E-cig Use Research Articles

Inflammatory biomarkers and growth factors in saliva and gingival crevicular fluid of e-cigarette users, cigarette smokers, and dual smokers: A pilot study.

Cigarette smoking remains one of the leading public health threats worldwide. Electronic cigarettes (e-cigs) provide an alternative to conventional cigarette smoking; however, the evidence base of risks and benefits of e-cig use is new and growing. In this cross-sectional pilot study, the effect of e-cig use on biological profiles in saliva and gingival crevicular fluid (GCF) was assessed and compared with the profiles of cigarette smokers (CS), dual users, and non-users. The systemic inflammatory mediators between e-cig users (EC) and these other groups were also assessed. This pilot cross-sectional study recruited volunteer participants consisting of four groups, non-smokers (NS), CS, EC, and dual EC and cigarette smokers (DS). Saliva and GCF samples were collected and analyzed for biomarkers of inflammation, oxidative stress, anti-inflammatory lipid mediators, tissue injury and repair, and growth factors with immunoassay (enzyme-linked immunosorbent assay and Luminex). Smoking status was confirmed via salivary cotinine. Prostaglandin E2 level was significantly increased in CS compared with EC and DS, but not significantly different in EC and DS groups compared with non-smokers (NS). Statistically significant differences were observed between groups of EC and NS (myeloperoxidase [MPO], matrix metalloproteinase-9) as well as between DS and EC for biomarkers of inflammatory mediators (receptor for advanced glycation end products [RAGE], MPO, uteroglobin/CC-10); between groups of DS and NS for extracellular newly identified RAGE binding protein and between CS and NS for MPO. No statistically significant differences in biomarkers of immunity (S100A8, S100A9, galectin-3), tissue injury and repair (Serpine1/PAI-1) and growth factors (brain-derived neurotrophic factor, fibroblast growth factors, platelet-derived growth factor-AA, vascular endothelial growth factor, and others) were found between any of groups. Statistically significant differences in measurable health outcomes were found between different smoking status groups, suggesting that smoking/vaping produces differential effects on oral health.

Hypomethylation of LINE-1 repeat elements and global loss of DNA hydroxymethylation in vapers and smokers

ABSTRACT The outbreak of vaping-related severe lung injuries and deaths and the epidemic of teen vaping in the U.S. underscore the urgent need for determining the biological consequences of electronic cigarette (e-cig) use. We have investigated the association between vaping and epigenetic changes by quantifying DNA methylation levels in Long Interspersed Nucleotide Element 1 (LINE-1) and global DNA hydroxymethylation (5-hmC) levels and measuring the expression level of enzymes catalysing the respective processes in peripheral blood of exclusive vapers, smokers, and controls, matched for age, gender, and race (n = 45). Both vapers and smokers showed significant loss of methylation in LINE-1 repeat elements in comparison to controls (P = 0.00854 and P = 0.03078, respectively). Similarly, vapers and smokers had significant reductions in 5-hmC levels relative to controls (P = 0.04884 and P = 0.0035, respectively). Neither the LINE-1 methylation levels nor the global 5-hmC levels were different between vapers and smokers. There was a direct correlation between methylation levels in the LINE-1 elements and global 5-hmC levels in the study subjects (r = 0.31696, P = 0.03389). Inverse and statistically significant correlations were found between both the LINE-1 methylation levels and the global 5-hmC levels and various vaping/smoking metrics in the study subjects. There were modest but not statistically significant changes in transcription of DNA methyltransferases and ten-eleven translocation enzymes in both vapers and smokers relative to controls. Our findings support follow-up genome-wide investigations into the epigenetic effects of vaping, which may further clarify the health consequences of e-cig use. Abbreviations 5-mC: 5-methylcytosine; 5-hmC: 5-hydroxymethylcytosine; 8-OHdG: 8-hydroxy-2ʹ-deoxyguanosine; ACTIN: actin beta; ANOVA: Analysis of Variance; BER: base excision repair; BMI: body mass index; CO: carbon monoxide; COHb: carboxyhaemoglobin; COBRA: combined bisulphite restriction analysis; COPD: chronic obstructive pulmonary disease; DNMT1: DNA methyltransferase 1; DNMT3A: DNA methyltransferase 3A; DNMT3B: DNA methyltransferase 3B; e-cigs: electronic cigarettes; ELISA: enzyme-linked immunosorbent assay; ENDS: electronic nicotine delivery systems; FDA: Food and Drug Administration; GAPDH; glyceraldehyde-3-phosphate dehydrogenase; HPLC: high-performance liquid chromatography; LINE-1: Long Interspersed Nucleotide Element 1; PBS: phosphate-buffered saline; RFU: relative fluorescence units; RT-qPCR: quantitative reverse-transcription polymerase chain reaction; ROS: reactive oxygen species; SAM, S-adenosylmethionine; SE: standard error; TET1: ten-eleven translocation 1; TET2: ten-eleven translocation 2; TET3: ten-eleven translocation 3.

Effects of Electronic Cigarette Constituents on the Human Lung: A Pilot Clinical Trial.

Electronic cigarette (e-cig) use is continuing to increase, particularly among youth never-smokers, and is used by some smokers to quit. The acute and chronic toxicity of e-cig use is unclear generally in the context of increasing reports of inflammatory-type pneumonia in some e-cig users. To assess lung effects of e-cigs without nicotine or flavors, we conducted a pilot study with serial bronchoscopies over 4 weeks in 30 never-smokers, randomized either to a 4-week intervention with the use of e-cigs containing only 50% propylene glycol (PG) and 50% vegetable glycerine or to a no-use control group. Compliance to the e-cig intervention was assessed by participants sending daily puff counts and by urinary PG. Inflammatory cell counts and cytokines were determined in bronchoalveolar lavage (BAL) fluids. Genome-wide expression, miRNA, and mRNA were determined from bronchial epithelial cells. There were no significant differences in changes of BAL inflammatory cell counts or cytokines between baseline and follow-up, comparing the control and e-cig groups. However, in the intervention but not the control group, change in urinary PG as a marker of e-cig use and inhalation was significantly correlated with change in cell counts (cell concentrations, macrophages, and lymphocytes) and cytokines (IL8, IL13, and TNFα), although the absolute magnitude of changes was small. There were no significant changes in mRNA or miRNA gene expression. Although limited by study size and duration, this is the first experimental demonstration of an impact of e-cig use on inflammation in the human lung among never-smokers.

Prenatal electronic cigarette exposure decreases brain glucose utilization and worsens outcome in offspring hypoxic-ischemic brain injury.

It has been shown that prenatal nicotine and tobacco smoke exposure can cause different neurobehavioral disorders in the offspring. We hypothesize that prenatal exposure to nicotine-containing electronic cigarette (e-Cig) vapor can predispose newborn to enhanced sensitivity to hypoxic-ischemic (HI) brain injury and impaired motor and cognitive functions. In this study, pregnant CD1 mice were exposed to e-Cig vapor (2.4% nicotine). Primary cortical neurons isolated from e-Cig exposed fetus were exposed to oxygen-glucose deprivation followed by reoxygenation (OGD/R) to mimic HI brain injury. Cell viability and glucose utilization were analyzed in these neurons. HI brain injury was induced in 8-9-day-old pups. Short-term brain injury was evaluated by triphenyltetrazolium chloride staining. Long-term motor and cognitive functions were evaluated by open field, novel object recognition, Morris water maze, and foot fault tests. Western blotting and immunofluorescence were done to characterize glucose transporters in offspring brain. We found that e-Cig exposed neurons demonstrated decreased cell viability and glucose utilization in OGD/R. Prenatally e-Cig exposed pups also had increased brain injury and edema 24hr after HI brain injury. Further, in utero e-Cig exposed offspring with HI brain injury displayed impaired memory, learning, and motor coordination at adolescence. Additionally, the expression of glucose transporters decreased in e-Cig exposed offspring brain after HI brain injury. These results indicate that reduced glucose utilization can contribute to prenatal e-Cig exposure induced worsened HI brain injury in offspring. This study is instrumental in elucidating the possible deleterious effects of e-Cig use in the general population.

Effects of Electronic Cigarettes on Indoor Air Quality and Health

With the rapid increase in electronic cigarette (e-cig) users worldwide, secondhand exposure to e-cig aerosols has become a serious public health concern. We summarize the evidence on the effects of e-cigs on indoor air quality, chemical compositions of mainstream and secondhand e-cig aerosols, and associated respiratory and cardiovascular effects. The use of e-cigs in indoor environments leads to high levels of fine and ultrafine particles similar to tobacco cigarettes (t-cigs). Concentrations of chemical compounds in e-cig aerosols are generally lower than those in t-cig smoke, but a substantial amount of vaporized propylene glycol, vegetable glycerin, nicotine, and toxic substances, such as aldehydes and heavy metals, has been reported. Exposures to mainstream e-cig aerosols have biologic effects but only limited evidence shows adverse respiratory and cardiovascular effects in humans. Long-term studies are needed to better understand the dosimetry and health effects of exposures to secondhand e-cig aerosols.

An Electronic Aerosol Delivery System for Functional Magnetic Resonance Imaging.

Background:Public health concerns over the addictive potential of electronic cigarettes (e-cigs) have heightened in recent years. Brain function during e-cig use could provide an objective measure of the addictive potential of new vaping products to facilitate research; however, there are limited methods for delivering e-cig aerosols during functional magnetic resonance imaging (fMRI). The current study describes the development and feasibility testing of a prototype to deliver up to four different e-cig aerosols during fMRI.Methods:Standardized methods were used to test the devices’ air flow variability, nicotine yield, and free radical production. MRI scans were run with and without the device present to assess its safety and effects on MRI data quality. Five daily smokers were recruited to assess plasma nicotine absorption from e-liquids containing nicotine concentrations of 8, 11, 16, 24, and 36 mg/ml. Feedback was collected from participants through a semi-structured interview and computerized questionnaire to assess comfort and subjective experiences of inhaling aerosol from the device.Results:Nicotine yield captured from the aerosol produced by the device was highly correlated with the nicotine concentration of the e-liquids used (R2 = 0.965). Nicotine yield was reduced by a mean of 48% and free radical production by 17% after traveling through the device. The e-liquid containing the highest nicotine concentration tested (36 mg/ml) resulted in the highest plasma nicotine boost (6.6 ng/ml). Overall, participants reported that the device was comfortable to use and inhaling the e-cig aerosols was tolerable. The device was determined to be safe for use during fMRI and had insignificant effects on scan quality.Conclusions:With the current project, we were able to design a working prototype that safely and effectively delivers e-cig aerosols during fMRI. The device has the potential to be used to assess brain activation during e-cig use and to compare brain reactivity to varying flavors, nicotine concentrations, and other e-cig characteristics.

Psychosocial and behavioral characteristics of still smokers at 6 months after acute cerebro or cardiovascular events: Findings from INEV@L, a prospective pilot study

Considering the benefits of smoking cessation, and evolving new tobacco-product consumption, such as e-cigarettes (e-cig), contemporary behavioral and psychosocial factors (PSF) associated with smoking after acute stroke or myocardial infarction (MI) remain to be investigated. From INEV@L, a prospective pilot study in 128 workers hospitalized for MI or stroke (MI/stroke: 199/57) < 65 y, between 2016 and 2017 in CHU Dijon. Among them, 67 (52%) current smokers were analyzed. PSF (education level (EL), socioeconomic status (SES), perceived disease severity (PDS), anxiety/depression), and health behavior (adhesion to Mediterranean diet (AMD), BMI, physical activity (PA), smoking) were collected at the acute phase and at 6 months follow-Up. Patients who quit smoking were compared with non-quitting patients at FU. Still smokers at FU were frequent (30(45%)) and had similar risk factors including age (51 ± 7 y) than quitters. Rate of overweight/obese patients and AMD were similar (52 vs. 65%, P = 0.281 and 29 ± 6 vs. 26 ± 7, P = 0.207). SES and EL were slightly higher in still smokers group. The level of anxiety or depression was as high in the 2 groups (63 vs. 68%, and 19 vs. 20%, P = 0.717 and 0.911). Although similar at the acute phase ( P = 0.867), PDS at 6-M FU, trended to be lower in non-quitters (57 vs. 78%, P = 0.057). At FU, only few returned to work (57% for both groups). Overweight/obese who reduced their weight were more common in non-quitters (60 vs. 38%, P = 0.170). Patients who improved AMD or PA level were similar (62 vs. 78%, P = 0.166, and 67 vs. 92%, P = 0.317). The vast majority of non-quitters introduced the use of e-cig (80% vs. 0%, P < 0.001). Our pilot study in young workers highlights the low rate of smoking cessation, and generalized dual use of electronic + conventional cigarette at mid-term after acute MI or stroke. Our findings further suggest specific PSF pattern of non-quitters, associated with loss of perceived disease severity.

Instagram's #JUUL: who's posting what.

Exposure to e-cigarette (e-cig) marketing through traditional and online media can increase the risk of e-cig use among adolescents. Though popular e-cig brand JUUL has scaled back its social media promotions, outside vendors and individual users create posts about JUUL unregulated. Instagram's image-focus offers an opportunity to document promotions that may appeal to adolescents. To assess the visual representation of JUUL on social media, we systematically classified discussion topics and themes of posts to Instagram. Of 25,428 unique Instagram images using the hashtag #JUUL retrieved between June 18 and July 18, 2018, a random subsample of 3,000 images (approximately 12% of the full data set) was drawn for human coding and analyses. Coded categories included relevance to JUUL, type of image, image appeal, and user type. Based on the number of relevant images, percentages of image type and appeal for each user type were calculated. There were 583 images that were coded as relevant. The majority of image types (64%) were classified as product (n =; 374). The most frequently coded type of appeal was flavors, found in 54% of images with appeal (n =; 149), followed by cartoons, found in 21% (n =; 57). Vendors were responsible for posting most of the images (n =; 291), followed by e-cig enthusiasts (n =; 99). Continued surveillance of e-cig products, such as JUUL, remains necessary to provide a foundation for potential regulatory protections against marketing and promotions that may appeal to youth.

Electronic Cigarette Vapor with Nicotine Causes Airway Mucociliary Dysfunction Preferentially via TRPA1 Receptors.

Rationale: Electronic cigarette (e-cig) use has been widely adopted under the perception of safety. However, possibly adverse effects of e-cig vapor in never-smokers are not well understood.Objectives: To test the effects of nicotine-containing e-cig vapors on airway mucociliary function in differentiated human bronchial epithelial cells isolated from never-smokers and in the airways of a novel, ovine large animal model.Methods: Mucociliary parameters were measured in human bronchial epithelial cells and in sheep. Systemic nicotine delivery to sheep was quantified using plasma cotinine levels, measured by ELISA.Measurements and Main Results:In vitro, exposure to e-cig vapor reduced airway surface liquid hydration and increased mucus viscosity of human bronchial epithelial cells in a nicotine-dependent manner. Acute nicotine exposure increased intracellular calcium levels, an effect primarily dependent on TRPA1 (transient receptor potential ankyrin 1). TRPA1 inhibition with A967079 restored nicotine-mediated impairment of mucociliary parameters including mucus transport in vitro. Sheep tracheal mucus velocity, an in vivo measure of mucociliary clearance, was also reduced by e-cig vapor. Nebulized e-cig liquid containing nicotine also reduced tracheal mucus velocity in a dose-dependent manner and elevated plasma cotinine levels. Importantly, nebulized A967079 reversed the effects of e-cig liquid on sheep tracheal mucus velocity.Conclusions: Our findings show that inhalation of e-cig vapor causes airway mucociliary dysfunction in vitro and in vivo. Furthermore, they suggest that the main nicotine effect on mucociliary function is mediated by TRPA1 and not nicotinic acetylcholine receptors.

Impact of electronic cigarette heating coil resistance on the production of reactive carbonyls, reactive oxygen species and induction of cytotoxicity in human lung cancer cells in vitro

Electronic cigarette (e-cigarette; e-cig) use has grown exponentially in recent years despite their unknown health effects. E-cig aerosols are now known to contain hazardous chemical compounds, including carbonyls and reactive oxygen species (ROS), and these compounds are directly inhaled by consumers during e-cig use. Both carbonyls and ROS are formed when the liquid comes into contact with a heating element that is housed within an e-cig's atomizer. In the present study, the effect of coil resistance (1.5 Ω and 0.25 Ω coils, to obtain a total wattage of 8 ± 2 W and 40 ± 5 W, respectively) on the generation of carbonyls (formaldehyde, acetaldehyde, acrolein) and ROS was investigated. The effect of the aerosols generated by different coils on the viability of H1299 human lung carcinoma cells was also evaluated. Our results show a significant (p < 0.05) correlation between the low resistance coils and the generation of higher concentrations of the selected carbonyls and ROS in e-cig aerosols. Moreover, exposure to e-cig vapor reduced the viability of H1299 cells by up to 45.8%, and this effect was inversely related to coil resistance. Although further studies are needed to better elucidate the potential toxicity of e-cig emissions, our results suggest that these devices may expose users to hazardous compounds which, in turn, may promote chronic respiratory diseases.

Electronic-cigarette smoke induces lung adenocarcinoma and bladder urothelial hyperplasia in mice

Electronic-cigarettes (E-cigs) are marketed as a safe alternative to tobacco to deliver the stimulant nicotine, and their use is gaining in popularity, particularly among the younger population. We recently showed that mice exposed to short-term (12 wk) E-cig smoke (ECS) sustained extensive DNA damage in lungs, heart, and bladder mucosa and diminished DNA repair in lungs. Nicotine and its nitrosation product, nicotine-derived nitrosamine ketone, cause the same deleterious effects in human lung epithelial and bladder urothelial cells. These findings raise the possibility that ECS is a lung and bladder carcinogen in addition to nicotine. Given the fact that E-cig use has become popular in the past decade, epidemiological data on the relationship between ECS and human cancer may not be known for a decade to come. In this study, the carcinogenicity of ECS was tested in mice. We found that mice exposed to ECS for 54 wk developed lung adenocarcinomas (9 of 40 mice, 22.5%) and bladder urothelial hyperplasia (23 of 40 mice, 57.5%). These lesions were extremely rare in mice exposed to vehicle control or filtered air. Current observations that ECS induces lung adenocarcinomas and bladder urothelial hyperplasia, combined with our previous findings that ECS induces DNA damage in the lungs and bladder and inhibits DNA repair in lung tissues, implicate ECS as a lung and potential bladder carcinogen in mice. While it is well established that tobacco smoke poses a huge threat to human health, whether ECS poses any threat to humans is not yet known and warrants careful investigation.

A content analysis of the promotional strategies employed by e-cigarette brands on Twitter

Cigarette smoking in the U.S. is declining, but e-cigarette (e-cig) use is rapidly expanding. E-cig brands utilize social media for promotion and have the autonomy to disseminate messages that encourage the use of their products. The current study categorized the most frequent strategies among popular e-cig brands on Twitter. A content analysis of over 1800 tweets was performed based on Philip Morris brand personality characteristics. Most tweets emphasized e-cigs’ economic value (24.2%) and normalized their use by portraying e-cigs as “cool” (23.1%). E-cig brands are employing similar strategies as tobacco companies and easily connecting to young adults through social media.

E-cigarette users commonly stealth vape in places where e-cigarette use is prohibited

Introduction‘Stealth vaping’ is the practice of vaping discreetly in places where electronic cigarette (e-cigarette) use is prohibited. While anecdotal evidence suggests that stealth vaping is common, there have been no...

Safety of Electronic Cigarette Use During Breastfeeding: Qualitative Study Using Online Forum Discussions.

BackgroundElectronic cigarettes (e-cigs) are an increasingly popular alternative to smoking, helping to prevent relapse in those trying to quit and with the potential to reduce harm as they are likely to be safer than standard cigarettes. Many women return to smoking in the postpartum period having stopped during pregnancy, and while this can affect their decisions about breastfeeding, little is known about women’s opinions on using e-cigs during this period.ObjectiveThe aim of this study is to explore online forum users’ current attitudes, motivations, and barriers to postpartum e-cig use, particularly as a breastfeeding mother.MethodsData were collected via publicly accessible (identified by Google search) online forum discussions, and a priori codes identified. All transcripts were entered into NVivo for analysis, with a template approach to thematic analysis being used to code all transcripts from which themes were derived.ResultsFour themes were identified: use, perceived risk, social support and evidence, with a number of subthemes identified within these. Women were using e-cigs to prevent postpartum return to smoking, but opinions on their safety were conflicting. They were concerned about possible transfer of harmful products from e-cigs via breastmilk and secondhand exposure, so they were actively seeking and sharing information on e-cigs from a variety of sources. Although some women were supportive of e-cig use, others provided harsh judgement for mothers who used them.ConclusionsE-cigs have the potential to reduce the number of women who return to smoking in the postpartum period and potentially improve breastfeeding rates, if breastfeeding mothers have access to relevant and reliable information. Health care providers should consider discussing e-cigs with mothers at risk of returning to smoking in the postpartum period.

The Customizable E-cigarette Resistance Influences Toxicological Outcomes: Lung Degeneration, Inflammation, and Oxidative Stress-Induced in a Rat Model.

Despite the knowledge gap regarding the risk-benefit ratio of the electronic cigarette (e-cig), its use has grown exponentially, even in teenagers. E-cig vapor contains carcinogenic compounds (eg, formaldehyde, acetaldehyde, and acrolein) and free radicals, especially reactive oxygen species (ROS) that cause toxicological effects, including DNA damage. The role of e-cig voltage customization on molecule generation has been reported, but the effects of the resistance on e-cig emissions and toxicity are unknown. Here, we show that the manipulation of e-cig resistance influences the carbonyls production from nonnicotine vapor and the oxidative and inflammatory status in a rat model. Fixing the voltage at the conventional 3.5 V, we observed that the amount of the selected aldehydes increased as the resistance decreased from 1.5 to 0.25 Ω. Under these conditions, we exposed Sprague Dawley rats to e-cig aerosol for 28 days, and we studied the pulmonary inflammation, oxidative stress, tissue damage, and blood homeostasis. We found a perturbation of the antioxidant and phase II enzymes, probably related to the increased ROS levels due to the enhanced xanthine oxidase and P450-linked monooxygenases. Furthermore, frames from scanning electron microscope showed a disorganization of alveolar and bronchial epithelium in 0.25 Ω group. Overall, various toxicological outcomes, widely recognized as smoke-related injuries, can potentially occur in e-cig consumers who use low-voltage and resistance device. Our study suggests that certain "tips for vaping safety" cannot be established, and encourages further independent investigations to help public health agencies in regulating the e-cig use.

A mouse model for chronic intermittent electronic cigarette exposure exhibits nicotine pharmacokinetics resembling human vapers

Electronic cigarettes (E-cig) use is increasing rapidly, particularly among youths. Animal models for E-cig exposure with pharmacokinetics resembling human E-cig users are lacking. We developed an E-cig aerosol exposure system for rodents and a chronic intermittent delivery method that simulates E-cig users who vape episodically during wakefulness and abstain during sleep. Mice were exposed to E-cig in a programmed schedule at very low, low, medium, or high doses defined by duration of each puff, number of puffs per delivery episode and frequency of episodes in the dark phase of a 12/12-h circadian cycle for 9 consecutive days. The plasma nicotine/cotinine levels and their time courses were determined using LC/MS-MS. We assessed the body weight, food intake and locomotor activity of Apolipoprotein E null (ApoE-/-) mice exposed to chronic intermittent E-cig aerosol. Plasma nicotine and cotinine levels were positively correlated with exposure doses. Nicotine and cotinine levels showed a circadian variation as they increased with time up to the maximum nicotine level of 21.8 ± 7.1 ng/mL during the daily intermittent E-cig exposure in the 12-h dark phase and then declined during the light phase when there was no E-cig delivery. Chronic E-cig exposure to ApoE-/- mice decreased body weight, food intake and increased locomotion. Our rodent E-cig exposure system and chronic intermittent exposure method yield clinically relevant nicotine pharmacokinetics associated with behavioral and metabolic changes. The methodologies are essential tools for in vivo studies of the health impacts of E-cig exposure on CNS, cardiovascular, pulmonary, hepatic systems, metabolism and carcinogenesis.

Abstract 664: Microbial and inflammatory response to electronic cigarette and cigarette use

Abstract Background: As electronic cigarette (e-cig) use increases in the US, investigation of their effects are critical. Alteration of the lung microbiome, oral microbiome, and inflammation are well established effects of cigarettes; however the effects of e-cigs are yet unknown. Individuals with smoking-related lung disease have alterations in their lung microbiome compared to healthy individuals and their lung microbiomes appear more similar to their oral microbiomes when compared to healthy individuals. To our knowledge, only one study has examined smoking tobacco’s concurrent effects in the oral and lung microbiome and none have examined e-cig use. Further, none have studied e-cigs’ effect on the lung microbiome and inflammation. We hypothesized that e-cig use would affect the lung microbiome, and that the effects are different from smokers and never-smokers; alteration of the lung microbiome will also affect inflammatory gene expression in the lungs. Methods: A cross-sectional study of bronchoscopy with bronchoalveolar lavage (BAL) of 10 never-smokers, 8 cigarette smokers, and 10 e-cig users was conducted. RNA was extracted from BAL samples for total transcriptome RNA-seq analysis, allowing measurement of the microbiome and human gene expression. Differences in the microbiome by smoking status were determined by the Kruskal-Wallis test. Pairwise Wilcoxon rank sum tests with Holm correction was used. Effect size (fold change &amp;gt;1.5) and adjusted P-value cutoffs (&amp;lt;0.05) were used to identify microbes of potential interest. The limma-voom package in R was used to determine associations with human gene expression. Results: We identified 53 differentially-abundant bacterial species in BAL samples by smoking group. Among them, the majority were less abundant in the lung of smokers and ~20 are normally found in the oral microbiome. While there were significant differences in differentially-abundant microbes between e-cig users and smokers and between smokers and never-smokers, the microbiome of e-cig users did not differ from that of never-smokers. In preliminary analyses of gene expression, there were 2,400 differentially-expressed human genes among the three groups, of which 58 are inflammatory pathway genes. Conclusion: The majority of differentially-abundant microbes observed by smoking group are largely due to smokers. The microbiome of e-cig users is more similar to that of never-smokers. Interestingly, nearly half of microbes that are altered in the lung microbiome due to smoking use are bacterial species normally found in the oral microbiome. These findings suggest that the alterations in the oral microbiome associated with smoking cigarettes may also be reflected in the lung microbiome. Citation Format: Kevin L. Ying, Min-Ae Song, Daniel Y. Weng, Quentin A. Nickerson, Joseph P. McElroy, Theodore M. Brasky, Mark D. Wewers, Ewy Mathé, Jo L. Freudenheim, Peter G. Shields. Microbial and inflammatory response to electronic cigarette and cigarette use [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 664.

Abstract 1756: Electronic cigarettes induce DNA damage in the oral epithelium of users

Abstract Background: The use of electronic cigarettes (e-cigs) has skyrocketed among adolescents and young adults. E-cigs are promoted as safer than combustible cigarettes but their long term effects on human health are still unknown. E-cig aerosols contain significantly lower number of chemicals than tobacco smoke, however they also contain known carcinogens, reactive oxygen species (ROS), and unique chemicals poorly studied. In vitro and animal studies revealed that e-cig aerosols increases DNA damage and reduces DNA repair. There have been no studies assessing e-cig-induced DNA damage in human subjects. This reflects, at least in part, technical limitations that make it quite challenging to measure the in vivo steady-state levels of DNA damage, particularly for relatively low levels of genotoxic exposure. Our lab has previously developed and validated a novel quantitative primer anchored DNA damage detection assay (q-PADDA) to quantify in vivo DNA damage. We have also reported that, in an in vitro setting, q-PADDA has high sensitivity to detect e-cig-induced DNA damage. Here, we take advantage of this assay to start assessing the potential long-term impact of e-cig use on human health. Aim: To determine whether e-cig users have higher levels of DNA damage on oral epithelial cells than non-users. Methods: Ethics Committee approval was obtained. Participants were recruited through internet ads, leaflets, flyers and word-of-mouth. After written informed consent, a total of 35 individuals were included in this study: 20 exclusive e-cigarette users and 15 individuals reporting no e-cig or tobacco use. Self-report of tobacco use was biochemically confirmed by salivary cotinine and by measuring exhaled carbon monoxide (CO). Oral mucosa samples were collected by cytobrush and used for DNA extraction and damage quantification. DNA damage was quantified by q-PADDA within p53, the most frequently mutated gene in human cancer. Plasma nicotine levels were analyzed by liquid chromatography-mass spectrometry. Data was analyzed by Student’s t test. Results: The study including participants using high and low voltage e-cig devices. E-cig users (33 ± 8) and non-users (33 ± 7) had similar age distribution. We observed that oral epithelial cells collected from e-cig users have significantly higher levels of DNA damage in both transcribed and non-transcribed DNA strands of the p53gene when compared to never users. Conclusion: Our work is the first study to measure DNA damage in e-cig users. Our study shows for the first time that e-cig users have significant levels of DNA damage in their oral mucosa epithelium. These data has major clinical implications and suggest that e-cig users might have an increased cancer risk. Further studies are urgently needed to expand these kind of studies and to characterize the molecular mechanisms underlying e-cig induced DNA damage which may leads to cancer. Citation Format: Vengatesh Ganapathy, Theodore Wagener, Lurdes Queimado. Electronic cigarettes induce DNA damage in the oral epithelium of users [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1756.

Teen e-cig use is epidemic, while many adults vape to quit smoking

Teen e-cig use is epidemic, while many adults vape to quit smoking

A comparison of risk factors for cigarette and e-cigarette use in the United States adult population.

1546 Background: The US CDC and public health agencies have reported alarming increases in e-cigarette (ecig) use among youth, even as cigarette (cig) use among youth decline. In this study, other risk factors for cig and ecig use are compared. Methods: This study used data from the Health Information National Trends Survey 5 Cycle 1 survey, conducted in 2017. Univariate survey-weighted logistic regression analyzed responses as a nationally representative US population. Results: Inverted trends included being 35 or older (cig: OR=1.22, p&lt;0.01; ecig: OR=0.79, p&lt;0.01), being a student (cig: OR=0.77, p&lt;0.01; ecig: OR=1.24, p&lt;0.01) or retired (cig: OR=1.09, p&lt;0.01; ecig: OR=0.89, p&lt;0.01) compared to being employed, and being single (cig: OR=0.92, p&lt;0.03; ecig: OR=1.18, p&lt;0.01). Having considered quitting smoking was not significantly associated with ecig use. Conclusions: Segments of the US adult population educated with anti-tobacco campaigns may remain at increased risk for ecig use.[Table: see text]