Association between prenatal exposure to ambient diesel particulate matter and perchloroethylene with children's 3rd grade standardized test scores.
ABSTRACT: The objective of this research was to determine if prenatal exposure to two common urban air pollutants, diesel and perchloroethylene, affects children's 3rd grade standardized test scores in mathematics and English language arts (ELA). Exposure estimates consisted of annual average ambient concentrations of diesel particulate matter and perchloroethylene obtained from the Environmental Protection Agency's 1996 National Air Toxics Assessment for the residential census tract at birth. Outcome data consisted of linked birth and educational records for 201,559 singleton, non-anomalous children born between 1994 and 1998 who attended New York City public schools. Quantile regression models were used to estimate the effects of these exposures on multiple points within the continuous distribution of standardized test scores. Modified Poisson regression models were used to calculate risk ratios (RR) and 95% confidence intervals (CI) of failing to meet curricula standards, an indicator derived from test scores. Models were adjusted for a number of maternal, neighborhood and childhood factors. Results showed that math scores were approximately 6% of a standard deviation lower for children exposed to the highest levels of both pollutants as compared to children with low levels of both pollutants. Children exposed to high levels of both pollutants also had the largest risk of failing to meet math test standards when compared to children with low levels of exposure to the pollutants (RR 1.10 95%CI 1.07,1.12 RR high perchloroethylene only 1.03 95%CI 1.00,1.06; RR high diesel PM only 1.02 95%CI 0.99,1.06). There was no association observed between exposure to the pollutants and failing to meet ELA standards. This study provides preliminary evidence of associations between prenatal exposure to urban air pollutants and lower academic outcomes. Additionally, these findings suggest that individual pollutants may additively impact health and point to the need to study the collective effects of air pollutant mixtures.air toxics, academic outcomes, urban health, tetrachloroethylene, air pollutant mixtures.
Project description:Genetic and environmental factors are believed to contribute to the development of autism, but relatively few studies have considered potential environmental risks. Here, we examine risks for autism in children related to in utero exposure to monitored ambient air toxics from urban emissions.Among the cohort of children born in Los Angeles County, California, 1995-2006, those whose mothers resided during pregnancy in a 5-km buffer around air toxics monitoring stations were included (n = 148,722). To identify autism cases in this cohort, birth records were linked to records of children diagnosed with primary autistic disorder at the California Department of Developmental Services between 1998 and 2009 (n = 768). We calculated monthly average exposures during pregnancy for 24 air toxics selected based on suspected or known neurotoxicity or neurodevelopmental toxicity. Factor analysis helped us identify the correlational structure among air toxics, and we estimated odds ratios (ORs) for autism from logistic regression analyses.Autism risks were increased per interquartile range increase in average concentrations during pregnancy of several correlated toxics mostly loading on 1 factor, including 1,3-butadiene (OR = 1.59 [95% confidence interval = 1.18-2.15]), meta/para-xylene (1.51 [1.26-1.82]), other aromatic solvents, lead (1.49 [1.23-1.81]), perchloroethylene (1.40 [1.09-1.80]), and formaldehyde (1.34 [1.17-1.52]), adjusting for maternal age, race/ethnicity, nativity, education, insurance type, parity, child sex, and birth year.Risks for autism in children may increase following in utero exposure to ambient air toxics from urban traffic and industry emissions, as measured by community-based air-monitoring stations.
Project description:Numerous studies have associated air pollutant exposures with adverse birth outcomes, but there is still relatively little information to attribute effects to specific emission sources or air toxics. We used three exposure data sources to examine risks of preterm birth in Los Angeles women when exposed to high levels of traffic-related air pollutants--including specific toxics--during pregnancy.We identified births during 6/1/04-3/31/06 to women residing within five miles of a Southern California Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. We identified preterm cases and, using a risk set approach, matched cases to controls based on gestational age at birth. Pregnancy period exposure averages were estimated for a number of air toxics including polycyclic aromatic hydrocarbons (PAHs), source-specific PM2.5 (fine particulates with aerodynamic diameter less than 2.5 ?m) based on a Chemical Mass Balance model, criteria air pollutants based on government monitoring data, and land use regression (LUR) estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of preterm birth were estimated using conditional logistic regression.Odds of preterm birth increased 6-21% per inter-quartile range increase in entire pregnancy exposures to organic carbon (OC), elemental carbon (EC), benzene, and diesel, biomass burning and ammonium nitrate PM2.5, and 30% per inter-quartile increase in PAHs; these pollutants were positively correlated and clustered together in a factor analysis. Associations with LUR exposure metrics were weaker (3-4% per inter-quartile range increase).These latest analyses provide additional evidence of traffic-related air pollution's impact on preterm birth for women living in Southern California and indicate PAHs as a pollutant of concern that should be a focus of future studies. Other PAH sources besides traffic were also associated with higher odds of preterm birth, as was ammonium nitrate PM2.5, the latter suggesting potential importance of secondary pollutants. Future studies should focus on accurate modeling of both local and regional spatial and temporal distributions, and incorporation of source information.
Project description:Numerous studies have linked criteria air pollutants with adverse birth outcomes, but there is less information on the importance of specific emission sources, such as traffic, and air toxics.We used three exposure data sources to examine odds of term low birth weight (LBW) in Los Angeles, California, women when exposed to high levels of traffic-related air pollutants during pregnancy.We identified term births during 1 June 2004 to 30 March 2006 to women residing within 5 miles of a South Coast Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. Pregnancy period average exposures were estimated for air toxics, including polycyclic aromatic hydrocarbons (PAHs), source-specific particulate matter < 2.5 ?m in aerodynamic diameter (PM2.5) based on a chemical mass balance model, criteria air pollutants from government monitoring data, and land use regression (LUR) model estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of term LBW (< 2,500 g) were examined using logistic regression.Odds of term LBW increased approximately 5% per interquartile range increase in entire pregnancy exposures to several correlated traffic pollutants: LUR measures of NO, NO2, and NOx, elemental carbon, and PM2.5 from diesel and gasoline combustion and paved road dust (geological PM2.5).These analyses provide additional evidence of the potential impact of traffic-related air pollution on fetal growth. Particles from traffic sources should be a focus of future studies.
Project description:We examined ambient exposure to specific air toxics in the perinatal period in relation to retinoblastoma development. Cases were ascertained from California Cancer Registry records of children diagnosed between 1990 and 2007 and matched to California birth certificates. Controls were randomly selected from state birth records for the same time period. We chose 27 air toxics for the present study that had been listed as possible, probable, or established human carcinogens by the International Agency for Research on Cancer. Children (103 cases and 30,601 controls) included in the study lived within 5 miles of an air pollution monitor. Using logistic regression analyses, we modeled the risk of retinoblastoma due to air toxic exposure, separately for exposures in pregnancy and the first year of life. With a per interquartile range increase in air toxic exposure, retinoblastoma risk was found to be increased with pregnancy exposure to benzene (OR=1.67, 95% CI: 1.06, 2.64) and other toxics which primarily arise from gasoline and diesel combustion: toluene, 1,3-butadiene, ethyl benzene, ortho-xylene, and meta/para-xylene; these six toxics were highly correlated. Retinoblastoma risk was also increased with pregnancy exposure to chloroform (OR=1.35, 95% CI: 1.07, 1.70), chromium (OR=1.29, 95% CI: 1.04, 1.60), para-dichlorobenzene (OR=1.24, 95% CI: 1.04, 1.49), nickel (OR=1.48, 95% CI: 1.08, 2.01), and in the first year of life, acetaldehyde (OR=1.62, 95% CI: 1.06, 2.48). Sources of these agents are discussed.
Project description:OBJECTIVE:To study prenatal air toxic exposure and Wilms' tumor in children. METHODS:We identified 337 Wilms' tumor cases among children younger than 6 years (1988 to 2008) from the California Cancer Registry, randomly selected 96,514 controls from California birth rolls in 20:1 ratio matched to all cancer cases, then linked birth addresses to air monitors within 15 miles to assess exposures. Multiple logistic regressions were applied to estimate effects. RESULTS:Children prenatally exposed to formaldehyde, polycyclic aromatic hydrocarbons, perchloroethylene, or acetaldehyde in the third trimester had an increased odds of Wilms' tumor per interquartile increase in concentration (odds ratio [95% confidence interval]: 1.28 [1.12 to 1.45], 1.10 [0.99 to 1.22], 1.09 [1.00 to 1.18], 1.25 [1.07 to 1.45], respectively). CONCLUSIONS:We found positive associations for four air toxics. This is the first study of this kind. Future studies are needed to confirm our findings.
Project description:Few studies have examined associations of birth outcomes with toxic air pollutants (air toxics) in traffic exhaust. This study included 8,181 term low birth weight (LBW) children and 370,922 term normal-weight children born between January 1, 1995, and December 31, 2006, to women residing within 5 miles (8 km) of an air toxics monitoring station in Los Angeles County, California. Additionally, land-use-based regression (LUR)-modeled estimates of levels of nitric oxide, nitrogen dioxide, and nitrogen oxides were used to assess the influence of small-area variations in traffic pollution. The authors examined associations with term LBW (?37 weeks' completed gestation and birth weight <2,500 g) using logistic regression adjusted for maternal age, race/ethnicity, education, parity, infant gestational age, and gestational age squared. Odds of term LBW increased 2%-5% (95% confidence intervals ranged from 1.00 to 1.09) per interquartile-range increase in LUR-modeled estimates and monitoring-based air toxics exposure estimates in the entire pregnancy, the third trimester, and the last month of pregnancy. Models stratified by monitoring station (to investigate air toxics associations based solely on temporal variations) resulted in 2%-5% increased odds per interquartile-range increase in third-trimester benzene, toluene, ethyl benzene, and xylene exposures, with some confidence intervals containing the null value. This analysis highlights the importance of both spatial and temporal contributions to air pollution in epidemiologic birth outcome studies.
Project description:Air pollution contains many toxicants known to affect neurological function and to have effects on the fetus in utero. Recent studies have reported associations between perinatal exposure to air pollutants and autism spectrum disorder (ASD) in children. We tested the hypothesis that perinatal exposure to air pollutants is associated with ASD, focusing on pollutants associated with ASD in prior studies.We estimated associations between U.S. Environmental Protection Agency-modeled levels of hazardous air pollutants at the time and place of birth and ASD in the children of participants in the Nurses' Health Study II (325 cases, 22,101 controls). Our analyses focused on pollutants associated with ASD in prior research. We accounted for possible confounding and ascertainment bias by adjusting for family-level socioeconomic status (maternal grandparents' education) and census tract-level socioeconomic measures (e.g., tract median income and percent college educated), as well as maternal age at birth and year of birth. We also examined possible differences in the relationship between ASD and pollutant exposures by child's sex.Perinatal exposures to the highest versus lowest quintile of diesel, lead, manganese, mercury, methylene chloride, and an overall measure of metals were significantly associated with ASD, with odds ratios ranging from 1.5 (for overall metals measure) to 2.0 (for diesel and mercury). In addition, linear trends were positive and statistically significant for these exposures (p < .05 for each). For most pollutants, associations were stronger for boys (279 cases) than for girls (46 cases) and significantly different according to sex.Perinatal exposure to air pollutants may increase risk for ASD. Additionally, future studies should consider sex-specific biological pathways connecting perinatal exposure to pollutants with ASD.
Project description:Association rule mining (ARM) has been widely used to identify associations between various entities in many fields. Although some studies have utilized it to analyze the relationship between chemicals and human health effects, fewer have used this technique to identify and quantify associations between environmental and social stressors. Socio-demographic variables were generated based on U.S. Census tract-level income, race/ethnicity population percentage, education level, and age information from the 2010-2014, 5-Year Summary files in the American Community Survey (ACS) database, and chemical variables were generated by utilizing the 2011 National-Scale Air Toxics Assessment (NATA) census tract-level air pollutant exposure concentration data. Six mobile- and industrial-source pollutants were chosen for analysis, including acetaldehyde, benzene, cyanide, particulate matter components of diesel engine emissions (namely, diesel PM), toluene, and 1,3-butadiene. ARM was then applied to quantify and visualize the associations between the chemical and socio-demographic variables. Census tracts with a high percentage of racial/ethnic minorities and populations with low income tended to have higher estimated chemical exposure concentrations (fourth quartile), especially for diesel PM, 1,3-butadiene, and toluene. In contrast, census tracts with an average population age of 40-50 years, a low percentage of racial/ethnic minorities, and moderate-income levels were more likely to have lower estimated chemical exposure concentrations (first quartile). Unsupervised data mining methods can be used to evaluate potential associations between environmental inequalities and social disparities, while providing support in public health decision-making contexts.
Project description:Air pollution has been linked to hypertension in the general population, but data on gestational hypertension (GH) are limited. We investigated criteria air pollutants and air toxics during the period before conception and in early gestation in relation to GH risk in the Consortium on Safe Labor/Air Quality and Reproductive Health Study (United States, 2002-2008). Modified Community Multi-scale Air Quality models estimated air pollution exposures for 6,074 singleton pregnancies in which GH was present and 199,980 normotensive pregnancies. Generalized estimating equations estimated relative risks per interquartile-range increment for pollutants and high exposure (?75th percentile) for air toxics after adjustment for major risk factors. For an interquartile-range increment, GH risk was significantly increased by 18% for sulfur dioxide during the 3 months before conception and, during gestational weeks 1-20, 17% for nitrogen oxides, 10% for particulate matter with an aerodynamic diameter <2.5 ?m, 7% for particulate matter with an aerodynamic diameter <10 ?m, and 22% for sulfur dioxide. High exposures to several polycyclic aromatic hydrocarbons before conception and during the first trimester were significantly associated with 8%-20% higher risk of GH. Further, preconceptional exposures to several volatile organic compounds were significantly associated with 11%-19% higher risk. Our findings suggest that early exposures to criteria air pollutants, particularly from transport emissions, and high exposure to several air toxics before conception may increase GH risk.
Project description:BACKGROUND:Previous research shows that environmental and social factors contribute to the development of attention-deficit/hyperactivity disorder (ADHD). OBJECTIVE:To determine the relationship between early-life exposure to common ambient air pollutants (benzene, toluene, ethylbenzene, and xylene, also known as BTEX), household material hardship (a measure of socio-economic status), and ADHD-suggestive behaviours in kindergarten-age children. METHODS:Pollutant exposure estimated from the 2002 National Air Toxics Assessment at each child's residential ZIP code at enrolment was linked to the Early Childhood Longitudinal Study Birth Cohort (n = 4650). Material hardship was assigned as a composite score of access to food, health care, and housing. Kindergarten teachers rated children's behaviours and activity in the classroom using a five-point Likert scale. Children with summary scores in the bottom decile were classified as displaying ADHD-suggestive behaviours. Logistic regression models were constructed to estimate the association between both BTEX exposure and material hardship on ADHD-suggestive behaviours. RESULTS:The odds of displaying ADHD-suggestive behaviours were greater in children with combined high-level exposure to BTEX and in those experiencing material hardship (odds ratio 1.54, 95% confidence interval [CI] 1.12, 2.11, and OR 2.12, 95% CI 1.25, 3.59, respectively), adjusting for covariates. These associations were stronger when restricting the study population to urban areas. There was no evidence of interaction between early life BTEX exposure and material hardship, although the effects of BTEX exposure were slightly greater in magnitude among those with higher material hardship scores. CONCLUSIONS:Children exposed to air toxics, material hardship, or both early in life are more likely to display signs of ADHD-suggestive behaviours as assessed by their kindergarten teachers. The associations between exposures to air pollution and to socio-economic hardship were observed in all children but were particularly strong in those living in urban areas.