# Placental Functional Networks Linking Developmental Pesticide Exposure and Offspring Neurodevelopment

> **NIH NIH R01** · EMORY UNIVERSITY · 2020 · $547,219

## Abstract

SUMMARY/ABSTRACT
There continues to be an increase in the incidence and prevalence of neurobehavioral disorders.
Considerable evidence has accumulated linking environmental toxicants, including pesticides, to these
disorders and generally to detriments in neurobehavioral development. The placenta serves as a conduit of
maternal signals and directs the developmental program through key roles it plays in nutrient transfer,
metabolism, gas exchange, neuroendocrine signaling, growth hormone production, and immunologic control.
These critical functions may be controlled by, as well as be reflected in, placenta genomics. Data from our
group and others have demonstrated that environmental exposures including chemical and psychosocial
factors can impact these placental functions reflected in variation in the molecular character of the placenta.
Pyrethroid pesticides are a group of common insecticides and due to their persistence and widespread use are
found with high prevalence throughout human populations. Increased pyrethroid exposures have been linked
to a greater risk for attention deficit hyperactivity disorder (ADHD) in children as well as to cognitive defects.
These insecticides can accumulate in and transfer through mammalian placentas and prenatal exposures have
been linked to altered placental and neuronal functions including effects on the dopaminergic system. The
scientific premise of this project is that the prenatal environment can disrupt critical functions of the
placenta, reflected in placental gene networks, leading to alterations in communication of
environmental signals between mother and fetus, and ultimately the development of postnatal health
and disease. Thus, the placenta is the central organ for the developmental origins of health and
diseases (DOHaD) paradigm. We specifically hypothesize that disruption of gene networks in the placenta by
in utero exposures to common pyrethroids acts as a mediator of the impact leading to cognition and behavior
deficit in the offspring. In a prospective pregnancy and birth cohort, with a primary focus on effects of prenatal
pesticide exposure on newborn and early life neurobehavioral function, we will thoroughly interrogate the
placenta genome to provide evidence for the molecular underpinnings of these effects. In parallel, we will
utilize a highly characterized murine model of exposure to the one common pyrethroid, i.e. deltamethrin, to
provide causal evidence of these placental genomic features as mediators of the environment’s effect on
offspring neurodevelopment, and more importantly, to shed lights on relevance of placental gene networks to
the programming in the brain, which will also be comprehensively interrogated. Our innovative, integrated
modelling takes advantage of this bidirectional translational research approach and will provide an opportunity
to define prevention or intervention strategies that can optimize the chances for successful pregnancy and
health outcomes in children, ...

## Key facts

- **NIH application ID:** 9940716
- **Project number:** 5R01ES029212-03
- **Recipient organization:** EMORY UNIVERSITY
- **Principal Investigator:** William Michael Caudle
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $547,219
- **Award type:** 5
- **Project period:** 2018-07-01 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9940716

## Citation

> US National Institutes of Health, RePORTER application 9940716, Placental Functional Networks Linking Developmental Pesticide Exposure and Offspring Neurodevelopment (5R01ES029212-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9940716. Licensed CC0.

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