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The Toxicity of Electronic Cigarette Vapor on Human Oral Cells
Author(s) -
Urena Jose Francisco,
Ebersol Lauren,
Silakov Alexey,
Lambert Joshua
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.786.6
Subject(s) - chemistry , cytotoxic t cell , oxidative stress , toxicity , cytotoxicity , in vitro , apoptosis , cell culture , viability assay , nicotine , neutral red , cell , pharmacology , biochemistry , medicine , biology , organic chemistry , genetics
Electronic cigarettes (ECs) have emerged as a popular alternative to conventional cigarettes. These devices operate by using resistive heating to vaporize a fluid consisting of a propylene glycol‐glycerol base, flavorings, and nicotine. Although considered safer than conventional cigarettes, recent studies have shown that EC vapor contains harmful compounds such as free radicals and carbonyls. A limited number of studies have shown that EC liquid and vapor can cause oxidative stress and cell death in vitro . While the majority of in vitro studies have focused on the toxicity in respiratory tract cell lines, the tissues in the oral cavity, which are exposed to high local concentrations of EC vapor, have been under‐studied. Our objective was to investigate the ability of EC vapor to induce cytotoxicity and oxidative stress in human oral cell lines. HGF‐1 human gingival fibroblasts and SCC‐25 human oral squamous cell carcinoma cells were exposed to a panel of commercially‐available fruit and tobacco‐flavored EC vapors using an air‐liquid interface exposure model, which mimics physiological exposures in vitro . Cytotoxicity and markers of oxidative stress were assessed after ecologically‐relevant exposure protocols. Cytotoxic EC vapors caused a greater than 30% reduction in cell viability. Nicotine was shown to ablate the effects of the cytotoxic EC vapors. There was no difference in the cytotoxic response to EC vapor between the cell lines tested. Treatment of SCC‐25 cells with a cytotoxic EC vapor caused a significant increase in intracellular ROS after a single 15 puff exposure. This increase occurred for both nicotine‐containing and nicotine‐free vapors. The differential effects of nicotine on cytotoxicity and oxidative stress suggest that either (1) cytotoxicity is not driven by ROS or (2) that nicotine protects cells by a mechanism that does not impact intracellular ROS levels. Ongoing studies are investigating the role of nicotine in this aerosolized system and the relationship between EC vapor constituents and cytotoxicity in human oral cells. Support or Funding Information Penn State Tobacco Center of Regulatory Science; Penn State Department of Food Science This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .