# Defining the Impact of E-Cigarettes on Cardiac Pathophysiology

> **NIH NIH R01** · OHIO STATE UNIVERSITY · 2020 · $390,000

## Abstract

Project Summary/Abstract
 Both cigarettes and air pollution are sources of toxic gases and fine particulate matter (PM2.5; particles
<2.5 µm) that are linked with adverse CV outcomes, characterized by increased inflammation. and subsequent
collagen deposition. Recently, a new source of emissions, the electronic cigarette (EC), was introduced and is
gaining unprecedented popularity, especially among young people. Although e-cigarettes are an artificial
source of nicotine similar to tobacco cigarettes, they are a source of potentially toxic gases, fine particulates,
and nicotine. However, it remains unknown if e-cigarette use increases inflammation and fibrosis long-term,
leading to structural and functional damage to heart and vasculature; these critical questions will be answered
by the present proposal using in vivo models and, for the first time, primary human myocytes. Aerosol from
ECs are comprised of fine and ultrafine particles which makes it relevant to investigate plausible effects of EC
exposure on inflammatory and calcium regulatory pathway. Studies from our team demonstrate that exposure
to fine particulate matter cause long-term cardiac dysfunction. In fact, our data are the first to examine the
adverse CV consequences of exposure to PM2.5, and will be expanded to include similar studies on EC-
generated aerosol. While our findings in mice support the critical impact of EC aerosol in mice, given the
growing population already exposed to EC aerosols, it is critical that we now translate our studies to define the
impact on key surrogate cardiac cell populations. We have established a live cell repository of key cardiac cell
populations from non-failing and diseased human heart. We will take advantage of this now well validated
resource to perform parallel functional experiments in both mice and human. We hypothesize that EC aerosol
promotes both acute and chronic damage to multiple cardiac cell populations resulting in severe organ and
organism dysfunction. The goals of this investigation are to define the impact of EC aerosol (in clinically-
relevant concentrations) on animals and well phenotyped human cardiac myocytes. We will 1) define the in
vivo impact of acute and chronic EC aerosol exposure on cardiac physiology, 2) define the impact of acute and
chronic EC aerosol exposure on the function of key cardiac cell populations, and 3), Define the impact of EC
aerosol exposure on key primary human cardiac cell populations.

## Key facts

- **NIH application ID:** 9993605
- **Project number:** 5R01HL139348-04
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** Loren Eugene Wold
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $390,000
- **Award type:** 5
- **Project period:** 2017-09-15 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9993605

## Citation

> US National Institutes of Health, RePORTER application 9993605, Defining the Impact of E-Cigarettes on Cardiac Pathophysiology (5R01HL139348-04). Retrieved via AI Analytics 2026-06-03 from https://api.ai-analytics.org/grant/nih/9993605. Licensed CC0.

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