E-cigarette aerosols induce lower oxidative stress in vitro when compared to tobacco smoke

Taylor, Mark; Carr, Tony; Oke, Oluwatobiloba; Jaunky, Tomasz; Breheny, Damien; Lowe, Frazer; Gaça, Marianna

doi:10.1080/15376516.2016.1222473

Cited by 103 publications

(81 citation statements)

References 67 publications

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“…Alternatively, the absence of oxidative stress induction in our model could be due differences in our model compared to other studies. Our findings are in accordance with a study by Tayler et al, which found that nicotine flavored e-liquid resulted in lower oxidative stress in H292 human bronchial epithelial cells than in cells exposed to cigarette smoke [40]. Additional studies into the varying effects of flavor and solvent additives of e-liquid, on oxidative stress would aid in determining the overall effect of e-cigarettes on A549 cells.…”

Section: Discussionsupporting

confidence: 92%

E-Cigarette Vapor Decreases Cellular Proliferation through Nicotine-Dependent Mechanisms

Rigg¹,

Gielda²

2019

JBM

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Electronic cigarette (e-cigarette) use has risen as individuals look for healthier nicotine delivery systems than conventional cigarettes, but recent studies have demonstrated variable physiological responses to e-cigarette vapor. The safety of e-cigarette vapor remains an open question. We investigated the molecular cellular response of adenocarcinoma human alveolar basal epithelial (A549) cells to flavored e-cigarette vapor. E-cigarette and cigarette vapor were extracted via a vacuum-percolating system into PBS. The effects of a flavored e-liquid containing nicotine (eCSE) and nicotine free e-liquid (NFeCSE) were compared to cigarette smoke extract (CSE), pure nicotine, glycerol, and PBS. Cells exposed to eCSE and NFeCSE had decreased cell viability and proliferation. An increase in active caspase-3 was observed in cells exposed to NFeCSE, while cells exposed to eCSE and CSE displayed no change, suggesting nicotine-mediated protection from apoptosis. However, phosphorylated Akt, which regulates cellular proliferation, was elevated in response to eCSE, NFeCSE, CSE, and glycerol. As the glutathione-oxidative stress response was known to integrate cellular factors including carcinogenesis, inflammation, and cell proliferation, GSH/GSSG levels were measured in cells exposed to e-cigarette smoke. An increase in oxidative stress was observed in cells treated with CSE, but not eCSE, suggesting components in CSE independent of nicotine may be contributing to an imbalance in the stress response. These results indicate e-cigarette vapor affects A549 cell viability dependent on nicotine, and is distinct from CSE-induced mechanisms of oxidative-stress.

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Section: Discussionsupporting

confidence: 92%

E-Cigarette Vapor Decreases Cellular Proliferation through Nicotine-Dependent Mechanisms

Rigg¹,

Gielda²

2019

JBM

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“…For instance, Misra et al (2014) found no cytotoxicity or mutagenicity of EC aerosols, but found high cytotoxicity and mutagenicity of CC smoke in human lung epithelial cells (A549). Also, Scheffler et al (2015b) discovered reduced viability and increased oxidative stress when human bronchial epithelial (NHBE) cells were exposed to EC humectants, but much lower viability and higher oxidative stress when the same cells were exposed to CC smoke (see also Taylor et al 2016 for similar results). Carnevale et al (2016) found similar results in healthy subjects with increased oxidative stress while vaping.…”

Section: Cellular Level Effectssupporting

confidence: 59%

Electronic cigarettes—A review of the physiological health effects

Zucchet

Schmaltz

2017

FACETS

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Electronic cigarettes (ECs) are devices that are used recreationally or as smoking cessation tools, and have become increasingly popular in recent years. We conducted a review of the available literature to determine the health effects caused by the use of these devices. A heating element in the EC aerosolizes a solution of propylene glycol, glycerol, nicotine (optional), and flavouring (optional). These compounds are generally harmless on their own. However, upon heating, they produce various carcinogens and irritants. We found that concentrations of these toxicants vary significantly depending on the type of EC device, the type of EC liquid, and the smoking behaviour of the user. Exposure to these vapours can cause inflammation and oxidative damage to in vitro and in vivo cells. EC aerosol can also potentially affect organ systems and especially cardiovascular and lung function. We concluded that EC use causes acute effects on health but not as severe as those of conventional cigarettes (CCs). These devices could, therefore, be of use for smokers of CCs wishing to quit. However, as EC aerosol introduces new toxicants not found in CCs, long-term studies are needed to investigate possible chronic effects associated with EC use.

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“…As compared to the exposure with TCIG, there was less impact on host defense, inflammation and gene expression. Other studies have shown that ECIGs induce antioxidant defenses and oxidative DNA damage in primary epithelial cells [60][61][62][63]. We used two different cell lines and pHBEs to account for different reactivity to TCIG and ECIG vapor.…”

Section: Resultsmentioning

confidence: 99%

Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

et al. 2020

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Background: The use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (pHBE). Methods: We exposed pHBEs and several cell lines to TCIG-smoke or ECIG-vapor. Epithelial host defense and barrier integrity were determined. The transcriptome of airway epithelial cells was compared by gene expression array analysis. Gene interaction networks were constructed and differential gene expression over all groups analyzed. The expression of several candidate genes was validated by qRT-PCR. Results: Bacterial killing, barrier integrity and the expression of antimicrobial peptides were not affected by ECIG-vapor compared to control samples. In contrast, TCIGs negatively affected host defense and reduced barrier integrity in a significant way. Furthermore ECIG-exposure significantly induced IL-8 secretion from Calu-3 cells but had no effect on NCI-H292 or primary cells. The gene expression based on array analysis distinguished TCIG-exposed cells from ECIG and room air-exposed samples. Conclusion: The transcriptome patterns of host defense and inflammatory genes are significantly distinct between ECIG-exposed and TCIG-treated cells. The overall effects of ECIGs on epithelial cells are less in comparison to TCIG, and ECIG-vapor does not affect host defense. Nevertheless, although acute exposure to ECIG-vapor induces inflammation, and the expression of S100 proteins, long term in vivo data is needed to evaluate the chronic effects of ECIG use. Background The contribution of exposure to cigarette smoke (CS) to the development and progression of chronic obstructive pulmonary disease (COPD), cancer, and cardiovascular diseases is widely recognized [1, 2]. Electronic cigarettes (ECIGs) are commercially available since 2004, but patents for similar devices reach back to 1965 [3, 4]. ECIGs are devices that produce a vapor by heating a liquid [3] that usually contains a mixture of glycerol, propylene-glycol, water, flavors, and different concentrations of nicotine. The flavors cover a broad range of tastes from fruit or spices, to different brands of tobacco. An intense scientific and political discussion about the toxicity and potential harm reduction of ECIGs is ongoing. Glycerol-propylene-glycol-water mixtures have been in use for a long time as artificial fog in aviation emergency training and entertainment business, but only a few studies about possible side effects exist before the emergence of ECIGs [5, 6]. Several studies have analyzed the effects of ECIGs on lung cells with the goal to evaluate toxic effects on cells and tissues [7]. A number of negative outcomes on different tissue culture systems (cell death, impaired repair, oxidative stress) have been reported [7-9]. In parallel, several ...

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E-cigarette aerosols induce lower oxidative stress in vitro when compared to tobacco smoke

Cited by 103 publications

References 67 publications

E-Cigarette Vapor Decreases Cellular Proliferation through Nicotine-Dependent Mechanisms

E-Cigarette Vapor Decreases Cellular Proliferation through Nicotine-Dependent Mechanisms

Electronic cigarettes—A review of the physiological health effects

Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

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