Hydroxyl Radicals in E-Cigarette Vapor and E-Vapor Oxidative Potentials under Different Vaping Patterns

Son, Yeongkwon; Mishin, Vladimir; Laskin, Jeffrey D.; Mainelis, Gediminas; Wackowski, Olivia A; Delnevo, Cristine D.; Schwander, Stephan; Khlystov, Andrey; Samburova, Vera; Meng, Qingyu

doi:10.1021/acs.chemrestox.8b00400

Cited by 57 publications

(56 citation statements)

References 52 publications

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“…that is commonly incorporated in a wide range of consumer goods, [2,3] whereas incidental NM may be generated from activities such as steel welding, printing, and vaping (e-cigarette). [4][5][6] Due to their increased demand and rampant production, the annual flux of anthropogenic NM circulating within our earth system was estimated to be in the astonishing range of 1-10 million metric tons per year. [1] Because of their ubiquitous presence in the environment, human exposure to NM by means of inhalation in our everyday life is inadvertent.…”

Section: Doi: 101002/smll202000963mentioning

confidence: 99%

Inflammation Increases Susceptibility of Human Small Airway Epithelial Cells to Pneumonic Nanotoxicity

Shi

Lim

et al. 2020

Small

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Exposure to inhaled anthropogenic nanomaterials (NM) with dimension <100 nm has been implicated in numerous adverse respiratory outcomes. Although studies have identified key NM physiochemical determinants of pneumonic nanotoxicity, the complex interactive and cumulative effects of NM exposure, especially in individuals with preexisting inflammatory respiratory diseases, remain unclear. Herein, the susceptibility of primary human small airway epithelial cells (SAEC) exposed to a panel of reference NM, namely, CuO, ZnO, mild steel welding fume (MSWF), and nanofractions of copier center particles (Nano‐CCP), is examined in normal and tumor necrosis factor alpha (TNF‐α)‐induced inflamed SAEC. Compared to normal SAEC, inflamed cells display an increased susceptibility to NM‐induced cytotoxicity by 15–70% due to a higher basal level of intracellular reactive oxygen species (ROS). Among the NM screened, ZnO, CuO, and Nano‐CCP are observed to trigger an overcompensatory response in normal SAEC, resulting in an increased tolerance against subsequent oxidative insults. However, the inflamed SAEC fails to adapt to the NM exposure due to an impaired nuclear factor erythroid 2‐related factor 2 (Nrf2)‐mediated cytoprotective response. The findings reveal that susceptibility to pulmonary nanotoxicity is highly dependent on the interplay between NM properties and inflammation of the alveolar milieu.

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Section: Doi: 101002/smll202000963mentioning

confidence: 99%

Inflammation Increases Susceptibility of Human Small Airway Epithelial Cells to Pneumonic Nanotoxicity

Shi

Lim

et al. 2020

Small

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“…E-vapors were generated based on the protocols used in our previous studies [27][28][29]. In brief, vaping topographies of 23 current e-cigarette users measured in our lab.…”

Section: E-vapor Generation Conditions and Materialsmentioning

confidence: 99%

The Impact of Device Settings, Use Patterns, and Flavorings on Carbonyl Emissions from Electronic Cigarettes

Son

Weisel

Wackowski

et al. 2020

IJERPH

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Health impacts of electronic cigarette (e-cigarette) vaping are associated with the harmful chemicals emitted from e-cigarettes such as carbonyls. However, the levels of various carbonyl compounds under real-world vaping conditions have been understudied. This study evaluated the levels of carbonyl compounds (e.g., formaldehyde, acetaldehyde, glyoxal, and diacetyl, etc.) under various device settings (i.e., power output), vaping topographies, and e-liquid compositions (i.e., base liquid, flavor types). The results showed that e-vapor carbonyl levels were the highest under higher power outputs. The propylene glycol (PG)-based e-liquids generated higher formaldehyde and acetaldehyde than vegetable glycerin (VG)-based e-liquids. In addition, fruit flavored e-liquids (i.e., strawberry and dragon fruit) generated higher formaldehyde emissions than mint/menthol and creamy/sweet flavored e-liquids. While single-top coils formed 3.5-fold more formaldehyde per puff than conventional cigarette smoking, bottom coils generated 10–10,000 times less formaldehyde per puff. In general, increases in puff volume and longer puff durations generated significantly higher amounts of formaldehyde. While e-cigarettes emitted much lower levels of carbonyl compounds compared to conventional cigarettes, the presence of several toxic carbonyl compounds in e-cigarette vapor may still pose potential health risks for users without smoking history, including youth. Therefore, the public health administrations need to consider the vaping conditions which generated higher carbonyls, such as higher power output with PG e-liquid, when developing e-cigarette product standards.

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“…In this study, we also observed significant acellular and cellular ROS generation by cartridges and their major components. These highly reactive species vary based on vaping patterns and can lead to lung pathogenesis [19]. Increased levels of IL-6 and IL-8 are clear indicators of an ongoing inflammatory response in epithelial cells and monocytes.…”

Section: Resultsmentioning

confidence: 99%

Pulmonary toxicity and inflammatory response of e-cigarettes containing medium-chain triglyceride oil and vitamin E acetate: Implications in the pathogenesis of EVALI but independent of SARS-COV-2 COVID-19 related proteins

Muthumalage

Lucas

Wang

et al. 2020

Preprint

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Recently, there has been an outbreak associated with the use of e-cigarette or vaping products, associated lung injury (EVALI). The primary components of vaping products, vitamin E acetate (VEA) and medium-chain triglycerides (MCT) may be responsible for acute lung toxicity. Currently, little information is available on the physiological and biological effects of exposure to these products. We hypothesized that these e-cig cartridges and their constituents (VEA and MCT) induce pulmonary toxicity, mediated by oxidative damage and inflammatory responses, leading to acute lung injury. We studied the potential mechanisms of cartridge aerosol induced inflammatory response by evaluating the generation of reactive oxygen species by MCT, VEA, and cartridges, and their effects on the inflammatory state of pulmonary epithelium and immune cells both in vitro and in vivo. Cells exposed to these aerosols generated reactive oxygen species, caused cytotoxicity, induced epithelial barrier dysfunction, and elicited an inflammatory response. Using a murine model, the parameters of acute toxicity to aerosol inhalation were assessed. Infiltration of neutrophils and lymphocytes was accompanied by significant increases in IL-6, eotaxin, and G-CSF in the bronchoalveolar lavage fluid (BALF). In mouse plasma, eicosanoid inflammatory mediators, leukotrienes, were significantly increased. Plasma from e-cig users also showed increased levels of hydroxyeicosatetraenoic acid (HETEs) and various eicosanoids. Exposure to e-cig cartridge aerosols showed the most significant effects and toxicity compared to MCT and VEA. In addition, we determined at SARS-COV-2 related proteins and found no impact associated with aerosol exposures from these tested cartridges. Overall, this study demonstrates acute exposure to specific e-cig cartridges induces in vitro cytotoxicity, barrier dysfunction, and inflammation and in vivo mouse exposure induces acute inflammation with elevated pro-inflammatory markers in the pathogenesis of EVALI.

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Hydroxyl Radicals in E-Cigarette Vapor and E-Vapor Oxidative Potentials under Different Vaping Patterns

Cited by 57 publications

References 52 publications

Inflammation Increases Susceptibility of Human Small Airway Epithelial Cells to Pneumonic Nanotoxicity

Inflammation Increases Susceptibility of Human Small Airway Epithelial Cells to Pneumonic Nanotoxicity

The Impact of Device Settings, Use Patterns, and Flavorings on Carbonyl Emissions from Electronic Cigarettes

Pulmonary toxicity and inflammatory response of e-cigarettes containing medium-chain triglyceride oil and vitamin E acetate: Implications in the pathogenesis of EVALI but independent of SARS-COV-2 COVID-19 related proteins

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