Acute impact of active and passive electronic cigarette smoking on serum cotinine and lung function

Flouris, Andreas D.; Chorti, Maria; Poulianiti, Konstantina; Jamurtas, Athanasios Z.; Κostikas, Κonstantinos; Tzatzarakis, Manolis; Hayes, A. Wallace; Tsatsakis, Aristidis; Koutedakis, Yiannis

doi:10.3109/08958378.2012.758197

Cited by 350 publications

(296 citation statements)

References 33 publications

(56 reference statements)

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“…Our results revealed that there were significant levels of cotinine in the mice exposed to e‐cigarettes, whereas it was not detectable in the clean air control mice. Importantly, the measured mean plasma levels (ie, average of 53.97±3.61 ng/mL; Figure 1) were in fact comparable to those observed in humans and other animal e‐cigarette exposure models, that is, 30 to 250 ng/mL 46, 47, 48…”

Section: Resultssupporting

confidence: 75%

“…Thus, key markers to be noted of this system are (1) the cotinine levels found in the plasma of our e‐cigarette–exposed mice (average of 53.97 ng/mL) overlaps with those observed in established human and animal e‐cigarette exposure models46, 47, 48 but undetectable in clean air samples, (2) which were obtained/observed using a device and an e‐liquid mixture that are widely used by humans34, 35, 36, 73 and (3) under real‐life puffing topography experimental conditions. 24–33 …”

Section: Discussionmentioning

confidence: 57%

“…Notably, our whole‐body exposure system, much like active and passive e‐cigarette exposure,47, 74 did increase cotinine (plasma) levels supporting the systematic delivery of nicotine, and further undermining the claim that e‐cigarettes are emission‐free devices; this finding also casts doubt regarding the notion that e‐cigarette are a safer/safe alternative to tobacco. Further support for the validity and the clinical applicability of our animal model derives from literature documenting that mouse studies do “map” very well to humans in the context of tobacco exposure 14, 75, 76.…”

Section: Discussionmentioning

confidence: 78%

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Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

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BackgroundCardiovascular disease is the main cause of death in the United States, with smoking being the primary preventable cause of premature death, and thrombosis being the main mechanism of cardiovascular mortality in smokers. Due to the perception that electronic/e‐cigarettes are “safer/less harmful” than conventional cigarettes, their usage—among a variety of ages—has increased tremendously during the past decade. Notably, there are limited studies regarding the negative effects of e‐cigarettes on the cardiovascular system, which is also the subject of significant debate.Methods and ResultsWe employed a passive e‐VapeTM vapor inhalation system and developed an in vivo whole‐body e‐cigarette mouse exposure protocol that mimics real‐life human exposure scenarios/conditions and investigated the effects of e‐cigarettes and clean air on platelet function and thrombogenesis. Our results show that platelets from e‐cigarette–exposed mice are hyperactive, with enhanced aggregation, dense and α granule secretion, activation of the αIIbβ3 integrin, phosphatidylserine expression, and Akt and ERK activation, when compared with clean air–exposed platelets. E‐cigarette–exposed platelets were also found to be resistant to inhibition by prostacyclin, relative to clean air. Furthermore, the e‐cigarette–exposed mice exhibited a shortened thrombosis occlusion and bleeding times.ConclusionsTaken together, our data demonstrate for the first time that e‐cigarettes alter physiological hemostasis and increase the risk of thrombogenic events. This is attributable, at least in part, to the hyperactive state of platelets. Thus, the negative health consequences of e‐cigarette exposure should not be underestimated and warrant further investigation.

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Section: Resultssupporting

confidence: 75%

Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 78%

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Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

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“…People passively exposed to e-cigarette aerosol may absorb nicotine at levels comparable to passive smokers. Flouris et al (2013) found that e-cigarettes and tobacco cigarettes generated similar effects on serum cotinine levels after passive…”

Section: E-cigarettes and Thirdhand Smokementioning

confidence: 99%

Measurements of dermal uptake of nicotine directly from air and clothing

et al. 2016

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In this preliminary study, we have investigated whether dermal uptake of nicotine directly from air or indirectly from clothing can be a meaningful exposure pathway. Two participants wearing only shorts and a third participant wearing clean cotton clothes were exposed to environmental tobacco smoke (ETS), generated by mechanically “smoking” cigarettes, for three hours in a chamber while breathing clean air from head-enveloping hoods. The average nicotine concentration (420 μg/m3) was comparable to the highest levels reported for smoking sections of pubs. Urine samples were collected immediately before exposure and 60 hour post-exposure for bare-skinned participants. For the clothed participant, post-exposure urine samples were collected for 24 hour. This participant then entered the chamber for another three-hour exposure wearing a hood and clothes, including a shirt that had been exposed for five days to elevated nicotine levels. The urine samples were analyzed for nicotine and two metabolites—cotinine and 3OH-cotinine. Peak urinary cotinine and 3OH-cotinine concentrations for the bare-skinned participants were comparable to levels measured among non-smokers in hospitality environments before smoking bans. The amount of dermally absorbed nicotine for each bare-skinned participant was conservatively estimated at 570 μg, but may have been larger. For the participant wearing clean clothes, uptake was ~20 μg, and while wearing a shirt previously exposed to nicotine, uptake was ~80 μg. This study demonstrates meaningful dermal uptake of nicotine directly from air or from nicotine-exposed clothes. The findings are especially relevant for children in homes with smoking or vaping

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“…More and more attention is paid to the problem of ''indirect'' smoking, i.e., secondhand smoking (SHS), but also third-hand smoking (THS) (WHO 2010; US Department of Health and Human Services 2006;Hu and DesMeules 2007;IARC 2004;State of California EPA 2005;Nebot et al 2009;Matt et al 2011;Petrick et al 2011;Sleiman et al 2014;Al-sarraf et al 2015). This problem refers not only to traditional cigarettes, but to e-cigarettes (Flouris et al 2013;Stillman et al 2015;Czogała et al 2014) as well. Furnishing textile materials constitute a significant element in different rooms: residential, office, public buildings or means of transport.…”

Section: Introductionmentioning

confidence: 99%

Removal of nicotine from indoor air using titania-modified polypropylene fibers: nicotine decomposition by titania-modified polypropylene fibers

Cieślak

Schmidt

Twarowska-Schmidt

et al. 2017

Int. J. Environ. Sci. Technol.

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Textile materials, because of their specific character, can affect the content of volatile pollutants in the indoor air, including the constituents of tobacco smoke (ETS-environmental tobacco smoke). Polypropylene fibers have a particularly high susceptibility for the sorption of nicotine. Textiles made of polypropylene are often used in different rooms or offices. The aim of the research was to give polypropylene fibers the photocatalytic properties by modifying their surface, using titanium dioxide doped with nanoparticles of silver (TiO 2 /Ag). Modification of polypropylene fibers with TiO 2 /Ag increases their susceptibility to sorption of nicotine and accelerates its decomposition. A comparison of the decomposition rate constants for the modified and unmodified fibers shows that the decomposition process runs from 1.6 to 2.9 times faster for the modified fibers depending on the nature of modification, the source of the nicotine and the ambient conditions. It was also found that the strength of modified fibers does not change under irradiation.

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Acute impact of active and passive electronic cigarette smoking on serum cotinine and lung function

Abstract: Regarding short-term usage, the studied e-cigarettes generate smaller changes in lung function but similar nicotinergic impact to tobacco cigarettes. Future research should target the health effects of long-term e-cigarette usage, including the effects of nicotine dosage.

Cited by 350 publications

References 33 publications

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Measurements of dermal uptake of nicotine directly from air and clothing

Removal of nicotine from indoor air using titania-modified polypropylene fibers: nicotine decomposition by titania-modified polypropylene fibers

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