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Abstract Background A large body of data shows that fetal brain development is vulnerable to disruption by air pollution experienced by the mother during pregnancy, adversely affecting cognitive and psychomotor capabilities during childhood (De Asis-Cruz et al., Biol Psychiatry 7:480–90, 2022; Morgan ZEM et al., Environ Health 22:11, 2023). This study has sought to identify gestational windows of susceptibility to prenatal exposure to air pollution. Methods 470 African American and Latina mother/child pairs participated in a prospective cohort study based in the low-income communities of Northern Manhattan and the South Bronx, New York City. Gestational exposure to respirable particulate matter (PM2.5) and nitrogen dioxide (NO2) was assessed through validated models in relation to cognitive and motor development assessed at ages 1, 2, and 3 years using the Bayley-II Scales. Multiple linear regression models and distributed lag models (DLM) were used to identify critical windows of exposure by trimester and week of pregnancy. Results By linear regression, average exposures to NO2 during the first and second trimesters and the entire pregnancy were significantly and negatively associated with the mental developmental index (MDI) at age 1. Average exposures to PM2.5 during the second trimester and the entire pregnancy were also significantly, inversely associated with age 1 MDI. No significant associations were found between these exposures and MDI at age 2. NO2 exposure during the first trimester was significantly negatively associated with MDI at age 3. Using DLM, exposures to NO2 at lags 29–30 weeks (within the first trimester) and PM2.5 at lags 17–18 weeks (second trimester) were significantly and inversely associated with MDI at age 1. Significant, inverse associations were found between exposures to NO2 at lag 29 weeks and PM2.5 at lags 27–29 weeks and children’s MDI at age 3. No significant associations were found between psychomotor index (PDI) and prenatal exposures to NO2 or PM2.5 at ages 1, 2 or 3. Conclusions Our finding that prenatal exposure to air pollution in the first and second trimesters was associated with lower scores for cognitive development at ages 1 and 3 is of concern because of the potential consequences of these outcomes for long-term functioning. They underscore the need for stronger policies to protect pregnant individuals and offspring, particularly during vulnerable, early life-stage of development.

Abstract Background Parental psychological distress is a well-known risk factor for developmental psychopathology, with longer term parental distress associated with worse youth mental health. Neurotoxicant exposure during pregnancy is a risk factor for both poor maternal and youth mental health. The impact of one class of pollutant, polycyclic aromatic hydrocarbons (PAH), on long-term trajectories of maternal distress and youth self-reported mental health symptoms in adolescence has been understudied. Methods PAH exposure was measured by DNA adducts in maternal blood sampled during the third trimester of pregnancy. Maternal distress, operationalized as maternal demoralization, was measured at 11 timepoints (prenatal to child age 16). Adolescent mental health symptoms were measured at age 13–15. Follow up analyses examined a subset of measures available at age 15–20 years. Structural equation modeling examined associations between PAH exposure during pregnancy and latent growth metrics of maternal distress, and between maternal distress (intercept and slope) and youth mental health symptoms in a prospective longitudinal birth cohort (N = 564 dyads). Results Higher prenatal PAH exposure was associated with higher concurrent maternal distress. Prenatal maternal distress was associated with adolescent’s self-reported anxiety, depression, and externalizing problems. On average, maternal distress declined over time; a slower decline in mother’s distress across the course of the child’s life was associated with greater self-reported anxiety and externalizing problems in youth. Conclusions Our findings are consistent with an intergenerational framework of environmental effects on mental health: PAH exposure during pregnancy affects maternal mental health, which in turn influences mental health outcomes for youth well into adolescence. Future research is necessary to elucidate the possible social and biological mechanisms (e.g., parenting, epigenetics) underlying the intergenerational transmission of the negative effects of pollution on mental health in caregiver-child dyads.

IntroductionAir pollution poses serious health risks to humans, with particular harm to children.ObjectivesTo address the gap in understanding the efficacy of policies to reduce exposure to air pollution, we sought to assess the temporal relationship between the enactment of major air pollution and climate policies in NYC and trends in air quality during the period 1998–2021. We used previously available data from citywide monitoring and new data from the Columbia Center for Children’s Environmental Health (CCCEH) longitudinal cohort studies of mothers and children living in communities in Northern Manhattan and the South Bronx.MethodsWe utilized publicly available citywide air monitoring data for particulate matter (PM2.5) and nitrogen dioxide (NO2) from 2009 to 2021 from the New York City Community Air Survey (NYCCAS) database and CCCEH cohort data on residential exposure to PM2.5 and NO2 and personal exposure to polycyclic aromatic hydrocarbons (PAH) during pregnancies occurring from 1998–2016 and 1998–2021, respectively. We compared annual and overall reductions in PM2.5 and NO2 citywide and reductions in PAH concentrations in the cohort studies.ResultsAs previously reported, annual average concentrations of pollutants in NYC dropped significantly over time. Between 1998 and 2021, PM2.5 and NO2 concentrations were reduced citywide by 37 and 31%, respectively. In our CCCEH cohorts, between 1998 and 2016, the annual average PM2.5 and NO2 concentrations also decreased significantly by 51 and 48%, respectively. Between 1998 and 2020, PAH concentrations decreased significantly by 66%.Discussion/conclusionWhile it is not possible to link improved air quality to a single policy, our analysis provides evidence of a cumulative beneficial effect of clean air and climate policies enacted between 1998 and 2021 both city-wide and in our cohorts residing in communities that have been disproportionately affected by air pollution. There are important implications for health benefits, particularly for children, who are known to be especially vulnerable to these exposures. The results support further environmental and social policy changes to prevent the serious health impacts of air pollution from fossil fuel emissions.

Report-back of research results (RBRR) is becoming standard practice for environmental health research studies. RBRR is thought to increase environmental health literacy (EHL), although standardized measurements are limited. For this study, we developed a report back document on exposure to air pollutants, Polycyclic Aromatic Hydrocarbons, during pregnancy through community engaged research and evaluated whether the report increased EHL. We used focus groups and surveys to gather feedback on the report document from an initial group of study participants (Group 1, n = 22) and then sent the revised report to a larger number of participants (Group 2, n = 168). We conducted focus groups among participants in Group 1 and discussed their suggested changes to the report and how those changes could be implemented. Participants in focus groups demonstrated multiple levels of EHL. While participant engagement critically informed report development, a survey comparing feedback from Group 1 (initial report) and Group 2 (revised report) did not show a significant difference in the ease of reading the report or knowledge gained about air pollutants. We acknowledge that our approach was limited by a lack of EHL tools that assess knowledge and behavior change, and a reliance on quantitative methodologies. Future approaches that merge qualitative and quantitative methodologies to evaluate RBRR and methodologies for assessing RBRR materials and subsequent changes in knowledge, attitudes, and behavior, may be necessary.

BackgroundChildren from socioeconomically disadvantaged backgrounds are at elevated risk for reading problems. They are also likely to live in neighborhoods with high levels of air pollution and to experience material hardship. Despite these risk factors, the links between prenatal chemical exposures, socioeconomic adversities, and reading problems in youth from disadvantaged backgrounds remain understudied. Here we examine associations between prenatal exposure to polycyclic aromatic hydrocarbons (PAH), a common air pollutant, and reading skills, and determine if this relationship is exacerbated by material hardship among Black and/or Latinx children who have been followed as part of a longitudinal urban birth cohort.MethodsMothers and their children, who were participants in a prospective birth cohort followed by the Columbia Center for Children’s Environmental Health, were recruited for the current study. Personal prenatal PAH exposure was measured during the third-trimester of pregnancy using a personal air monitoring backpack. Mothers reported their level of material hardship when their child was age 5 and children completed measures of pseudoword and word reading [Woodcock Johnson III Tests of Achievement (WJ-III) Basic Reading Index] at age 7. We used multiple linear regression to examine the effects of the interaction between prenatal PAH and material hardship on Basic Reading Index, controlling for ethnicity/race, sex, birthweight, presence of a smoker in the home (prenatal), and maternal education (prenatal) (N = 53).ResultsA prenatal PAH × material hardship interaction significantly associated with WJ-III Basic Reading Index scores at age 7 (β = −0.347, t(44) = −2.197, p = 0.033). Exploratory analyses suggested that this effect was driven by untimed pseudoword decoding (WJ-III Word Attack: β = −0.391, t(44) = −2.550, p = 0.014).ConclusionEnvironmental chemical exposures can be particularly toxic during the prenatal period when the fetal brain undergoes rapid development, making it uniquely vulnerable to chemical perturbations. These data highlight the interactive effects of environmental neurotoxicants and unmet basic needs on children’s acquisition of reading skill, specifically phonemic processing. Such findings identify potentially modifiable environmental risk factors implicated in reading problems in children from economically disadvantaged backgrounds.

OBJECTIVES/GOALS: This study models a framework for integrating epidemiological and experimental approaches to investigate the effect of prenatal polycyclic aromatic hydrocarbon (PAH) exposure on mitochondrial function (mtDNAcn, superoxide production and membrane potential) as a potential mechanism of toxicity. METHODS/STUDY POPULATION: The epidemiological aim of this study characterizes mitochondrial outcomes in samples of umbilical cord tissue and blood from two Manhattan based birth cohorts. Prenatal PAH exposure is quantified using silicone wristbands worn for 48 hours during the third trimester of pregnancy. Experimentally, we are applying a PAH mixture designed to emulate the exposure profile of the human cohorts to mouse preimplantation embryos on various dosing schedules and quantifying the same mitochondrial outcomes. mtDNAcn is quantified using rtPCR while superoxide production and membrane potential are measured using fluorescence microscopy. The goal of this study design is to leverage the strengths of each approach to draw more robust conclusions than could be derived from either alone. RESULTS/ANTICIPATED RESULTS: Preliminary results of this study have found associations between higher levels of PAH exposure and increased mitochondrial superoxide production and hyperpolarization of the mitochondrial membrane potential in mouse preimplantation embryos. We anticipate these findings to persist across dosing schedules. We furthermore expect a decrease in mtDNAcn in association with higher PAH exposure in umbilical cord tissue samples and decreased mtDNAcn with exposure to the PAH mixture in mouse embryos. DISCUSSION/SIGNIFICANCE: Characterizing the effect of prenatal PAH exposure on the mitochondria is a critical step in understanding the mechanisms that underlie the toxicity of this exposure. By employing a similar exposure mixture and mitochondrial outcomes across epidemiological and experimental approaches, we offer a model of true interdisciplinary research design.

Objective: Many studies have shown that severe (hospitalized) bronchiolitis during infancy is a risk factor for developing childhood asthma. However, the population subgroups at the highest risk remain unclear. Using large nationwide pediatric cohort data, namely the NIH Environmental influences on Child Health Outcomes (ECHO) Program, we aimed to quantify the longitudinal relationship of bronchiolitis hospitalization during infancy with asthma in a generalizable dataset and to examine potential heterogeneity in terms of major demographics and clinical factors. Methods: We analyzed data from infants (age Results: The analytic cohort consisted of 11,762 infants, 10% of whom had bronchiolitis hospitalization. Overall, 15% subsequently developed asthma. In the Cox proportional hazards model adjusting for 10 patient-level factors, compared with the no-bronchiolitis hospitalization group, the bronchiolitis hospitalization group had a significantly higher rate of asthma (14% vs. 24%, HR = 2.77, 95%CI = 2.24–3.43, p < 0.001). There was significant heterogeneity by race and ethnicity (Pinteraction = 0.02). The magnitude of the association was greater in non-Hispanic White (HR = 3.77, 95%CI = 2.74–5.18, p < 0.001) and non-Hispanic Black (HR = 2.39, 95%CI = 1.60–3.56; p < 0.001) infants, compared with Hispanic infants (HR = 1.51, 95%CI = 0.77–2.95, p = 0.23). Conclusions: According to the nationwide cohort data, infants hospitalized with bronchiolitis are at a higher risk for asthma, with quantitative heterogeneity in different racial and ethnic groups.

Background and Objectives: Prenatal exposure to environmental tobacco smoke (ETS) is associated with increased attention problems in children, however, the effects of such exposure on children’s brain structure and function have not been studied. Herein, we probed effects of prenatal ETS on children’s cognitive control circuitry and behavior. Methods: Forty-one children (7–9 years) recruited from a prospective longitudinal birth cohort of non-smoking mothers completed structural and task-functional magnetic resonance imaging to evaluate effects of maternal ETS exposure, measured by maternal prenatal urinary cotinine. Attention problems and externalizing behaviors were measured by parent report on the Child Behavior Checklist. Results: Compared to non-exposed children, exposed children had smaller left and right thalamic and inferior frontal gyrus (IFG) volumes, with large effect sizes (p-FDR

Background: Emerging evidence suggests that phthalate exposure may be associated with behavior problems in children and that these associations may be sex specific. Methods: In a follow up study of 411 inner-city minority mothers and their children, mono-n-butyl phthalate (MnBP), monobenzyl phthalate (MBzP), monoisobutyl phthalate (MiBP), monethyl phthalate (MEP) and four di-2-ethylhexyl phthalate metabolites (DEHP) were quantified in maternal urine samples collected during the third trimester and in child urine samples at ages 3 and 5 years. The Conners’ Parent Rating Scale-Revised: Long Form (CPRS) and Child Behavior Checklist (CBCL) were administered to the mothers to assess children’s behavior problems at 7 years of age. The analysis included children with available measures of CBCL, CPRS and phthalates measured in maternal urine. We performed both Quasi-Poisson regression and a mixture analysis using Weighted Quantile Sum(WQS) regression to assess the risk for CPRS scores and for internalizing and externalizing behaviors (from the CBCL) following intra-uterine exposure to the phthalate metabolites for boys and girls separately. Results: Among boys, increases in in anxious-shy behaviors were associated with prenatal exposure to MBzP (Mean Ratio [MR] = 1.20, 95%CI 1.05–1.36) and MiBP (Mean Ratio (MR) = 1.22, 95%CI 1.02–1.47). Among girls, increases in perfectionism were associated with MBzP (MR = 1.15, 95%CI 1.01–1.30). In both boys and girls, increases in psychosomatic problems were associated with MiBP (MR = 1.28, 95%CI 1.02–1.60), and MnBP (MR = 1.28, 95%CI 1.02–1.59), respectively. Among girls, decreased hyperactivity was associated with two DEHP metabolites, mono(2-ethyl-5-oxohexyl) phthalate (MR = 0.83, 95%CI 0.71–0.98) and mono(2-ethyl-5-hydroxyhexyl) phthalate (MR = 0.85, 95%CI 0.72–0.99). Using weighted Quantile Sum logistic regression, no associations were found between the Weighted Quantile Sum (WQS) of phthalate metabolites and CPRS scores or externalizing and internalizing behaviors. Nonetheless, when the analysis was performed separately for DEHP and non-DEHP metabolites significant associations were found between the WQS of DEHP metabolites and social problems in boys (OR = 2.15, 95%CI 1.13–4.06, p-value = 0.02) anxious-shy problems in girls (OR = 2.19, 95%CI 1.15–4.16, p = 0.02), and emotional lability problems in all children (OR = 0.61, 95%CI 0.38–0.97, p = 0.04). MEHP and MEOHP were the most highly weighted DEHP metabolites in WQS mixture. The analysis performed with CBCL scale corroborated these associations. Conclusion: Concentration of non-DEHP metabolites was associated with anxious-shy behaviors among boys. DEHP phthalate metabolites were associated with decreased hyperactivity and impulsivity among girls on CPRS scores. These findings lend further support to the adverse associations between prenatal phthalate exposure and childhood outcomes, and clearly suggest that such associations are sex and mixture specific.

Introduction: Phthalates are a group of high production chemicals, generally used as plasticizers and odor enhancers. Phthalates cross the blood-placenta barrier and are associated with deficits in cognitive functions and behavior problems in offspring. We previously reported sex-specific associations with motor function when phthalates are considered singly. Because exposure to phthalates usually occurs as mixtures, here we assess these associations between a mixture of phthalates and motor function at age 11 years. Methods: Data come from the prospective cohort study of mothers and offspring who participated in the Columbia Center for Children’s Environmental Health birth cohort (CCCEH). Seven phthalate metabolites were measured in maternal spot urine obtained during the third trimester and motor function was evaluated using the short form of the Bruininks-Oseretsky Test of Motor Proficiency, 2nd edition (BOT-2) at the age of 11 years. We used Weighted Quartile Sum (WQS) regression models to examine the effect of phthalate metabolites in males and females separately. The models were adjusted for child age in months, child BMI, maternal race (African-American vs. Dominican), prenatal alcohol consumption, maternal demoralization score, HOME score, and urine specific gravity. In a secondary analysis we used linear regression models to examine the association between the sum of molar concentrations of both DEHP and non-DEHP metabolites, and outcomes of gross and fine motor functions. Results: 209 mother-child pairs were eligible for this analysis. A significant decrease in fine-motor functions was observed among females, but not among males, following exposure to high levels of weighted quartile sum of seven phthalate metabolites (Covariates-adjusted coefficient estimate B = −2.7, 95% Confidence Interval [CI] −4.64 to −0.75, p = 0.01 for females [n = 116] and B = −1.63, 95%CI −3.94 to 0.69, p = 0.16 for males [n = 93]). The most highly weighted phthalate metabolites, associated with fine-motor functions among females, were MBP, MBZP, and MIBP, all non-DEHP phthalates.No significant associations were found between the weighted quartile sum of seven phthalate metabolites and gross-motor functions at the age of 11 years for males (B = −0.81, 95%CI −1.17 to 1.96, p = 0.23).With the molar sum of four non-DEHP phthalates as main predictor of linear regression models, we found significant decrease in gross and fine motor functions among females prenatally exposed to non-DEHP phthalates B = −0.98, 95%CI −1.98 to 0.03, p = 0.05 and B = −0.85, 95%CI −1.49 to −0.20, p = 0.01, respectively). Conclusions: Phthalate exposure during pregnancy was associated with decreased motor functions among 11-year-old girls. Keywords: Phthalates, Motor functions

Background: Polycyclic aromatic hydrocarbons (PAH) are carcinogenic, neurotoxic environmental pollutants generated during incomplete combustion of fossil fuel and other organic material. PAH exposure has been associated with adverse fetal development and epigenetic alterations in cord blood. Several molecular epidemiology studies have established PAH-DNA adducts as biomarkers of PAH exposure. Objectives: We investigated the relationship between LINE1 DNA methylation and PAH-DNA adduct levels in cord blood, and with neurodevelopmental outcomes. Methods: In Tongliang County, China, the current study enrolled two population-based cohorts of nonsmoking pregnant women before (2002) and after (2005) the closure of a local coal-fired power plant in May 2004. We analyzed cord blood samples collected from mothers in the two cohorts (n = 110 from 2002 cohort and n = 107 from 2005 cohort) for PAH-DNA adducts and genomic LINE1 DNA methylation. Neurodevelopmental data on children were collected using the Gesell Developmental Scales (GDS) at age 2 and using the Wechsler Intelligence Scale for Children (WISC) at age 5. Results: A significant inverse relationship was observed between PAH-DNA adducts and LINE1 DNA methylation (β = −0.010, p

To assess differences and trends in personal chemical exposure, volunteers from 14 communities in Africa (Senegal, South Africa), North America (United States (U.S.)) and South America (Peru) wore 262 silicone wristbands. We analysed wristband extracts for 1530 unique chemicals, resulting in 400 860 chemical data points. The number of chemical detections ranged from 4 to 43 per wristband, with 191 different chemicals detected, and 1339 chemicals were not detected in any wristband. No two wristbands had identical chemical detections. We detected 13 potential endocrine disrupting chemicals in over 50% of all wristbands and found 36 chemicals in common between chemicals detected in three geographical wristband groups (Africa, North America and South America). U.S. children (less than or equal to 11 years) had the highest percentage of flame retardant detections compared with all other participants. Wristbands worn in Texas post-Hurricane Harvey had the highest mean number of chemical detections (28) compared with other study locations (10–25). Consumer product-related chemicals and phthalates were a high percentage of chemical detections across all study locations (36–53% and 18–42%, respectively). Chemical exposures varied among individuals; however, many individuals were exposed to similar chemical mixtures. Our exploratory investigation uncovered personal chemical exposure trends that can help prioritize certain mixtures and chemical classes for future studies.

Polycyclic aromatic hydrocarbons are widespread urban air pollutants from combustion of fossil fuel and other organic material shown previously to be neurotoxic.In a prospective cohort study, we evaluated the relationship between Attention Deficit Hyperactivity Disorder behavior problems and prenatal polycyclic aromatic hydrocarbon exposure, adjusting for postnatal exposure.Children of nonsmoking African-American and Dominican women in New York City were followed from in utero to 9 years. Prenatal polycyclic aromatic hydrocarbon exposure was estimated by levels of polycyclic aromatic hydrocarbon- DNA adducts in maternal and cord blood collected at delivery. Postnatal exposure was estimated by the concentration of urinary polycyclic aromatic hydrocarbon metabolites at ages 3 or 5. Attention Deficit Hyperactivity Disorder behavior problems were assessed using the Child Behavior Checklist and the Conners Parent Rating Scale- Revised.High prenatal adduct exposure, measured by elevated maternal adducts was significantly associated with all Conners Parent Rating Scale-Revised subscales when the raw scores were analyzed continuously (N = 233). After dichotomizing at the threshold for moderately to markedly atypical symptoms, high maternal adducts were significantly associated with the Conners Parent Rating Scale-Revised DSM-IV Inattentive (OR = 5.06, 95% CI [1.43, 17.93]) and DSM-IV Total (OR = 3.37, 95% CI [1.10, 10.34]) subscales. High maternal adducts were positivity associated with the DSM-oriented Attention Deficit/Hyperactivity Problems scale on the Child Behavior Checklist, albeit not significant. In the smaller sample with cord adducts, the associations between outcomes and high cord adduct exposure were not statistically significant (N = 162).The results suggest that exposure to polycyclic aromatic hydrocarbons encountered in New York City air may play a role in childhood Attention Deficit Hyperactivity Disorder behavior problems.

In a longitudinal cohort of approximately 700 children in New York City, the prevalence of asthma (>25%) is among the highest in the US. This high risk may in part be caused by transplacental exposure to traffic-related polycyclic aromatic hydrocarbons (PAHs) but biomarkers informative of PAH-asthma relationships is lacking. We here hypothesized that epigenetic marks associated with transplacental PAH exposure and/or childhood asthma risk could be identified in fetal tissues. Mothers completed personal prenatal air monitoring for PAH exposure determination. Methylation sensitive restriction fingerprinting was used to analyze umbilical cord white blood cell (UCWBC) DNA of 20 cohort children. Over 30 DNA sequences were identified whose methylation status was dependent on the level of maternal PAH exposure. Six sequences were found to be homologous to known genes having one or more 5'-CpG island(s) (5'-CGI). Of these, acyl-CoA synthetase long-chain family member 3 (ACSL3) exhibited the highest concordance between the extent of methylation of its 5'-CGI in UCWBCs and the level of gene expression in matched fetal placental tissues in the initial 20 cohort children. ACSL3 was therefore chosen for further investigation in a larger sample of 56 cohort children. Methylation of the ACSL3 5'-CGI was found to be significantly associated with maternal airborne PAH exposure exceeding 2.41 ng/m(3) (OR = 13.8; p

Background:Thyroid function is dynamic during the perinatal period with many factors potentially influencing maternal, fetal and neonatal TSH and thyroid hormone levels. We sought to identify the impact of numerous maternal, fetal and delivery attributes on thyroid parameters in newborns.Methods:This was a cross sectional study of 300 newborns. Detailed information was obtained from medical records and multiple characteristics from the record were tested as predictors of cord blood serum total T4, free T4 and TSH and infant T4 levels from the Maryland newborn screening program.Main outcome:Outcomes are levels of thyroid stimulating hormone (TSH), thyroxine (T4), and free T4in newborn cord serum and total T4in postnatal heelstick bloodspot samples.Results:Multivariate models identified a number of variables that are independently associated with thyroid hormone levels: higher birth order (lower cord TSH); older maternal age (lower cord total T4); pregnancy-induced hypertension and/or preeclampsia (lower cord total T4and free T4); gestational diabetes (higher cord free T4); sexually transmitted disease during pregnancy (lower cord TSH); alcohol use during pregnancy (lower cord TSH); thyroid condition/medications (higher bloodspot total T4, both neonatal and subsequent); Asian ancestry (higher cord TSH); male sex (higher TSH and lower neonatal bloodspot total T4); and C-section (lower cord TSH). Gestational age was independently associated with lower cord TSH, higher cord total T4, and higher neonatal and subsequent bloodspot total T4.Conclusions:Fetal and newborn thyroid hormone levels during the perinatal period are dynamic and influenced by several biological and delivery related factors. Efforts to identify fetal thyroid disruptors in late gestation must carefully consider these factors. [ABSTRACT FROM AUTHOR]