# Stress-Air Pollution Interactions and Adolescent Neurobehavior

> **NIH NIH R01** · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · 2024 · $560,829

## Abstract

PROJECT SUMMARY
Research shows that environmental exposures during sensitive life periods affect key physiological processes
that orchestrate the development of multiple organ systems, including brain development and growth/obesity.
The perinatal period is particularly important, as cells and tissues differentiate most rapidly then. Inhibitory
control and negative affect (i.e. depression, anxiety) have been linked to obesity, although most research is
cross-sectional or in adults. Brain development and later life obesity may have roots in perinatal life- consistent
with the Developmental Origins of Health and Disease concept (DOHaD). There is substantial overlap among
perinatal environmental risk factors for depression/anxiety, learning disabilities and obesity. Despite shared
vulnerabilities, no studies have addressed if perinatal environmental exposures create a temporally dependent
network linking obesity with negative affect and inhibitory control, nor have they addressed the sequential
nature of their relationships during child life stages that predate adolescent obesity. Bringing all these concepts
and observations together, we propose that prevalent, perinatal neurotoxic exposures to air pollution and
psychological stress program adolescent obesity by first causing obesity associated neurophenotypes that
arise in children prior to adolescence, the age at which obesity incidence peaks. Because neurophenotypes
are continuous and overlapping, we use transdiagnostic approaches to better capture the relationships among
environment, behavior and obesity. Our proposed framework means that longitudinal pathways from
environment to later onset disease should consider other phenotypic traits as intermediates in a larger causal
pathway that arises during age dependent developmental stages. We believe this is a paradigm shifting
concept in neurodevelopment and obesity research that can unify several widely observed relationships. In
addition, the path from environment to behavior to obesity may depend as much on exposure timing as on
differences in exposure levels. We combine prospective longitudinal exposure measures of perinatal stress
and air pollution with novel statistical approaches to allow us to objectively define susceptibility windows. We
conduct this work in PROGRESS, a prospective child health cohort that has collected longitudinal exposure,
covariate and phenotype data from pregnancy to age 12 years already. In this proposal, we will assess the role
of perinatal environment, negative affect and inhibitory control on obesity phenotypes from 13-16 years, an age
during which child obesity rates rise dramatically, ensuring adequate power and justifying data collection in an
additional grant cycle. Only a cohort like PROGRESS with longitudinal, prospective measures starting in
perinatal life across multiple health domains and across time could address these questions on adolescent
health in a single 5 year grant. In sum, we will explain connec...

## Key facts

- **NIH application ID:** 10898909
- **Project number:** 5R01ES013744-17
- **Recipient organization:** ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
- **Principal Investigator:** Robert O Wright
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $560,829
- **Award type:** 5
- **Project period:** 2007-01-15 → 2028-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10898909

## Citation

> US National Institutes of Health, RePORTER application 10898909, Stress-Air Pollution Interactions and Adolescent Neurobehavior (5R01ES013744-17). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10898909. Licensed CC0.

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