A Latent Trait-based Measure as a Data Harmonization and Missing Data Solution Applied to the Environmental Influences on Child Health Outcomes Cohort.

Background: Collaborative research consortia provide an efficient method to increase sample size, enabling evaluation of subgroup heterogeneity and rare outcomes. In addition to missing data challenges faced by all cohort studies like nonresponse and attrition, collaborative studies have missing data due to differences in study design and measurement of the contributing studies.

Methods: We extend ROSETTA, a latent variable method that creates common measures across datasets collecting the same latent constructs with only partial overlap in measures, to define a common measure of socioeconomic status (SES) across cohorts with varying indicators in the Environmental influences on Child Health Outcomes Cohort, a consortium of pregnancy and pediatric cohorts.

Associations between maternal plasma concentrations of corticotrophin releasing hormone and the placental transcriptome.

Introduction: The placenta produces corticotrophin releasing hormone (CRH), which rises exponentially in maternal plasma across pregnancy. CRH plays a functional role in fetal development, labor initiation, and the regulation of gestational length. We aimed to understand how maternal plasma CRH during pregnancy reflects placental physiology during parturition by characterizing placental transcriptomic signatures of maternal plasma CRH and comparing to transcriptomic signatures of gestational age at birth.

The influence of early childhood education and care on the relation between early-life social adversity and children's mental health in the environmental influences for Child Health Outcomes Program.

Early adversity increases risk for child mental health difficulties. Stressors in the home environment (e.g.

Environmental and dietary factors associated with urinary OH-PAHs in mid-pregnancy in a large multi-site study.

Background: PAH exposure is associated with adverse health outcomes, but exposure sources in pregnancy are not well-understood.

Objectives: We examined associations between urinary OH-PAHs during pregnancy and environmental tobacco smoke (ETS) and short-term ambient air pollution exposure. Participants included 1603 pregnant non-smokers in three cohorts from 7 sites across the USA.

Associations Between Prenatal Vitamin D and Placental Gene Expression.

Background: Vitamin D is a hormone that regulates gene transcription. Prenatal vitamin D has been linked to immune and vascular function in the placenta, a key organ of pregnancy. Transcriptome-wide RNA sequencing can provide a more complete representation of the placental effects of vitamin D.

Association of prenatal vitamin E levels with child asthma and wheeze.

Background: We investigated the individual and interaction effects of maternal plasma 𝛂- and ϒ-tocopherol levels (vitamin E isomers) on child asthma and wheeze at age 8-9.

Methods: Mother-child dyads were enrolled between 2006 and 2011 into the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) prenatal cohort. Maternal second-trimester samples were analyzed for tocopherol and lipid concentrations.

Urinary polycyclic aromatic hydrocarbon (PAH) metabolite concentrations in three pregnancy cohorts from 7 U.S. study sites.

Objective: Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with adverse birth and developmental outcomes in children. We aimed to describe prenatal PAH exposures in a large, multisite U.S.

A genome scale transcriptional regulatory model of the human placenta.

Gene regulation is essential to placental function and fetal development. We built a genome-scale transcriptional regulatory network (TRN) of the human placenta using digital genomic footprinting and transcriptomic data. We integrated 475 transcriptomes and 12 DNase hypersensitivity datasets from placental samples to globally and quantitatively map transcription factor (TF)-target gene interactions.

Associations Between Prenatal Vitamin D and Placental Gene Expression.

Background: Vitamin D is a hormone regulating gene transcription. Prenatal vitamin D has been linked to immune and vascular function in the placenta, a key organ of pregnancy. To date, studies of vitamin D and placental gene expression have focused on a limited number of candidate genes.

Measurement bias in caregiver-report of early childhood behavior problems across demographic factors in an ECHO-wide diverse sample.

Background: Research and clinical practice rely heavily on caregiver-report measures, such as the Child Behavior Checklist 1.5-5 (CBCL/1.5-5), to gather information about early childhood behavior problems and to screen for child psychopathology.

Associations of prenatal ambient air pollution exposures with asthma in middle childhood.

We examined associations between prenatal fine particulate matter (PM), nitrogen dioxide (NO), and ozone (O) exposures and child respiratory outcomes through age 8-9 years in 1279 ECHO-PATHWAYS Consortium mother-child dyads. We averaged spatiotemporally modeled air pollutant exposures during four fetal lung development phases: pseudoglandular (5-16 weeks), canalicular (16-24 weeks), saccular (24-36 weeks), and alveolar (36+ weeks). We estimated adjusted relative risks (RR) for current asthma at age 8-9 and asthma with recent exacerbation or atopic disease, and odds ratios (OR) for wheezing trajectories using modified Poisson and multinomial logistic regression, respectively.

Sex-specific associations between placental corticotropin releasing hormone and problem behaviors in childhood.

Placental corticotropin-releasing hormone (pCRH) is a neuroactive peptide produced in high concentrations in mid-late pregnancy, during key periods of fetal brain development. Some evidence suggests that higher pCRH exposure during gestation is associated with adverse neurodevelopment, particularly in female offspring. In 858 mother-child dyads from the sociodemographically diverse CANDLE cohort (Memphis, TN), we examined: (1) the slope of pCRH rise in mid-late pregnancy and (2) estimated pCRH at delivery as a measure of cumulative prenatal exposure.