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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 and Health | Climate Change and Mental Health | Systemic Environmental Racism | Vehicles/Traffic
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.
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.
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. (https://www.sciencedirect.com/science/article/pii/S0013935121000487)
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.
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.
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
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
Electricity generation is a large contributor to fine particulate matter (PM2.5) air pollution. However, the demographic distribution of the resulting exposure is largely unknown. We estimate exposures to and health impacts of PM2.5 from electricity generation in the US, for each of the seven Regional Transmission Organizations (RTOs), for each US state, by income and by race. We find that average exposures are the highest for blacks, followed by non-Latino whites. Exposures for remaining groups (e.g., Asians, Native Americans, Latinos) are somewhat lower. Disparities by race/ethnicity are observed for each income category, indicating that the racial/ethnic differences hold even after accounting for differences in income. Levels of disparity differ by state and RTO. Exposures are higher for lower-income than for higher-income, but disparities are larger by race than by income. Geographically, we observe large differences between where electricity is generated and where people experience the resulting PM2.5 health consequences; some states are net exporters of health impacts, other are net importers. For 36 US states, most of the health impacts are attributable to emissions in other states. Most of the total impacts are attributable to coal rather than other fuels.
Published Nov 20, 2020
Maninder P. S. Thind, Christopher W. Tessum, Inês L. Azevedo, and Julian D. Marshall Environmental Science & Technology 2019 53 (23), 14010-14019 DOI: 10.1021/acs.est.9b02527
Assessing whether long-term exposure to air pollution increases the severity of COVID-19 health outcomes, including death, is an important public health objective. Limitations in COVID-19 data availability and quality remain obstacles to conducting conclusive studies on this topic. At present, publicly available COVID-19 outcome data for representative populations are available only as area-level counts. Therefore, studies of long-term exposure to air pollution and COVID-19 outcomes using these data must use an ecological regression analysis, which precludes controlling for individual-level COVID-19 risk factors. We describe these challenges in the context of one of the first preliminary investigations of this question in the United States, where we found that higher historical PM2.5 exposures are positively associated with higher county-level COVID-19 mortality rates after accounting for many area-level confounders. Motivated by this study, we lay the groundwork for future research on this important topic, describe the challenges, and outline promising directions and opportunities.
Published Nov 4, 2020
Wu, X., Nethery, R. C., Sabath, M. B., Braun, D., & Dominici, F. (2020). Air pollution and COVID-19 mortality in the United States: Strengths and limitations of an ecological regression analysis. Science Advances, 6(45). doi:10.1126/sciadv.abd4049
Accumulating evidence links fine particulate matter (PM2·5) to premature mortality, cardiovascular disease, and respiratory disease. However, less is known about the influence of PM2·5 on neurological disorders. We aimed to investigate the effect of long-term PM2·5 exposure on development of Parkinson's disease or Alzheimer's disease and related dementias.
Between Jan 1, 2000, and Dec 31, 2016, of 63 038 019 individuals who were aged 65 years or older during the study period, we identified 1·0 million cases of Parkinson's disease and 3·4 million cases of Alzheimer's disease and related dementias based on primary and secondary diagnosis billing codes. For each 5 μg/m3 increase in annual PM2·5 concentrations, the HR was 1·13 (95% CI 1·12–1·14) for first hospital admission for Parkinson's disease and 1·13 (1·12–1·14) for first hospital admission for Alzheimer's disease and related dementias. For both outcomes, there was strong evidence of linearity at PM2·5 concentrations less than 16 μg/m3 (95th percentile of the PM2·5 distribution), followed by a plateaued association with increasingly larger confidence bands.
Published Oct 19, 2020
Shi, L., Wu, X., Danesh Yazdi, M., Braun, D., Abu Awad, Y., Wei, Y., Liu, P., Di, Q., Wang, Y., Schwartz, J., Dominici, F., Kioumourtzoglou, M.-A., & Zanobetti, A. (2020). Long-term effects of PM2·5 on neurological disorders in the American Medicare population: a longitudinal cohort study. The Lancet Planetary Health, 0(0). https://doi.org/10.1016/S2542-5196(20)30227-8
Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents.
Published Oct 16, 2020
Prunicki, M., Cauwenberghs, N., Ataam, J.A. et al. Immune biomarkers link air pollution exposure to blood pressure in adolescents. Environ Health 19, 108 (2020). https://rdcu.be/cdiQM