# World Trade Center Particulate Matter-Associated End Organ Dysfunction: Targeting Early Vascular Dysfunction and Injury

> **NIH ALLCDC K01** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2024 · $160,804

## Abstract

PROJECT SUMMARY. This K01 grant proposal will investigate the early vascular injury and end organ
dysfunction in World Trade Center (WTC)-Particulate Matter (WTC-PM) exposed and affected by
gastroesophageal reflux disease (GERD). PM is the main component of WTC dust, and the exposure of WTC-
PM includes effects such as systemic inflammation, vascular dysfunction, and subsequent end-organ damage.
Epidemiologic investigations have documented associations between increased PM, lung, cardiovascular and
kidney diseases such as chronic kidney diseases (CKD). Additionally, metabolic syndrome (MetSyn) is often
associated with kidney damage, and we have seen MetSyn in a large population of our Fire Department of New
York (FDNY) study cohort. This leads to the possible risk of end organ damage such as cardio-renal disease in
WTC-PM exposed FDNY first responders. Further, CKD remains one of the leading causes of mortality and are
characterized by a marked and reduction of renal artery flow. This yields tissue ischemia, renal injury and fibrosis.
Hence, there is an urgent need to explore relevant early phenotypic changes and identify related kidney
biomarkers and cardio-renal vascular setting. Further, a greater understanding of the cellular and molecular
mechanisms underlying cardio-renal injury could lead to the development of new therapeutic approaches.
This proposal will focus on exploring cardio-renal/ vascular injury biomarkers in FDNY cohort serum samples as
well as understanding the role of macrophages and transforming growth factor-beta (TGF-β) in the development
of renal vascular dysfunction (RVD) in WTC-PM–exposed GERD model, and subsequent cardio-renal failure in
this murine model. Earlier studies showed that immune cells in particular macrophages play a critical role in
mediating cardio-renal injury, repair, and fibrosis. Interestingly, our recent preliminary work shows that there is
macrophage hyperplasia in WTC-PM exposed mice with loss of lung function. Fibrosis is the hallmark of
progressive CKD, which leads to an end organ failure. Our earlier studies indicate that activation of inflammatory
cells can mediate fibrosis in both the heart and kidney through TGF-β. Our preliminary findings demonstrate that
with an increased inflammation, and collagen deposition in inter-tubular region in the kidneys. This proposal
consists of 3 aims. Aim 1 will quantify WTC-cardio-renal vascular risk biomarkers from first responders (FDNY).
Aim 2 will further determine cardio-renal vascular injury by quantifying functional/histopathologic and
complementary imaging modalities in a murine WTC-PM exposure model. Aim 3 will further assess whether
WTC-PM induced cardio-renal vascular injury has an influence in a GERD murine model. Results of the proposed
research will help provide insights into WTC-PM induced cardio-renal associated with GERD risk biomarkers in
first responders as well as how macrophage and TGF-β influence RVD in the remodeling of WTC-PM -induced
ca...

## Key facts

- **NIH application ID:** 10995060
- **Project number:** 1K01OH012794-01
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Arul Veerappan
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** ALLCDC
- **Fiscal year:** 2024
- **Award amount:** $160,804
- **Award type:** 1
- **Project period:** 2024-07-01 → 2027-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10995060

## Citation

> US National Institutes of Health, RePORTER application 10995060, World Trade Center Particulate Matter-Associated End Organ Dysfunction: Targeting Early Vascular Dysfunction and Injury (1K01OH012794-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10995060. Licensed CC0.

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