Research Hub

Background
Growing evidence suggests that air pollution exposure may adversely affect the brain and increase risk for psychiatric disorders such as schizophrenia and depression. However, little is known about the potential role of air pollution in severity and relapse following illness onset.

Aims
To examine the longitudinal association between residential air pollution exposure and mental health service use (an indicator of illness severity and relapse) among individuals with first presentations of psychotic and mood disorders.

Method
We identified individuals aged ≥15 years who had first contact with the South London and Maudsley NHS Foundation Trust for psychotic and mood disorders in 2008–2012 (n = 13 887). High-resolution (20 × 20 m) estimates of nitrogen dioxide (NO2), nitrogen oxides (NOx) and particulate matter (PM2.5 and PM10) levels in ambient air were linked to residential addresses. In-patient days and community mental health service (CMHS) events were recorded over 1-year and 7-year follow-up periods.

Results
Following covariate adjustment, interquartile range increases in NO2, NOx and PM2.5 were associated with 18% (95% CI 5–34%), 18% (95% CI 5–34%) and 11% (95% CI 3–19%) increased risk for in-patient days after 1 year. Similarly, interquartile range increases in NO2, NOx, PM2.5 and PM10 were associated with 32% (95% CI 25–38%), 31% (95% CI 24–37%), 7% (95% CI 4–11%) and 9% (95% CI 5–14%) increased risk for CMHS events after 1 year. Associations persisted after 7 years.

Conclusions
Residential air pollution exposure is associated with increased mental health service use among people recently diagnosed with psychotic and mood disorders. Assuming causality, interventions to reduce air pollution exposure could improve mental health prognoses and reduce healthcare costs.

Published Aug 19, 2021

Newbury, J. B., Stewart, R., Fisher, H. L., Beevers, S., Dajnak, D., Broadbent, M., Pritchard, M., Shiode, N., Heslin, M., Hammoud, R., Hotopf, M., Hatch, S. L., Mudway, I. S., & Bakolis, I. (2021). Association between air pollution exposure and mental health service use among individuals with first presentations of psychotic and mood disorders: retrospective cohort study. The British Journal of Psychiatry, 219(6), 678–685. https://doi.org/10.1192/BJP.2021.119

The year 2020 brought unimaginable challenges in public health, with the confluence of the COVID-19 pandemic and wildfires across the western United States. Wildfires produce high levels of fine particulate matter (PM2.5). Recent studies reported that short-term exposure to PM2.5 is associated with increased risk of COVID-19 cases and deaths. We acquired and linked publicly available daily data on PM2.5, the number of COVID-19 cases and deaths, and other confounders for 92 western U.S. counties that were affected by the 2020 wildfires. We estimated the association between short-term exposure to PM2.5 during the wildfires and the epidemiological dynamics of COVID-19 cases and deaths. We adjusted for several time-varying confounding factors (e.g., weather, seasonality, long-term trends, mobility, and population size). We found strong evidence that wildfires amplified the effect of short-term exposure to PM2.5 on COVID-19 cases and deaths, although with substantial heterogeneity across counties.

Published Aug 13, 2021

Zhou, X., Josey, K., Kamareddine, L., Caine, M. C., Liu, T., Mickley, L. J., Cooper, M., & Dominici, F. (2021). Excess of COVID-19 cases and deaths due to fine particulate matter exposure during the 2020 wildfires in the United States. Science Advances, 7(33), 8789–8802. https://doi.org/10.1126/SCIADV.ABI8789

Alzheimer’s disease (AD), non-AD dementia, and Parkinson’s disease (PD) are increasingly common in older adults, yet all risk factors for their onset are not fully understood. Consequently, environmental exposures, including air pollution, have been hypothesized to contribute to the etiology of neurodegeneration. Because persistently elevated rates of AD mortality in the southern Piedmont area of North Carolina (NC) have been documented, we studied mortality and hospital admissions for AD, non-AD dementia, and PD in residential populations aged 65+ with long-term exposures to elevated levels of ambient air particulate matter 2.5 (PM2.5) exceeding the World Health Organization (WHO) air quality standards (≥10μg/m3). Health data were obtained from the State Center for Health Statistics and the Healthcare Cost and Utilization Project. PM2.5 levels were obtained from the MODIS/MISR and SeaWiFS datafiles. Residents in the Study group of elevated air particulate matter (87 zip codes with PM2.5≥10μg/m3) were compared to the residents in the Control group with low levels of air particulate matter (81 zip codes with PM2.5≤7.61μg/m3), and were found to have higher age-adjusted rates of mortality and hospital admissions for AD, non-AD dementia, and PD, including a most pronounced increase in AD mortality (323/100,000 vs. 257/100,000, respectively). After adjustment for multiple co-factors, the risk of death (odds ratio, or OR) from AD in the Study group (OR = 1.35, 95%CI[1.24–1.48]) was significantly higher than ORs of non-AD dementia or PD (OR = 0.97, 95%CI[0.90–1.04] and OR = 1.13, 95%CI[0.92–1.31]). The OR of hospital admissions was significantly increased only for AD as a primary case of hospitalization (OR = 1.54, 95%CI[1.31–1.82]). Conclusion: NC residents aged 65+ with long-term exposures to ambient PM2.5 levels exceeding the WHO standard had significantly increased risks of death and hospital admissions for AD. The effects for non-AD dementia and PD were less pronounced.

Published Jul 9, 2021

Rhew, S. H., Kravchenko, J., & Lyerly, H. K. (2021). Exposure to low-dose ambient fine particulate matter PM2.5 and Alzheimer’s disease, non-Alzheimer’s dementia, and Parkinson’s disease in North Carolina. PLOS ONE, 16(7), e0253253. https://doi.org/10.1371/JOURNAL.PONE.0253253

Ambient fine particulate matter (PM2.5) is the world’s leading environmental health risk factor. Reducing the PM2.5 disease burden requires specific strategies that target dominant sources across multiple spatial scales. We provide a contemporary and comprehensive evaluation of sector- and fuel-specific contributions to this disease burden across 21 regions, 204 countries, and 200 sub-national areas by integrating 24 global atmospheric chemistry-transport model sensitivity simulations, high-resolution satellite-derived PM2.5 exposure estimates, and disease-specific concentration response relationships. Globally, 1.05 (95% Confidence Interval: 0.74–1.36) million deaths were avoidable in 2017 by eliminating fossil-fuel combustion (27.3% of the total PM2.5 burden), with coal contributing to over half. Other dominant global sources included residential (0.74 [0.52–0.95] million deaths; 19.2%), industrial (0.45 [0.32–0.58] million deaths; 11.7%), and energy (0.39 [0.28–0.51] million deaths; 10.2%) sectors. Our results show that regions with large anthropogenic contributions generally had the highest attributable deaths, suggesting substantial health benefits from replacing traditional energy sources.

Published Jun 14, 2021

McDuffie, E. E., Martin, R. v., Spadaro, J. v., Burnett, R., Smith, S. J., O’Rourke, P., Hammer, M. S., van Donkelaar, A., Bindle, L., Shah, V., Jaeglé, L., Luo, G., Yu, F., Adeniran, J. A., Lin, J., & Brauer, M. (2021). Source sector and fuel contributions to ambient PM2.5 and attributable mortality across multiple spatial scales. Nature Communications, 12(1), 1–12. https://doi.org/10.1038/S41467-021-23853-Y;TECHMETA

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

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.