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Air pollution has been associated with a number of detrimental health effects for children. Another potentially substantive, but previously unappreciated, effect of air pollution on children is diminished academic performance, presumably resulting in reduced human capital accumulation and reduced future earnings. In this paper we investigate the relationship between outdoor air pollution levels and standardized state test scores of California public school children. To do this we combine individual family data and community pollution data from the Children's Health Study (CHS), a longitudinal respiratory health study of Southern California school children, with publicly available information on California standardized test scores by grade, school, and year. We find that a 10% decrease in outdoor PM 10 , PM 2.5 , or NO 2 would raise math test scores by 0.15%, 0.34%, or 0.18%, while a 10% decrease in outdoor PM 2.5 increases reading scores by 0.21%. To put these effects in perspective, if it were possible to reduce PM 2.5 by 10% for low-income students but not for high-income students, the gap in math test scores between high-and low-income 8 th grade students would fall by nearly one thirtieth. 2

Published Dec 1, 2009

Zweig, J. S., Ham, J. C., & Avol, E. L. (2009). Air Pollution and Academic Performance: Evidence from California Schools. https://radic8.com/wp-content/uploads/2017/12/test-scores-submit-1.pdf

OBJECTIVE: This study evaluated the relationship between prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAHs) and child intelligence.

METHODS: Children of nonsmoking black or Dominican-American women residing in New York City were monitored from in utero to 5 years of age, with determination of prenatal PAH exposure through personal air monitoring for the mothers during pregnancy. At 5 years of age, intelligence was assessed for 249 children by using the Wechsler Preschool and Primary Scale of Intelligence-Revised. Multivariate linear regression models were used to estimate and to test the associations between prenatal PAH exposure and IQ.

RESULTS: After adjustment for maternal intelligence, quality of the home caretaking environment, environmental tobacco smoke exposure, and other potentially confounding factors, high PAH levels (above the median of 2.26 ng/m3) were inversely associated with full-scale IQ (P = .007) and verbal IQ (P = .003) scores. Children in the high-exposure group had full-scale and verbal IQ scores that were 4.31 and 4.67 points lower, respectively, than those of less-exposed children (≤2.26 ng/m3). The associations between logarithmically transformed, continuous, PAH levels and these IQ measures also were significant (full-scale IQ: β = −3.00; P = .009; verbal IQ: β = −3.53; P = .002).

CONCLUSION: These results provide evidence that environmental PAHs at levels encountered in New York City air can affect children's IQ adversely.

Published Aug 1, 2009

Perera, F. P., Li, Z., Whyatt, R., Hoepner, L., Wang, S., Camann, D., & Rauh, V. (2009). Prenatal airborne polycyclic AROMATIC hydrocarbon exposure and Child IQ at age 5 years. PEDIATRICS, 124(2). doi:10.1542/peds.2008-3506

An investigation of the potential environmental and health impacts in the immediate aftermath of one of the largest coal ash spills in U.S. history at the Tennessee Valley Authority (TVA) Kingston coal-burning power plant has revealed three major findings. First, the surface release of coal ash with high levels of toxic elements (As = 75 mg/kg; Hg = 150 μg/kg) and radioactivity (226Ra + 228Ra = 8 pCi/g) to the environment has the potential to generate resuspended ambient fine particles (<10 μm) containing these toxics into the atmosphere that may pose a health risk to local communities. Second, leaching of contaminants from the coal ash caused contamination of surface waters in areas of restricted water exchange, but only trace levels were found in the downstream Emory and Clinch Rivers due to river dilution. Third, the accumulation of Hg- and As-rich coal ash in river sediments has the potential to have an impact on the ecological system in the downstream rivers by fish poisoning and methylmercury formation in anaerobic river sediments.

Published May 4, 2009

Ruhl, L., Vengosh, A., Dwyer, G. S., Hsu-Kim, H., Deonarine, A., Bergin, M., & Kravchenko, J. (2009). Survey of the Potential Environmental and Health Impacts in the Immediate Aftermath of the Coal Ash Spill in Kingston, Tennessee. Environmental Science & Technology, 43(16), 6326–6333. https://doi.org/10.1021/es900714p

Outdoor air pollution at levels occurring in many urban areas around the world has substantial adverse effects on health. Children in general, and children with asthma in particular, are sensitive to the adverse effects of outdoor air pollutants, including ozone, nitrogen oxides, and respirable particulate matter. A growing number of studies also show that children living in environments near traffic have increased risks of new-onset asthma, asthma symptoms, exacerbations, school absences, and asthma-related hospitalizations. The large population of children exposed to high levels of outdoor air pollutants and the substantial risks for adverse health effects present unexploited opportunities to reduce the burden of asthma. Because the evidence indicates significant adverse effects of air pollution at current levels, there is clearly a need to reduce levels of regulated pollutants such as ozone, as well as unregulated pollutants in tailpipe emissions from motor vehicles. Achieving this long-term goal requires the active involvement of physicians and medical providers to ensure that the health of children is at the top of the list of competing priorities for regulatory policy decision-making. Clinical approaches include treatment to control asthma and patient education to reduce adverse effects of the disease. Reduction in exposures also can be approached at a policy level through changes in schools and school bus operations. Beyond clinical and public health approaches to reduce exposure, another strategy to be used before clean air goals are met is to decrease the susceptibility of children to air pollution. Emerging research indicates that dietary supplementation for individuals with low antioxidant levels is one promising ap- proach to reducing susceptibility to air pollution. A second approach involves induction of enzymatic antioxidant defenses, especially for individuals with at-risk genetic variants of key antioxidant enzymes. Copyright © 2009 by the American Academy of Pediatrics.

Published Mar 1, 2009

Gilliland, F. D. (2009). Outdoor air pollution, genetic susceptibility, and asthma management: Opportunities for intervention to reduce the burden of asthma. Pediatrics, 123(SUPPL. 3), 14–16. https://doi.org/10.1542/peds.2008-2233G

Rationale: There are unexplained geographical and seasonal differences in the short-term effects of fine particulate matter (PM 2.5) on human health. The hypothesis has been advanced to include the possibility that such differences might be due to variations in the PM 2.5 chemical composition, but evidence supporting this hypothesis is lacking. Objectives: To examine whether variation in the relative risks (RR) of hospitalization associated with ambient exposure to PM 2.5 total mass reflects differences in PM 2.5 chemical composition. Methods: We linked two national datasets by county and by season: (1) long-term average concentrations of PM 2.5 chemical components for 2000-2005 and (2) RRs of cardiovascular and respiratory hospitalizations for persons 65 years or older associated with a 10-mg/m 3 increase in PM 2.5 total mass on the same day for 106 U.S. counties for 1999 through 2005. Measurements and Main Results: We found a positive and statistically significant association between county-specific estimates of the short-term effects of PM 2.5 on cardiovascular and respiratory hospitalizations and county-specific levels of vanadium, elemental carbon , or nickel PM 2.5 content. Conclusions: Communities with higher PM 2.5 content of nickel, vanadium, and elemental carbon and/or their related sources were found to have higher risk of hospitalizations associated with short-term exposure to PM 2.5. Statistically significant associations between short-term exposure to airborne particulate matter (PM) and mortality and morbidity have been reported in numerous multicity studies (1-6). Several studies also found that health effect estimates vary substantially across communities and seasons (4, 7, 8). The findings of these studies support the hypothesis that geographical and seasonal heteroge-neity of community-specific relative rates could be explained by differences in the chemical composition of PM 2.5 (PM with aerodynamic diameter <2.5 mm). Animal and human toxicological studies support this hypothesis (9-12). However, empirical population-based evidence supporting this hypothesis is lacking. Understanding the basis of the variation in PM effects is critical to further characterize the biological mechanisms of toxicity and to move toward more focused regulatory approaches for PM (13). We investigated whether particular PM 2.5 chemical components are responsible for observed geographical and seasonal variation in the short-term association of PM 2.5 with hospital admissions (4, 7). We also performed a similar analysis based on effect estimates for PM 10 and mortality (see online supplement). METHODS We analyzed whether community-specific estimates of the impact of PM on health risk (cardiovascular and respiratory hospital admissions and mortality) were higher or lower in communities or seasons with particular PM 2.5 chemical composition, as indicated by the fraction of PM 2.5 total mass that is a particular component (e.g., elemental carbon [EC]). We estimated county-and season-specific relative risks (RR) of cardiovascular and respiratory hospitalization associated with a 10-mg/m 3 increase in PM 2.5 total mass on the same day for 106 U.S. counties for the years 1999 through 2005 (Figures 1 and 2). Counties were selected based on data availability for PM 2.5 total mass and chemical components and on having a population of 200,000 or more persons to allow for sufficient sample size and to allow a distribution of counties across the United States. The population criterion results in more urban counties. We conducted similar analysis for PM 10 and total nonaccidental mortality in 100 U.S. communities for 1987 through 2000 (see Figure E1 in the online supplement) (8). All county-and season-specific effect estimates were adjusted for day of the week, seasonality, and long-term trends based on a smooth function of a variable representing time by including these variables in the county-specific regression models. We adjusted for daily temperature and dew point temperature and for the previous 3 days' temperature and dew point temperature. Details of the methods are provided elsewhere (4, 7, 8). We generated a national database of PM 2.5 chemical component concentrations from February 2000 to December 2005 based on data obtained from the U.S. Environmental Protection Agency (USEPA) (14). We calculated county-and season-specific averages of PM 2.5 chemical components that were demonstrated to contribute a substantial fraction of PM 2.5 total mass (14) or to have been implicated as potentially toxic in earlier research (11, 15-18) (Table 1). Detailed information on the spatial and temporal variation of the PM 2.5 chemical components is provided elsewhere (14). We then calculated the fraction of PM 2.5 total mass for each component by season and county. Chemical composition data were available for 106 of the 200 AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Although airborne particulate matter (PM) has been linked to adverse human health effects, the chemical constituents that cause harm are unknown. The relationship between PM and health varies seasonally and regionally , as does the particle's chemical composition. What This Study Adds to the Field This work provides evidence that the chemical composition of PM affects its toxicity. In places and during seasons when PM had higher fractions of nickel, vanadium, and elemental carbon, the risks of hospital admission associated with PM with aerodynamic diameter < 2.5 mm were higher.

Published Oct 7, 2008

Bell, M. L., Ebisu, K., Peng, R. D., Samet, J. M., & Dominici, F. (2009). Hospital Admissions and Chemical Composition of Fine Particle Air Pollution. Am J Respir Crit Care Med, 179, 1115–1120. https://doi.org/10.1164/rccm.200808-1240OC

The question of whether air pollution contributes to asthma onset remains unresolved. Objectives: In this study, we assessed the association between asthma onset in children and traffic-related air pollution. Methods: We selected a sample of 217 children from participants in the Southern California Children's Health Study, a prospective cohort designed to investigate associations between air pollution and respiratory health in children 10-18 years of age. Individual covariates and new asthma incidence (30 cases) were reported annually through questionnaires during 8 years of follow-up. Children had nitrogen dioxide monitors placed outside their home for 2 weeks in the summer and 2 weeks in the fall-winter season as a marker of traffic-related air pollution. We used multilevel Cox models to test the associations between asthma and air pollution. Results: In models controlling for confounders, incident asthma was positively associated with traffic pollution, with a hazard ratio (HR) of 1.29 [95% confidence interval (CI), 1.07-1.56] across the average within-community interquartile range of 6.2 ppb in annual residential NO2. Using the total interquartile range for all measurements of 28.9 ppb increased the HR to 3.25 (95% CI, 1.35-7.85). Conclusions: In this cohort, markers of traffic-related air pollution were associated with the onset of asthma. The risks observed suggest that air pollution exposure contributes to new-onset asthma.

Published Oct 1, 2008

Jerrett, M., Shankardass, K., Berhane, K., Gauderman, W. J., Künzli, N., Avol, E., Gilliland, F., Lurmann, F., Molitor, J. N., Molitor, J. T., Thomas, D. C., Peters, J., & McConnell, R. (2008). Traffic-related air pollution and asthma onset in children: A prospective cohort study with individual exposure measurement. Environmental Health Perspectives, 116(10), 1433–1438. https://doi.org/10.1289/ehp.10968

Background
Coal burning provides 70% of the energy for China’s industry and power, but releases large quantities of polycyclic aromatic hydrocarbons (PAHs) and other pollutants. PAHs are reproductive and developmental toxicants, mutagens, and carcinogens.

Objective
We evaluated the benefit to neurobehavioral development from the closure of a coal-fired power plant that was the major local source of ambient PAHs.

Methods
The research was conducted in Tongliang, Chongqing, China, where a coal-fired power plant operated seasonally before it was shut down in May 2004. Two identical prospective cohort studies enrolled nonsmoking women and their newborns in 2002 (before shutdown) and 2005 (after shutdown). Prenatal PAH exposure was measured by PAH–DNA adducts (benzo[a]pyrene–DNA) in umbilical cord blood. Child development was assessed by the Gesell Developmental Schedules at 2 years of age. Prenatal exposure to other neurotoxicants and potential confounders (including lead, mercury, and environmental tobacco smoke) was measured. We compared the cohorts regarding the association between PAH–DNA adduct levels and neurodevelopmental outcomes.

Results
Significant associations previously seen in 2002 between elevated adducts and decreased motor area developmental quotient (DQ) (p = 0.043) and average DQ (p = 0.047) were not observed in the 2005 cohort (p = 0.546 and p = 0.146). However, the direction of the relationship did not change.

Conclusion
The findings indicate that neurobehavioral development in Tongliang children benefited by elimination of PAH exposure from the coal-burning plant, consistent with the significant reduction in PAH–DNA adducts in cord blood of children in the 2005 cohort. The results have implications for children’s environmental health in China and elsewhere.

Published Oct 1, 2008

Frederica Perera, Tin-yu Li, Zhi-jun Zhou, Tao Yuan, Yu-hui Chen, Lirong Qu, Virginia A. Rauh, Yiguan Zhang, and Deliang Tang 2008 Benefits of Reducing Prenatal Exposure to Coal-Burning Pollutants to Children’s Neurodevelopment in China Environmental Health Perspectives 116:10 CID: https://doi.org/10.1289/ehp.11480

Background: Environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs), lead, and mercury are released by combustion of coal and other fossil fuels.

Objectives: In the present study we evaluated the association between prenatal exposure to these pollutants and child development measured by the Gesell Developmental Schedules at 2 years of age.

Methods: The study was conducted in Tongliang, Chongqing, China, where a seasonally operated coal-fired power plant was the major source of ambient PAHs and also contributed lead and mercury to the air. In a cohort of nonsmoking women and their newborns enrolled between March 2002 and June 2002, we measured levels of PAH-DNA adducts, lead, and mercury in umbilical cord blood. PAH-DNA adducts (specifically benzo[a]pyrene adducts) provided a biologically relevant measure of PAH exposure. We also obtained developmental quotients (DQs) in motor, adaptive, language, and social areas.

Results: Decrements in one or more DQs were significantly associated with cord blood levels of PAH-DNA adducts and lead, but not mercury. Increased adduct levels were associated with decreased motor area DQ (p = 0.043), language area DQ (p = 0.059), and average DQ (p = 0.047) after adjusting for cord lead level, environmental tobacco smoke, sex, gestational age, and maternal education. In the same model, high cord blood lead level was significantly associated with decreased social area DQ (p = 0.009) and average DQ (p = 0.038).

Conclusion: The findings indicate that exposure to pollutants from the power plant adversely affected the development of children living in Tongliang; these findings have implications for environmental health policy.

Published May 1, 2008

Tang, D., Li, T. Y., Liu, J. J., Zhou, Z. J., Yuan, T., Chan, Y. H., Rauh, V. A., Xie, J., & Perera, F. (2008). Effects of prenatal exposure to coal-burning pollutants on children’s development in China. Environmental Health Perspectives, 116(5), 674–679. https://doi.org/10.1289/EHP.10471

We used data from a survey of 16493 West Virginians merged with county-level coal production and other covariates to investigate the relations between health indicators and residential proximity to coal mining. Results of hierarchical analyses indicated that high levels of coal production were associated with worse adjusted health status and with higher rates of cardiopulmonary disease, chronic obstructive pulmonary disease, hypertension, lung disease, and kidney disease. Research is recommended to ascertain the mechanisms, magnitude, and consequences of a community coal-mining exposure effect.

Published Apr 1, 2008

Hendryx, M., & Ahern, M. M. (2008). Relations between health indicators and residential proximity to coal mining in West Virginia. American Journal of Public Health, 98(4), 669–671. https://doi.org/10.2105/AJPH.2007.113472

Since Hurricane Katrina made landfall, there have been accusations of blatant racism in the government's response, on the one hand, and adamant denials that race played any role at all, on the other. We propose that both perspectives reflect oversimplifications of the processes involved, and the resulting debate may obscure a deeper understanding of the dynamics of the situation. Specifically, we discuss the potential roles of institutional discrimination, subtle contemporary biases, and racial mistrust. The operation of these processes is illustrated with events associated with Hurricane Katrina. In addition, drawing on these principles, we offer suggestions for present and future recovery efforts.© 2006 The Society for the Psychological Study of Social Issues.

Published Dec 21, 2006

Henkel, K. E., Dovidio, J. F., & Gaertner, S. L. (2006). Institutional Discrimination, Individual Racism, and Hurricane Katrina. Analyses of Social Issues and Public Policy, 6(1), 99–124. https://doi.org/10.1111/j.1530-2415.2006.00106.x