# Proj3:Role of cytochrome P450 (CYP)1A/1B1 enzymes in the potentiation of neonatal lung injury in newbron mice exposed prenatally to PHs, and increased risk of premature infants to chronic lung disease

> **NIH NIH P42** · BAYLOR COLLEGE OF MEDICINE · 2021 · $360,875

## Abstract

Project Summary
 Pregnant women, living in the vicinity of superfund sites, who may be exposed to polyclic
aromatic hydrocarbons (PAHs) that emanate from these sites, are at a higher risk for preterm
delivery. Preterm delivery requires the neonate to be subjected to supplemental oxygen
(hyperoxia), and this in turn could lead to chronic lung disease/ bronchopulmonary dysplasia
(BPD). We hypothesize that prenatal PAH exposure will exacerbate the effects of postnatal
supplemental oxygen in preterm neonates. The mechanisms by which PAHs potentiate BPD in
infants are not well understood. The central hypothesis of this project is that prenatal
administration of PAHs [i.e. benzo[a]pyrene (BP), or a mixture of benzo(a)pyrene (BP),
benzo(b)fluoranthrene (BbF), and dibenz[a]anthracene (DBA)], which are which are defined as
class B2 carcinogens by USEPA, will differentially exacerbate lung injury and alveolar
simplification in neonatal mice following postnatal hyperoxia, and that this effect will be altered in
mice lacking the gene for cytochrome P450 (Cyp)1a1 or 1a2 genes by mechanisms entailing a
combination of genotoxic and epigenetic mechanisms. We will also test the hypothesis that the
infants exposed prenatally to PAHs have a greater risk of developing BPD than those exposed to
lesser or no PAHs, and that human pulmonary cells exposed to remediated PAHs will exhibit
lesser toxicity than parent PAHs. In order to test these hypotheses, we propose the following Specific
Aims: (1). Specific Aim 1. To test the hypothesis that prenatal exposure of wild type (WT) (C57BL/6J)
mice to the PAH BP or a mixture of PAHs (BP + BbF + DBA) will result in exacerbation of lung injury and
alveolar simplification following postnatal hyperoxia, and this effect will be altered in mice lacking the gene
for Cyp1a1, 1a2 or 1b1. 2. To determine the mechanisms by which prenatal PAHs will alter the
susceptibility of neonatal mice to hyperoxia. 3. To test the hypothesis that mothers exposed to
PAHs (that are present in superfund sites) are at a greater risk for preterm delivery, and that these
infants will show increased susceptibility to develop BPD than those with lesser or no exposure.
Accomplishments of these aims could lead to novel strategies for the prevention/treatment in
premature infants of BPD, which is probably potentiated by maternal PAHs that emanate from
Superfund sites.

## Key facts

- **NIH application ID:** 10116394
- **Project number:** 5P42ES027725-02
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **Principal Investigator:** BHAGAVATULA MOORTHY
- **Activity code:** P42 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $360,875
- **Award type:** 5
- **Project period:** 2020-02-28 → 2025-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10116394

## Citation

> US National Institutes of Health, RePORTER application 10116394, Proj3:Role of cytochrome P450 (CYP)1A/1B1 enzymes in the potentiation of neonatal lung injury in newbron mice exposed prenatally to PHs, and increased risk of premature infants to chronic lung disease (5P42ES027725-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10116394. Licensed CC0.

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