2021
DOI: 10.1016/j.tiv.2021.105234
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E-cigarette fluids and aerosol residues cause oxidative stress and an inflammatory response in human keratinocytes and 3D skin models

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Cited by 16 publications
(15 citation statements)
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“…IL-6, a pro-inflammatory cytokine, was significantly higher after 3h exposure to THS and remained elevated at 22 h. Similar increases in inflammatory cytokines occurred in a 3D model of human epidermis (EpiDerm) exposed to the residue from exhaled electronic cigarette aerosol. 26 Furthermore, the top scored biofunctions network were "inflammatory response" at 3 h and "inflammation of organs" at 22 h. Together, our results demonstrate that exposure to THS increases hemostasis ("adhesion of blood cells") and initiates a pro-inflammatory response, which are risk factors for thrombosis. Upregulation of "RhoA signaling" and "signaling of Rho family GTPases" in the 3-h THS exposure group provides further evidence for activation of the innate immune system.…”
Section: Articlesmentioning
confidence: 56%
See 1 more Smart Citation
“…IL-6, a pro-inflammatory cytokine, was significantly higher after 3h exposure to THS and remained elevated at 22 h. Similar increases in inflammatory cytokines occurred in a 3D model of human epidermis (EpiDerm) exposed to the residue from exhaled electronic cigarette aerosol. 26 Furthermore, the top scored biofunctions network were "inflammatory response" at 3 h and "inflammation of organs" at 22 h. Together, our results demonstrate that exposure to THS increases hemostasis ("adhesion of blood cells") and initiates a pro-inflammatory response, which are risk factors for thrombosis. Upregulation of "RhoA signaling" and "signaling of Rho family GTPases" in the 3-h THS exposure group provides further evidence for activation of the innate immune system.…”
Section: Articlesmentioning
confidence: 56%
“…Our data, which contribute to the growing literature on THS, 51 will be useful in devising regulatory policies to limit exposure to THS in contaminated properties and will enable healthcare workers to advise their patients on the risks associated with THS exposure. Electronic cigarettes also deposit a residue that comes into contact with the skin, 26 , 52 , 53 and this should be evaluated in future studies. The evaluation of larger populations exposed for longer periods of exposure would further characterise human health responses to dermal THS exposure.…”
Section: Discussionmentioning
confidence: 99%
“…ECEAR generated using “Dewberry Cream” and “Churrios” in tank style ECs contained nicotine, nicotine alkaloids, tobacco specific nitrosamines (TSNAs), and flavor chemicals . ECEAR derived from “Churrios” e-liquid induced IL-1α secretion following air–liquid interface exposure of EpiDerm tissue, a 3D human skin model . Some ECEAR chemicals caused oxidative damage and inflammation to human skin .…”
Section: Introductionmentioning
confidence: 99%
“…35 ECEAR derived from "Churrios" e-liquid induced IL-1α secretion following air−liquid interface exposure of EpiDerm tissue, a 3D human skin model. 37 Some ECEAR chemicals caused oxidative damage and inflammation to human skin. 37 No data have previously been reported on ECEAR associated with JUUL products.…”
Section: ■ Introductionmentioning
confidence: 99%
“…In vitro studies have shown that E-liquids and E-vapours are not as benign as originally believed. E-liquids and -vapours induce cellular toxicity , Willershausen., 2014, Hwang., 2016, Leig., 2016, Rowell., 2017, Ween., 2019, inflammatory cytokine release (Wu., 2014, Cervellati., 2014, Rubenstein., 2015, Lerner., 2015, Higham., 2016, Leigh., 2016, Khachatoorian., 2021 and impaired cellular function (Schweitzer., 2015, Hwang., 2016, Scott., 2018, Gómez., 2020 of airway epithelia and immune cells. Human alveolar macrophages secreted increased pro-inflammatory cytokines IL-8, IL-6, and TNFα along with reactive oxygen species (ROS) and were more susceptible to cell death when exposed to E-cigarette vapour extracts (Scott., 2018) Cell death and ROS are activators of inflammasomes, which regulates the activity and release of pro-inflammatory IL-1β and IL-18 (Martinon, Burns and Tschopp, 2002;Srinivasula., 2002).…”
Section: Introductionmentioning
confidence: 99%