Prenatal Exposure Research Articles

Prenatal exposure to pesticides has been linked to disrupted fetal growth, which contributes to cardiometabolic disease risk. The placenta, as the maternal–fetal interface, undergoes extensive DNA methylation remodeling that may record environmental exposures and mediate downstream metabolic effects, including those related to cardiometabolic risk in offspring. We hypothesized that placental DNA methylation patterns vary with maternal pesticide exposure, that exposure-associated CpG sites overlap with those predictive of neonatal anthropometry, and that genes with altered methylation may represent pathways relevant to cardiometabolic health. We analyzed 254 term placentas from the Study of Asian Women and their Offspring's Development and Environmental Exposures (SAWASDEE) cohort using the Illumina EPIC v2.0 array. Robust linear regression models assessed associations between placental DNA methylation and infant head circumference, birth length, and birth weight z-scores. Each outcome was analyzed separately, adjusting for estimated proportions of eight placental cell types, infant sex, maternal age, BMI, and gestational age. Parallel analyses examined urinary organophosphate metabolites (OP), pyrethroid metabolites (PYR), and a composite exposure index (MIX). CpGs with Benjamini–Hochberg FDR < 0.05 were considered significant. Significant CpGs were intersected across exposures and outcomes and mapped to genes for Gene Ontology and KEGG pathway enrichment (FDR < 0.05). EWAS of growth traits identified 26, 1,626, and 1,729 CpGs associated with head circumference, birth length, and birthweight, respectively. CpGs associated with weight and length were enriched for pathways including insulin resistance and MAPK signaling. Exposure-related EWAS identified 46,519 significant CpGs for OP and 46,564 for MIX; none for PYR. MAPK signaling was the top enriched pathway for both OP and MIX. Intersection of OP and MIX signatures yielded 46,417 shared CpGs, with 102 and 135 overlapping length- and weight-associated sites, respectively. Nine genes were common to both exposure and growth signatures, with IRS1 identified as a central node linking insulin and MAPK pathways. Placental methylation patterns associated with prenatal pesticide exposure overlap with epigenetic signals linked to neonatal growth, particularly involving insulin resistance and MAPK signaling, highlighting mechanisms of fetal programming relevant to long-term cardiometabolic health.

Background: Regionalization is the direction of patients to centers with appropriate levels of care and is key to optimizing outcomes. However, the role of prenatal care in perinatal regionalization for congenital heart defect (CHD) care is poorly understood. Objective: To estimate associations between prenatal care initiation or visit frequency, and probability of delivery at a pediatric cardiac center. Methods: Cross-sectional analysis of neonates with CHDs in Illinois, 2013-2021. Data were obtained from the Illinois Department of Public Health’s Adverse Pregnancy Outcomes Reporting System. The two exposure variables were: (1) prenatal care initiation – none vs. inadequate prenatal care (initiated after the fourth month or <50% of recommended visits); and (2) prenatal visit frequency – intermediate (50-79% of recommended visits) vs. adequate (80-109%) or adequate plus ( > 110%) prenatal care. The outcome was delivery at a pediatric cardiac surgical center. Multivariable linear probability models estimating associations between both prenatal care exposures and delivery hospital, controlling for demographic and clinical characteristics, were stratified by CHD severity (mild, moderate, severe) to account for the modifying effect of CHD severity. Results: Of 12,113 neonates with CHD, 25.4% were born at a cardiac center; 2.3% had no prenatal care, 13.4% had inadequate prenatal care, 10.8% had intermediate prenatal care, and 73.6% had adequate or adequate plus prenatal care; 13.0% had severe CHD and 73.0% had mild CHD. In multivariable models, prenatal care initiation was associated with a 10.5 percentage-point (pp) higher probability of delivery at a cardiac center for those with fetuses who had mild CHD (95%CI 4.7-16.2pp) and 30.2pp higher probability for severe CHD (95%CI 13.6-46.9pp). For mild CHD, adequate plus prenatal care was associated with a 6.7 pp (95%CI 4.0 to -9.4pp) lower probability of delivery at a cardiac center than intermediate prenatal care. Prenatal visit frequency was not associated with delivery at a cardiac center for severe CHD ( Table 1 ). Conclusion: Initiating prenatal care, even if delayed, is associated with a higher probability of delivery at a cardiac center, especially for severe CHDs. However, more prenatal visits may direct mild CHDs to non-cardiac centers. Both prenatal care components are crucial to achieve efficient perinatal regionalization of CHD care.

Prenatal exposure to dietary levels of glyphosate disrupts metabolic, immune, and behavioral markers across generations in mice.

Immunotoxic effects in children resulting from prenatal and early childhood exposure to pesticides: A systematic review and meta-analysis.

Reduced exosomal miR-215-5p activates the NEAT1/MAPK1/p-CRMP2 pathway and contributes to social dysfunction in a VPA-induced autism model.

Comparative effectiveness of moderate treadmill training and venlafaxine treatment on long-lasting brain changes induced by prenatal dexamethasone exposure.

Prenatal phthalate exposures and childhood allergies: Combined linear/nonlinear modeling reveals critical windows and sex differences.

Mouse model of prenatal valproic acid exposure: Effects on cortical morphogenesis and behavioral outcomes across environmental conditions.

Prenatal fentanyl exposure affects social dominance and myelination patterns in the adult mouse brain.

Impact of prenatal and childhood exposure to pyrethroids and chlorpyrifos on motor skills in 7-year-old children from the Odense Child Cohort.

Perinatal and prenatal alcohol exposure impairs striatal cholinergic function and cognitive flexibility in adult offspring.

The association of preconception and prenatal cannabis and tobacco exposure with autism symptoms in offspring: A population-based longitudinal study.

Associations between prenatal exposure to air pollution and infant growth trajectories in the first two years: Exploring potential sexual dimorphism and sensitive windows.

Impact of prenatal alcohol exposure in midlife: an assessment of the retina in the vervet monkey.

Developmental programming: Differing impact of prenatal testosterone and prenatal bisphenol-A -treatment on hepatic methylome in female sheep.

Endocrine Disruptors and Attention Deficit Hyperactivity Disorder: A Systematic Review.

Ethanol exposure impaired mitotic division in apical radial glial cells and disrupted early cortical development in human forebrain organoids: Implications for ethanol-induced microcephaly.

Maternal exposure to polycyclic aromatic hydrocarbons and visual developmental outcomes in early childhood.

Spatial disparities in perfluoroalkyl and polyfluoroalkyl substances exposure and immunosuppressive effects on vaccine induced antibody levels in Guangzhou children.

Neurodevelopmental impact of prenatal regional or general anaesthesia: An ambidirectional pilot cohort study.