood anaemia prevalence is greatest. We aimed to determine if long-term ambient fine particulate matter (≤2.5 μm in aerodynamic diameter [PM 2.5 ]) exposure was associated with Hb levels and the prevalence of anaemia in children aged <5 years living in 36 LMICs. We used Demographic and Health Survey data, collected between 2010 and 2019, which included blood Hb measurements. Satellite-derived estimates of annual average PM 2.5 was the main exposure variable, which was linked to children's area of residence. Anaemia was defined according to standard World Health Organization guidelines (Hb < 11 g/dL). The association of PM 2.5 with Hb levels and anaemia prevalence was examined using multivariable linear and logistic regression models, respectively. We examined whether the effects of ambient PM 2.5 were modified by a child's sex and age, household wealth index, and urban/rural place of residence. Models were adjusted for relevant covariates, including other outdoor pollutants and household cooking fuel. The study included 154,443 children, of which 89,904 (58.2%) were anaemic. The country-level prevalence of anaemia ranged from 15.8% to 87.9%. Mean PM 2.5 exposure was 33.0 (±21.6) μg/m 3 . The adjusted model showed that a 10 μg/m 3 increase in annual PM 2.5 concentration was associated with greater odds of anaemia (OR = 1.098 95% CI: 1.087, 1.109). The same increase in PM 2.5 was associated with a decrease in average Hb levels of 0.075 g/dL (95% CI: 0.081, 0.068). There was evidence of effect modification by household wealth index and place of residence, with greater adverse effects in children from lower wealth quintiles and children in rural areas. Exposure to annual PM 2.5 was cross-sectionally associated with decreased blood Hb levels, and greater risk of anaemia, in children aged <5 years living in 36 LMICs., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

High-resolution simulations are essential to resolve fine-scale air pollution patterns due to localized emissions, nonlinear chemical feedbacks, and complex meteorology. However, high-resolution global simulations of air quality remain rare, especially of the Global South. Here, we exploit recent developments to the GEOS-Chem model in its high-performance implementation to conduct 1-year simulations in 2015 at cubed-sphere C360 (∼25 km) and C48 (∼200 km) resolutions. We investigate the resolution dependence of population exposure and sectoral contributions to surface fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ), focusing on understudied regions. Our results indicate pronounced spatial heterogeneity at high resolution (C360) with large global population-weighted normalized root-mean-square difference (PW-NRMSD) across resolutions for primary (62-126%) and secondary (26-35%) PM 2.5 species. Developing regions are more sensitive to spatial resolution resulting from sparse pollution hotspots, with PW-NRMSD for PM 2.5 in the Global South (33%), 1.3 times higher than globally. The PW-NRMSD for PM 2.5 for discrete southern cities (49%) is substantially higher than for more clustered northern cities (28%). We find that the relative order of sectoral contributions to population exposure depends on simulation resolution, with implications for location-specific air pollution control strategies.

Background: Numerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter ≤ 2.5 μ m in aerodynamic diameter ( PM 2.5 )] on mortality even at relatively low levels. However, methodological challenges remain to consider potential regulatory intervention's complexity and provide actionable evidence on the predicted benefits of interventions. We propose the parametric g-computation as an alternative analytical approach to such challenges., Method: We applied the parametric g-computation to estimate the cumulative risks of nonaccidental death under different hypothetical intervention strategies targeting long-term exposure to PM 2.5 in the Canadian Community Health Survey cohort from 2005 to 2015. On both relative and absolute scales, we explored the benefits of hypothetical intervention strategies compared with the natural course that a ) set the simulated exposure value at each follow-up year to a threshold value if exposure was above the threshold ( 8.8   μ g / m 3 , 7.04   μ g / m 3 , 5   μ g / m 3 , and 4   μ g / m 3 ), and b ) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average PM 2.5 concentration with 1-y lag at the postal code of respondents' annual mailing addresses as their long-term exposure to PM 2.5 . We considered baseline and time-varying confounders, including demographics, behavior characteristics, income level, and neighborhood socioeconomic status. We also included the R syntax for reproducibility and replication., Results: All hypothetical intervention strategies explored led to lower 11-y cumulative mortality risks than the estimated value under the natural course without intervention, with the smallest reduction of 0.20 per 1,000 participants (95% CI: 0.06, 0.34) under the threshold of 8.8   μ g / m 3 , and the largest reduction of 3.40 per 1,000 participants (95% CI: - 0.23 , 7.03) under the relative reduction of 10% per interval. The reductions in cumulative risk, or numbers of deaths that would have been prevented if the intervention was employed instead of maintaining the status quo, increased over time but flattened toward the end of the follow-up period. Estimates among those ≥ 65 years of age were greater with a similar pattern. Our estimates were robust to different model specifications., Discussion: We found evidence that any intervention further reducing the long-term exposure to PM 2.5 would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient PM 2.5 . The parametric g-computation used in this study provides flexibilities in simulating real-world interventions, accommodates time-varying exposure and confounders, and estimates adjusted survival curves with clearer interpretation and more information than a single hazard ratio, making it a valuable analytical alternative in air pollution epidemiological research. https://doi.org/10.1289/EHP11095.

Exposure to ambient air pollution may affect cognitive functioning and development in children. Unfortunately, there is little evidence available for low- and middle-income countries (LMICs), where air pollution levels are highest. We analysed the association between exposure to ambient fine particulate matter (≤2.5 μm [PM 2.5 ]) and cognitive development indicators in a cross-sectional analysis of children (aged 3-4 years) in 12 LMICs. We linked Demographic and Health Survey data, conducted between 2011 and 2018, with global estimates of PM 2.5 mass concentrations to examine annual average exposure to PM 2.5 and cognitive development (literacy-numeracy and learning domains) in children. Cognitive development was assessed using the United Nations Children's Fund's early child development indicators administered to each child's mother. We used multivariable logistic regression models, adjusted for individual- and area-level covariates, and multi-pollutant models (including nitrogen dioxide and surface-level ozone). We assessed if sex and urban/rural status modified the association of PM 2.5 with the outcome. We included 57,647 children, of whom, 9613 (13.3%) had indicators of cognitive delay. In the adjusted model, a 5 μg/m 3 increase in annual all composition PM 2.5 was associated with greater odds of cognitive delay (OR = 1.17; 95% CI: 1.13, 1.22). A 5 μg/m 3 increase in anthropogenic PM 2.5 was also associated with greater odds of cognitive delay (OR = 1.05; 95% CI: 1.00, 1.10). These results were robust to several sensitivity analyses, including multi-pollutant models. Interaction terms showed that urban-dwelling children had greater odds of cognitive delay than rural-dwelling children, while there was no significant difference by sex. Our findings suggest that annual average exposure to PM 2.5 in young children was associated with adverse effects on cognitive development, which may have long-term consequences for educational attainment and health., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Studies examining long-term effects of ambient air pollution exposure, measured as annual averages, on pulmonary tuberculosis (TB) incidence are scarce, particularly in endemic, rural settings. We performed a small-area study in Ningxia Hui Autonomous Region (NHAR), a high TB-burden area in rural China, using township-level (n = 358 non-overlapping townships) annual TB notification data (2005-2017). We aimed to determine if annual average concentrations of ambient air pollution (particulate matter <2·5 μm [PM 2·5 ], nitrogen dioxide [NO 2 ] ozone [O 3 ]) were associated with TB notification rates (as a proxy for incidence). Air pollution effects on TB notification rates at township-level were estimated as incidence rate ratios (IRR), fitted using a generalised estimating equation (GEE) adjusted for covariates (age, sex, occupation, education, ethnicity, remoteness [urban or rural], household crowding and solid fuel use). A total of 38,942 TB notifications were reported in NHAR between 2005 and 2017. The mean annual TB notification rate was 67 (standard deviation [SD]; 7) per 100,000 people. Median concentrations of PM 2·5 , NO 2 , and O 3 were 42 μg/m 3 (interquartile range [IQR]; 38-48 μg/m 3 ), 15 ppb (IQR; 12-16 ppb), and 56 ppb (IQR; 56-57 ppb), respectively. In single pollutant models, adjusted for covariates, an interquartile range (IQR) increase (10 μg/m 3 ) in PM 2·5 was significantly associated with higher TB notification rates (IRR: 1∙35; 95% CI: 1·25-1·48). Comparable effects on notifications of TB were observed for increases in NO 2 exposure (IRR: 1·20 per IQR (4 ppb) increase; 95% CI: 1·08-1·31). Ground-level ozone was not associated with TB notification rate in any models. The observed effects were consistent over time, in multi-pollutant models, and appeared robust to additional adjustment for indicators of household crowding, solid fuel use and remoteness. More rigorous study designs are needed to understand if improving air quality has population-level benefits on TB disease incidence in endemic settings., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

This retrospective cohort study examined associations of autism spectrum disorder (ASD) with prenatal exposure to major fine particulate matter (PM 2.5 ) components estimated using two independent exposure models. The cohort included 318 750 mother-child pairs with singleton deliveries in Kaiser Permanente Southern California hospitals from 2001 to 2014 and followed until age five. ASD cases during follow-up ( N = 4559) were identified by ICD codes. Prenatal exposures to PM 2.5 , elemental (EC) and black carbon (BC), organic matter (OM), nitrate (NO 3 - ), and sulfate (SO 4 2- ) were constructed using (i) a source-oriented chemical transport model and (ii) a hybrid model. Exposures were assigned to each maternal address during the entire pregnancy, first, second, and third trimester. In single-pollutant models, ASD was associated with pregnancy-average PM 2.5 , EC/BC, OM, and SO 4 2- exposures from both exposure models, after adjustment for covariates. The direction of effect estimates was consistent for EC/BC and OM and least consistent for NO 3 - . EC/BC, OM, and SO 4 2- were generally robust to adjustment for other components and for PM 2.5 . EC/BC and OM effect estimates were generally larger and more consistent in the first and second trimester and SO 4 2- in the third trimester. Future PM 2.5 composition health effect studies might consider using multiple exposure models and a weight of evidence approach when interpreting effect estimates.

Growing evidence suggests that fine particulate matter (PM 2.5 ) 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 integrating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM 2.5 major chemical composition, including black carbon (BC), organic matter (OM), nitrate (NO 3 - ), sulfate (SO 4 2- ), ammonium (NH 4 + ), and soil dust (DUST). To investigate the impact of long-term exposure to PM 2.5 constituents 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 PM 2.5 and its major constituents. An interquartile range increase in PM 2.5 mass was associated with a 6 to 7% increase in dementia incidence and a 9% increase in AD incidence. For different PM 2.5 constituents, associations remained significant for BC, OM, SO 4 2- , and NH 4 + for both end points (even after adjustments of other constituents), among which BC and SO 4 2- 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 PM 2.5 is significantly associated with higher rates of incident dementia and AD and that SO 4 2- , BC, and OM related to traffic and fossil fuel combustion might drive the observed associations.

Background Long-term exposure to outdoor fine particulate matter (PM 2.5 ) is the leading environmental risk factor for premature mortality worldwide. Characterizing important pathways through which PM 2.5 increases individuals' mortality risk can clarify the PM 2.5 -mortality relationship and identify possible points of interventions. Recent evidence has linked PM 2.5 to the onset of diabetes and cardiovascular disease, but to what extent these associations contribute to the effect of PM 2.5 on mortality remains poorly understood. Methods and Results We conducted a population-based cohort study to investigate how the effect of PM 2.5 on nonaccidental mortality is mediated by its impacts on incident diabetes, acute myocardial infarction, and stroke. Our study population comprised ≈200 000 individuals aged 20 to 90 years who participated in population-based health surveys in Ontario, Canada, from 1996 to 2014. Follow-up extended until December 2017. Using causal mediation analyses with Aalen additive hazards models, we decomposed the total effect of PM 2.5 on mortality into a direct effect and several path-specific indirect effects mediated by diabetes, each cardiovascular event, or both combined. A series of sensitivity analyses were also conducted. After adjusting for various individual- and neighborhood-level covariates, we estimated that for every 1000 adults, each 10 μg/m 3 increase in PM 2.5 was associated with ≈2 incident cases of diabetes, ≈1 major cardiovascular event (acute myocardial infarction and stroke combined), and ≈2 deaths annually. Among PM 2.5 -related deaths, 31.7% (95% CI, 17.2%-53.2%) were attributable to diabetes and major cardiovascular events in relation to PM 2.5 . Specifically, 4.5% were explained by PM 2.5 -induced diabetes, 22.8% by PM 2.5 -induced major cardiovascular events, and 4.5% through their interaction. Conclusions This study suggests that a significant portion of the estimated effect of long-term exposure to PM 2.5 on deaths can be attributed to its effect on diabetes and cardiovascular diseases, highlighting the significance of PM 2.5 on deteriorating cardiovascular health. Our findings should raise awareness among professionals that improving metabolic and cardiovascular health may reduce mortality burden in areas with higher exposure to air pollution.

Background: Preharvest burning of sugarcane is a common agricultural practice in Florida, which produces fine particulate matter [particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 )] that is associated with higher mortality., Objectives: We estimated premature mortality associated with exposure to PM 2.5 from sugarcane burning in people age 25 y and above for 20 counties in South Florida., Methods: We combined information from an atmospheric dispersion model, satellites, and surface measurements to quantify PM 2.5 concentrations in South Florida and the fraction of PM 2.5 from sugarcane fires. From these concentrations, estimated mortalities attributable to PM 2.5 from sugarcane fires were calculated by census tract using health impact functions derived from literature for six causes of death linked to PM 2.5 . Confidence intervals (CI) are provided based on Monte Carlo simulations that propagate uncertainty in the emissions, dispersion model, health impact functions, and demographic data., Results: Sugarcane fires emitted an amount of primary PM 2.5 similar to that of motor vehicles in Florida. PM 2.5 from sugarcane fires is estimated to contribute to mortality rates within the Florida Sugarcane Growing Region (SGR) by 0.4 death per 100,000 people per year (95% CI: 0.3, 1.6 per 100,000). These estimates imply 2.5 deaths per year across South Florida were associated with PM 2.5 from sugarcane fires (95% CI: 1.2, 6.1), with 0.16 in the SGR (95% CI: 0.09, 0.6) and 0.72 in Palm Beach County (95% CI: 0.17, 2.2)., Discussion: PM 2.5 from sugarcane fires was estimated to contribute to mortality risk across South Florida, particularly in the SGR. This is consistent with prior studies that documented impacts of sugarcane fire on air quality but did not quantify mortality. Additional health impacts of sugarcane fires, which were not quantified here, include exacerbating nonfatal health conditions such as asthma and cardiovascular problems. Harvesting sugarcane without field burning would likely reduce PM 2.5 and health burdens in this region. https://doi.org/10.1289/EHP9957.

Background: The tremendous global health burden related to COVID-19 means that identifying determinants of COVID-19 severity is important for prevention and intervention. We aimed to explore long-term exposure to ambient air pollution as a potential contributor to COVID-19 severity, given its known impact on the respiratory system., Methods: We used a cohort of all people with confirmed SARS-CoV-2 infection, aged 20 years and older and not residing in a long-term care facility in Ontario, Canada, during 2020. We evaluated the association between long-term exposure to fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ) and ground-level ozone (O 3 ), and risk of COVID-19-related hospital admission, intensive care unit (ICU) admission and death. We ascertained individuals' long-term exposures to each air pollutant based on their residence from 2015 to 2019. We used logistic regression and adjusted for confounders and selection bias using various individual and contextual covariates obtained through data linkage., Results: Among the 151 105 people with confirmed SARS-CoV-2 infection in Ontario in 2020, we observed 8630 hospital admissions, 1912 ICU admissions and 2137 deaths related to COVID-19. For each interquartile range increase in exposure to PM 2.5 (1.70 μg/m 3 ), we estimated odds ratios of 1.06 (95% confidence interval [CI] 1.01-1.12), 1.09 (95% CI 0.98-1.21) and 1.00 (95% CI 0.90-1.11) for hospital admission, ICU admission and death, respectively. Estimates were smaller for NO 2 . We also estimated odds ratios of 1.15 (95% CI 1.06-1.23), 1.30 (95% CI 1.12-1.50) and 1.18 (95% CI 1.02-1.36) per interquartile range increase of 5.14 ppb in O 3 for hospital admission, ICU admission and death, respectively., Interpretation: Chronic exposure to air pollution may contribute to severe outcomes after SARS-CoV-2 infection, particularly exposure to O 3 ., Competing Interests: Competing interests: Jeff Kwong is supported by a Clinician Scientist Award from the Department of Family and Community Medicine, University of Toronto. Chen Chen reports receiving salary support by the funding of this project, from Health Canada. Megan Kirby-Mcgregor reports receiving doctoral student funding from Health Canada, paid through McGill University. Jay Kaufman reports receiving payments from Health Canada (paid to institution) for student salaries and other research expenses associated with this work. Hong Chen reports receiving support for the present manuscript from Health Canada. No other competing interests were declared., (© 2022 CMA Impact Inc. or its licensors.)

Objectives. To compare fine particulate matter (PM 2.5 ) concentrations in American Indian (AI)-populated with those in non-AI-populated counties over time (2000-2018) in the contiguous United States. Methods. We used a multicriteria approach to classify counties as AI- or non--AI-populated. We ran linear mixed effects models to estimate the difference in countywide annual PM 2.5 concentrations from well-validated prediction models and monitoring sites (modeled and measured PM 2.5 , respectively) in AI- versus non-AI-populated counties. Results. On average, adjusted modeled PM 2.5 concentrations in AI-populated counties were 0.38 micrograms per cubic meter (95% confidence interval [CI] = 0.23, 0.54) lower than in non-AI-populated counties. However, this difference was not constant over time: in 2000, modeled concentrations in AI-populated counties were 1.46 micrograms per cubic meter (95% CI = 1.25, 1.68) lower, and by 2018, they were 0.66 micrograms per cubic meter (95% CI = 0.45, 0.87) higher. Over the study period, adjusted modeled PM 2.5 mean concentrations decreased by 2.13 micrograms per cubic meter in AI-populated counties versus 4.26 micrograms per cubic meter in non-AI-populated counties. Results were similar for measured PM 2.5 . Conclusions. This study highlights disparities in PM 2.5 trends between AI- and non-AI-populated counties over time, underscoring the need to strengthen air pollution regulations and prevention implementation in tribal territories and areas where AI populations live. ( Am J Public Health . 2022;112(4): 615-623. https://doi.org/10.2105/AJPH.2021.306650).

Background: Few studies have evaluated long-term cardiovascular effects of fine particulate matter (PM 2.5 ) and its constituents in countries with high air pollution levels. We aimed to investigate the associations of long-term exposure to PM 2.5 and constituents with cardiovascular mortality in China., Methods: We conducted a prospective cohort study of 90,672 adults ≥ 18 years from 2010 to 2017 in 161 districts/counties across China. The residential annual-average exposure to PM 2.5 and 6 main components from 2011 to 2017 were estimated by satellite-based and chemical transport models. Associations of PM 2.5 and constituents with cardiovascular mortality were analyzed by competing-risk Cox proportional hazards regression., Results: The average PM 2.5 exposure throughout the whole period was 46 ± 22 μg/m 3 . The hazard ratios of mortality (95% confidence intervals) per 10 μg/m 3 increase in PM 2.5 concentrations were 1.02 (1.00, 1.05) for overall cardiovascular disease, 1.05 (1.01, 1.09) for ischemic heart disease, 1.03 (1.00, 1.06) for overall stroke, 0.99 (0.94, 1.04) for hemorrhagic stroke, and 1.11 (1.04, 1.19) for ischemic stroke. PM 2.5 constituents from fossil fuel combustion (i.e., black carbon, organic matter, nitrate, ammonium, and sulfate) showed larger hazard ratios than PM 2.5 total mass, while soil dust showed no risks., Conclusions: This nationwide cohort study demonstrated associations of long-term exposure to PM 2.5 and its constituents with increased risks of cardiovascular mortality in the general population of China. Our study highlighted the importance of PM 2.5 constituents from fossil fuel combustion in the long-term cardiovascular effects of PM 2.5 in China., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

We used a large national cohort in Canada to assess the incidence of acute myocardial infarction (AMI) and stroke hospitalizations in association with long-term exposure to fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ). The study population comprised 2.7 million respondents from the 2006 Canadian Census Health and Environment Cohort (CanCHEC), followed for incident hospitalizations of AMI or stroke between 2006 and 2016. We estimated 10-year moving average estimates of PM 2.5 , NO 2 , and O 3 , annually. We used Cox proportional hazards models to examine the associations adjusting for various covariates. For AMI, each interquartile range (IQR) increase in exposure was found to be associated with a hazard ratio of 1.026 (95% CI: 1.007-1.046) for PM 2.5 , 1.025 (95% CI: 1.001-1.050) for NO 2 , and 1.062 (95% CI: 1.041-1.084) for O 3 , respectively. Similarly, for stroke, an IQR increase in exposure was associated with a hazard ratio of 1.078 (95% CI: 1.052-1.105) for PM 2.5 , 0.995 (95% CI: 0.965-1.030) for NO 2 , and 1.055 (95% CI: 1.028-1.082) for O 3 , respectively. We found consistent evidence of positive associations between long-term exposures to PM 2.5 , and O 3 , and to a lesser degree NO 2 , with incident AMI and stroke hospitalizations., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Growing evidence has linked fine particulate matter (PM 2.5 ) exposure to elevated blood pressure, but the effects of PM 2.5 components are unclear, particularly in children and adolescents. Based on a cross-sectional investigation in China, we analyzed the associations between long-term exposure to PM 2.5 and its major components with elevated blood pressure in children and adolescents. A representative sample (N = 37,610) of children and adolescents with age 7-18 years was collected in seven Chinese provinces. Exposures to PM 2.5 and five of its major components, including black carbon (BC), organic matter (OM), inorganic nitrate (NO 3 - ), sulfate (SO 4 2- ), and soil particles (SOIL), were estimated using satellite-based spatiotemporal models. The associations between long-term exposures to PM 2.5 and its components and diastolic blood pressure (DBP), systolic blood pressure (SBP), and hypertension were investigated using mixed-effects logistic and linear regression models. Within the populations, 11.5 % were classified as hypertension. After adjusting for a variety of covariates, per interquartile range (IQR) increment in PM 2.5 mass and BC levels were significantly associated with a higher hypertension prevalence with odds ratios (ORs) of 1.56 (95% confidence interval (CI): 1.08, 2.25) for PM 2.5 and 1.19 (95% CI: 1.04, 1.35) for BC. Long-term exposures to PM 2.5 and BC have also been associated with elevated SBP and DBP. Additionally, OM and NO 3 - were significantly associated with increased SBP, while SOIL was significantly associated with increased DBP. In the subgroup analysis, the associations between long-term exposures to BC and blood pressure vary significantly by urbanicity of residential area and diet habits. Our study suggests that long-term exposure to PM 2.5 mass and specific PM 2.5 components, especially for BC, are significantly associated with elevated blood pressure and a higher hypertension prevalence in Chinese children and adolescents., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Fine particulate matter (PM 2.5 ) exposure has been reported to adversely affect birth outcomes, but the evidence is limited, particularly in low- and middle-income countries (LMICs). We assessed the associations between maternal PM 2.5 exposure and low birth weight (LBW) and preterm birth (PTB) in Africa., Methods: We used standard Demographic and Health Surveys (DHS) data (2005-2015) from 15 countries in Africa to conduct a cross-sectional study. The study population was composed of 131,594 births with detailed information on maternal and household variables. LBW was defined as a birth weight of < 2500 g after 37 weeks, and PTB was defined as live birth occurring before 37 weeks of gestation. Average exposure to PM 2.5 during pregnancy was estimated using satellite-based models. Multivariable logistic regression models were constructed, and analyses of data by region (Western, Eastern, Central, and Southern Africa) and data stratified by potential effect modifiers were conducted., Results: A total of 13,214 (10%) LBW and 4,377 (3.3%) PTB cases were identified. An interquartile range (IQR) (33.9 μg/m 3 ) increase in PM 2.5 during pregnancy was associated with increased odds of LBW and PTB, with odds ratios (ORs) of 1.28 (95% CI: 1.23, 1.34) and 1.08 (95% CI: 1.01, 1.16), respectively. Region-specific analyses revealed significant associations between PM 2.5 and LBW in all regions, and significant associations between PM 2.5 and PTB in Western and Southern Africa. Subgroup analyses revealed that the association between PM 2.5 and LBW was present in all subgroups, and stronger associations were observed in female infants, while the association between PM 2.5 and PTB was larger in subgroups of older individuals living in urban areas., Conclusion: This multicountry study in Africa demonstrated significant associations between maternal exposure to PM 2.5 and higher odds of LBW and PTB. Our findings may facilitate air quality control strategies that address adverse birth outcomes in LMICs., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: With much of the world's population residing in urban areas, an understanding of air pollution exposures at the city level can inform mitigation approaches. Previous studies of global urban air pollution have not considered trends in air pollutant concentrations nor corresponding attributable mortality burdens. We aimed to estimate trends in fine particulate matter (PM 2·5 ) concentrations and associated mortality for cities globally., Methods: We use high-resolution annual average PM 2·5 concentrations, epidemiologically derived concentration response functions, and country-level baseline disease rates to estimate population-weighted PM 2·5 concentrations and attributable cause-specific mortality in 13 160 urban centres between the years 2000 and 2019., Findings: Although regional averages of urban PM 2·5 concentrations decreased between the years 2000 and 2019, we found considerable heterogeneity in trends of PM 2·5 concentrations between urban areas. Approximately 86% (2·5 billion inhabitants) of urban inhabitants lived in urban areas that exceeded WHO's 2005 guideline annual average PM 2·5 (10 μg/m 3 ), resulting in an excess of 1·8 million (95% CI 1·34 million-2·3 million) deaths in 2019. Regional averages of PM 2·5 -attributable deaths increased in all regions except for Europe and the Americas, driven by changes in population numbers, age structures, and disease rates. In some cities, PM 2·5 -attributable mortality increased despite decreases in PM 2·5 concentrations, resulting from shifting age distributions and rates of non-communicable disease., Interpretation: Our study showed that, between the years 2000 and 2019, most of the world's urban population lived in areas with unhealthy levels of PM 2·5 , leading to substantial contributions to non-communicable disease burdens. Our results highlight that avoiding the large public health burden from urban PM 2·5 will require strategies that reduce exposure through emissions mitigation, as well as strategies that reduce vulnerability to PM 2·5 by improving overall public health., Funding: NASA, Wellcome Trust., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Evidence from developed countries suggests that fine particulate matter (≤2.5 µm [PM 2.5 ]) contributes to childhood respiratory morbidity and mortality. However, few analyses have focused on resource-limited settings, where much of this burden occurs. We aimed to investigate the cross-sectional associations between annual average exposure to ambient PM 2.5 and acute respiratory infection (ARI) in children aged <5 years living in low- and middle-income countries (LMICs)., Methods: We combined Demographic and Health Survey (DHS) data from 35 countries with gridded global estimates of annual PM 2.5 mass concentrations. We analysed the association between PM 2.5 and maternal-reported ARI in the two weeks preceding the survey among children aged <5 years living in 35 LMICs. We used multivariable logistic regression models that adjusted for child, maternal, household and cluster-level factors. We also fitted multi-pollutant models (adjusted for nitrogen dioxide [NO 2 ] and surface-level ozone [O 3 ]), among other sensitivity analyses. We assessed whether the associations between PM 2.5 and ARI were modified by sex, age and place of residence., Results: The analysis comprised 573,950 children, among whom the prevalence of ARI was 22,506 (3.92%). The mean (±SD) estimated annual concentration of PM 2.5 to which children were exposed was 48.2 (±31.0) µg/m 3 . The 5th and 95th percentiles of PM 2.5 were 9.8 µg/m 3 and 110.9 µg/m 3 , respectively. A 10 µg/m 3 increase in PM 2.5 was associated with greater odds of having an ARI (OR: 1.06; 95% CI: 1.05-1.07). The association between PM 2.5 and ARI was robust to adjustment for NO 2 and O 3 . We observed evidence of effect modification by sex, age and place of residence, suggesting greater effects of PM 2.5 on ARI in boys, in younger children, and in children living in rural areas., Conclusions: Annual average ambient PM 2.5 , as an indicator for long-term exposure, was associated with greater odds of maternal-reported ARI in children aged <5 years living in 35 LMICs. Longitudinal studies in LMICs are required to corroborate our cross-sectional findings, to further elucidate the extent to which lowering PM 2.5 may have a role in the global challenge of reducing ARI-related morbidity and mortality in children., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Long-term exposure to fine particulate matter (PM 2.5 ) mass has been associated with adverse health effects. However, the health effects of PM 2.5 components have been less studied. There is a pressing need to better understand the relative contribution of components of PM 2.5 , which can lay the scientific basis for designing effective policies and targeted interventions., Methods: We conducted a population-based cohort study, comprising all Medicare enrollees aged 65 or older in the southeastern United States from 2000 to 2016, to explore the associations between long-term exposure to PM 2.5 major components and all-cause mortality among the elderly. Based on well-validated prediction models, we estimated ZIP code-level annual mean concentrations for five major PM 2.5 components, including black carbon (BC), nitrate (NIT), organic matter (OM), sulfate (SO 4 ), and soil particles. Data were analyzed using Cox proportional hazards models, adjusting for potential confounders., Results: The cohort comprised 13,590,387 Medicare enrollees and a total of 107,191,652 person-years. In single-component models, all five major PM 2.5 components were significantly associated with elevated all-cause mortality. The hazard ratios (HR) per interquartile range (IQR) increase in exposure were 1.027 (95% CI: 1.025-1.030), 1.012 (95% CI: 1.010-1.013), 1.018 (95% CI: 1.017-1.020), 1.021 (95% CI: 1.017-1.024), and 1.004 (95% CI: 1.003-1.006) for BC, NIT, OM, SO 4 , and soil particles, respectively. While the effect estimate of soil component was statistically significant, it is much smaller than those of combustion-related components., Conclusion: Our study provides epidemiological evidence that long-term exposure to major PM 2.5 components is significantly associated with elevated mortality., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Maternal prenatal exposure to air pollution has been associated with adverse birth outcomes. However, previous studies focused on a priori time intervals such as trimesters reported inconsistent associations., Objectives: We investigated time-varying vulnerability of birth weight to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) using flexible time intervals., Methods: We analyzed 1,300 live, full-term births from Maternal-Infant Research on Environmental Chemicals, a Canadian prospective pregnancy cohort spanning 10 cities (2008-2011). Daily PM2.5 and NO2 concentrations were estimated from ground-level monitoring, satellite models, and land-use regression, and assigned to participants from pre-pregnancy through delivery. We developed a flexible two-stage modeling method-using a Bayesian Metropolis-Hastings algorithm and empirical density threshold-to identify time-dependent vulnerability to air pollution without specifying exposure periods a priori. This approach identified critical windows with varying lengths (2-363 days) and critical windows that fell within, or straddled, predetermined time periods (i.e., trimesters). We adjusted the models for detailed infant and maternal covariates., Results: Critical windows associated with reduced birth weight were identified during mid- to late-pregnancy for both PM2.5 and NO2: -6 g (95% credible interval: -11, -1 g) and -5 g (-10, -0.1 g) per µg/m3 PM2.5 during gestational days 91-139 and 249-272, respectively; and -3 g (-5, -1 g) per ppb NO2 during days 55-145., Discussion: We used a novel, flexible selection method to identify critical windows when maternal exposures to air pollution were associated with decrements in birth weight. Our results suggest that air pollution impacts on fetal development may not be adequately captured by trimester-based analyses., Competing Interests: The authors report no conflicts of interest., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

The COVID-19 global pandemic and associated government lockdowns dramatically altered human activity, providing a window into how changes in individual behavior, enacted en masse, impact atmospheric composition. The resulting reductions in anthropogenic activity represent an unprecedented event that yields a glimpse into a future where emissions to the atmosphere are reduced. Furthermore, the abrupt reduction in emissions during the lockdown periods led to clearly observable changes in atmospheric composition, which provide direct insight into feedbacks between the Earth system and human activity. While air pollutants and greenhouse gases share many common anthropogenic sources, there is a sharp difference in the response of their atmospheric concentrations to COVID-19 emissions changes, due in large part to their different lifetimes. Here, we discuss several key takeaways from modeling and observational studies. First, despite dramatic declines in mobility and associated vehicular emissions, the atmospheric growth rates of greenhouse gases were not slowed, in part due to decreased ocean uptake of CO 2 and a likely increase in CH 4 lifetime from reduced NO x emissions. Second, the response of O 3 to decreased NO x emissions showed significant spatial and temporal variability, due to differing chemical regimes around the world. Finally, the overall response of atmospheric composition to emissions changes is heavily modulated by factors including carbon-cycle feedbacks to CH 4 and CO 2 , background pollutant levels, the timing and location of emissions changes, and climate feedbacks on air quality, such as wildfires and the ozone climate penalty., Competing Interests: The authors declare no competing interest., (Copyright © 2021 the Author(s). Published by PNAS.)

Annual global satellite-based estimates of fine particulate matter (PM 2.5 ) are widely relied upon for air-quality assessment. Here, we develop and apply a methodology for monthly estimates and uncertainties during the period 1998-2019, which combines satellite retrievals of aerosol optical depth, chemical transport modeling, and ground-based measurements to allow for the characterization of seasonal and episodic exposure, as well as aid air-quality management. Many densely populated regions have their highest PM 2.5 concentrations in winter, exceeding summertime concentrations by factors of 1.5-3.0 over Eastern Europe, Western Europe, South Asia, and East Asia. In South Asia, in January, regional population-weighted monthly mean PM 2.5 concentrations exceed 90 μg/m 3 , with local concentrations of approximately 200 μg/m 3 for parts of the Indo-Gangetic Plain. In East Asia, monthly mean PM 2.5 concentrations have decreased over the period 2010-2019 by 1.6-2.6 μg/m 3 /year, with decreases beginning 2-3 years earlier in summer than in winter. We find evidence that global-monitored locations tend to be in cleaner regions than global mean PM 2.5 exposure, with large measurement gaps in the Global South. Uncertainty estimates exhibit regional consistency with observed differences between ground-based and satellite-derived PM 2.5 . The evaluation of uncertainty for agglomerated values indicates that hybrid PM 2.5 estimates provide precise regional-scale representation, with residual uncertainty inversely proportional to the sample size.

The associations of long-term exposure to various constituents of fine particulate matter (≤2.5 μm in aerodynamic diameter, PM 2.5 ) air pollution with lung function were not clearly elucidated in developing countries. The aim was to evaluate the associations of long-term exposure to main constituents of PM 2.5 with lung function in China. This is a nationwide, cross-sectional analysis among 50,991 study participants from the China Pulmonary Health study. Multivariable linear regression models were used to obtain differences of forced expiratory volume in 1 s (FEV 1 ), forced vital capacity (FVC), FEV 1 /FVC, peak expiratory flow (PEF), and forced expiratory flow at 25-75% of exhaled FVC (FEF 25-75% ) associated with an interquartile range (IQR) change of PM 2.5 or its constituents. Residential annual PM 2.5 levels varied from 26 μg/m 3 to 92 μg/m 3 (average: 53 μg/m 3 ). An IQR increase of PM 2.5 concentrations was associated with lower FEV 1 (19.82 mL, 95% CI: 11.30-28.33), FVC (17.45 mL, 95% CI: 7.16-27.74), PEF (86.64 mL/s, 95% CI: 59.77-113.52), and FEF 25-75% (31.93 mL/s, 95% CI: 16.64-47.22). Black carbon, organic matter, ammonium, sulfate, and nitrate were negatively associated with most lung function indicators, with organic matter and nitrate showing consistently larger magnitude of associations than PM 2.5 mass. This large-scale study provides first-hand epidemiological evidence that long-term exposure to ambient PM 2.5 and some constituents, especially organic matter and nitrate, were associated with lower large- and small- airway function., (Copyright © 2021. Published by Elsevier Ltd.)

Background: Few studies have investigated the association between exposure to fine particulate matter (PM 2.5 ) and infant mortality in developing countries, especially for the health effects of specific PM 2.5 constituents., Objective: We aimed to examine the association of long-term exposure to specific PM 2.5 constituents with infant mortality in 15 African countries from 2005 to 2015., Methods: Based on the Demographic and Health Surveys (DHS) dataset, we included birth history records from 15 countries in Africa and conducted a multicountry cross-sectional study to examine the associations between specific PM 2.5 constituents and infant mortality. We estimated annual residential exposure using satellite-derived PM 2.5 for mass and a chemical transport model (GEOS-Chem) for its six constituents, including organic matter (OM), black carbon (BC), sulfate (SO 4 2- ), nitrate (NO 3 - ), ammonium (NH 4 + ), and soil dust (DUST). Multivariable logistic regression analysis was employed by fitting single-constituent models, the constituent-PM 2.5 models, and the constituent-residual models. We also conducted stratified analyses by potential effect modifiers and examined the specific associations for each country., Results: We found positive and significant associations between PM 2.5 total mass and most of its constituents with infant mortality. In the single-constituent model, for an IQR increase in pollutant concentrations, the odds ratio (OR) of infant mortality was 1.03 (95 %CI; 1.01, 1.06) for PM 2.5 total mass, and was 1.04 (95 %CI: 1.02, 1.06), 1.04 (95 %CI: 1.02, 1.05), 1.02 (95 %CI: 1.00, 1.03), 1.04 (1.01, 1.06) for BC, OM, SO 4 2- , and DUST, respectively. The associations of BC, OM, and SO 4 2- remained significant in the other two models. We observed larger estimates in subgroups with older maternal age, living in urban areas, using unclean cooking energy, and with access to piped water. The associations varied among countries, and by different constituents., Conclusions: The carbonaceous fractions and sulfate play a major important role among PM 2.5 constituents on infant mortality. Our findings have certain policy implications for implementing effective measures for targeted reduction in specific sources (fossil fuel combustion and biomass burning) of PM 2.5 constituents against the risk of infant mortality., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Objective: To investigate the association between changes in long term residential exposure to ambient fine particulate matter (PM 2.5 ) and premature mortality in Canada., Design: Population based quasi-experimental study., Setting: Canada., Participants: 663 100 respondents to the 1996, 2001, and 2006 Canadian censuses aged 25-89 years who had consistently lived in areas with either high or low PM 2.5 levels over five years preceding census day and moved during the ensuing five years., Interventions: Changes in long term exposure to PM 2.5 arising from residential mobility., Main Outcome Measures: The primary outcome was deaths from natural causes. Secondary outcomes were deaths from any cardiometabolic cause, any respiratory cause, and any cancer cause. All outcomes were obtained from the national vital statistics database., Results: Using a propensity score matching technique with numerous personal, socioeconomic, health, and environment related covariates, each participant who moved to a different PM 2.5 area was matched with up to three participants who moved within the same PM 2.5 area. In the matched groups that moved from high to intermediate or low PM 2.5 areas, residential mobility was associated with a decline in annual PM 2.5 exposure from 10.6 μg/m 3 to 7.4 and 5.0 μg/m 3 , respectively. Conversely, in the matched groups that moved from low to intermediate or high PM 2.5 areas, annual PM 2.5 increased from 4.6 μg/m 3 to 6.7 and 9.2 μg/m 3 . Five years after moving, individuals who experienced a reduction in exposure to PM 2.5 from high to intermediate levels showed a 6.8% (95% confidence interval 1.7% to 11.7%) reduction in mortality (2510 deaths in 56 025 v 4925 deaths in 101 960). A greater decline in mortality occurred among those exposed to a larger reduction in PM 2.5 . Increased mortality was found with exposure to PM 2.5 from low to high levels, and to a lesser degree from low to intermediate levels. Furthermore, the decreases in PM 2.5 exposure were most strongly associated with reductions in cardiometabolic deaths, whereas the increases in PM 2.5 exposure were mostly related to respiratory deaths. No strong evidence was found for the changes in PM 2.5 exposure with cancer related deaths., Conclusions: In Canada, decreases in PM 2.5 were associated with lower mortality, whereas increases in PM 2.5 were associated with higher mortality. These results were observed at PM 2.5 levels considerably lower than many other countries, providing support for continuously improving air quality., Competing Interests: Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/disclosure-of-interest/ and declare: support from funded by Health Canada for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work., (© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Few cohort studies explored the associations of long-term exposure to ambient fine particulate matter with an aerodynamic diameter of 2.5 μm or less (PM 2.5 ) and its chemical constituents with mortality risk in rural China. We conducted a 12-year prospective study of 28,793 adults in rural Deqing, China from 2006 to 2018. Annual mean PM 2.5 and its constituents, including black carbon (BC), organic carbon (OC), ammonium (NH 4 + ), nitrate (NO 3 - ), sulfate (SO 4 2- ), and soil dust were measured at participants' addresses at enrollment from a satellite-based exposure predicting model. Cox proportional hazard model was used to estimate hazard ratios (HRs) and 95% confidence intervals (95%CIs) of long-term exposure to PM 2.5 for mortality. A total of 1960 deaths were identified during the follow-up. We found PM 2.5 , BC, OC, NH 4 + , NO 3 - , and SO 4 2- were significantly associated with an increased risk of non-accidental mortality. The HR for non-accidental mortality was 1.17 (95%CI: 1.07, 1.28) for each 10 μg/m 3 increase in PM 2.5 . As for constituents, the strongest association was found for BC (HR = 1.21, 95%CI: 1.11, 1.33), followed by NO 3 - , NH 4 + , SO 4 2- , and OC (HR = 1.14-1.17 per interquartile range). A non-linear relationship was found between PM 2.5 and non-accidental mortality. Similar associations were found for cardio-cerebrovascular and cancer mortality. Associations were stronger among men and ever smokers. Conclusively, we found long-term exposure to ambient PM 2.5 and its chemical constituents (especially BC and NO 3 - ) increased mortality risk. Our results suggested the importance of adopting effective targeted emission control to improve air quality for health protection in rural East China., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Background: Long-term exposure to fine particulate matter (PM 2.5 ) has been associated with neurodegenerative diseases, including disease aggravation in Parkinson's disease (PD), but associations with specific PM 2.5 components have not been evaluated., Objective: To characterize the association between specific PM 2.5 components and PD first hospitalization, a surrogate for disease aggravation., Methods: We obtained data on hospitalizations from the New York Department of Health Statewide Planning and Research Cooperative System (2000-2014) to calculate annual first PD hospitalization counts in New York State per county. We used well-validated prediction models at 1 km 2 resolution to estimate county level population-weighted annual black carbon (BC), organic matter (OM), nitrate, sulfate, sea salt (SS), and soil particle concentrations. We then used a multi-pollutant mixed quasi-Poisson model with county-specific random intercepts to estimate rate ratios (RR) of one-year exposure to each PM 2.5 component and PD disease aggravation. We evaluated potential nonlinear exposure-outcome relationships using penalized splines and accounted for potential confounders., Results: We observed a total of 197,545 PD first hospitalizations in NYS from 2000 to 2014. The annual average count per county was 212 first hospitalizations. The RR (95% confidence interval) for PD aggravation was 1.06 (1.03, 1.10) per one standard deviation (SD) increase in nitrate concentrations and 1.06 (1.04, 1.09) for the corresponding increase in OM concentrations. We also found a nonlinear inverse association between PD aggravation and BC at concentrations above the 96th percentile. We found a marginal association with SS and no association with sulfate or soil exposure., Conclusion: In this study, we detected associations between the PM 2.5 components OM and nitrate with PD disease aggravation. Our findings support that PM 2.5 adverse effects on PD may vary by particle composition., (Copyright © 2021. Published by Elsevier Inc.)

Background: Studies have reported that prenatal exposure to fine particulate matter (PM 2.5 ) might be associated with adverse birth outcomes in offspring. However, evidence with regard to the effects of prenatal exposure to PM 2.5 and, especially, its main chemical constituents on offspring's weight in childhood is limited and inconsistent., Objectives: The present study aimed to examine associations of prenatal exposure to PM 2.5 total mass and its chemical constituents in each trimester with children's weight from birth to 6 years of age using data from Shanghai-Minhang Birth Cohort Study., Methods: A total of 1,084 mother-infant pairs were included with both PM 2.5 exposure data and at least one measurement of weight and height. Weight-for-Length (WLZ), BMI-for-Age (BMIz), and Weight-for-Age (WAZ) z-scores were generated according to the World Health Organization guidelines. Exposure to PM 2.5 total mass and its chemical constituents [organic carbon (OC), black carbon (BC), ammonium (NH 4 + ), nitrate (NO 3 - ), sulfate (SO 4 2- ), and soil dust (SOIL)] during pregnancy was estimated from a satellite based modelling framework. We used multiple informant model to estimate the associations of trimester-specific PM 2.5 total mass and its specific constituents concentrations with WLZ/BMIz and WAZ of offspring at birth and 1, 4, and 6 years of age., Results: In multiple informant model, we observed consistent patterns of associations between exposure to PM 2.5 total mass, OC, BC, NH 4 + , NO 3 - , and SO 4 2- during the 2 nd and 3 rd trimesters and decreased WLZ/BMIz and WAZ at 1, 4, and 6 years of age in boys. We observed associations between prenatal exposure to PM 2.5 total mass, NH 4 + , and NO 3 - during the 1 st and 2 nd trimesters and increased WLZ/BMIz and WAZ in girls at birth. However, there were null associations at 1 and 4 years of age and inverse associations at 6 years of age., Conclusions: Prenatal exposure to PM 2.5 total mass and its main chemical constituents was associated with decreased weight in boys from 1 to 6 years of age, with increased weight at birth and decreased weight at 6 years of age in girls. Our findings suggest that prenatal exposure to PM 2.5 and its chemical constituents may have a lasting effect on offspring's weight in childhood., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Air pollution has been associated with increased mortality. However, updated evidence from cohort studies with detailed information on various risk factors is needed, especially in regions with low air pollution levels. We investigated the associations between long-term exposure to air pollution and mortality in a prospective cohort., Methods: We studied 88,615 participants aged ≥30 years from an ongoing cohort study in Ontario, Canada from 2009 to 2017. Exposure to ambient fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) was estimated at participants' residence. Cox proportional hazard models were used to investigate the associations between air pollution and non-accidental, cardiovascular, and respiratory mortality, adjusted for a wide array of individual-level and contextual covariates. Potential effect modification by socio-demographic and behavioral factors was also examined in exploratory stratified analyses., Results: The fully adjusted hazard ratios (HRs) per 1 µg/m 3 increment in PM 2.5 were 1.037 [95% confidence interval (CI): 1.018, 1.057]¸ 1.083 (95% CI: 1.040, 1.128) and 1.109 (95% CI: 1.035, 1.187) for non-accidental, cardiovascular, and respiratory mortality, respectively. Positive associations were also found for NO 2 ; the corresponding HRs per 1 ppb increment were 1.027 (95% CI: 1.021, 1.034), 1.032 (95% CI: 1.019, 1.046) and 1.044 (95% CI: 1.020, 1.068). We found suggestive evidence of stronger associations in physically active participants, smokers, and those with lower household income., Conclusions: Long-term exposure to PM 2.5 and NO 2 was associated with increased risks for non-accidental, cardiovascular, and respiratory mortality, suggesting potential benefits of further improvement in air quality even in low-exposure environments., (Copyright © 2021. Published by Elsevier Ltd.)

Background: Ecologic analyses suggest that living in areas with higher levels of ambient fine particulate matter air pollution (PM 2.5 ) is associated with higher risk of adverse COVID-19 outcomes. Studies accounting for individual-level health characteristics are lacking., Methods: We leveraged the breadth and depth of the US Department of Veterans Affairs national healthcare databases and built a national cohort of 169,102 COVID-19 positive United States Veterans, enrolled between March 2, 2020 and January 31, 2021, and followed them through February 15, 2021. Annual average 2018 PM 2.5 exposure, at an approximately 1 km 2 resolution, was linked with residential street address at the year prior to COVID-19 positive test. COVID-19 hospitalization was defined as first hospital admission between 7 days prior to, and 15 days after, the first COVID-19 positive date. Adjusted Poisson regression assessed the association of PM 2.5 with risk of hospitalization., Results: There were 25,422 (15.0%) hospitalizations; 5,448 (11.9%), 5,056 (13.0%), 7,159 (16.1%), and 7,759 (19.4%) were in the lowest to highest PM 2.5 quartile, respectively. In models adjusted for State, demographic and behavioral factors, contextual characteristics, and characteristics of the pandemic a one interquartile range increase in PM 2.5 (1.9 µg/m 3 ) was associated with a 10% (95% CI: 8%-12%) increase in risk of hospitalization. The association of PM 2.5 and risk of hospitalization among COVID-19 individuals was present in each wave of the pandemic. Models of non-linear exposure-response suggested increased risk at PM 2.5 concentrations below the national standard 12 µg/m 3 . Formal effect modification analyses suggested higher risk of hospitalization associated with PM 2.5 in Black people compared to White people (p = 0.045), and in those living in socioeconomically disadvantaged neighborhoods (p < 0.001)., Conclusions: Exposure to higher levels of PM 2.5 was associated with increased risk of hospitalization among COVID-19 infected individuals. The risk was evident at PM 2.5 levels below the regulatory standards. The analysis identified those of Black race and those living in disadvantaged neighborhoods as population groups that may be more susceptible to the untoward effect of PM 2.5 on risk of hospitalization in the setting of COVID-19., (Published by Elsevier Ltd.)

Owing to their greater outdoor activity and ongoing lung development, children are particularly vulnerable to the harmful effects of exposure to fine particulate matter (PM 2.5 ) . However, the effects of PM 2.5 components are poorly understood. This study aimed to use a longitudinal birth cohort of children with physician-diagnosed incident asthma to investigate the effect of PM 2.5 components at birth on morbidity measured by health services utilization. Of 1277 Toronto Child Health Evaluation Questionnaire (T-CHEQ) participants, the study population included 362 children diagnosed with asthma who were followed for a mean of 13 years from birth until March 31, 2016, or loss-to-follow-up. Concentrations of PM 2.5 and its components were assigned based on participants' postal codes at birth. Study outcomes included counts of asthma, asthma-related, and all-cause health services use. Poisson regression in single-, two-, and multi-pollutant models was used to estimate rate ratios (RR) per interquartile range (IQR) increase of exposures. Covariates were included in all models to further adjust for potential confounding. The adjusted RR for sulfate (SO 4 ) and all-cause hospitalizations was statistically significant with RR = 2.23 (95% confidence interval [CI]: 1.25-3.96) in a multi-pollutant model with nitrogen dioxide (NO 2 ) and ozone (O 3 ). In multi-pollutant models with oxidants, the adjusted RRs for SO 4 of all-cause hospitalizations and emergency department (ED) visits were also statistically significant with RR = 2.31 (95% CI: 1.32-4.03) and RR = 1.39 (95% CI: 1.02-1.90), respectively. While unadjusted single-pollutant RRs for asthma-specific and asthma-related health services use with the SO 4 component of PM 2.5 were above one, none were statistically significant. This study found significant associations with exposure to SO 4 in PM 2.5 and all-cause acute care, chiefly for hospitalizations, in children with asthma., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)

Fine particulate air pollution (PM 2.5 ) is a leading contributor to the overall global burden of disease. Traditionally, outdoor PM 2.5 has been characterized using mass concentrations which treat all particles as equally harmful. Oxidative potential (OP) (per μg) and oxidative burden (OB) (per m 3 ) are complementary metrics that estimate the ability of PM 2.5 to cause oxidative stress, which is an important mechanism in air pollution health effects. Here, we provide the first national estimates of spatial variations in multiple measures (glutathione, ascorbate, and dithiothreitol depletion) of annual median outdoor PM 2.5 OB across Canada. To do this, we combined a large database of ground-level OB measurements collected monthly prospectively across Canada for 2 years (2016-2018) with PM 2.5 components estimated using a chemical transport model (GEOS-Chem) and satellite aerosol observations. Our predicted ground-level OB values of all three methods were consistent with ground-level observations (cross-validation R 2 = 0.63-0.74). We found that forested regions and urban areas had the highest OB, predicted primarily by black carbon and organic carbon from wildfires and transportation sources. Importantly, the dominant components associated with OB were different than those contributing to PM 2.5 mass concentrations (secondary inorganic aerosol); thus, OB metrics may better indicate harmful components and sources on health than the bulk PM 2.5 mass, reinforcing that OB estimates can complement the existing PM 2.5 data in future national-level epidemiological studies.

Background: Several studies have found positive associations between outdoor fine particulate air pollution (≤2.5 μm, PM 2.5 ) and childhood asthma incidence. However, the impact of PM 2.5 composition on children's respiratory health remains uncertain., Objective: We examined whether joint exposure to PM 2.5 mass concentrations and its major chemical components was associated with childhood asthma development., Methods: We conducted a population-based cohort study by identifying 1,130,855 singleton live births occurring between 2006 and 2014 in the province of Ontario, Canada. Concentrations of PM 2.5 and its seven major chemical components were assigned to participants based on their postal codes using chemical transport models and remote sensing. The joint impact of outdoor PM 2.5 concentrations and its major components and childhood asthma incidence (up to age 6) were estimated using Cox proportional hazards models, allowing for potential nonlinearity., Results: We identified 167,080 children who developed asthma before age 6. In adjusted models, outdoor PM 2.5 mass concentrations during childhood were associated with increased incidence of childhood asthma (Hazard Ratio (HR) for each 1 μg/m 3 increase = 1.026, 95% CI: 1.021-1.031). We found that the joint effects of PM 2.5 and its components on childhood asthma incidence may be 24% higher than the conventional approach. Specific components/source markers such as black carbon, ammonium, and nitrate appeared to play an important role., Conclusions: Early life exposure to PM 2.5 and its chemical components is associated with an increased risk of asthma development in children. The heterogeneous nature of PM 2.5 should be considered in future health risk assessments., (Crown Copyright © 2021. Published by Elsevier Ltd. All rights reserved.)

Background: Exposure to fine particulate (PM2.5) air pollution is associated with increased cardiovascular disease (CVD), but less is known about its specific components, such as metals originating from non-tailpipe emissions. We investigated the associations of long-term exposure to metal components [iron (Fe) and copper (Cu)] in PM2.5 with CVD incidence., Methods: We conducted a population-based cohort study in Toronto, Canada. Exposures to Fe and Cu in PM2.5 and their combined impact on the concentration of reactive oxygen species (ROS) in lung fluid were estimated using land use regression models. Incidence of acute myocardial infarction (AMI), congestive heart failure (CHF) and CVD death was ascertained using health administrative datasets. We used mixed-effects Cox regression models to examine the associations between the exposures and health outcomes. A series of sensitivity analyses were conducted, including indirect adjustment for individual-level cardiovascular risk factors (e.g. smoking), and adjustment for PM2.5 and nitrogen dioxide (NO2)., Results: In single-pollutant models, we found positive associations between the three exposures and all three outcomes, with the strongest associations detected for the estimated ROS. The associations of AMI and CHF were sensitive to indirect adjustment, but remained robust for CVD death in all sensitivity analyses. In multi-pollutant models, the associations of the three exposures generally remained unaltered. Interestingly, adjustment for ROS did not substantially change the associations between PM2.5 and CVD, but attenuated the associations of NO2., Conclusions: Long-term exposure to Fe and Cu in PM2.5 and their combined impact on ROS were consistently associated with increased CVD death., (© The Author(s) 2020; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Epidemiologic studies have found associations between fine particulate matter (PM 2.5 ) exposure and adverse health effects using exposure models that incorporate monitoring data and other relevant information. Here, we use nine PM 2.5 concentration models (i.e., exposure models) that span a wide range of methods to investigate i) PM 2.5 concentrations in 2011, ii) potential changes in PM 2.5 concentrations between 2011 and 2028 due to on-the-books regulations, and iii) PM 2.5 exposure for the U.S. population and four racial/ethnic groups. The exposure models included two geophysical chemical transport models (CTMs), two interpolation methods, a satellite-derived aerosol optical depth-based method, a Bayesian statistical regression model, and three data-rich machine learning methods. We focused on annual predictions that were regridded to 12-km resolution over the conterminous U.S., but also considered 1-km predictions in sensitivity analyses. The exposure models predicted broadly consistent PM 2.5 concentrations, with relatively high concentrations on average over the eastern U.S. and greater variability in the western U.S. However, differences in national concentration distributions (median standard deviation: 1.00 μg m -3 ) and spatial distributions over urban areas were evident. Further exploration of these differences and their implications for specific applications would be valuable. PM 2.5 concentrations were estimated to decrease by about 1 μg m -3 on average due to modeled emission changes between 2011 and 2028, with decreases of more than 3 μg m -3 in areas with relatively high 2011 concentrations that were projected to experience relatively large emission reductions. Agreement among models was closer for population-weighted than uniformly weighted averages across the domain. About 50% of the population was estimated to experience PM 2.5 concentrations less than 10 μg m -3 in 2011 and PM 2.5 improvements of about 2 μg m -3 due to modeled emission changes between 2011 and 2028. Two inequality metrics were used to characterize differences in exposure among the four racial/ethnic groups. The metrics generally yielded consistent information and suggest that the modeled emission reductions between 2011 and 2028 would reduce absolute exposure inequality on average., (Published by Elsevier Inc.)

Rationale: Current evidence on the relationship between long-term exposure to air pollution and new onset of chronic lung disease is inconclusive. Objectives: To examine associations of incident chronic obstructive pulmonary disease (COPD) and adult-onset asthma with past exposure to fine particulate matter ≤ 2.5 μm in diameter (PM 2.5 ), nitrogen dioxide (NO 2 ), ozone (O 3 ), and the redox-weighted average of NO 2 and O 3 (O x ) and characterize the concentration-response relationship. Methods: We conducted a population-based cohort study of all Ontarians, aged 35-85 years, from 2001 to 2015. A 3-year moving average of residential exposures to selected pollutants with a 1-year lag were estimated during follow-up. We used Cox proportional hazard models and Aalen additive-hazard models to quantify the pollution-disease associations and characterized the shape of these relationships using newly developed nonlinear risk models. Measurements and Main Results: Among 5.1 million adults, we identified 340,733 and 218,005 incident cases of COPD and asthma, respectively. We found positive associations of COPD with PM 2.5 per interquartile-range (IQR) increase of 3.4 μg/m 3 (hazard ratio, 1.07; 95% confidence interval, 1.06-1.08), NO 2 per IQR increase of 13.9 ppb (1.04; 1.02-1.05), O 3 per IQR increase of 6.3 ppb (1.04; 1.03-1.04), and O x per IQR increase of 4.4 ppb (1.03; 1.03-1.03). By contrast, we did not find strong evidence linking these pollutants to adult-onset asthma. In addition, we quantified that each IQR increase in pollution exposure yielded 3.0 (2.4-3.6), 3.2 (2.0-4.3), 1.9 (1.3-2.5), and 2.3 (1.7-2.9) excess cases of COPD per 100,000 adults for PM 2.5 , NO 2 , O 3 , and O x , respectively. Furthermore, most pollutant-COPD relationships exhibited supralinear shapes. Conclusions: Air pollution was associated with a higher incidence of COPD but was not associated with a higher incidence of adult-onset asthma.

Background: Experimental evidence and studies of children and adolescents suggest that ambient fine particulate matter [particulate matter ≤ 2.5 μ m in aerodynamic diameter ( PM 2.5 )] air pollution may be obesogenic, but the relationship between PM 2.5 and the risk of body weight gain and obesity in adults is uncertain., Objectives: Our goal was to characterize the association between PM 2.5 and the risks of weight gain and obesity., Methods: We followed 3,902,440 U.S. Veterans from 2010 to 2018 (median 8.1 y, interquartile range: 7.3-8.4) and assigned time-updated PM 2.5 exposures by linking geocoded residential street addresses with satellite-based estimates of surface-level PM 2.5 mass (at ∼ 1 -km 2 resolution). Associations with PM 2.5 were estimated using Cox proportional hazards models for incident obesity [body mass index ( BMI ) ≥ 30   kg / m 2 ] and a 10 -lb increase in weight relative to baseline and linear mixed models for associations with intra-individual changes in BMI and weight., Results: A 10 - μ g / m 3 higher average annual PM 2.5 concentration was associated with risk of incident obesity [ n = 2,325,769 ; hazard ratio  ( HR ) = 1.08 (95% CI: 1.06, 1.11)] and the risk of a 10 -lb ( 4.54   kg ) increase in weight [ HR = 1.07 (95% CI: 1.06, 1.08)] and with higher intra-individual changes in BMI [ 0.140   kg / m 2  per year (95% CI: 0.139, 0.142)] and weight [ 0.968  lb / y (95% CI: 0.955, 0.981)]. Nonlinear exposure-response models indicated associations at PM 2.5 concentrations below the national standard of 12   μ g / m 3 . As expected, a negative exposure control (ambient air sodium) was not associated with obesity or weight gain. Associations were consistent in direction and magnitude across sensitivity analyses that included alternative outcomes and exposures assigned at different spatial resolutions., Discussion: PM 2.5 air pollution was associated with the risk of obesity and weight gain in a large predominantly male cohort of U.S. Veterans. Discussions about health effects of PM 2.5 should include its association with obesity, and deliberations about the epidemiology of obesity should consider its association with PM 2.5 . Investigation in other cohorts will deepen our understanding of the relationship between PM 2.5 and weight gain and obesity. https://doi.org/10.1289/EHP7944.

Metal components in fine particulate matter (PM 2.5 ) from nontailpipe emissions may play an important role in underlying the adverse respiratory effects of PM 2.5 . We investigated the associations between long-term exposure to iron (Fe) and copper (Cu) in PM 2.5 and their combined impact on reactive oxygen species (ROS) generation in human lungs, and the incidence of asthma, chronic obstructive pulmonary disease (COPD), COPD mortality, pneumonia mortality, and respiratory mortality. We conducted a population-based cohort study of ∼0.8 million adults in Toronto, Canada. Land-use regression models were used to estimate the concentrations of Fe, Cu, and ROS. Outcomes were ascertained using validated health administrative databases. We found positive associations between long-term exposure to Fe, Cu, and ROS and the risks of all five respiratory outcomes. The associations were more robust for COPD, pneumonia mortality, and respiratory mortality than for asthma incidence and COPD mortality. Stronger associations were observed for ROS than for either Fe or Cu. In two-pollutant models, adjustment for nitrogen dioxide somewhat attenuated the associations while adjustment for PM 2.5 had little influence. Long-term exposure to Fe and Cu in PM 2.5 and estimated ROS concentration in lung fluid was associated with increased incidence of respiratory diseases, suggesting the adverse respiratory effects of nontailpipe emissions.

It has been posited that populations being exposed to long-term air pollution are more susceptible to COVID-19. Evidence is emerging that long-term exposure to ambient PM 2.5 (particulate matter with aerodynamic diameter 2.5 μm or less) associates with higher COVID-19 mortality rates, but whether it also associates with the speed at which the disease is capable of spreading in a population is unknown. Here, we establish the association between long-term exposure to ambient PM 2.5 in the United States (US) and COVID-19 basic reproduction ratio R 0 - a dimensionless epidemic measure of the rapidity of disease spread through a population. We inferred state-level R 0 values using a state-of-the-art susceptible, exposed, infected, and recovered (SEIR) model initialized with COVID-19 epidemiological data corresponding to the period March 2-April 30. This period was characterized by a rapid surge in COVID-19 cases across the US states, implementation of strict social distancing measures, and a significant drop in outdoor air pollution. We find that an increase of 1 μg/m 3 in PM 2.5 levels below current national ambient air quality standards associates with an increase of 0.25 in R 0 (95% CI: 0.048-0.447). A 10% increase in secondary inorganic composition, sulfate-nitrate-ammonium, in PM 2.5 associates with ≈10% increase in R 0 by 0.22 (95% CI: 0.083-0.352), and presence of black carbon (soot) in the ambient environment moderates this relationship. We considered several potential confounding factors in our analysis, including gaseous air pollutants and socio-economical and meteorological conditions. Our results underscore two policy implications - first, regulatory standards need to be better guided by exploring the concentration-response relationships near the lower end of the PM 2.5 air quality distribution; and second, pollution regulations need to be continually enforced for combustion emissions that largely determine secondary inorganic aerosol formation., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Background: Limited evidence is available on the associations of long-term exposure to various fine particulate matter (PM 2.5 ) constituents with sub-clinical outcomes of cardiovascular disease (CVD) in China., Objectives: We aimed to explore the associations of PM 2.5 and its constituents with blood pressure (BP), fasting glucose, and cardiac electrophysiological (ECG) properties based on a national survey of 5852 Chinese adults, who participated in the Sub-Clinical Outcome of Polluted Air study, from July 2017 to March 2019., Methods: Annual residential exposure to PM 2.5 and its constituents of each subject was predicted by a satellite-based mode. We assessed the associations between five main constituents [organic matter (OM), black carbon (BC), sulfate (SO 4 2- ), nitrate (NO 3 - ), ammonium (NH 4 + )] of PM 2.5 and systolic BP (SBP), diastolic BP (DBP), fasting glucose, and ECG measurements (PR, QRS, QT, and QTc interval) using multivariable linear regression models., Results: Long-term PM 2.5 exposure was significantly associated with increased levels of fasting glucose, DBP, and ECG measurements. An IQR increase in OM (8.2 μg/m 3 ) showed considerably stronger associations with an elevated fasting glucose of 0.39 mmol/L (95%CI confidence interval: 0.28, 0.49) compared with other PM 2.5 constituents. Meanwhile, an IQR increase in NO 3 - , NH 4 + and OM had stronger associations with DBP and ECG parameters compared with BC and SO 4 2- ., Conclusions: This nationwide multi-center study in China indicated that some constituents (i.e., OM, NO 3 - , and NH 4 + ) might be mainly responsible for the association of PM 2.5 with sub-clinical outcomes of CVD including BP, fasting glucose, and ECG measurements., Competing Interests: Declaration of competing interest The authors declared no conflicts of interests., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Background: Air pollution-attributable disease burdens reported at global, country, state, or county levels mask potential smaller-scale geographic heterogeneity driven by variation in pollution levels and disease rates. Capturing within-city variation in air pollution health impacts is now possible with high-resolution pollutant concentrations., Objectives: We quantified neighborhood-level variation in air pollution health risks, comparing results from highly spatially resolved pollutant and disease rate data sets available for the Bay Area, California., Methods: We estimated mortality and morbidity attributable to nitrogen dioxide ( NO 2 ), black carbon (BC), and fine particulate matter [PM ≤ 2.5 μ m in aerodynamic diameter ( PM 2.5 )] using epidemiologically derived health impact functions. We compared geographic distributions of pollution-attributable risk estimates using concentrations from a ) mobile monitoring of NO 2 and BC; and b ) models predicting annual NO 2 , BC and PM 2.5 concentrations from land-use variables and satellite observations. We also compared results using county vs. census block group (CBG) disease rates., Results: Estimated pollution-attributable deaths per 100,000 people at the 100 -m grid-cell level ranged across the Bay Area by a factor of 38, 4, and 5 for NO 2 [ mean = 30 (95% CI: 9, 50)], BC [ mean = 2 (95% CI: 1, 2)], and PM 2.5 , [ mean = 49 (95% CI: 33, 64)]. Applying concentrations from mobile monitoring and land-use regression (LUR) models in Oakland neighborhoods yielded similar spatial patterns of estimated grid-cell-level NO 2 -attributable mortality rates. Mobile monitoring concentrations captured more heterogeneity [mobile monitoring mean = 64 (95% CI: 19, 107) deaths per 100,000 people; LUR mean = 101 (95% CI: 30, 167)]. Using CBG-level disease rates instead of county-level disease rates resulted in 15% larger attributable mortality rates for both NO 2 and PM 2.5 , with more spatial heterogeneity at the grid-cell-level [ NO 2 CBG mean = 41 deaths per 100,000 people (95% CI: 12, 68); NO 2 county mean = 38 (95% CI: 11, 64); PM 2.5 CBG mean = 59 (95% CI: 40, 77); and PM 2.5 county mean = 55 (95% CI: 37, 71)]., Discussion: Air pollutant-attributable health burdens varied substantially between neighborhoods, driven by spatial variation in pollutant concentrations and disease rates. https://doi.org/10.1289/EHP7679.

Background: Adult-onset neurodegenerative diseases affect millions and negatively impact health care systems worldwide. Evidence suggests that air pollution may contribute to aggravation of neurodegeneration, but studies have been limited., Objective: We examined the potential association between long-term exposure to particulate matter ≤ 2.5 μ m in aerodynamic diameter [fine particulate matter ( PM 2.5 )] and disease aggravation in Alzheimer's (AD) and Parkinson's (PD) diseases and amyotrophic lateral sclerosis (ALS), using first hospitalization as a surrogate of clinical aggravation., Methods: We used data from the New York Department of Health Statewide Planning and Research Cooperative System (SPARCS 2000-2014) to construct annual county counts of first hospitalizations with a diagnosis of AD, PD, or ALS (total, urbanicity-, sex-, and age-stratified). We used annual PM 2.5 concentrations estimated by a prediction model at a 1 -km 2 resolution, which we aggregated to population-weighted county averages to assign exposure to cases based on county of residence. We used outcome-specific mixed quasi-Poisson models with county-specific random intercepts to estimate rate ratios (RRs) for a 1-y PM 2.5 exposure. We allowed for nonlinear exposure-outcome relationships using penalized splines and accounted for potential confounders., Results: We found a positive nonlinear PM 2.5 - PD association that plateaued above 11   μ g / m 3 ( RR = 1.09 , 95% CI: 1.04, 1.14 for a PM 2.5 increase from 8.1 to 10.4   μ g / m 3 ). We also found a linear PM 2.5 - ALS positive association ( RR = 1.05 , 95% CI: 1.01, 1.09 per 1 - μ g / m 3 PM 2.5 increase), and suggestive evidence of an association with AD. We found effect modification by age for PD and ALS with a stronger positive association in patients < 70  years of age but found insufficient evidence of effect modification by sex or urbanization level for any of the outcomes., Conclusion: Our findings suggest that annual increase in county-level PM 2.5 concentrations may contribute to clinical aggravation of PD and ALS. Importantly, the average annual PM 2.5 concentration in our study was 8.1   μ g / m 3 , below the current American national standards, suggesting the standards may not adequately protect the aging population. https://doi.org/10.1289/EHP7425.

The long-term effects of ambient PM 2.5 and chemical constituents on childhood pneumonia were still unknown. A cross-sectional study was conducted in 30,315 children in the China Children, Homes, Health (CCHH) project, involving 205 preschools in six cities in China, to investigate the long-term effects of PM 2.5 constituents on lifetime-ever diagnosed pneumonia. Information on the lifetime-ever pneumonia and demographics were collected by validated questionnaires. The lifetime annual average ambient PM 2.5 , ozone and five main PM 2.5 constituents, including SO 4 2- , NO 3 - , NH 4 + , organic matter (OM) and black carbon (BC), were estimated according to preschool addresses by a combination of satellite remote sensing, chemical transport modeling and ground-based monitors. The prevalence of lifetime-ever diagnosed pneumonia was 34.5% across six cities and differed significantly among cities (p = 0.004). The two-level logistic regression models showed that the adjusted odds ratio for PM 2.5 (per 10 µg/m 3 ) and its constituents (per 1 µg/m 3 )-SO 4 2- , NO 3 - , NH 4 + , and OM were 1.12 (95% CI:1.07-1.18), 1.02 (1.00-1.04), 1.06 (1.04-1.09), 1.05 (1.03-1.07) and 1.09 (1.06-1.12), respectively. Children in urban area, aged < 5 years and breastfeeding time < 6 months enhanced the risks of pneumonia. Our study provided robust results that long-term levels of ambient PM 2.5 and its constituents increased the risk of childhood pneumonia, especially NH 4 + , NO 3 - and OM., (Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

We developed Europe-wide models of long-term exposure to eight elements (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in particulate matter with diameter <2.5 μm (PM 2.5 ) using standardized measurements for one-year periods between October 2008 and April 2011 in 19 study areas across Europe, with supervised linear regression (SLR) and random forest (RF) algorithms. Potential predictor variables were obtained from satellites, chemical transport models, land-use, traffic, and industrial point source databases to represent different sources. Overall model performance across Europe was moderate to good for all elements with hold-out-validation R -squared ranging from 0.41 to 0.90. RF consistently outperformed SLR. Models explained within-area variation much less than the overall variation, with similar performance for RF and SLR. Maps proved a useful additional model evaluation tool. Models differed substantially between elements regarding major predictor variables, broadly reflecting known sources. Agreement between the two algorithm predictions was generally high at the overall European level and varied substantially at the national level. Applying the two models in epidemiological studies could lead to different associations with health. If both between- and within-area exposure variability are exploited, RF may be preferred. If only within-area variability is used, both methods should be interpreted equally.

Background: Individual and neighbourhood-scale socioeconomic characteristics modify associations between exposure to air pollution and mortality. The role of stress, which may integrate effects of social and environmental exposures on health, is unknown. We examined whether an individual's perspective on their own well-being, as assessed using self-rated measures of stress and health, modifies the pollutant-mortality relationship., Methods: The Canadian Community Health Survey (CCHS)-mortality cohort includes respondents from surveys administered between 2001 and 2012 linked to vital statistics and postal codes from 1981 until 2016. Annual fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) exposure estimates were attached to a sample of cohort members aged 30-89 years (n = 398,300 respondents/3,848,400 person-years). We examined whether self-rated stress, distress, mental health, and general health modified associations between long-term exposure to each pollutant (three-year moving average with one-year lag) and non-accidental mortality using Cox survival models, adjusted for individual- (i.e. socioeconomic and behavioural) and neighbourhood-scale covariates., Results: In fully-adjusted models, the relationship between exposure to pollutants and mortality was stronger among those with poor self-rated mental health, including a significant difference for NO 2 (hazard ratio (HR) = 1.15, 95% CI 1.06-1.25 per IQR) compared to those with very good/excellent mental health (HR = 1.05, 95% CI 1.01-1.08; Cochran's Q = 4.01; p < 0.05). Poor self-rated health was similarly associated with higher pollutant-associated HRs, but only in unadjusted models. Stress and distress did not modify pollutant-mortality associations., Conclusions: Poor self-rated mental and general health were associated with increased mortality attributed to exposure to ambient pollutants., (Crown Copyright © 2020. Published by Elsevier Inc. All rights reserved.)

Background: Ambient air pollution has been associated with childhood cancer. However, little is known about the possible impact of ambient ultrafine particles (<0.1 μm) (UFPs) on childhood cancer incidence., Objective: This study aimed to evaluate the association between prenatal and childhood exposure to UFPs and development of childhood cancer., Methods: We conducted a population-based cohort study of within-city spatiotemporal variations in ambient UFPs across the City of Toronto, Canada using 653,702 singleton live births occurring between April 1, 1998 and March 31, 2017. Incident cases of 13 subtypes of paediatric cancers among children up to age 14 were ascertained using a cancer registry. Associations between ambient air pollutant concentrations and childhood cancer incidence were estimated using random-effects Cox proportional hazards models. We investigated both single- and multi-pollutant models accounting for co-exposures to PM 2.5 and NO 2 ., Results: A total of 1,066 childhood cancers were identified. We found that first trimester exposure to UFPs (Hazard Ratio (HR) per 10,000/cm 3 increase = 1.13, 95% CI: 1.03-1.22) was associated with overall cancer incidence diagnosed before 6 years of age after adjusting for PM 2.5 , NO 2 , and for personal and neighborhood-level covariates. Association between UFPs and overall cancer incidence exhibited a linear shape. No statistically significant associations were found for specific cancer subtypes., Conclusion: Ambient UFPs may represent a previously unrecognized risk factor in the aetiology of cancers in children. Our findings reinforce the importance of conducting further research on the effects of UFPs given their high prevalence of exposure in urban areas., (Crown Copyright © 2020. Published by Elsevier Ltd. All rights reserved.)