Impact of Model Spatial Resolution on Global Geophysical Satellite-Derived Fine Particulate Matter.

Global geophysical satellite-derived ambient fine particulate matter (PM2.5) inference relies upon a geophysical relationship (η) from a chemical transport model to relate satellite retrievals of aerosol optical depth (AOD) to surface PM2.5. The resolution dependence of simulated η warrants further investigation. In this study, we calculate geophysical PM2.5 with simulated η from the GEOS-Chem model in its high-performance configuration (GCHP) at cubed-sphere resolutions of C360 (∼25 km) and C48 (∼200 km) and satellite AOD at 0.01° (∼1 km). Annual geophysical PM2.5 concentrations inferred from satellite AOD and GCHP simulations at ∼25 km and ∼200 km resolutions exhibit remarkable similarity (R 2 = 0.96, slope = 1.03). This similarity in part reflects opposite resolution responses across components with population-weighted normalized mean difference (PW-NMD) increasing by 5% to 11% for primary species while decreasing by -30% to -5% for secondary species at finer resolution. Despite global similarity, our results also identify larger resolution sensitivities of η over isolated pollution sources and mountainous regions, where spatial contrast of aerosol concentration and composition is better represented at fine resolution. Our results highlight the resolution dependence of representing near-surface concentrations and the vertical distribution of chemically different species with implications for inferring ground-level PM2.5 from columnar AOD.

Effect modification by statin use status on the association between fine particulate matter (PM2.5) and cardiovascular mortality.

BACKGROUND: Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. METHODS: In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). RESULTS: Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032-1.053) vs OR = 1.009 (95% CI, 0.996-1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019-1.047), RERI = 0.039 (95% CI, 0.025-0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. CONCLUSIONS: The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users.

Understanding Reductions of PM2.5 Concentration and Its Chemical Composition in the United States: Implications for Mitigation Strategies.

Motivated by the recent tightening of the US annual standard of fine particulate matter (PM2.5) concentrations from 12 to 9 µg/m3, there is a need to understand the spatial variation and drivers of historical PM2.5 reductions. We evaluate and interpret the variability of PM2.5 reductions across the contiguous US using high-resolution estimates of PM2.5 and its chemical composition over 1998-2019, inferred from satellite observations, air quality modeling, and ground-based measurements. We separated the 3092 counties into four characteristic regions sorted by PM2.5 trends. Region 1 (primarily Central Atlantic states, 25.9% population) exhibits the strongest population-weighted annual PM2.5 reduction (-3.6 ± 0.4%/yr) versus Region 2 (primarily rest of the eastern US, -3.0 ± 0.3%/yr, 39.7% population), Region 3 (primarily western Midwest, -1.9 ± 0.3%/yr, 25.6% population), and Region 4 (primarily the Mountain West, -0.4 ± 0.5%/yr, 8.9% population). Decomposition of these changes by chemical composition elucidates that sulfate exhibits the fastest reductions among all components in 2720 counties (76% of population), mostly over Regions 1-3, with the 1998-2019 mean sulfate mass fraction in PM2.5 decreasing from Region 1 (29.5%) to Region 4 (11.8%). Complete elimination of the remaining sulfate may be insufficient to meet the new standard for many regions in exceedance. Additional measures are needed to reduce other PM2.5 sources and components for further progress.

Epidemiological studies likely need to consider PM2.5 composition even if total outdoor PM2.5 mass concentration is the exposure of interest.

Background: Outdoor fine particulate air pollution, <2.5 µm (PM2.5) mass concentrations can be constructed through many different combinations of chemical components that have varying levels of toxicity. This poses a challenge for studies interested in estimating the health effects of total outdoor PM2.5 (i.e., how much PM2.5 mass is present in the air regardless of composition) because we must consider possible confounders of the version of treatment-outcome relationships. Methods: We evaluated the extent of possible bias in mortality hazard ratios for total outdoor PM2.5 by examining models with and without adjustment for sulfate and nitrate in PM2.5 as examples of potential confounders of version of treatment-outcome relationships. Our study included approximately 3 million Canadians and Cox proportional hazard models were used to estimate hazard ratios for total outdoor PM2.5 adjusting for sulfate and/or nitrate and other relevant covariates. Results: Hazard ratios for total outdoor PM2.5 and nonaccidental, cardiovascular, and respiratory mortality were overestimated due to the confounding version of treatment-outcome relationships, and associations for lung cancer mortality were underestimated. Sulfate was most strongly associated with nonaccidental, cardiovascular, and respiratory mortality suggesting that regulations targeting this specific component of outdoor PM2.5 may have greater health benefits than interventions targeting total PM2.5. Conclusions: Studies interested in estimating the health impacts of total outdoor PM2.5 (i.e., how much PM2.5 mass is present in the air) need to consider potential confounders of the version of treatment-outcome relationships. Otherwise, health risk estimates for total PM2.5 will reflect some unknown combination of how much PM2.5 mass is present in the air and the kind of PM2.5 mass that is present.

Enhancing Global Estimation of Fine Particulate Matter Concentrations by Including Geophysical a Priori Information in Deep Learning.

Global fine particulate matter (PM2.5) assessment is impeded by a paucity of monitors. We improve estimation of the global distribution of PM2.5 concentrations by developing, optimizing, and applying a convolutional neural network with information from satellite-, simulation-, and monitor-based sources to predict the local bias in monthly geophysical a priori PM2.5 concentrations over 1998-2019. We develop a loss function that incorporates geophysical a priori estimates and apply it in model training to address the unrealistic results produced by mean-square-error loss functions in regions with few monitors. We introduce novel spatial cross-validation for air quality to examine the importance of considering spatial properties. We address the sharp decline in deep learning model performance in regions distant from monitors by incorporating the geophysical a priori PM2.5. The resultant monthly PM2.5 estimates are highly consistent with spatial cross-validation PM2.5 concentrations from monitors globally and regionally. We withheld 10% to 99% of monitors for testing to evaluate the sensitivity and robustness of model performance to the density of ground-based monitors. The model incorporating the geophysical a priori PM2.5 concentrations remains highly consistent with observations globally even under extreme conditions (e.g., 1% for training, R2 = 0.73), while the model without exhibits weaker performance (1% for training, R2 = 0.51).

A comparison of PM2.5 exposure estimates from different estimation methods and their associations with cognitive testing and brain MRI outcomes.

BACKGROUND: Reported associations between particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5) and cognitive outcomes remain mixed. Differences in exposure estimation method may contribute to this heterogeneity. OBJECTIVES: To assess agreement between PM2.5 exposure concentrations across 11 exposure estimation methods and to compare resulting associations between PM2.5 and cognitive or MRI outcomes. METHODS: We used Visit 5 (2011-2013) cognitive testing and brain MRI data from the Atherosclerosis Risk in Communities (ARIC) Study. We derived address-linked average 2000-2007 PM2.5 exposure concentrations in areas immediately surrounding the four ARIC recruitment sites (Forsyth County, NC; Jackson, MS; suburbs of Minneapolis, MN; Washington County, MD) using 11 estimation methods. We assessed agreement between method-specific PM2.5 concentrations using descriptive statistics and plots, overall and by site. We used adjusted linear regression to estimate associations of method-specific PM2.5 exposure estimates with cognitive scores (n = 4678) and MRI outcomes (n = 1518) stratified by study site and combined site-specific estimates using meta-analyses to derive overall estimates. We explored the potential impact of unmeasured confounding by spatially patterned factors. RESULTS: Exposure estimates from most methods had high agreement across sites, but low agreement within sites. Within-site exposure variation was limited for some methods. Consistently null findings for the PM2.5-cognitive outcome associations regardless of method precluded empirical conclusions about the potential impact of method on study findings in contexts where positive associations are observed. Not accounting for study site led to consistent, adverse associations, regardless of exposure estimation method, suggesting the potential for substantial bias due to residual confounding by spatially patterned factors. DISCUSSION: PM2.5 estimation methods agreed across sites but not within sites. Choice of estimation method may impact findings when participants are concentrated in small geographic areas. Understanding unmeasured confounding by factors that are spatially patterned may be particularly important in studies of air pollution and cognitive or brain health.

Quantifying Prescribed-Fire Smoke Exposure Using Low-Cost Sensors and Satellites: Springtime Burning in Eastern Kansas.

Prescribed fires (fires intentionally set for mitigation purposes) produce pollutants, which have negative effects on human and animal health. One of the pollutants produced from fires is fine particulate matter (PM2.5). The Flint Hills (FH) region of Kansas experiences extensive prescribed burning each spring (March-May). Smoke from prescribed fires is often understudied due to a lack of monitoring in the rural regions where prescribed burning occurs, as well as the short duration and small size of the fires. Our goal was to attribute PM2.5 concentrations to the prescribed burning in the FH. To determine PM2.5 increases from local burning, we used low-cost PM2.5 sensors (PurpleAir) and satellite observations. The FH were also affected by smoke transported from fires in other regions during 2022. We separated the transported smoke from smoke from fires in eastern Kansas. Based on data from the PurpleAir sensors, we found the 24-hr median PM2.5 to increase by 3.0-5.3 µg m-3 (based on different estimates) on days impacted by smoke from fires in the eastern Kansas region compared to days unimpacted by smoke. The FH region was the most impacted by smoke PM2.5 compared to other regions of Kansas, as observed in satellite products and in situ measurements. Additionally, our study found that hourly PM2.5 estimates from a satellite-derived product aligned with our ground-based measurements. Satellite-derived products are useful in rural areas like the FH, where monitors are scarce, providing important PM2.5 estimates.

Increasing Racial and Ethnic Disparities in Ambient Air Pollution-Attributable Morbidity and Mortality in the United States.

BACKGROUND: Ambient nitrogen dioxide (NO2) and fine particulate matter with aerodynamic diameter ≤2.5µm (PM2.5) 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 NO2- and PM2.5-attributable health burdens, considering NO2-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 NO2 and PM2.5 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 NO2 and PM2.5, racial and ethnic relative disparities in NO2-attributable pediatric asthma and PM2.5-attributable premature mortality have widened in the US during the last decade. Racial relative disparities in PM2.5-attributable premature mortality and NO2-attributable pediatric asthma have increased by 16% and 19%, respectively, between 2010 and 2019. Similarly, ethnic relative disparities in PM2.5-attributable premature mortality have increased by 40% and NO2-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.

Comparison of PM2.5 Air Pollution Exposures and Health Effects Associations Using 11 Different Modeling Approaches in the Women's Health Initiative Memory Study (WHIMS).

BACKGROUND: Many approaches to quantifying air pollution exposures have been developed. However, the impact of choice of approach on air pollution estimates and health-effects associations remains unclear. OBJECTIVES: Our objective is to compare particulate matter with aerodynamic diameter ≤2.5µm (PM2.5) concentrations and resulting health effects associations using multiple estimation approaches previously used in epidemiologic analyses. METHODS: We assigned annual PM2.5 exposure estimates from 1999 to 2004 derived from 11 different approaches to Women's Health Initiative Memory Study (WHIMS) participant addresses within the contiguous US. Approaches included geostatistical interpolation approaches, land-use regression or spatiotemporal models, satellite-derived approaches, air dispersion and chemical transport models, and hybrid models. We used descriptive statistics and plots to assess relative and absolute agreement among exposure estimates and examined the impact of approach on associations between PM2.5 and death due to natural causes, cardiovascular disease (CVD) mortality, and incident CVD events, adjusting for individual-level covariates and climate-based region. RESULTS: With a few exceptions, relative agreement of approach-specific PM2.5 exposure estimates was high for PM2.5 concentrations across the contiguous US. Agreement among approach-specific exposure estimates was stronger near PM2.5 monitors, in certain regions of the country, and in 2004 vs. 1999. Collectively, our results suggest but do not quantify lower agreement at local spatial scales for PM2.5. There was no evidence of large differences in health effects associations with PM2.5 among estimation approaches in analyses adjusted for climate region. CONCLUSIONS: Different estimation approaches produced similar spatial patterns of PM2.5 concentrations across the contiguous US and in areas with dense monitoring data, and PM2.5-health effects associations were similar among estimation approaches. PM2.5 estimates and PM2.5-health effects associations may differ more in samples drawn from smaller areas or areas without substantial monitoring data, or in analyses with finer adjustment for participant location. Our results can inform decisions about PM2.5 estimation approach in epidemiologic studies, as investigators balance concerns about bias, efficiency, and resource allocation. Future work is needed to understand whether these conclusions also apply in the context of other air pollutants of interest. https://doi.org/10.1289/EHP12995.

Inequality in the Distribution of Air Pollution Attributable Mortality Within Canadian Cities.

Recent studies have identified inequality in the distribution of air pollution attributable health impacts, but to our knowledge this has not been examined in Canadian cities. We evaluated the extent and sources of inequality in air pollution attributable mortality at the census tract (CT) level in seven of Canada's largest cities. We first regressed fine particulate matter (PM2.5) and nitrogen dioxide (NO2) attributable mortality against the neighborhood (CT) level prevalence of age 65 and older, low income, low educational attainment, and identification as an Indigenous (First Nations, Métis, Inuit) or Black person, accounting for spatial autocorrelation. We next examined the distribution of baseline mortality rates, PM2.5 and NO2 concentrations, and attributable mortality by neighborhood (CT) level prevalence of these characteristics, calculating the concentration index, Atkinson index, and Gini coefficient. Finally, we conducted a counterfactual analysis of the impact of reducing baseline mortality rates and air pollution concentrations on inequality in air pollution attributable mortality. Regression results indicated that CTs with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality. Concentration index, Atkinson index, and Gini coefficient values revealed different degrees of inequality among the cities. Counterfactual analysis indicated that inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities. Reducing inequality in air pollution attributable mortality requires reducing disparities in both baseline mortality and air pollution exposure.

Reversal of trends in global fine particulate matter air pollution.

Ambient fine particulate matter (PM2.5) is the world's leading environmental health risk factor. Quantification is needed of regional contributions to changes in global PM2.5 exposure. Here we interpret satellite-derived PM2.5 estimates over 1998-2019 and find a reversal of previous growth in global PM2.5 air pollution, which is quantitatively attributed to contributions from 13 regions. Global population-weighted (PW) PM2.5 exposure, related to both pollution levels and population size, increased from 1998 (28.3 µg/m3) to a peak in 2011 (38.9 µg/m3) and decreased steadily afterwards (34.7 µg/m3 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 PM2.5-attributable mortality and increasing health benefits per µg/m3 marginal reduction in exposure, implying increasing urgency and benefits of PM2.5 mitigation with aging population and cleaner air.

Fine particulate matter composition in American Indian vs. Non-American Indian communities.

BACKGROUND: Fine particulate matter (PM2.5) exposure is a known risk factor for numerous adverse health outcomes, with varying estimates of component-specific effects. Populations with compromised health conditions such as diabetes can be more sensitive to the health impacts of air pollution exposure. Recent trends in PM2.5 in primarily American Indian- (AI-) populated areas examined in previous work declined more gradually compared to the declines observed in the rest of the US. To further investigate components contributing to these findings, we compared trends in concentrations of six PM2.5 components in AI- vs. non-AI-populated counties over time (2000-2017) in the contiguous US. METHODS: We implemented component-specific linear mixed models to estimate differences in annual county-level concentrations of sulfate, nitrate, ammonium, organic matter, black carbon, and mineral dust from well-validated surface PM2.5 models in AI- vs. non-AI-populated counties, using a multi-criteria approach to classify counties as AI- or non-AI-populated. Models adjusted for population density and median household income. We included interaction terms with calendar year to estimate whether concentration differences in AI- vs. non-AI-populated counties varied over time. RESULTS: Our final analysis included 3108 counties, with 199 (6.4%) classified as AI-populated. On average across the study period, adjusted concentrations of all six PM2.5 components in AI-populated counties were significantly lower than in non-AI-populated counties. However, component-specific levels in AI- vs. non-AI-populated counties varied over time: sulfate and ammonium levels were significantly lower in AI- vs. non-AI-populated counties before 2011 but higher after 2011 and nitrate levels were consistently lower in AI-populated counties. CONCLUSIONS: This study indicates time trend differences of specific components by AI-populated county type. Notably, decreases in sulfate and ammonium may contribute to steeper declines in total PM2.5 in non-AI vs. AI-populated counties. These findings provide potential directives for additional monitoring and regulations of key emissions sources impacting tribal lands.

Prenatal air pollution, maternal immune activation, and autism spectrum disorder.

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 (PM2.5) 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 PM2.5 or major PM2.5 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 PM2.5 and four PM2.5 components, black carbon (BC), organic matter (OM), nitrate (NO3-), and sulfate (SO42-), 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 PM2.5 [1.07; 1.03-1.12 per interquartile (3.73 µg/m3) increase] and with all four PM2.5 components. However, there were no interactions of each category of MIA-related conditions with PM2.5 or its components on either multiplicative or additive scales. CONCLUSIONS: MIA-related conditions and pregnancy PM2.5 were independently associations with ASD risk. There were no statistically significant interactions of MIA conditions and prenatal PM2.5 exposure with ASD risk.

Source Contributions to Fine Particulate Matter and Attributable Mortality in India and the Surrounding Region.

Fine particulate matter (PM2.5) 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 PM2.5 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 PM2.5, 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 PM2.5 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 PM2.5-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 PM2.5 (>95 µg/m3). 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 PM2.5 mass and improve population health by reducing emissions from traditional energy sources across multiple sectors in South Asia.

Advances in Simulating the Global Spatial Heterogeneity of Air Quality and Source Sector Contributions: Insights into the Global South.

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 (PM2.5) and nitrogen dioxide (NO2), 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%) PM2.5 species. Developing regions are more sensitive to spatial resolution resulting from sparse pollution hotspots, with PW-NRMSD for PM2.5 in the Global South (33%), 1.3 times higher than globally. The PW-NRMSD for PM2.5 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.

National Cohort Study of Long-Term Exposure to PM2.5 Components and Mortality in Medicare American Older Adults.

There is increasing evidence linking long-term fine particulate matter (PM2.5) exposure to negative health effects. However, the relative influence of each component of PM2.5 on health risk is poorly understood. In a cohort study in the contiguous United States between 2000 and 2017, we examined the effect of long-term exposure to PM2.5 main components and all-cause mortality in older adults who had to be at least 65 years old and enrolled in Medicare. We estimated the yearly mean concentrations of six key PM2.5 compounds, including black carbon (BC), organic matter (OM), soil dust (DUST), nitrate (NO3-), sulfate (SO42-), and ammonium (NH4+), using two independently sourced well-validated prediction models. We applied Cox proportional hazard models to evaluate the hazard ratios for mortality and penalized splines for assessing potential nonlinear concentration-response associations. Results suggested that increased exposure to PM2.5 mass and its six main constituents were significantly linked to elevated all-cause mortality. All components showed linear concentration-response relationships in the low exposure concentration ranges. Our research indicates that long-term exposure to PM2.5 mass and its essential compounds are strongly connected to increased mortality risk. Reductions of fossil fuel burning may yield significant air quality and public health benefit.

Using Parametric g-Computation to Estimate the Effect of Long-Term Exposure to Air Pollution on Mortality Risk and Simulate the Benefits of Hypothetical Policies: The Canadian Community Health Survey Cohort (2005 to 2015).

BACKGROUND: Numerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter ≤2.5µm in aerodynamic diameter (PM2.5)] 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 PM2.5 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 µg/m3, 7.04 µg/m3, 5 µg/m3, and 4 µg/m3), and b) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average PM2.5 concentration with 1-y lag at the postal code of respondents' annual mailing addresses as their long-term exposure to PM2.5. 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 µg/m3, 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 PM2.5 would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient PM2.5. 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.

A cross-sectional analysis of ambient fine particulate matter (PM2.5) exposure and haemoglobin levels in children aged under 5 years living in 36 countries.

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 [PM2.5]) 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 PM2.5 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 PM2.5 with Hb levels and anaemia prevalence was examined using multivariable linear and logistic regression models, respectively. We examined whether the effects of ambient PM2.5 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 PM2.5 exposure was 33.0 (±21.6) µg/m3. The adjusted model showed that a 10 µg/m3 increase in annual PM2.5 concentration was associated with greater odds of anaemia (OR = 1.098 95% CI: 1.087, 1.109). The same increase in PM2.5 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 PM2.5 was cross-sectionally associated with decreased blood Hb levels, and greater risk of anaemia, in children aged <5 years living in 36 LMICs.