Exposure to nicotine-free and flavor-free e-cigarette vapors modifies the pulmonary response to tobacco cigarette smoke in female mice

2020 ◽  
Vol 319 (4) ◽  
pp. L717-L727 ◽  
Author(s):  
Ariane Lechasseur ◽  
Carol-Ann Huppé ◽  
Maude Talbot ◽  
Joanie Routhier ◽  
Sophie Aubin ◽  
...  

Most of electronic cigarette (e-cigarette) users are also smoking tobacco cigarettes. Because of the relative novelty of this habit, very little is known on the impact of vaping on pulmonary health, even less on the potential interactions of dual e-cigarette and tobacco cigarette use. Therefore, we used well-established mouse models to investigate the impact of dual exposure to e-cigarette vapors and tobacco cigarette smoke on lung homeostasis. Groups of female BALB/c mice were exposed to room air, tobacco smoke only, nicotine-free flavor-free e-cigarette vapors only or both tobacco smoke and e-cigarette vapors. Moreover, since tobacco smoke and electronic cigarette vapors both affect circadian processes in the lungs, groups of mice were euthanized at two different time points during the day. We found that dual-exposed mice had altered lung circadian gene expression compared with mice exposed to tobacco smoke alone. Dual-exposed mice also had different frequencies of dendritic cells, macrophages, and neutrophils in the lung tissue compared with mice exposed to tobacco smoke alone, an observation also valid for B-lymphocytes and CD4+ and CD8+ T lymphocytes. Exposure to e-cigarette vapors also impacted the levels of immunoglobulins in the bronchoalveolar lavage and serum. Finally, e-cigarette and dual exposures increased airway resistance compared with mice exposed to room air or tobacco smoke alone, respectively. Taken together, these data suggest that e-cigarette vapors, even without nicotine or flavors, could affect how the lungs react to tobacco cigarette smoke exposure in dual users, potentially altering the pathological course triggered by smoking.

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.


2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Maude Talbot ◽  
Mélanie Hamel-Auger ◽  
Marie-Josée Beaulieu ◽  
Morgan Gazzola ◽  
Ariane Lechasseur ◽  
...  

2018 ◽  
Vol 21 (10) ◽  
pp. 1394-1400 ◽  
Author(s):  
Ashley N Dowd ◽  
Stephen T Tiffany

Abstract Introduction Up to 24% of electronic cigarette (e-cigarette) users are concurrent users of both tobacco and e-cigarettes (dual users). Dual users provide an opportunity to assess key motivational processes supporting e-cigarette use, such as the reward value of e-cigarettes. This study used the Choice Behavior Under Cued Conditions procedure to examine cue-specific reactions to tobacco and e-cigarettes with a primary focus on evaluating the relative reward value of both forms of cigarettes. Methods Fifty-four dual users were exposed to a lit tobacco cigarette, their own e-cigarette, or a cup of water across multiple trials. On each trial, participants rated their craving for both tobacco and e-cigarettes and indicated the amount of money they would spend to access the cue. Key measures included craving, amount of money spent to access the cue, latency to access the cue, spending choice time, and consumption. Results Participants reported significantly higher craving and spent significantly more money on tobacco and e-cigarette trials than on water trials. The magnitude of cue-specific craving was comparable across tobacco and e-cigarettes, but participants spent significantly more to access tobacco cigarettes than e-cigarettes. Conclusions This is the first study to demonstrate cue-specific reactivity to e-cigarettes utilizing a neutral comparison condition and to examine the reward value of e-cigarettes relative to tobacco cigarettes. Overall, the data suggest that e-cigarette puffs are less valued and generate less craving than tobacco cigarette puffs for dual users. The data provide clear support for the utility of Choice Behavior Under Cued Conditions for examining a range of motivational processes supporting e-cigarette use. Implications The test procedure used in this research generates multiple indices of nicotine and tobacco motivation and allows for an explicit comparison of those variables in people who use both e-cigarettes and tobacco cigarettes.


2015 ◽  
Vol 35 (2) ◽  
pp. 179-185 ◽  
Author(s):  
A. Marsot ◽  
N. Simon

Background: Since their introduction in 2004, electronic cigarettes (e-cigarettes) have gained popularity worldwide. E-cigarettes are marketed as nicotine delivery devices. Commonly reported reasons for use include to quit smoking, to reduce urge to smoke, or the perceived lower risk alternative to smoking. But what are the actual amounts of nicotine delivered? Aim: This review summarizes all the published studies concerning nicotine or cotinine levels following e-cigarette use. Methods: A literature search was conducted from the PubMed database, from 1985 to January 2014, using the following terms: electronic cigarette(s), e-cigarette(s), electronic nicotine delivery system, cotinine, and nicotine. Articles were excluded if they were not pertinent according to our criteria. References of all relevant articles were also evaluated. Results: Eight studies were included in this review. The following information was extracted from the articles: population size, age of participants, recruitment, inclusion and exclusion criteria, concentration of nicotine in refills liquids, study sample design, and observed concentrations. Following design of studies, plasma nicotine Cmax was observed between 0 and 5 ng/mL (no significant changes) or between 13.9 and 16.3 ng/mL (similar to a tobacco cigarette) with a Tmax between 70 and 75 minutes. Cotinine levels after “vaping” an e-cigarette are similar to a tobacco cigarette. Conclusion: This review summarizes e-cigarette studies that contain information on nicotine or cotinine levels. The peak concentration of nicotine appears to be dependent on the use and dose level of e-cigarette cartridge. The value of this peak concentration is similar to the value found with a tobacco cigarette. However, the time corresponding to the peak concentration is delayed compared to a tobacco cigarette.


2006 ◽  
Vol 291 (1) ◽  
pp. L19-L29 ◽  
Author(s):  
Carolyn J. Baglole ◽  
Seth M. Bushinsky ◽  
Tatiana M. Garcia ◽  
Aruna Kode ◽  
Irfan Rahman ◽  
...  

Cigarette smoke is the principal cause of emphysema. Recent attention has focused on the loss of alveolar fibroblasts in the development of emphysema. Fibroblasts may become damaged by oxidative stress and undergo apoptosis as a result of cigarette smoke exposure. Not all smokers develop lung diseases associated with tobacco smoke, a fact that may reflect individual variation among human fibroblast strains. We hypothesize that fibroblasts from different human beings vary in their ability to undergo apoptosis after cigarette smoke exposure. This could account for emphysematous changes that occur in the lungs of some but not all smokers. Primary human lung fibroblast strains were exposed to cigarette smoke extract (CSE) and assessed for viability, morphological changes, and mitochondrial transmembrane potential as indicators of apoptosis. We also examined the generation of intracellular reactive oxygen species (ROS), 4-hydroxy-2-nonenal, and changes in glutathione (GSH) and glutathione disulfide (GSSG) levels. Each human lung fibroblast strain exhibited a differential sensitivity to CSE as judged by changes in mitochondrial membrane potential, viability, ROS generation, and glutathione production. Interestingly, the thiol antioxidants N-acetyl-l-cysteine and GSH eliminated CSE-induced changes in fibroblast morphology such as membrane blebbing, nuclear condensation, and cell size and prevented alterations in mitochondrial membrane potential and the generation of ROS. These findings support the concept that oxidative stress and apoptosis are responsible for fibroblast death associated with exposure to tobacco smoke. Variations in the sensitivity of fibroblasts to cigarette smoke may account for the fact that only some smokers develop emphysema.


2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Kim Romijnders ◽  
Marlieke Beijaert ◽  
Liesbeth van Osch ◽  
Hein de Vries ◽  
Reinskje Talhout

Author(s):  
Maya Ayu Riestiyowati ◽  
◽  
Setyo Sri Rahardjo ◽  
Vitri Widyaningsih ◽  
◽  
...  

Background: Acute Respiratory Infections are classified into the upper and lower respiratory tract infections, contributing to the leading cause of death among children under five globally. The estimation showed the deaths of more than 800,000 children under five every year or about 2,200 per day. One of the risk factors for ARI in children under five years of age is secondary exposure to tobacco smoke. This study aimed to examine the effect of cigarette smoke exposure and acute respiratory infection in children under five. Subjects and Method: This was meta analysis and systematic review. The study was conducted by collecting published articles from Google Scholar, Pubmed, and Springer Link databases, from year 2010 to 2019. Keywords used “risk factor” OR “passive smoking” OR “secondhand smoking” AND “ARI due to children under five”. The inclusion criteria were full text, using English language, using cross-sectional study design, and reporting adjusted odds ratio. The collected articles were selected by PRISMA flow chart. The quantitative data were analyzed by fixed effect model using Revman 5.3. Results: 6 studies from Cameroon, Ethiopia, India, Nepal, and Nigeria reported that tobacco smoke exposure increased the risk of acute respiratory infection in children under five (aOR=1.39; 95% CI= 1.22 to 1.58; p<0.001). Conclusion: Tobacco smoke exposure increases the risk of acute respiratory infection in children under five. Keywords: tobacco smoke, acute respiratory infection, children under five Correspondence: Maya Ayu Riestiyowati. Masters Program in Public Health. Universitas Sebelas Maret, Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: [email protected]. Mobile: 081235840067.


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