Faculty Bibliography

OBJECTIVES/OBJECTIVE:To assess relations of prepregnancy maternal and paternal obesity with offspring behavioral problems and psychiatric symptoms at 7-8 years in the Upstate KIDS study, a prospective cohort study. STUDY DESIGN/METHODS:Maternal body mass index (BMI) was calculated from prepregnancy height and weight provided in vital records or self-report at 4 months postpartum. Mothers reported paternal height and weight. At 7-8 years, mothers indicated if their children had been diagnosed with ADHD or anxiety (n = 1915). Additionally, children's behavior was measured with the Strengths and Difficulties Questionnaire at 7 years of age (n = 1386) and the Vanderbilt ADHD Diagnostic Parent Rating Scale at 8 years of age (n = 1484). Based on Strengths and Difficulties Questionnaire scores, we identified children with borderline behavioral problems. Adjusted risk ratios (aRR) and 95% CIs were estimated with robust multivariable Poisson regression. RESULTS:had higher risks of reported ADHD (aRR, 1.14, 95% CI, 0.78-1.69; aRR, 1.96, 95% CI, 1.29-2.98; and aRR, 1.82, 95% CI,1.21-2.74, respectively). Risks of hyperactivity problems identified by the Strengths and Difficulties Questionnaire and a positive screen for inattentive or hyperactive/impulsive behavior with the Vanderbilt ADHD Diagnostic Parent Rating Scale were also higher with increasing maternal prepregnancy BMI. Paternal BMI was not associated with child outcomes. CONCLUSIONS:Our findings suggest that maternal, rather than paternal, obesity is associated with maternal report of child ADHD diagnosis and inattentive or hyperactivity problems. Further research is needed to understand how maternal obesity might influence these behavioral changes during or after pregnancy.

The aims of the NYU Children's Health and Environment Study (CHES) are to evaluate influences of prenatal non-persistent chemical exposures on fetal and postnatal growth and pool our data with the US National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) Program to answer collaborative research questions on the impact of the preconceptual, prenatal, and postnatal environment on childhood obesity, neurodevelopment, pre/peri/postnatal outcomes, upper and lower airway outcomes, and positive health. Eligible women were ≥ 18 years old, < 18 weeks pregnant, had a pregnancy that is not medically threatened, and planned to deliver at NYU Langone Hospital-Manhattan, Bellevue Hospital, or NYU Langone Hospital-Brooklyn. Between March 22, 2016 and April 15, 2019, we recruited 2469 pregnant women, from whom 2193 completed an initial questionnaire and continued into NYU CHES. Of the 2193, 88 miscarried, 28 terminated, and 20 experienced stillbirth, while 57 were lost to follow up. We report here demographic and other characteristics of the 2000 live deliveries (2037 children), from whom 1624 (80%) consented to postnatal follow-up. Data collection in pregnancy was nested in clinical care, with questionnaire and specimen collection conducted during routine prenatal visits at < 18, 18-25, and > 25 weeks gestation. These have been followed by questionnaire and specimen collection at birth and regular postpartum intervals.

OBJECTIVE:To study the associations between maternal polycystic ovary syndrome (PCOS) and hirsutism with offspring attention-deficit/hyperactivity disorder (ADHD), anxiety, conduct disorder, and behavioral problems. DESIGN/METHODS:Prospective birth cohort study. SETTING/METHODS:Not applicable. PATIENT(S)/METHODS:A total of 1,915 mother-child dyads. INTERVENTION(S)/METHODS:None. MAIN OUTCOME MEASURE(S)/METHODS:Maternal report of offspring ADHD, anxiety, or conduct disorder diagnosis at 7 to 8 years; emotional symptoms, behavioral problems (including peer relationship, conduct, hyperactivity/inattention), and prosocial problems measured with the Strengths and Difficulties Questionnaire (SDQ) at 7 years. RESULT(S)/RESULTS:Prevalence of PCOS and hirsutism were 12.0% and 3.9%; 84% of women with hirsutism had PCOS. After adjustment for sociodemographic covariates, prepregnancy body mass index, and parental history of affective disorders, children born to mothers with PCOS had higher risk of anxiety (adjusted risk ratio [aRR] 1.62; 95% confidence interval [CI], 1.02-2.57) and borderline emotional symptoms (aRR 1.66; 95% CI, 1.18-2.33) compared with children born to mothers without PCOS. The associations between maternal PCOS and offspring ADHD were positive but imprecise. Maternal hirsutism was related to a higher risk of children's ADHD (aRR 2.33; 95% CI, 1.28-4.24), conduct disorder (aRR 2.54; 95% CI 1.18-5.47), borderline emotional symptoms, peer relationship problems, and conduct problems (aRRs 2.61; 95% CI, 1.69-4.05; 1.92; 95% CI, 1.16-3.17; and 2.22; 95% CI, 1.30-3.79, respectively). CONCLUSION(S)/CONCLUSIONS:Maternal PCOS was associated with offspring anxiety, and hirsutism was related to other offspring behavioral problems. These findings should be interpreted with caution as replication is needed in prospective cohort studies that assess PCOS and hirsutism diagnoses using medical records.

BACKGROUND:Impaired neuromotor development is often one of the earliest observations in children with autism spectrum disorder (ASD). We investigated whether a genetic predisposition to developmental disorders was associated with nonoptimal neuromotor development during infancy and examined the genetic correlation between nonoptimal neuromotor development and autistic traits in the general population. METHODS:In a population-based cohort in The Netherlands (2002-2006), we calculated polygenic risk scores (PRSs) for ASD and attention-deficit/hyperactivity disorder (ADHD) using genome-wide association study summary statistics. In 1921 children with genetic data, parents rated autistic traits at 6 years of age. Among them, 1174 children (61.1%) underwent neuromotor examinations (tone, responses, senses, and other observations) during infancy (9-20 weeks of age). We used linear regressions to examine associations of PRSs with neuromotor scores and autistic traits. We performed a bivariate genome-based restricted maximum likelihood analysis to explore whether genetic susceptibility underlies the association between neuromotor development and autistic traits. RESULTS:Higher PRSs for ASD were associated with less optimal overall infant neuromotor development, in particular low muscle tone. Higher PRSs for ADHD were associated with less optimal senses. PRSs for ASD and those for ADHD both were associated with autistic traits. The single nucleotide polymorphism-based heritability of overall motor development was 20% (SE = .21) and of autistic traits was 68% (SE = .26). The genetic correlation between overall motor development and autistic traits was .35 (SE = .21, p < .001). CONCLUSIONS:We found that genetic liabilities for ASD and ADHD covary with neuromotor development during infancy. Shared genetic liability might partly explain the association between nonoptimal neuromotor development during infancy and autistic traits in childhood.

Importance/UNASSIGNED:Many children begin interacting with screen media as early as infancy. Although screen time is associated with negative developmental consequences, few longitudinal studies in the United States have examined covariates of screen time among children under 3 years of age. Objectives/UNASSIGNED:To identify trajectories of screen time among children aged 1 to 3 years, to examine their association with screen use at 8 years of age, and to assess potential determinants of screen time. Design, Setting, and Participants/UNASSIGNED:This prospective birth cohort study included 3895 children (3083 singletons and 812 unrelated multiples) in New York State who had screen time data available for at least 1 time point from 1 to 3 years of age; 1156 children had data at 8 years. The study spanned September 4, 2007, through June 12, 2014, in the first phase, and August 29, 2014, through November 15, 2019, in the second phase. Data analysis for the present study was conducted from September 28, 2018, to July 15, 2019. Main Outcomes and Measures/UNASSIGNED:Maternal reports of children's television, movie, and computer game times were summed for total daily screen time at 12, 18, 24, 30, and 36 months of age. Two screen time trajectories (low and increasing use) were classified by cluster analysis, and logistic regression was used to model risk factors for the increasing trajectory. Children exhibiting the highest 10th percentile of screen use at each point were examined, and linear mixed models were used to identify risk factors of this high exposure category. Results/UNASSIGNED:Among the 3895 children included in the analysis (2031 boys [52.1%] and 1864 girls [47.9%]), median daily screen time increased from 30 (interquartile range, 0-60) minutes at 12 months of age to 120 (interquartile range, 75-200) minutes at 36 months of age. Of 1045 children with complete data at all 5 time points, 279 (26.7%) had an increasing screen time trajectory. Female child sex (adjusted odds ratio [aOR], 0.90; 95% CI, 0.81-0.99) and graduate school levels of paternal (aOR, 0.73; 95% CI, 0.56-0.95) and maternal (aOR, 0.60; 95% CI, 0.47-0.77) education, compared with having completed college, were associated with lower risk of increasing trajectory. Maternal nulliparity was associated with higher risk of increasing trajectory (aOR, 1.14; 95% CI, 1.00-1.30). Children with an increasing trajectory from 1 to 3 years of age had an additional 22 (95% CI, 11-33) minutes per day of screen time at 8 years of age. Covariates associated with the highest 10th percentile of screen exposure included paterman graduate school education compared with college (aOR, 0.63; 95% CI, 0.39-0.99), maternal graduate school education compared with college (aOR, 0.55; 95% CI, 0.37-0.82), maternal nulliparity (aOR, 1.98; 95% CI, 1.50-2.61), twins compared with singletons (aOR, 1.41; 95% CI, 1.05-1.91), non-Hispanic black compared with non-Hispanic white race/ethnicity (aOR, 4.77; 95% CI, 2.25-10.10), and type of care (home-based care aOR, 2.17 [95% CI, 1.38-3.41]; parental care aOR, 2.11 [95% CI, 1.41-3.15]) compared with center-based care. Conclusions and Relevance/UNASSIGNED:These findings suggest that a range of parental and child characteristics are associated with screen time. Screen time habits appear to track from as early as infancy, emphasizing the need for earlier interventions.

Endocrine disrupting chemicals are known to cause neurodevelopmental toxicity through direct and indirect pathways. In this study we used data from the National Health and Nutrition Examination Surveys, along with known exposure-disease relationships, to quantify the intellectual disability burden attributable to in utero exposure to polybrominated diphenyl ethers (PBDEs), organophosphates, and methylmercury and early life exposure to lead. We also estimated the cost of the IQ points lost and cases of intellectual disability. PBDE exposure was the greatest contributor to intellectual disability burden, resulting in a total of 162 million IQ points lost and over 738,000 cases of intellectual disability. This was followed by lead, organophosphates, and methylmercury. From 2001 to 2016, IQ loss from PBDEs, methylmercury, and lead have decreased or remained stagnant. Organophosphate exposure measurements were only available up to 2008 but did show an increase in organophosphate-attributable IQ loss. Although most of these trends show benefit for children's neurodevelopmental health, they may also point towards the use of potentially harmful substitutions for chemicals that are being phased out.

Importance/UNASSIGNED:Air pollutants interact with estrogen nuclear receptors, but their effect on thyroid signaling is less clear. Thyroid function is of particular importance for pregnant women because of the thyroid's role in fetal brain development. Objective/UNASSIGNED:To determine the short-term association of exposure to air pollution in the first trimester with thyroid function throughout pregnancy. Design, Setting, and Participants/UNASSIGNED:In this cohort study, 9931 pregnant women from 4 European cohorts (the Amsterdam Born Children and Their Development Study, the Generation R Study, Infancia y Medio Ambiente, and Rhea) and 1 US cohort (Project Viva) with data on air pollution exposure and thyroid function during pregnancy were included. The recruitment period for the Amsterdam Born Children and Their Development Study was January 2003 to March 2004; for Generation R, April 2002 to January 2006; for Infancia y Medio Ambiente, November 2003 to January 2008; for Rhea, February 2007 to February 2008; and for Project Viva, April 1999 to November 2002. Statistical analyses were conducted from January 2018 to April 2019. Main Outcomes and Measures/UNASSIGNED:Residential air pollution concentrations (ie, nitrogen oxide and particulate matter [PM]) during the first trimester of pregnancy were estimated using land-use regression and satellite-derived aerosol optical depth models. Free thyroxine, thyrotropin, and thyroid peroxidase antibody levels were measured across gestation. Hypothyroxinemia was defined as free thyroxine below the fifth percentile of the cohort distribution with normal thyrotropin levels, following the American Thyroid Association guidelines. Results/UNASSIGNED:Among 9931 participants, the mean (SD) age was 31.2 (4.8) years, 4853 (48.9%) had more than secondary educational levels, 5616 (56.6%) were nulliparous, 404 (4.2%) had hypothyroxinemia, and 506 (6.7%) tested positive for thyroid peroxidase antibodies. Concentrations of nitrogen dioxide and PM with an aerodynamic diameter of 2.5 μm or less (PM2.5) were lower and had less variation in women in the US cohort than those in European cohorts. No associations of nitrogen oxide with thyroid function were found. Higher exposures to PM2.5 were associated with higher odds of hypothyroxinemia in pregnant women (odds ratio per 5-μg/m3 change, 1.21; 95% CI, 1.00-1.47). Although exposure to PM with an aerodynamic diameter of 10 μm or less was not significantly associated with hypothyroxinemia, the coefficient was similar to that for the association of PM2.5 with hypothyroxinemia (odds ratio per 10-μg/m3 change, 1.18; 95% CI, 0.93-1.48). Absorbances of PM2.5 and PM with aerodynamic diameter from 2.5 to 10 μg and were not associated with hypothyroxinemia. There was substantial heterogeneity among cohorts with respect to thyroid peroxidase antibodies (P for heterogeneity, <.001), showing associations of nitrogen oxide and PM with thyroid autoimmunity only in the women in the Generation R Study. Conclusions and Relevance/UNASSIGNED:The findings of this study suggest that first-trimester exposures to PM2.5 were associated with mild thyroid dysfunction throughout pregnancy. The association of PM2.5 exposure with thyroid function during pregnancy is of global health importance because air pollution exposure is widespread and hypothyroxinemia may adversely influence the brain development of offspring.

BACKGROUND:) are linked to poor fetal outcomes but their relationship with childhood development is unclear. OBJECTIVES/OBJECTIVE:increase the risk of early developmental delays. STUDY DESIGN/METHODS:Prospective cohort. SETTINGS/METHODS:New York State excluding New York City. PARTICIPANTS/METHODS:4089 singletons and 1016 twins born between 2008 and 2010. EXPOSURES/UNASSIGNED:estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care. OUTCOMES/RESULTS:, and for those living <1000 m away from a major roadway compared to those living further. Models adjusted for potential confounders. RESULTS:exposures. CONCLUSIONS:were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted.