Prenatal and early-life chemical exposures linked to faster cellular aging in children and adolescents
Official title: Early-life environmental exposure mixtures and biological age acceleration in children and adolescents: susceptibility, potential interactions and underlying mechanisms
Funded at Icahn School of Medicine at Mount Sinai · NIH-11469427 · Data updated 2026-11-12
Researchers will look at whether prenatal and early-life mixtures of chemicals and factors like diet and obesity speed up cellular aging in children and teens.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Icahn School of Medicine at Mount Sinai NIH-funded |
| Lab location | 1 site (New York, United States) |
| Project start | March 5, 2024 |
| Project end | December 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $69,858 |
| NIH project number | 3R01ES035773-03S1 |
| Project ID | NIH-11469427 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal participants include pregnant people and their children (from birth through adolescence) who can provide biological samples, exposure information, and agree to periodic follow-up visits.
✕Less likely to help
This observational study does not provide a treatment, so people seeking immediate therapy or adults without prenatal/birth data or unwilling to provide samples and follow-up would not directly benefit.
What this research studies
This project follows children from before birth through adolescence to measure prenatal chemical exposures, diet, body size, and markers of cellular aging such as telomere length. Scientists will analyze blood and other biological samples using multi-omics methods to identify molecular pathways linking mixtures of endocrine-disrupting chemicals (EDCs) and other stressors to accelerated biological aging. The study combines data from existing birth cohorts with repeated measurements to track how exposures relate to changes over time. The aim is to identify who is most susceptible and which exposures could be modified to lower long-term risk of age-related diseases.
Why it matters
Potential benefit: If successful, the findings could point to specific exposures and biological pathways to target for prevention efforts that reduce early cellular aging and future chronic disease risk.
How similar studies have gone: Prior smaller studies have linked prenatal EDC exposures to shorter telomeres in children, but no large longitudinal multi-omics study has followed the prenatal exposome through adolescence to test interactions and mechanisms.
Where this research is happening
-
Icahn School of Medicine at Mount Sinai
New York, United States Active
Researchers
- Principal investigator: Valvi, Damaskini — Icahn School of Medicine at Mount Sinai
- Study coordinator: Valvi, Damaskini
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.