# From the womb to the classroom: Linking perinatal micronutrients and toxicants to neural and behavioral development in utero and in childhood

> **NIH NIH R01** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2021 · $505,480

## Abstract

PROJECT SUMMARY
Maternal toxicant exposure and nutritional status during pregnancy contribute to the emergence of attention
deficit hyperactivity disorder (ADHD) and serious externalizing behavioral problems. A prevailing belief is that
toxicants and fetal micronutrient deficiencies disrupt fetal brain development, with subsequent long-term
implications for offspring health and development. However, evidence that prenatal toxicant exposure and
micronutrient imbalances influence fetal neural systems in humans is lacking, as is evidence that changes in
the fetal brain precede nutrient- and toxicant-related developmental concerns of childhood. Filling these gaps
in knowledge is critical, given the high prevalence of prenatal toxicant exposure worldwide and evidence that
events during gestation influence long-range health and well-being. The central objective of this proposal is to
examine development of human neural networks in utero, and to link variation in prenatal brain development to
prenatal toxicant and nutrient levels (measured in the fetus) and to child outcomes. This will be done in a way
that is sensitive both to chemical mixture effects and to time-variant exposure across the course of gestation,
which are both likely to have specific neurodevelopmental consequences. We will pair advances in fetal
resting-state functional connectivity (RSFC) MRI with innovations in tooth-biomarker assays to rigorously
investigate associations between prenatal chemical/micronutrient exposures and human fetal neural
connectome development, and will determine how exposome and connectome development in utero relate to
child neurobehavioral development. Data collection in a Detroit-based pregnancy cohort was initiated more
than 7 years ago, beginning with fetal brain RSFC MRI. Children have been followed over time, with
assessments at birth, 7 months, age 3 and age 5, and have begun to naturally shed their deciduous teeth. The
primary aims of this project are to (i) identify fetal brain connectome abnormalities associated with prenatal
toxicant exposure and micronutrient imbalance, and identify key windows of gestational vulnerability; (ii)
evaluate prenatal exposures and fetal neural connectivity as longitudinal predictors of executive function,
externalizing problems and school readiness at age 5; and (iii) isolate protective factors in the postnatal
environment that promote resilient outcomes in children with prenatal micronutrient deficiency and toxicant
exposure. We will thus be able to meaningfully evaluate whether and how prenatal nutrient availability and
toxic exposure events affect functional neurocircuitry of the developing fetal brain, and the longer-term
neurobehavioral consequences of those associations. Such work would constitute a substantial advance in our
understanding of both the longitudinal effects of micronutrient and toxicant exposures in the prenatal period
and the origins of child neurobehavioral disorders.

## Key facts

- **NIH application ID:** 10247799
- **Project number:** 5R01ES032294-02
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Christine Austin
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $505,480
- **Award type:** 5
- **Project period:** 2020-08-26 → 2025-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10247799

## Citation

> US National Institutes of Health, RePORTER application 10247799, From the womb to the classroom: Linking perinatal micronutrients and toxicants to neural and behavioral development in utero and in childhood (5R01ES032294-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10247799. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*
