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Evidence is growing on the adverse neurodevelopmental effects of exposure to combustion-related air pollution. Project TENDR (Targeting Environmental Neurodevelopmental Risks), a unique collaboration of leading scientists, health professionals, and children’s and environmental health advocates, has identified combustion-related air pollutants as critical targets for action to protect healthy brain development. We present policy recommendations for maintaining and strengthening federal environmental health protections, advancing state and local actions, and supporting scientific research to inform effective strategies for reducing children’s exposures to combustion-related air pollution. Such actions not only would improve children’s neurological development but also would have the important co-benefit of climate change mitigation and further improvements in other health conditions.

Published Aug 26, 2019

Payne-Sturges, D. C., Marty, M. A., Perera, F., Miller, M. D., Swanson, M., Ellickson, K., Cory-Slechta, D. A., Ritz, B., Balmes, J., Anderko, L., Talbott, E. O., Gould, R., & Hertz-Picciotto, I. (2019). Healthy air, healthy brains: Advancing air pollution policy to protect children’s health. American Journal of Public Health, 109(4), 550–554. https://doi.org/10.2105/AJPH.2018.304902

The search for the genetic factors underlying complex neuropsychiatric disorders has proceeded apace in the past decade. Despite some advances in identifying genetic variants associated with psychiatric disorders, most variants have small individual contributions to risk. By contrast, disease risk increase appears to be less subtle for disease-predisposing environmental insults. In this study, we sought to identify associations between environmental pollution and risk of neuropsychiatric disorders. We present exploratory analyses of 2 independent, very large datasets: 151 million unique individuals, represented in a United States insurance claims dataset, and 1.4 million unique individuals documented in Danish national treatment registers. Environmental Protection Agency (EPA) county-level environmental quality indices (EQIs) in the US and individual-level exposure to air pollution in Denmark were used to assess the association between pollution exposure and the risk of neuropsychiatric disorders. These results show that air pollution is significantly associated with increased risk of psychiatric disorders. We hypothesize that pollutants affect the human brain via neuroinflammatory pathways that have also been shown to cause depression-like phenotypes in animal studies.

Published Aug 20, 2019

Khan, A., Plana-Ripoll, O., Antonsen, S., Brandt, J., Geels, C., Landecker, H., Sullivan, P. F., Pedersen, C. B., & Rzhetsky, A. (2019). Environmental pollution is associated with increased risk of psychiatric disorders in the US and Denmark. PLOS Biology, 17(8), e3000353. https://doi.org/10.1371/JOURNAL.PBIO.3000353

BACKGROUND: Telomere length is a molecular marker of biological aging. OBJECTIVE: Here we investigated whether early-life exposure to residential air pollution was associated with leukocyte telomere length (LTL) at 8 y of age. METHODS: In a multicenter European birth cohort study, HELIX (Human Early Life Exposome) (n= 1,396), we estimated prenatal and 1-y childhood exposure to nitrogen dioxide (NO2), particulate matter with aerodynamic diameter ≤2:5 lm (PM2:5), and proximity to major roads. Average relative LTL was measured using quantitative real-time polymerase chain reaction (qPCR). Effect estimates of the association between LTL and prenatal, 1-y childhood air pollution, and proximity to major roads were calculated using multiple linear mixed models with a random cohort effect and adjusted for relevant covariates. RESULTS: LTL was inversely associated with prenatal and 1-y childhood NO2 and PM2:5 exposures levels. Each standard deviation (SD) increase in prenatal NO2 was associated with a −1:5% (95% CI: −2:8, −0:2) change in LTL. Prenatal PM2:5 was nonsignificantly associated with LTL (−0:7% per SD increase; 95% CI: −2:0, 0.6). For each SD increment in 1-y childhood NO2 and PM2:5 exposure, LTL shortened by −1:6% (95% CI: −2:9, −0:4) and −1:4% (95% CI: −2:9, 0.1), respectively. Each doubling in residential distance to nearest major road during childhood was associated with a 1.6% (95% CI: 0.02, 3.1) lengthening in LTL. CONCLUSION: Lower exposures to air pollution during pregnancy and childhood were associated with longer telomeres in European children at 8 y of age. These results suggest that reductions in traffic-related air pollution may promote molecular longevity, as exemplified by telomere length, from early life onward.

Published Aug 8, 2019

Clemente, D. B. P., Vrijheid, M., Martens, D. S., Bustamante, M., Chatzi, L., Danileviciute, A., De Castro, M., Grazuleviciene, R., Gutzkow, K. B., Lepeule, J., Maitre, L., McEachan, R. R. C., Robinson, O., Schwarze, P. E., Tamayo, I., Vafeiadi, M., Wright, J., Slama, R., Nieuwenhuijsen, M., & Nawrot, T. S. (2019). Prenatal and childhood traffic-related air pollution exposure and telomere length in european children: The HELIX project. Environmental Health Perspectives, 127(8), 1–8. https://doi.org/10.1289/EHP4148

Telomere shortening is associated with early mortality and chronic disease. Recent studies indicate that environmental exposures, including urban and traffic-related air pollution, may shorten telomeres. Associations between exposure to household air pollution from solid fuel stoves and telomere length have not been evaluated. METHODS: Among 137 rural Chinese women using biomass stoves (mean = 55 y of age), we measured 48-h personal exposures to fine particulate matter [PM ≤ 2:5 μm in aerodynamic diameter (PM2:5)] and black carbon and collected oral DNA on up to three occasions over a period of 2.5 y. Relative telomere length (RTL) was quantified using a modified real-time polymerase chain reaction protocol. Mixed effects regression models were used to investigate the exposure-response associations between household air pollution and RTL, adjusting for key sociodemographic, behavioral, and environmental covariates. RESULTS: Women’s daily exposures to air pollution ranged from 13-1,136 μg=m3 for PM2:5 (mean = 154) and 0:1-34 μg=m3 for black carbon (mean = 3:6). Natural cubic spline models indicated a mostly linear association between increased exposure to air pollution and shorter RTL, except at very high concentrations where there were few observations. We thus modeled the linear associations with all observations, excluding the highest 3% and 5% of exposures. In covariate-adjusted models, an interquartile range (IQR) increase in exposure to black carbon (3:1 μg=m3) was associated with shorter RTL [all observations: −0:27 (95% CI: −0:48, −0:06); excluding highest 5% exposures: −1:10 (95% CI: −1:63, −0:57)]. Further adjustment for outdoor temperature brought the estimates closer to zero [all observations: −0:15 (95% CI: −0:36, 0.06); excluding highest 5% exposures: −0:68 (95% CI: −1:26, −0:10)]. Models with PM2:5 as the exposure metric followed a similar pattern. CONCLUSION: Telomere shortening, which is a biomarker of biological aging and chronic disease, may be associated with exposure to air pollution in settings where household biomass stoves are commonly used.

Published Aug 8, 2019

Li, S., Yang, M., Carter, E., Schauer, J. J., Yang, X., Ezzati, M., Goldberg, M. S., & Baumgartner, J. (2019). Exposure-response associations of household air pollution and buccal cell telomere length in women using biomass stoves. Environmental Health Perspectives, 127(8), 1–11. https://doi.org/10.1289/EHP4041

BACKGROUND: Surrounding green, air pollution, and noise have been associated with cardiometabolic diseases, but most studies have assessed only one of these correlated exposures. OBJECTIVES: We aimed to evaluate associations of combined exposures to green, air pollution, and road traffic noise with cardiometabolic diseases. METHODS: In this cross-sectional study, we studied associations between self-reported physician-diagnosed diabetes, hypertension, heart attack, and stroke from a Dutch national health survey of 387,195 adults and residential surrounding green, annual average air pollutant concentrations [including particulate matter with aerodynamic diameter ≤10 μm (PM10), PM with aerodynamic diameter ≤2:5 μm (PM2:5), nitrogen dioxide (NO2), and oxidative potential (OP) with the dithiothreitol (DTT) assay (OPDTT)] and road traffic noise. Logistic regression models were used to analyze confounding and interaction of surrounding green, air pollution, and noise exposure. RESULTS: In single-exposure models, surrounding green was inversely associated with diabetes, while air pollutants (NO2, OPDTT) and road traffic noise were positively associated with diabetes. In two-exposure analyses, associations with green and air pollution were attenuated but remained. The association between road traffic noise and diabetes was reduced to unity when adjusted for surrounding green or air pollution. Air pollution and surrounding green, but not road traffic noise, were associated with hypertension in single-exposure models. The weak inverse association of surrounding green with hypertension attenuated and lost significance when adjusted for air pollution. Only PM2:5 was associated with stroke and heart attack. CONCLUSIONS: Studies including only one of the correlated exposures surrounding green, air pollution, and road traffic noise may overestimate the association of diabetes and hypertension attributed to the studied exposure. https://doi.org/10.1289/EHP3857.

Published Aug 8, 2019

Klompmaker, J. O., Janssen, N. A. H., Bloemsma, L. D., Gehring, U., Wijga, A. H., Brink, C. Vanden, Lebret, E., Brunekreef, B., & Hoek, G. (2019). Associations of combined exposures to surrounding green, air pollution, and road traffic noise with cardiometabolic diseases. Environmental Health Perspectives, 127(8), 1–15. https://doi.org/10.1289/EHP3857

In the final sentence of the Acknowledgments section, the sentence “Findings and conclusions of this research are those of the authors and do not necessarily represent the views of the National Center for Health Statistics (NCHS) Research Data Center (RDC), the NCHS, the U.S. EPA, or the Centers for Disease Control and Prevention” should be “Findings and conclusions of this research are those of the authors and do not necessarily represent the views of the National Center for Health Statistics (NCHS) Research Data Center (RDC), the NCHS, the U.S. EPA, the Centers for Disease Control and Prevention, or Cornerstone Research.” The authors apologize for the error.

Published Jul 24, 2019

Pope, C. A., Lefler, J. S., Ezzati, M., Higbee, J. D., Marshall, J. D., Kim, S. Y., Bechle, M., Gilliat, K. S., Vernon, S. E., Robinson, A. L., & Burnett, R. T. (2019). Erratum: Mortality risk and fine particulate air pollution in a large, representative cohort of U.S. adults (Environ Health Perspect, (2019), 127, 7, 10.1289/EHP4438). Environmental Health Perspectives, 127(9), 099002–1. https://doi.org/10.1289/EHP6182

In recent decades, epidemiological and experimental research has yielded plenty of evidence that air pollution exposure is a key risk factor for asthma flare-ups and, potentially, new cases.1,2 A study in Environmental Health Perspectives offers the first estimates of the global asthma burden that may be attributable to specific air pollutants.3 Although preliminary, the authors’ conclusions are sobering. They estimated that in 2015, some 9–23 million asthma-induced emergency room visits worldwide resulted from ozone exposure, 5–10 million resulted from fine particulate matter (PM2.5) exposure, and 400,000–500,000 resulted from nitrogen dioxide (NO2) exposure.

Published Jul 17, 2019

Seltenrich, N. (2019). Asthma actors: Estimating how much specific air pollutants contribute to ER visits. Environmental Health Perspectives, 127(7), 9–10. https://doi.org/10.1289/EHP4799

Although several empirical studies and systematic reviews have documented the mental health impacts of global climate change, the range of impacts has not been well understood. This review examines mental health impacts of three types of climate-related events: (1) acute events such as hurricanes, floods, and wildfires; (2) subacute or long-term changes such as drought and heat stress; and (3) the existential threat of long-lasting changes, including higher temperatures, rising sea levels and a permanently altered and potentially uninhabitable physical environment. The impacts represent both direct (i.e. heat stress) and indirect (i.e. economic loss, threats to health and well-being, displacement and forced migration, collective violence and civil conflict, and alienation from a degraded environment) consequences of global climate change.

Published Jun 23, 2019

Palinkas, L. A., & Wong, M. (2020). Global climate change and mental health. In Current Opinion in Psychology (Vol. 32, pp. 12–16). Elsevier B.V. https://doi.org/10.1016/j.copsyc.2019.06.023

Environmental racism plagues the history and contemporary realities of globalization. To control resources, stake holders seek to
dominate lands and peoples in order to produce at a maximum profit. Left in the wake of consumerism are populations of ethnic,
religious, and racial minorities. These groups traditionally have an attachment to ancestral lands they wish to protect or are unable
to compete with large corporations who establish environmentally unfriendly conditions and unfair working situations for underserved populations. Since a mentality of ‘Not in My Backyard’ (NIMBY) perpetuates apathy for addressing iniquities, remediation of
these issues has been slow to non-existent. The value of exploring specific instances and recurring trends within regions of inequity
and destructive ecological policy cannot be understated. Without awareness, change is impossible. Inherently, methodologies used
to analyze current global systems are imperialist in nature and create further distance from the subjects exposed to detrimental
corporate and policy decisions. This research provides an historic overview of globalized environmental racism in order to address
and combat negative choices affecting marginalized communities throughout the world.

Published Jun 21, 2019

Mcintyre-Brewer, C. (2019). Environmental racism throughout the history of economic globalization. AUC Geographica, 54(1), 105–113. https://doi.org/10.14712/23361980.2019.10

Coal-based energy production is the most utilized method of electricity production worldwide and releases the highest concentration of gaseous, particulate, and metallic pollutants. This article aims to systematically review the public health impact of coal-fired power plant emissions on children’s health. PubMed, Web of Science, and Toxline databases were queried for the past 20 years. Inclusion criteria included original scientific articles with (a) coal-fired power plant exposure assessment, (b) at least one primary pediatric health outcome, and (c) assessment of potential sources of confounding and bias. Only morbidity and mortality studies were included; economic analysis and risk assessment studies without a primary health outcome were not included. Of 513 articles initially retrieved, 17 epidemiological articles were included in the final systematic review after screening and eligibility. The articles reviewed showed a statistically significant adverse effect on pediatric neurodevelopment; birth weight and pediatric respiratory morbidity was associated with exposure to coal-fired power plant emissions, primarily particulate matter and polyaromatic hydrocarbon exposure. There is a lack of consistency of exposure assessment and inadequate control of significant potential confounders such as social economic status. Future research should focus on improving exposure assessment models with an emphasis on source-apportionment and geographic information system methods to model power plant-specific emissions.

Published Jun 5, 2019

Amster, E., & Levy, C. L. (2019). Impact of Coal-fired Power Plant Emissions on Children’s Health: A Systematic Review of the Epidemiological Literature. International Journal of Environmental Research and Public Health, 16(11), 2008. https://doi.org/10.3390/IJERPH16112008