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[School] Buses/Vehicle Use around schools | Air Pollution and Academic Achievement | Air Pollution and Children's Health | Air Pollution and COVID-19 | Air Pollution/Climate Change and Health | Air Pollution/Climate Change and Mental Health | Data Center Resources & Research | Indoor Air Pollution | Systemic Environmental Racism | Vehicles/Traffic
The impact of prenatal and early childhood exposure of ambient particulate matters (PMs) on the risk of autism spectrum disorder (ASD) in children remained inconclusive, particularly at low levels below current National Ambient Air Quality Standards. The study summarizes the epidemiological association between PM exposure and risks of ASD in children. PubMed, Embase, Web of Science, Cochrane Library, Compendex, Biosis Previews, and Agricultural & Environmental Science Databases for studies published before February 2020. Original studies with the following information were included: (a) exposure of ambient PM (including PM2.5 and/or PM10); (b) ASD as the outcome of interest in children; (c) effect estimates of relative risk (RR), odds ratio (OR), or hazard ratio. The risks of ASD are summarized at different exposure windows (i.e. first, second, third trimesters, and early childhood period) by using a random-effects model. Exposure-response meta-regression was performed across various background levels of PM2.5. We used Newcastle–Ottawa Scale for quality assessment. Eleven studies (two cohort and nine case-control studies) and 313 301 children were enrolled. Overall, the risk of ASD increased by 64% (pooled RR = 1.64, 95% CI = 1.16–2.34) and 31% (pooled RR = 1.31, 95% CI = 1.08–1.58), with exposure to 10 μg m−3 increment of PM2.5 during early childhood and prenatal periods, respectively. Stratifying by three trimesters of prenatal period, the risk of ASD increased 35% per 10 μg m−3 difference of PM2.5 exposure during the third trimester (pooled RR = 1.35, 95% CI = 1.18–1.55), but not during the first and second trimesters. The risks of ASD persisted at the background PM2.5 levels from 8 μg m−3 (pooled RR = 1.30, 95% CI = 1.02–1.66) and onward. Our findings suggested an association between PM2.5 exposure and risks of ASD, particularly within specific exposure windows, even at low background levels of PM2.5.
Published May 28, 2021
Lin, C. K., Chang, Y. T., Lee, F. S., Chen, S. T., & Christiani, D. (2021). Association between exposure to ambient particulate matters and risks of autism spectrum disorder in children: a systematic review and exposure-response meta-analysis. Environmental Research Letters, 16(6), 063003. https://doi.org/10.1088/1748-9326/ABFCF7
Background
Previous studies have investigated the association of ambient air pollution with blood pressure (BP) in children and adolescents, however, the results are not consistent. We conducted a systematic review and meta‐analysis to assess the relationship between short‐term and long‐term ambient air pollutant exposure with BP values among children and adolescents.
Methods and Results
We searched PubMed, Web of Science, and Embase before September 6, 2020. Two reviewers independently searched and selected studies, extracted data, and assessed study quality. The studies were divided into groups by composition of air pollutants (NO2, particulate matter (PM) with diameter ≤10 μm or ≤2.5 μm) and length of exposure. The beta regression coefficients (β) and their 95% CIs were calculated to evaluate the strength of the effect with each 10 μg/m3 increase in air pollutants. Out of 36 650 articles, 14 articles were included in this meta‐analysis. The meta‐analysis showed short‐term exposure to PM with diameter ≤10 μm (β=0.267; 95% CI, 0.033‒0.501) was significantly associated with elevated systolic BP values. In addition, long‐term exposure to PM with diameter ≤2.5 μm (β=1.809; 95% CI, 0.962‒2.655), PM with diameter ≤10 μm (β=0.526; 95% CI, 0.095‒0.958), and NO2 (β=0.754; 95% CI, 0.541‒0.968) were associated with systolic BP values and long‐term exposure to PM with diameter ≤2.5 μm (β=0.931; 95% CI, 0.157‒1.705), and PM with diameter ≤10 μm (β=0.378; 95% CI, 0.022‒0.735) was associated with diastolic BP.
Conclusions
Our study indicates that both short‐term and long‐term exposure to some ambient air pollutants may increase BP values among children and adolescents.
Published May 4, 2021
Huang, M., Chen, J., Yang, Y., Yuan, H., Huang, Z., & Lu, Y. (2021). Effects of Ambient Air Pollution on Blood Pressure Among Children and Adolescents: A Systematic Review and Meta‐Analysis. Journal of the American Heart Association, 10(10), 17734. https://doi.org/10.1161/JAHA.120.017734
The SARS-COV-2 virus, also known as the coronavirus, has spread around the world. A growing literature suggests that exposure to pollution can cause respiratory illness and increase deaths among the elderly. However, little is known about whether increases in pollution could cause additional or more severe infections from COVID-19, which typically manifests as a respiratory infection. During the pandemic, the Environmental Protection Agency (EPA) rolled back enforcement of environmental regulation, causing an increase in pollution in counties with more TRI sites. We use the variation in pollution and a difference in differences design to estimate the effects of increased pollution on county-level COVID-19 deaths and cases. We find that counties with more Toxic Release Inventory (TRI) sites saw a 11.8 percent increase in pollution on average following the EPA’s rollback of enforcement, compared to counties with fewer TRI sites. We also find that these policy-induced increases in pollution are associated with a 53 percent increase in cases and a 10.6 percent increase in deaths from COVID-19.
Published May 1, 2021
Claudia L. Persico, Kathryn R. Johnson, The effects of increased pollution on COVID-19 cases and deaths, Journal of Environmental Economics and Management, Volume 107, 2021, 102431, ISSN 0095-0696, https://doi.org/10.1016/j.jeem.2021.102431.
Objectives. To investigate the effects of coal-fired power plant closures on zip code–level rates of emergency department visits for asthma-related conditions among 0- to 4-year-old children in Chicago, Illinois.
Methods. We used data on wind, population, PM2.5 (particulates measuring ≤ 2.5 µm in diameter), and zip code–level rates of emergency department visits for asthma-related conditions among 0- to 4-year-old children between 2009 and 2017 in Chicago. The difference-in-differences research design compared rates of emergency department visits in zip codes near 3 coal-fired power plants before and after their closures to rates in zip codes farther away during the same time period.
Results. We found that emergency department visits for asthma-related conditions among 0- to 4-year-old children decreased by 12% in zip codes near the 3 coal-fired power plants following their closures relative to rates in zip codes farther away during the same period. The crude and age-specific rates of emergency department visits decreased by 2.41 visits per ten thousand inhabitants and 35.63 visits per ten thousand children aged 0 to 4 years, respectively.
Conclusions. Our findings demonstrate that closing coal-fired power plants can lead to improvements in the respiratory health of young children.
Published May 1, 2021
Komisarow, S., & Pakhtigian, E. L. (2021). The Effect of Coal-Fired Power Plant Closures on Emergency Department Visits for Asthma-Related Conditions Among 0- to 4-Year-Old Children in Chicago, 2009–2017. American Journal of Public Health, 111(5), 881–889. https://doi.org/10.2105/AJPH.2021.306155
Importance Air pollution exposure damages the brain, but its associations with the development of psychopathology are not fully characterized.
Objective To assess whether air pollution exposure in childhood and adolescence is associated with greater psychopathology at 18 years of age.
Design, Setting, and Participants The Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born from January 1, 1994, to December 4, 1995, across England and Wales and followed up to 18 years of age. Pollution data generation was completed on April 22, 2020; data were analyzed from April 27 to July 31, 2020.
Exposures High-resolution annualized estimates of outdoor nitrogen oxides (NOx) and particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5) linked to home addresses at the ages of 10 and 18 years and then averaged.
Main Outcomes and Measures Mental health disorder symptoms assessed through structured interview at 18 years of age and transformed through confirmatory factor analysis into continuous measures of general psychopathology (primary outcome) and internalizing, externalizing, and thought disorder symptoms (secondary outcomes) standardized to a mean (SD) of 100 (15). Hypotheses were formulated after data collection, and analyses were preregistered.
Results A total of 2039 participants (1070 [52.5%] female) had full data available. After adjustment for family and individual factors, each interquartile range increment increase in NOx exposure was associated with a 1.40-point increase (95% CI, 0.41-2.38; P = .005) in general psychopathology. There was no association between continuously measured PM2.5 and general psychopathology (b = 0.45; 95% CI, −0.26 to 1.11; P = .22); however, those in the highest quartile of PM2.5 exposure scored 2.04 points higher (95% CI, 0.36-3.72; P = .02) than those in the bottom 3 quartiles. Copollutant models, including both NOx and PM2.5, implicated NOx alone in these significant findings. NOx exposure was associated with all secondary outcomes, although associations were weakest for internalizing (adjusted b = 1.07; 95% CI, 0.10-2.04; P = .03), medium for externalizing (adjusted b = 1.42; 95% CI, 0.53-2.31; P = .002), and strongest for thought disorder symptoms (adjusted b = 1.54; 95% CI, 0.50-2.57; P = .004). Despite NOx concentrations being highest in neighborhoods with worse physical, social, and economic conditions, adjusting estimates for neighborhood characteristics did not change the results.
Conclusions and Relevance Youths exposed to higher levels of outdoor NOx experienced greater psychopathology at the transition to adulthood. Air pollution may be a nonspecific risk factor for the development of psychopathology.
Published Apr 28, 2021
Reuben, A., Arseneault, L., Beddows, A., Beevers, S. D., Moffitt, T. E., Ambler, A., Latham, R. M., Newbury, J. B., Odgers, C. L., Schaefer, J. D., & Fisher, H. L. (2021). Association of Air Pollution Exposure in Childhood and Adolescence With Psychopathology at the Transition to Adulthood. JAMA Network Open, 4(4), e217508–e217508. https://doi.org/10.1001/JAMANETWORKOPEN.2021.7508
The burning of fossil fuels – especially coal, petrol, and diesel – is a major source of airborne fine particulate matter (PM2.5), and a key contributor to the global burden of mortality and disease. Previous risk assessments have examined the health response to total PM2.5, not just PM2.5 from fossil fuel combustion, and have used a concentration-response function with limited support from the literature and data at both high and low concentrations. This assessment examines mortality associated with PM2.5 from only fossil fuel combustion, making use of a recent meta-analysis of newer studies with a wider range of exposure. We also estimated mortality due to lower respiratory infections (LRI) among children under the age of five in the Americas and Europe, regions for which we have reliable data on the relative risk of this health outcome from PM2.5 exposure. We used the chemical transport model GEOS-Chem to estimate global exposure levels to fossil-fuel related PM2.5 in 2012. Relative risks of mortality were modeled using functions that link long-term exposure to PM2.5 and mortality, incorporating nonlinearity in the concentration response. We estimate a global total of 10.2 (95% CI: −47.1 to 17.0) million premature deaths annually attributable to the fossil-fuel component of PM2.5. The greatest mortality impact is estimated over regions with substantial fossil fuel related PM2.5, notably China (3.9 million), India (2.5 million) and parts of eastern US, Europe and Southeast Asia. The estimate for China predates substantial decline in fossil fuel emissions and decreases to 2.4 million premature deaths due to 43.7% reduction in fossil fuel PM2.5 from 2012 to 2018 bringing the global total to 8.7 (95% CI: −1.8 to 14.0) million premature deaths. We also estimated excess annual deaths due to LRI in children (0–4 years old) of 876 in North America, 747 in South America, and 605 in Europe. This study demonstrates that the fossil fuel component of PM2.5 contributes a large mortality burden. The steeper concentration-response function slope at lower concentrations leads to larger estimates than previously found in Europe and North America, and the slower drop-off in slope at higher concentrations results in larger estimates in Asia. Fossil fuel combustion can be more readily controlled than other sources and precursors of PM2.5 such as dust or wildfire smoke, so this is a clear message to policymakers and stakeholders to further incentivize a shift to clean sources of energy.
Published Apr 1, 2021
Karn Vohra, Alina Vodonos, Joel Schwartz, Eloise A. Marais, Melissa P. Sulprizio, Loretta J. Mickley, Global mortality from outdoor fine particle pollution generated by fossil fuel combustion: Results from GEOS-Chem, Environmental Research, Volume 195, 2021,110754, ISSN 0013-9351, https://doi.org/10.1016/j.envres.2021.110754.
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 (NO2), black carbon (BC), and fine particulate matter [PM ≤ 2.5μm in aerodynamic diameter (PM2.5)] using epidemiologically derived health impact functions. We compared geographic distributions of pollution-attributable risk estimates using concentrations from a) mobile monitoring of NO2 and BC; and b) models predicting annual NO2, BC and PM2.5 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 NO2 [mean=30 (95% CI: 9, 50)], BC [mean=2 (95% CI: 1, 2)], and PM2.5, [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 NO2-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 NO2 and PM2.5, with more spatial heterogeneity at the grid-cell-level [NO2 CBG mean=41 deaths per 100,000 people (95% CI: 12, 68); NO2 county mean=38 (95% CI: 11, 64); PM2.5 CBG mean=59 (95% CI: 40, 77); and PM2.5
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.
Published Mar 31, 2021
Southerland VA, Anenberg SC, Harris M, Apte J, Hystad P, van Donkelaar A, Martin RV, Beyers M, Roy A. Assessing the Distribution of Air Pollution Health Risks within Cities: A Neighborhood-Scale Analysis Leveraging High-Resolution Data Sets in the Bay Area, California. Environ Health Perspect. 2021 Mar;129(3):37006. doi: 10.1289/EHP7679. Epub 2021 Mar 31. PMID: 33787320; PMCID: PMC8011332.
Exposure to ambient PM2.5 pollution has been linked to multiple adverse health effects. Additional effects have been identified in the literature and there is a need to understand its potential role in high prevalence diseases. In response to recent indications of PM2.5 as a risk factor for dementia, we examine the evidence by systematically reviewing the epidemiologic literature, in relation to exposure from ambient air pollution, household air pollution, secondhand smoke, and active smoking. We develop preliminary exposure-response functions, estimate the uncertainty, and discuss sensitivities and model selection. We estimate the likely impact to be 2.1 M (1.4 M, 2.5 M; 5%–95% confidence) global incident dementia cases and 0.6 M (0.4 M, 0.8 M) deaths attributable to ambient PM2.5 pollution in 2015. This implies a combined toll from morbidity and mortality of dementia of 7.3 M (5.0 M, 9.1 M) lost disability-adjusted life years. China, Japan, India, and the United States had the highest estimated total burden, and the per capita burden was highest in developed countries with large elderly populations. Compared to 2000, most countries in Europe, the Americas, and Southern Africa reduced the burden in 2015, while other regions had a net increase. Based on a recent systematic review of cost of illness studies for dementia, our estimates imply economic costs of US$ 26 billion worldwide in 2015. Based on this estimation, ambient PM2.5 pollution may be responsible for 15% of premature deaths and 7% of DALYs associated with dementia. Our estimates also indicate substantial uncertainty in this relationship, and future epidemiological studies at high exposure levels are especially needed.
Published Mar 27, 2021
Ru, M., Brauer, M., Lamarque, J. F., & Shindell, D. (2021). Exploration of the Global Burden of Dementia Attributable to PM2.5: What Do We Know Based on Current Evidence? GeoHealth, 5(5), e2020GH000356. https://doi.org/10.1029/2020GH000356;SUBPAGE:STRING:FULL
Objective: To evaluate the short term associations between nitrogen dioxide (NO2) and total, cardiovascular, and respiratory mortality across multiple countries/regions worldwide, using a uniform analytical protocol.
Design: Two stage, time series approach, with overdispersed generalised linear models and multilevel meta-analysis.
Setting: 398 cities in 22 low to high income countries/regions.
Main outcome measures: Daily deaths from total (62.8 million), cardiovascular (19.7 million), and respiratory (5.5 million) causes between 1973 and 2018.
Results On average, a 10 μg/m3 increase in NO2 concentration on lag 1 day (previous day) was associated with 0.46% (95% confidence interval 0.36% to 0.57%), 0.37% (0.22% to 0.51%), and 0.47% (0.21% to 0.72%) increases in total, cardiovascular, and respiratory mortality, respectively. These associations remained robust after adjusting for co-pollutants (particulate matter with aerodynamic diameter ≤10 μm or ≤2.5 μm (PM10 and PM2.5, respectively), ozone, sulfur dioxide, and carbon monoxide). The pooled concentration-response curves for all three causes were almost linear without discernible thresholds. The proportion of deaths attributable to NO2 concentration above the counterfactual zero level was 1.23% (95% confidence interval 0.96% to 1.51%) across the 398 cities.
Conclusions This multilocation study provides key evidence on the independent and linear associations between short term exposure to NO2 and increased risk of total, cardiovascular, and respiratory mortality, suggesting that health benefits would be achieved by tightening the guidelines and regulatory limits of NO2.
Published Mar 24, 2021
Meng X, Liu C, Chen R, Sera F, Vicedo-Cabrera A M, Milojevic A et al. Short term associations of ambient nitrogen dioxide with daily total, cardiovascular, and respiratory mortality: multilocation analysis in 398 cities BMJ 2021; 372 :n534 doi:10.1136/bmj.n534
Coal has historically been a primary energy source in the United States (U.S.). The byproducts of coal combustion, such as fine particulate matter (PM2.5), have increasingly been associated with adverse birth outcomes. The goal of this study was to leverage the current progressive transition away from coal in the U.S. to assess whether coal PM2.5 is associated with preterm birth (PTB) rates and whether this association differs by maternal Black/White race/ethnicity. Using a novel dispersion modeling approach, we estimated PM2.5 pollution from coal-fired power plants nationwide at the county-level during the study period (2000–2018). We also obtained county-level PTB rates for non-Hispanic White and non-Hispanic Black mothers. We used a generalized additive mixed model to estimate the relationship between coal PM2.5 and PTB rates, overall and stratified by maternal race. We included a natural spline to allow for non-linearity in the concentration–response curve. We observed a positive non-linear relationship between coal PM2.5 and PTB rate, which plateaued at higher levels of pollution. We also observed differential associations by maternal race; the association was stronger for White women, especially at higher levels of coal PM2.5 (>2.0 μg m−3). Our findings suggest that the transition away from coal may reduce PTB rates in the U.S.
Published Mar 2, 2021
Daouda, M., Henneman, L., Kioumourtzoglou, M. A., Gemmill, A., Zigler, C., & Casey, J. A. (2021). Association between county-level coal-fired power plant pollution and racial disparities in preterm births from 2000 to 2018. Environmental Research Letters, 16(3), 034055. https://doi.org/10.1088/1748-9326/ABE4F7