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Open AccessJournal ArticleDOI

Vapors Produced by Electronic Cigarettes and E-Juices with Flavorings Induce Toxicity, Oxidative Stress, and Inflammatory Response in Lung Epithelial Cells and in Mouse Lung

TLDR
Exposure to e-cig aerosols/juices incurs measurable oxidative and inflammatory responses in lung cells and tissues that could lead to unrealized health consequences.
Abstract
Oxidative stress and inflammatory response are the key events in the pathogenesis of chronic airway diseases. The consumption of electronic cigarettes (e-cigs) with a variety of e-liquids/e-juices is alarmingly increasing without the unrealized potential harmful health effects. We hypothesized that electronic nicotine delivery systems (ENDS)/e-cigs pose health concerns due to oxidative toxicity and inflammatory response in lung cells exposed to their aerosols. The aerosols produced by vaporizing ENDS e-liquids exhibit oxidant reactivity suggesting oxidants or reactive oxygen species (OX/ROS) may be inhaled directly into the lung during a “vaping” session. These OX/ROS are generated through activation of the heating element which is affected by heating element status (new versus used), and occurs during the process of e-liquid vaporization. Unvaporized e-liquids were oxidative in a manner dependent on flavor additives, while flavors containing sweet or fruit flavors were stronger oxidizers than tobacco flavors. In light of OX/ROS generated in ENDS e-liquids and aerosols, the effects of ENDS aerosols on tissues and cells of the lung were measured. Exposure of human airway epithelial cells (H292) in an air-liquid interface to ENDS aerosols from a popular device resulted in increased secretion of inflammatory cytokines, such as IL-6 and IL-8. Furthermore, human lung fibroblasts exhibited stress and morphological change in response to treatment with ENDS/e-liquids. These cells also secrete increased IL-8 in response to a cinnamon flavored e-liquid and are susceptible to loss of cell viability by ENDS e-liquids. Finally, exposure of wild type C57BL/6J mice to aerosols produced from a popular e-cig increase pro-inflammatory cytokines and diminished lung glutathione levels which are critical in maintaining cellular redox balance. Thus, exposure to e-cig aerosols/juices incurs measurable oxidative and inflammatory responses in lung cells and tissues that could lead to unrealized health consequences.

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Citations
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E-cigarettes: an evidence update. A report commissioned by Public Health England.

TL;DR: There is no evidence that EC are undermining the long-term decline in cigarette smoking among adults and youth, and may in fact be contributing to it, and new regulations currently planned should also maximise the public health opportunities of EC.
Journal ArticleDOI

Overview of Electronic Nicotine Delivery Systems: A Systematic Review.

TL;DR: Analysis of published empirical research literature on ENDS indicates that ENDS are increasing in use, particularly among current smokers, pose substantially less harm to smokers than cigarettes, are being used to reduce/quit smoking, and are widely available.
Journal ArticleDOI

Cancer Progress and Priorities: Lung Cancer

TL;DR: In the United States, lung cancer is the second most common diagnosed cancer and the leading cause of cancer-related death and the major risk factor is tobacco smoking.
Journal ArticleDOI

Acute Impact of Tobacco vs Electronic Cigarette Smoking on Oxidative Stress and Vascular Function

TL;DR: The study showed that both cigarettes have unfavorable effects on markers of oxidative stress and FMD after single use, although e-Cigarettes seemed to have a lesser impact.
References
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Journal ArticleDOI

Advances in metal-induced oxidative stress and human disease

Klaudia Jomová, +1 more
- 10 May 2011 - 
TL;DR: An overview of redox and non-redox metal-induced formation of free radicals and the role of oxidative stress in toxic action of metals is provided.
Journal ArticleDOI

Assay for quantitative determination of glutathione and glutathione disulfide levels using enzymatic recycling method.

TL;DR: The spectrophotometric/microplate reader assay method for glutathione (GSH) can assay GSH in whole blood, plasma, serum, lung lavage fluid, cerebrospinal fluid, urine, tissues and cell extracts and can be extended for drug discovery/pharmacology and toxicology protocols to study the effects of drugs and toxic compounds on glutATHione metabolism.
Journal ArticleDOI

Skin penetration enhancers.

TL;DR: It is proposed that overall the effects of CPEs on the skin barrier may best be explained by a Diffusion-Partition-Solubility theory.
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