# Prenatal endocrine-disrupting chemicals and social/cognitive risk in mothers and infants: Potential biologic pathways

> **NIH NIH R01** · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · 2020 · $558,701

## Abstract

Mother-infant interaction sets the behavioral foundation and trajectory for infant social/cognitive development.
Parental social behaviors are especially vulnerable to endocrine-disrupting chemicals because these behaviors
are shaped by hormonal priming and by the organization of the social/parental brain. It is known that in utero
bisphenol A (BPA) exposure disturbs neurobehavioral development in animals and in humans. The pathways
linking in utero BPA exposure to neurobehavioral development likely involve direct effects in utero, and indirect
effects via disruption of postnatal mother-infant interactions. To date, little human study has linked prenatal
BPA exposure to altered mother-infant interaction or examined the consequence of this effect on
neurobehavioral development. Most of the human literature identifies effects of BPA in older children. In rodent
and primate models, prenatal exposure to BPA disrupts maternal care and offspring social behavior via
epigenetic changes. In humans, these indirect effects on mother-infant interaction and the associated
epigenetic mechanisms have not been examined. We thus risk underestimating the full impact of BPA
exposure, and we currently do not know the pathways through which BPA may disrupt development. Although
BPA has been removed from many consumer products, it has been replaced by structural analogs, bisphenol-s
(BPS) and bisphenol-f (BPF), which may have similar detrimental effects. This study aims to translate findings
from animal models to ask whether increased prenatal BPA, BPS, BPF (BP) exposure in humans predicts less
optimal maternal care/mother-infant interaction and infant/toddler development. Moreover we ask whether this
exposure is associated with corresponding epigenetic changes in mother and infant in genes previously shown
to be impacted by prenatal BPA exposure in rodents: estrogen receptor alpha (ESR1: implicated in maternal
behavior) and brain-derived neurotrophic factor (BDNF; implicated in infant neural plasticity and cognition). In
our translational approach, we recruit women during pregnancy, assess prenatal BP exposure using multiple
urine samples collected during the 3rd trimester of pregnancy. We assess mother-infant interaction with
measures of moment-by-moment reciprocal influences between mother and infant, providing a more nuanced
measure of the effects of BP in humans, and we assess infant/toddler social and cognitive development at 12
and 24 months. In serially collected buccal swabs, we assess DNA methylation of ESR1 in the mother and
infant and of BDNF in the infant to understand how early life BP exposure alters these pathways.
Understanding the effects of BP on maternal care and mother-infant interaction is essential to revealing the
pathways through which BP acts to disrupt neurodevelopment. This R01 addresses a critical gap in our
understanding of how prenatal endocrine-disrupting chemicals alter mother-infant interaction, infant/toddler
development, and associa...

## Key facts

- **NIH application ID:** 9854742
- **Project number:** 5R01ES027424-03
- **Recipient organization:** NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC
- **Principal Investigator:** Beatrice A Beebe
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $558,701
- **Award type:** 5
- **Project period:** 2018-02-15 → 2023-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9854742

## Citation

> US National Institutes of Health, RePORTER application 9854742, Prenatal endocrine-disrupting chemicals and social/cognitive risk in mothers and infants: Potential biologic pathways (5R01ES027424-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9854742. Licensed CC0.

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