# Electronic Cigarette Vapor Inhalation Adversely Affects Lung Cellular and Physiologic Function and Alters Systemic Inflammatory Pathways

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 2020 · $366,508

## Abstract

SUMMARY/ABSTRACT
 COPD is the 3rd leading cause of death and incidence continues to rise. Many people are trying to quit
smoking by using electronic (e)-cigarettes, even though data suggest that e-cigarette use adversely impacts
cessation rates. Patients are switching to or adding on e-cigarette use because advertisements say they are
completely safe. Young adult (18-40) never smokers are vaping e-cigarettes - inhaling vapor containing
nicotine and other chemicals from these drug delivery devices. Our in vivo, ex vivo and in vitro data suggest
significant adverse effects on host defenses, inflammation in the lung and systemically, and bacterial virulence.
Vaping may lead to long-term effects, such as development of COPD, heart disease, and kidney failure, but it
will be decades before epidemiologic data can demonstrate or disprove it.
 We propose experiments to evaluate effects of e-cigarette vapor on primary human airway cells of host
defense: macrophages (>90% of airway cells in normal human subjects) and neutrophils (elevated in the
airways of cigarette smokers - the largest population using e-cigarettes). These cells are directly exposed to
inhaled vapor in the airways and are the mainstays of host defense in lung and blood. Comparison to cigarette
smoke is important to answer one of the most urgent questions: Are e-cigarettes safer than conventional
cigarettes? We will determine whether e-cigarette vapor negatively impacts the ability of macrophages and
neutrophils to kill common pathogens and examine whether e-cigarettes dysregulate inflammatory responses,
as both increases and decreases in inflammation are known to cause chronic disease. We will use our
established mouse model of e-cigarette vapor inhalation, such that we may study effects of e-cigarettes in the
setting of common human diseases, such as gram-negative sepsis, acute lung injury, and gram-positive
pneumonia and bacteremia.
 Finally, the incidence of invasive disease and death due to antibiotic resistant bacteria is growing
rapidly. In particular, methicillin resistant Staphylococcus aureus (MRSA) is the leading cause of bloodstream,
skin and soft tissue infections. MRSA colonizes the nasopharynx of 20% of the population chronically. We
recently found that MRSA is harder to kill and more virulent after exposure to e-cigarette vapor as well as
conventional tobacco smoke. In this proposal we will: 1. Determine whether e-cigarette vapor promotes
virulence in colonizing S. aureus in vivo by isolating strains from e-cigarette users, cigarette smokers and
controls; and 2. Evaluate e-cigarette effects on both host defense and bacterial virulence in a physiologic
setting (mice colonized with MRSA and concomitantly inhaling e-cigarette vapor) to determine whether
deleterious effects of e-cigarettes on host defenses and bacterial pathogenicity occur in a more complex
setting, as would happen in human airways. These studies may have a major public health impact, laying
groundwork for fut...

## Key facts

- **NIH application ID:** 10220439
- **Project number:** 3R01HL137052-04S1
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO
- **Principal Investigator:** Laura Elise Crotty Alexander
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $366,508
- **Award type:** 3
- **Project period:** 2020-07-28 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10220439

## Citation

> US National Institutes of Health, RePORTER application 10220439, Electronic Cigarette Vapor Inhalation Adversely Affects Lung Cellular and Physiologic Function and Alters Systemic Inflammatory Pathways (3R01HL137052-04S1). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/10220439. Licensed CC0.

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