# Integrating environment-by-epigenome interactions into a tractable model of epigenetic aging

> **NIH NIH R56** · UNIVERSITY OF GEORGIA · 2022 · $273,430

## Abstract

Project Summary
The goal of the project is to discover how the environment interacts with epigenetic aging processes to affect
biological aging. Risk of radiation exposure occurring through occupational exposures, medical therapies, or
environmental disasters involving ionizing radiation (IR), either due to nuclear accidents, nuclear warfare,
and/or terrorist attacks (e.g., attacks on nuclear energy facilities, dirty bombs) are acutely relevant to
contemporary public health. However, health impacts resulting from such exposures are difficult to predict due
to variable dose rates, duration of exposure, age-specific effects, and the environmental and social context of
exposure. Although testing the outcome of each combinatorial scenario isn’t feasible, a fundamental
understanding of how environmental and age-dependent variables interact with IR exposure can be achieved
through approaches that incorporate environmental complexity and realistic dosing regimens.
Recent advances demonstrate a role for the epigenome in biological aging as it provides a molecular context
for integrating both genetic and environmental influences into aging programs. Epigenetic clocks summarize
the readout of age associated hyper- and hypo-methylation from a selection of loci across the genome which
are collectively capable of predicting chronological age with high accuracy. Despite their unprecedented
accuracy, the age indicated by epigenetic clocks can differ from an individual’s actual age. The magnitude and
directionality of this epigenetic-to-chronological age mismatch is associated with physiological function and
disease risk. For example, advanced epigenetic age relative to their chronological age is associated with
cancer, heart disease, and all-cause mortality. The underlying causes of epigenetic-to-chronological age
discordance are not resolved but both genetic and environmental factors appear to play a role. To empirically
address causal relationships between environmental conditions and epigenetic aging, this project will take
advantage of recently developed epigenetic clocks for the experimentally and genetically tractable medaka fish
(Oryzias latipes) model.
The work encompasses three primary objectives: (1) Test the hypothesis that chronic exposure to
environmentally relevant doses of ionizing radiation accelerate and shape epigenetic aging trajectories. (2)
Determine how an individual’s developmental exposure history interacts with subsequent radiation exposure to
affect biological aging trajectories. (3) Identify windows of vulnerability occurring across the lifespan in which
environmental exposures disproportionately impacts epigenetic aging trajectories. Together, this work will
advance a life course and toxicological understanding of how environmental challenges associated with
radiological disaster events shape biological aging and attendant organismal physiology.

## Key facts

- **NIH application ID:** 10674255
- **Project number:** 1R56AG078336-01
- **Recipient organization:** UNIVERSITY OF GEORGIA
- **Principal Investigator:** Benjamin Barrow Parrott
- **Activity code:** R56 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $273,430
- **Award type:** 1
- **Project period:** 2022-09-02 → 2024-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10674255

## Citation

> US National Institutes of Health, RePORTER application 10674255, Integrating environment-by-epigenome interactions into a tractable model of epigenetic aging (1R56AG078336-01). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10674255. Licensed CC0.

---

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