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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.

Lerner CA, Sundar IK, Yao H, Gerloff J, Ossip DJ, McIntosh S, Robinson R, Rahman I - PLoS ONE (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, United States of America.

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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Related in: MedlinePlus

Air-liquid interface deposition of fluorescent substance on human bronchial airway epithelial cells.Beas-2B cells exposed to Blu e-cigarette vapor with a puff of 3–4 sec for 15 min. After exposure cells were immediately collected and measured by flow cytometry. (A) Histogram showing increase in non-specific fluorescence in cells exposed to e-cig aerosols. (B) Average fluorescence for e-cig exposed cells versus air-sham control shown as Mean Fluorescence Intensity (MFI). Data are shown as mean ± SD, n = 3, * P< 0.05 compared to air-sham control cells.
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pone.0116732.g006: Air-liquid interface deposition of fluorescent substance on human bronchial airway epithelial cells.Beas-2B cells exposed to Blu e-cigarette vapor with a puff of 3–4 sec for 15 min. After exposure cells were immediately collected and measured by flow cytometry. (A) Histogram showing increase in non-specific fluorescence in cells exposed to e-cig aerosols. (B) Average fluorescence for e-cig exposed cells versus air-sham control shown as Mean Fluorescence Intensity (MFI). Data are shown as mean ± SD, n = 3, * P< 0.05 compared to air-sham control cells.

Mentions: Next, we observed evidence of a non-specific e-cig substance associated with its aerosol that could emit a fluorescent signature after aerosol deposition onto the cells in the air-liquid interface chamber that may be associated with oxidative and inflammatory responses. Beas-2B cells exposed for a 15 minute period (4 sec. puffs every 30 sec.) with Blu e-cig aerosols were harvested and analyzed by flow cytometry using 2 different colored lasers (488, and 405 nm). In cells exposed to e-cig aerosols, we detected a small but significant increase in fluorescence utilizing the 405 nm laser with 440/40 band pass filter (Fig. 6). This result alludes to the possibility that e-cig aerosol constituents can adhere to cell surfaces despite those surfaces being submerged under a thin layer (1–2 mm) of culture media, and become pro-oxidant and inflammatory.


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.

Lerner CA, Sundar IK, Yao H, Gerloff J, Ossip DJ, McIntosh S, Robinson R, Rahman I - PLoS ONE (2015)

Air-liquid interface deposition of fluorescent substance on human bronchial airway epithelial cells.Beas-2B cells exposed to Blu e-cigarette vapor with a puff of 3–4 sec for 15 min. After exposure cells were immediately collected and measured by flow cytometry. (A) Histogram showing increase in non-specific fluorescence in cells exposed to e-cig aerosols. (B) Average fluorescence for e-cig exposed cells versus air-sham control shown as Mean Fluorescence Intensity (MFI). Data are shown as mean ± SD, n = 3, * P< 0.05 compared to air-sham control cells.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4319729&req=5

pone.0116732.g006: Air-liquid interface deposition of fluorescent substance on human bronchial airway epithelial cells.Beas-2B cells exposed to Blu e-cigarette vapor with a puff of 3–4 sec for 15 min. After exposure cells were immediately collected and measured by flow cytometry. (A) Histogram showing increase in non-specific fluorescence in cells exposed to e-cig aerosols. (B) Average fluorescence for e-cig exposed cells versus air-sham control shown as Mean Fluorescence Intensity (MFI). Data are shown as mean ± SD, n = 3, * P< 0.05 compared to air-sham control cells.
Mentions: Next, we observed evidence of a non-specific e-cig substance associated with its aerosol that could emit a fluorescent signature after aerosol deposition onto the cells in the air-liquid interface chamber that may be associated with oxidative and inflammatory responses. Beas-2B cells exposed for a 15 minute period (4 sec. puffs every 30 sec.) with Blu e-cig aerosols were harvested and analyzed by flow cytometry using 2 different colored lasers (488, and 405 nm). In cells exposed to e-cig aerosols, we detected a small but significant increase in fluorescence utilizing the 405 nm laser with 440/40 band pass filter (Fig. 6). This result alludes to the possibility that e-cig aerosol constituents can adhere to cell surfaces despite those surfaces being submerged under a thin layer (1–2 mm) of culture media, and become pro-oxidant and inflammatory.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, United States of America.

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.

Show MeSH
Related in: MedlinePlus