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BACKGROUND AND AIM: Research supports the adverse effect of air pollution exposures on child cognitive performance and behavior, but few studies have utilized spatiotemporally resolved pollution predictions. METHODS: We investigated these associations in 1,894 mother-child dyads from three U.S. pregnancy cohorts (CANDLE, TIDES, GAPPS) in the ECHO-PATHWAYS Consortium. Child cognition was assessed using cohort-specific intelligence scales and quantified as the Full-Scale Intelligence Quotient (IQ). Child behavior was reported using the Child Behavior Checklist and quantified as the total problems raw score. Pre- and postnatal nitrogen dioxide (NO2) and particulate matter ≤2.5μm in aerodynamic diameter (PM2.5) were derived from an advanced spatiotemporal model. We fit multivariate linear regressions, adjusted for sociodemographic, behavioral, and psychological factors, to measure associations per 2-unit increase in pollutant in each window, and examined modification by child sex using interaction models. RESULTS: Mean PM2.5 and NO2 ranged from 8.4-9.1 µg/m3 and 8.4-9.0 ppb, respectively, across pre-and postnatal windows. Average child IQ and total problems raw score at 4-6 years were 102.7 (SD:15.3) and 22.6 (SD:18.3). Children with a higher 3rd trimester NO2 exposure had a lower IQ (β=-0.44, 95%CI: -0.81, -0.07). Each 2-ppb increase of NO2 in the 2nd trimester and averaged over pregnancy was associated with a 0.68 (95%CI: 0.09, 1.27) and a 0.85 (95%CI: 0.09, 1.61) higher total problems raw score, respectively. Prenatal PM2.5 was only associated with a higher total problems score (β=1.94, 95%CI: 0.11, 3.76), while PM2.5 at 2-4 years was associated with both outcomes (IQ: β=-2.30, 95%CI: -4.53, 0.08; Total problems: β=3.00, 95%CI: 0.21, 5.78). Other associations were null. No modification by child sex was suggested. CONCLUSIONS: The findings build on the current literature on air pollution and child neurodevelopment by using more refined exposure assessments across several pre- and postnatal windows in settings with modest air pollution levels.

Published Aug 23, 2021

Ni, Y., Loftus, C. T., Szpiro, A. A., Young, M. T., Hazlehurst, M. F., Murphy, L. E., Tylavsky, F. A., Mason, A. W., Lewinn, K. Z., Sathyanarayana, S., Barrett, E. S., Bush, N. R., & Karr, C. J. (2021). Associations of Pre- and Postnatal Air Pollution Exposures with Child Cognitive Performance and Behavior: A Multi-cohort Study. ISEE Conference Abstracts, 2021(1). https://doi.org/10.1289/ISEE.2021.P-492

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

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