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Pediatric and Adolescent Endocrinology

SAT-232 - Sex-Dependent Placental Mirna Responses to Insecticide Exposure in A Thai Agricultural Birth Cohort

Saturday, June 13, 2026
9:30 AM - 4:30 PM CT
Location: ENDOExpo; Poster Floor
Disclosure(s):
Yewei Wang, PhD, MD, MSc: No financial relationships to disclose
The placenta is a central endocrine organ that governs fetal growth and developmental programming through processes including steroidogenesis, peptide hormone signaling, and nutrient transport. Environmental insecticide exposures may disrupt placental endocrine function, yet their impacts on regulatory mechanisms remain understudied. Placental microRNAs (miRNAs), as potent post-transcriptional regulators of genes involved in hormone-related networks, may encode sex-dependent endocrine vulnerability.
In a rural Thai agricultural pregnancy cohort (SAWASDEE) with elevated insecticide exposure, we quantified maternal urinary metabolites of organophosphate and pyrethroid insecticide and profiled placental miRNA and mRNA expression by RNA sequencing (n=247). For each metabolite, we fit miRNA-specific linear models adjusting for maternal BMI, gestational age, maternal age, placental cell types, and infant sex, and examined sex-specific associations using stratified analyses (female n=131, male n=116). Significant miRNAs (FDR < 0.1) were mapped to validated and predicted mRNA targets (multiMiR), filtered to expressed placental genes, and prioritized by inverse miRNA–mRNA correlation across matched samples. We performed pathway enrichment using GO Biological Processes and pre-ranked GSEA.
Sex-stratified models identified substantially more exposure-associated placental miRNAs than pooled models, indicating sex-dependent placental sensitivity. In female placentas, inverse-supported mRNA targets were enriched for hormone-relevant pathways, including response to steroid and peptide hormones, ER calcium signaling, vesicle trafficking, membrane organization, and glycoprotein biosynthesis—suggesting disruption of hormone processing, maturation, and secretion. In males, enriched pathways involved growth factor signaling, protein ubiquitination, and DNA damage response, pointing to exposure-linked stress adaptation and genome maintenance.
These findings suggest that prenatal insecticide exposures may alter placental miRNA networks in a sex-dependent manner, particularly targeting hormone-related regulatory axes and secretory pathways essential to placental endocrine function. This supports a mechanistic model wherein environmental exposures disrupt fetal development via sex-specific effects on placental endocrine signaling, through multiple levels of molecular control, highlighting the value of multi-omic placenta profiling in high-exposure populations.

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