Faculty Bibliography

PURPOSE/OBJECTIVE:This study aimed to examine associations of bisphenol and phthalate exposure with arterial stiffness among women of reproductive age. METHODS:Participants include 637 adult women enrolled in the New York University Children's Health and Environment Study (NYU CHES), a prospective pregnancy cohort. The concentrations of eight bisphenols and 22 phthalate metabolites were quantified in up to three spot urine samples. Primary outcomes included brachial artery distensibility (BrachD) and carotid-femoral pulse wave velocity (cfPWV) as measures of peripheral and central arterial stiffness, respectively, along with blood pressure assessed at repeated study visits up to seven years from exposure measures. Associations between averaged, log2-transformed, creatinine-standardized chemical concentrations and subclinical vascular outcomes of interest were examined using linear mixed-effects models. RESULTS:In covariate-adjusted models, a doubling of bisphenol A was positively associated with BrachD (0.09%/mmHg, 95% confidence interval [CI] = 0.02, 0.16), a doubling of bisphenol S was negatively associated with mean arterial pressure (MAP) (-0.52 mmHg, 95% CI = -0.98, -0.05), a doubling of di(2-ethylhexyl) phthalate (DEHP) metabolites was negatively associated with diastolic blood pressure (DBP) (-0.81 mmHg, 95% CI = -1.38, -0.23) and MAP (-0.83 mmHg, 95% CI = -1.45, -0.21), and a doubling of antiandrogenic phthalate metabolites was associated with 0.62 mmHg lower DBP (95% CI = -1.22, -0.03) and 0.66 mmHg lower MAP (95% CI = -1.30, -0.02). CONCLUSION/CONCLUSIONS:These findings suggest that routine exposure to bisphenols and DEHP may be associated with vasorelaxation, potentially related to these chemicals' estrogenic and/or antiandrogenic effects.

BACKGROUND:Emerging data suggests that glyphosate, a non-selective herbicide, can influence reproductive health. We investigated associations of prenatal exposure to glyphosate and aminomethylphosphonic acid (AMPA), with preterm birth and its subtypes. METHODS:We used data from the NYU Children's Health and Environmental Study, a prospective birth cohort in New York City (2016-2019). Participants (n=1450) provided urine samples at 4 to <18 weeks and 18 to 25 weeks gestation. Exposure was adjusted for creatinine and natural log transformed. Preterm birth was defined as a birth occurring before 37 weeks of gestation. We also explored preterm birth subtypes, spontaneous preterm births and medically indicated preterm births as secondary outcomes. To examine associations between glyphosate and AMPA at both timepoints with preterm birth, we used generalized estimating equations with a logit link function. RESULTS:Overall, 7% (n=103) of births were preterm. Glyphosate concentrations at 18-25 weeks was associated with preterm birth (OR: 1.35, 95% CI: 1.04, 1.76) and spontaneous preterm birth (OR: 2.01, 95% CI: 1.40, 2.90). AMPA was not associated with preterm birth in any model. CONCLUSIONS:These results support evidence that glyphosate may act upon pathways leading to preterm birth and spontaneous preterm birth. Our study highlights pregnancy as a vulnerable period to glyphosate exposure.

PURPOSE OF REVIEW/OBJECTIVE:Diabetes care is characterized by the widespread use of plastics. With plastic-associated endocrine-disrupting chemicals (EDCs) implicated in diabetes pathogenesis, this review examines how medical plastics relate to diabetes and related disorders and proposes interventions to improve the situation. RECENT FINDINGS/RESULTS:Plastic-associated EDCs and micro-/nanoplastics (MNPs) are linked to metabolic dysfunction. Medical care exposes patients to these agents; however, the precise contribution of diabetes care to these exposures and their associated adverse health effects remains poorly defined. Diabetes care is an increasingly important contributor to plastic pollution and climate change, yet inadequate systems exist to mitigate its environmental impact. Plastic-associated EDCs and MNPs remain an underappreciated metabolic health threat. Mitigating the deleterious impacts of plastics on human and planetary health requires concerted actions from manufacturers, scientists, policymakers, professional organizations, healthcare providers, and patients. Doing so has the potential to improve metabolic health and promote health equity.

Relatively few epidemiologic studies in the US have measured the short-chain replacement per- or polyfluoroalkyl substance (PFAS) perfluorobutanesulfonic acid (PFBS), and little is known about its health impacts. We measured prenatal serum concentrations of 13 PFAS, including PFBS, among 500 participants in the New York University Children's Health and Environment Study (NYU CHES) between 2016 and 2019. We investigated associations of PFAS exposures with demographic characteristics, including location of residence, and conducted an exploratory factor analysis to investigate common sources of exposure. PFBS concentrations were quantified in 95.6% of samples (median 0.40 ng/mL), which was unexpectedly higher than serum PFBS concentrations reported in other US-based cohorts. PFBS concentrations were not correlated with other PFAS, though they were positively correlated with each other. Unlike other PFAS, PFBS concentrations were not associated with participant characteristics, and there was no evidence for spatial autocorrelation. The changing PFAS exposure landscape warrants further investigation into the health effects of short-chain replacements, particularly in vulnerable populations.

BACKGROUND:Emerging evidence suggests endocrine disrupting chemicals, including bisphenols and phthalates, may affect behavioral development in children and adolescents. Risk behavior constitutes a potentially sex hormone sensitive behavioral construct. Here, we examined longitudinal associations of phthalate and bisphenol exposure with performance-based tasks and self-reported risk-taking behaviors. METHODS:Within a population-based birth cohort in the Netherlands, urinary bisphenols and phthalate metabolite concentrations were measured in women during pregnancy (three times, n = 1379) and in children (once at 6 years, n = 775). At 10 years, child risk-taking behavior was assessed with the computerized experimental Columbia Card Task (CCT). At 14 years, adolescents completed a computerized self-assessment of real-life risk-taking behaviors. Linear regression and hurdle models adjusted for confounders were applied in the whole sample and stratified by sex at birth. RESULTS:After multiple testing correction, no associations in all children or in boys were found for prenatal or childhood phthalate exposure with the average CCT-score. In girls, prenatal mono-isobutyl phthalate was associated with a higher average CCT-score, indicting more risk-taking (B per 10-fold increase in creatinine-adjusted average prenatal levels = 2.10, 95% CI: 0.69,3.52). No associations were observed for bisphenol exposure nor for self-reported risk-taking. CONCLUSIONS:Prenatal phthalate exposure was associated with more risk-taking in an experimental task at 10 years-of-age in girls only. The task reflects risky decision-making, which may be a hormonally sensitive construct. Risky decision making potentially precedes real-life risk-taking, which was captured by the self-reported measure and was limited in this young sample.

Growing evidence suggests that exposure to air pollution during early life is associated with autism spectrum disorder (ASD). However, results have been inconsistent for autism-like traits and in low exposure settings. Here, we assessed sensitive windows of exposure to fine particulate matter (PM_2.5), nitrogen dioxide (NO₂), and ozone (O₃) and joint effects of exposure to sources and constituents of PM_2.5 on autism-like traits among 798 children in the Upstate KIDS cohort. Residential air pollution exposures were assessed with machine learning and land use regression models. Autism-like traits at age 10 were assessed via the ASD subscale on the Child Behavior Checklist. Treed distributed lag mixture model was used to identify critical windows of exposure to PM_2.5, NO₂, and O₃ and partial linear single index model was applied to estimate contributions of sources and constituents of PM_2.5 on autism-like traits. The median PM_2.5 exposures were 8.36 and 8.00 μg/m³ for pregnancy and the first year of life. We did not observe critical windows of exposure to PM_2.5, NO₂, or O₃ for autism-like traits. Exposures to elemental carbon (EC) PM_2.5 during gestation and to EC and traffic PM_2.5 during the first year of life were associated with higher odds of autism-like traits (prenatal EC adjusted odds ratio (aOR): 1.72, 95% CI: 1.04-2.83; first year EC aOR: 1.72, 95% CI: 1.21-2.46; traffic aOR: 1.31, 95% CI: 1.01-1.71). Our results suggest that exposure to motor vehicle traffic sources of PM_2.5 may drive previously reported associations between total PM_2.5 and autism-like traits.

IMPORTANCE/UNASSIGNED:Gestational environmental chemical exposures are widespread. Some chemicals are known to adversely affect birth outcomes, but many remain understudied. OBJECTIVE/UNASSIGNED:To evaluate associations of gestational exposure to a priori identified chemicals in 10 classes with birth outcomes in a large, diverse US cohort. DESIGN, SETTING, AND PARTICIPANTS/UNASSIGNED:In the prospective Environmental influences on Child Health Outcomes Cohort study, 5318 mother-child pairs were enrolled from January 1, 2000, to December 31, 2021, with data on gestational urinary chemical concentrations, gestational age at birth, and birth weight. Statistical analysis was performed from January 2024 to February 2026. EXPOSURES/UNASSIGNED:In single, midgestation (median, 25 weeks [IQR, 21-30 weeks]) urine samples, concentrations of 113 analytes (chemicals or their metabolites) from 10 chemical classes were simultaneously measured: fungicides and herbicides (n = 11), insecticides (n = 20), halogenated phenols (n = 5), organophosphate esters (n = 10), benzophenones (n = 6), bisphenols (n = 14), parabens (n = 6), antimicrobials (n = 2), phthalates or alternative plasticizers (n = 32), and polycyclic aromatic hydrocarbons (PAHs) (n = 7). MAIN OUTCOMES AND MEASURES/UNASSIGNED:Linear mixed-effects regression models with a random effect for site were used to estimate covariate-adjusted differences in gestational age at birth (days) and birth weight-for-gestational age (BW-GA) z scores per IQR increase in urinary analyte concentrations. In secondary analyses, odds ratios (ORs) for preterm birth and small for gestational age (SGA) were estimated. RESULTS/UNASSIGNED:In the sample of 5318 mother-child pairs, most infants (2667 female [50%]; median gestational age at birth, 39.0 weeks [IQR, 38.0-40.0 weeks]) were born to college-educated (67% [3218 of 4785]), parous (56% [2815 of 5007]) mothers (median age at delivery, 30.7 years [IQR, 26.1-34.3 years]). A total of 43 of 113 analytes (38%) were detected in 50% or more of samples. Multiple phthalates or alternative plasticizers were associated with younger gestational age at birth or lower BW-GA z scores; for example, summed diisononyl phthalate metabolites were associated with a 0.6-day (95% CI, -1.0 to -0.1 days) younger gestational age (preterm birth OR, 1.16 [95% CI, 1.01-1.34]), and summed phthalate or alternative plasticizers were associated with a 0.06 (95% CI, -0.11 to -0.02) lower BW-GA z score (SGA OR, 1.09 [95% CI, 0.93-1.27]). Two halogenated phenols, benzophenone 8, bisphenol F, and several PAHs were associated with lower BW-GA z scores; for example, 1- and 9-hydroxphenanthrene were associated with a 0.04 (95% CI, -0.08 to -0.01) lower BW-GA z score (SGA OR, 1.13 [95% CI, 1.01-1.27]). CONCLUSIONS AND RELEVANCE/UNASSIGNED:This large cohort study of diverse US pregnancies found widespread exposure to 10 classes of environmental chemicals, many of which were associated with differences in gestational age at birth or lower BW-GA z scores. These findings indicate that reducing gestational exposure to chemicals, particularly phthalates or alternative plasticizers and PAHs, could promote healthy deliveries and better child outcomes.

BACKGROUND/UNASSIGNED:Prior work has suggested poorer performance on Fluid, but not Crystallized, NIH Toolbox Cognition Battery (NTCB) subtests in autistic youth relative to neurotypical individuals. This study sought to extend previous findings using a larger sample from a nationwide multi-cohort study and to examine the effect of attention-deficit/hyperactivity disorder (ADHD) status on cognitive functioning. METHODS/UNASSIGNED: = 737) were included in the analyses. We used a general linear model framework to examine group differences in task performance, and we used latent profile analysis (LPA) to identify subgroups of individuals with similar cognitive profiles. RESULTS/UNASSIGNED:The AUT and AUT + ADHD groups had lower NTCB Fluid Cognition Index Scores compared to the noAUTADHD group, whereas no group differences in the Crystallized Cognition Index Score were observed. No significant differences in the NTCB subtest or index scores were found between the AUT and AUT + ADHD groups. Sex-stratified analyses revealed no sex differences. LPA identified four distinct NTCB groups, with a substantial proportion of the AUT group (19%) assigned to the class with higher Crystallized versus Fluid Cognition Index Scores; however, there was considerable overlap between the diagnostic groups within the LPA classes. CONCLUSIONS/UNASSIGNED:Autistic individuals experience difficulties with fluid NTCB tasks and those with co-occurring ADHD do not appear to face greater difficulties than those with autism alone. However, there was a notable proportion of autistic individuals with average or superior cognitive performance, highlighting the importance of strength-based and transdiagnostic research approaches.