# Environmental bisphenol exposure, infant brain and behavior: Human and animal models

> **NIH NIH R01** · COLUMBIA UNIVERSITY HEALTH SCIENCES · 2020 · $671,780

## Abstract

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 on
infant brain development, and indirect effects via disruption of postnatal mother-infant interactions. Parental
social behaviors may be especially vulnerable to endocrine-disrupting chemicals such as BPA as these
behaviors are shaped by hormonal priming and by the organization of the social/parental brain. Most of the
human literature identifies effects of BPA in older children, with little focus on the first year of life. In rodent and
primate models, in utero exposure to BPA disrupts offspring cognitive and social development and maternal care
via epigenetic changes. In humans, the direct effect of BPA on infant brain development and attention, and the
modulation of these effects by BP-induced changes to mother-infant interaction, have not been examined. We
thus 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from many consumer products, it has been replaced by structural analogs, bisphenol-s (BPS) and bisphenol-f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 will: 1) examine associations between in utero BP
(combined exposure) exposure and infant brain function and attention, 2) conduct a parallel rodent study of the
effects of in utero BP exposure on cellular and molecular changes in the brain, and 3) translate a human method
of studying mother-infant interaction for use in our rodent model and determine the effects of BP on these
caregiving interactions. In both humans and rodents, we ask whether associations detected between in utero BP
and brain and cognitive development are moderated by BP-induced change in mother-infant interaction. In our
translational approach, we recruit infants at 1- and 9-months old and assess infant brain function and attention
at two timepoints, and we leverage previously funded measurement of mother-infant interaction to test its
moderating effects on these associations. In our parallel rodent model, we measure effects of BP exposure on
offspring cortical gene expression, structure, attention and quality of mother-infant interactions.
Impact: This R01 addresses a critical gap in our understanding of how in utero exposure to endocrine-disrupting
chemicals alters infant brain and cognitive function. Understanding these effects is essential to developing
screening tools and intervention for downstream effects on neurodevelopment. The R01 also provides
preliminary data for use in future translational collaborations among this team. Future animal studies will
disentangle the direct and indirect effects of BP through cross-fostering experiments, and human studies will
follow this cohort into school age to investigate neural correlates of BP-induced effects on neurodevelopment.

## Key facts

- **NIH application ID:** 10064434
- **Project number:** 1R01ES030950-01A1
- **Recipient organization:** COLUMBIA UNIVERSITY HEALTH SCIENCES
- **Principal Investigator:** AMY MARGOLIS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $671,780
- **Award type:** 1
- **Project period:** 2020-09-10 → 2023-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10064434

## Citation

> US National Institutes of Health, RePORTER application 10064434, Environmental bisphenol exposure, infant brain and behavior: Human and animal models (1R01ES030950-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10064434. Licensed CC0.

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