E-cigarette Aerosol Research Articles

Abstract 19102: E-Cigarettes Induce Persistent Cardiac Autonomic Dysfunction and Molecular Signatures of Dilated and Arrhythmogenic Cardiomyopathy

Introduction: Evidence is mounting that use of e-cigarettes (e-cigs) promotes cardiopulmonary injury and dysfunction, but the long-term consequences remain unclear. Consumption of menthol e-cigs has surged amid imminent bans on combustible menthol cigarettes and cigars. Recently, we found e-cig aerosols with menthol (but not tobacco) flavor acutely induced spontaneous ventricular arrhythmias in mice. Hypothesis: Menthol e-cigs induces persistent cardiac autonomic imbalance. Methods: Adult C57BL/6J male mice with electrocardiogram (ECG) and blood pressure (BP) telemeters were exposed for 4 weeks to menthol e-cig aerosols (JUUL, 180 puffs/day, 5 days/week; n=8) or filtered air (Air; n=7) and challenged with restraint stress to determine cardiovascular reactivity to stress. Hearts (n=5/group) were collected immediately after final exposure for phosphoproteomics. Results: Menthol e-cig exposures increased HR, decreased HR variability, and evoked ventricular premature beats only on exposure day 1, but consistently increased BP throughout the 20-day exposure (+16 mmHg systolic BP vs. Air). Additional exposures in females (n=4) recapitulated these acute effects. Pre-treatment with atenolol (n=4 males) abolished e-cig-induced arrhythmias, suggesting β 1 -adrenergic mediation of e-cig-induced arrhythmias. After 4-week JUUL Menthol exposure, mice had basal sinus bradycardia and impaired stress reactivity, characterized by reduced maximal HR and rapid recovery to baseline. All three effects persisted up to 3 weeks following cessation and were accompanied by prolonged ventricular repolarization (QT c ). Phosphoproteomic analysis revealed upregulation of protein kinase A signaling, and mitochondrial dysfunction in e-cig-exposed mice. Phosphoproteins associated with dilated & arrhythmogenic cardiomyopathy (ATP2A2, FN1, CACNB2, PFKM, ADCY6, and PRKAR1A) were differentially regulated in e-cig-exposed mice. Conclusions: We demonstrate that menthol e-cigs induce persistent cardiac autonomic imbalance associated with molecular signatures of dilated & arrhythmogenic cardiomyopathy. Autonomic imbalance and cardiac electrical dysfunction may contribute to the long-term health effects of repeated use of e-cigarettes.

Abstract 13361: The Effect of Electronic Cigarette Exposure on Flow Mediated Vasodilation and LV Remodeling in a Chronic Myocardial Infarction Model

Introduction: There is little information about the effect of electronic cigarette (e-C) exposure on the cardiovascular system in the setting of myocardial infarction (MI) and whether e-C’s could alter vascular or cardiac function during the healing phase of MI. We determine the effect of e-C on endothelial function, cardiac remodeling and function during the healing phase of MI. Methods: Sprague Dawley rats (both sexes) were anesthetized and subjected to a proximal left coronary artery occlusion to induce a large anterior wall MI. At one week, rats were randomized to receive either 12 weeks of exposure to purified air (n=37) or e-cig vapor plus 15 mg/ml of nicotine (e-Cn=32). At 12 weeks endothelial function was tested by assessing femoral artery diameter and blood flow following a 5- minute femoral artery occlusion and reperfusion (ultrasound and flow probe). Cardiac function was assessed by echocardiography; remodeling was also assessed by quantitative histologic analysis. Results: Baseline blood flow in the femoral artery did not differ between groups, but peak reperfusion blood flow was blunted in the e-Cn group (1.59 ± 0.15 ml/min) vs. the air group (2.11 ± 0.18 ml/min; p=0.034). Femoral artery diameter after reperfusion was narrower in the e-Cn group (0.54 ± 0.02mm) compared to the air group (0.60 ± 0.02mm; p=0.023). Postmortem left ventricular (LV) volumes were similar in the e-Cn (0.69 ± 0.04 ml) and air groups (0.73 ± 0.04 ml; p=NS); and myocardial infarct expansion index did not differ between groups (1.4 ± 0.1 in e-Cn group versus 1.3 ± 0.1 in air group; p=NS). Gross pathology LV wall thickness was greater in the e-Cn group (1.38 ± 0.12 mm) versus the air group (1.04 ± 0.10 mm) despite no increase in blood pressure at 12 weeks in the e-CN group. LV fractional shortening by echo did not differ between groups at 12 weeks (e-Cn at 29 ± 2% and air at 27 ± 1%; p=NS). Conclusion: Exposure to e-Cn during the healing phase of MI was associated with altered endothelial function with reduced femoral artery blood flow and diameter at reperfusion, but not with worsened LV dilation or worsened cardiac function. E-Cn did increase gross pathologic LV wall thickness. E-Cn exposure during the healing phase of MI has deleterious effects on the CV system but does not dilate the LV.

Nicotine, THC, and Dolutegravir Modulate E-Cigarette-Induced Changes in Addiction- and Inflammation-Associated Genes in Rat Brains and Astrocytes.

E-cigarette use has been marketed as a safer alternative to traditional cigarettes, as a means of smoking cessation, and are used at a higher rate than the general population in people with HIV (PWH). Early growth receptor 2 (EGR2) and Activity-Regulated Cytoskeleton-Associated Protein (ARC) have a role in addiction, synaptic plasticity, inflammation, and neurodegeneration. This study showed that 10 days of exposure to e-cigarette vapor altered gene expression in the brains of 6-month-old, male, Sprague Dawley rats. Specifically, the e-cigarette solvent vapor propylene glycol (PG) downregulated EGR2 and ARC mRNA expression in frontal cortex, an effect which was reversed by nicotine (NIC) and THC, suggesting that PG could have a protective role against NIC and cannabis dependence. However, in vitro, PG upregulated EGR2 and ARC mRNA expression at 18 h in cultured C6 rat astrocytes suggesting that PG may have neuroinflammatory effects. PG-induced upregulation of EGR2 and ARC mRNA was reversed by NIC but not THC. The HIV antiretroviral DTG reversed the effect NIC had on decreasing PG-induced upregulation of EGR2, which is concerning because EGR2 has been implicated in HIV latency reversal, T-cell apoptosis, and neuroinflammation, a process that underlies the development of HIV-associated neurocognitive disorders.

Abstract 14730: The Effect of Electronic Cigarette Exposure With Nicotine on Expression of Inflammatory Genes and Blood Parameters in a Chronic Myocardial Infarction Model

Background: There are no data available regarding the effects of chronic electronic cigarette (eC) exposure on inflammatory gene expressions after myocardial infarction (MI) and whether eC could alter blood counts and chemistries in this setting. We determined the effect of eC on expression of genes for inflammatory cytokines and receptors and blood parameters during the healing phase of MI. Methods and Results: Sprague Dawley rats of either sex were subjected to a proximal left coronary artery occlusion to induce a large anterior wall MI. At 1 week, rats were randomized to exposure to air or E-cig with nicotine (eC Nic + ) for 12 weeks. After 12 weeks of exposure, rat inflammatory cytokine and receptor PCR array was performed (n=4 in each group). The data showed 70 out of 84 inflammatory-related genes were downregulated in the eC Nic+ group versus the air group and 11 downregulated genes reached a significant difference. Interleukin 6 (IL6), Tumor necrosis factor superfamily (TNF), Chemokine (C-C motif) ligand 12 (Ccl12), and C-X-C Motif Chemokine Receptor 3 (Cxcr3) gene expressions were significantly decreased by -6.49 fold, p=0.0048, -2.63 fold, p=0.0227, -2.71 fold, p=0.0146, and -2.28 fold, p=0.0067, respectively, in the eC Nic+ group vs air group. The rats in eC Nic+ group had significantly decreased white blood cell (WBC), lymphocyte and platelet count compared to the air group (Figure). Conclusions: Exposure to eC Nic+ alters the expression of inflammatory genes and decreases blood immune cells during the healing phase of MI. Our findings suggest that chronic inhalation of e-cigarette aerosols can suppress the immune and inflammatory response in the already compromised setting of MI.

The Effect of Moringa Leaf Extract (moringa oleifera) on the Microscopic Structure of the Lungs of Male Wistar Rats Given Inhalation of E-cigarette Liquid Vapor

Background: Moringa leaf extract is proven to have high antioxidant bioactive compounds and acts as an anti-inflammatory and prevents cell damage due to exposure to free radicals or oxidative. In the respiratory system exposed to Electronic Delivery Nicotine System liquid vapor, an inflammatory response and oxidative stress occur. Objective: This study aimed to determine the effect of Moringa leaf extract (Moringa oleifera) on the microscopic structure of the lungs of male Wistar rats given inhalation of e-cigarette liquid vapor. Methods: This research is an experimental laboratory with Post Test Only Control Group Design. Rats were divided into 4 groups containing 6 rats in each group, determined based on simple random sampling with the following divisions: Aquadest 3 mL (K1), gave inhalation of liquid vapours of electric cigarettes (K2), gave inhalation of liquid vapours of electric cigarettes + Moringa leaf extract with the dekoxy method dose of 500 mg/kgBW (P1), administration of vapor inhalation of e-cigarette liquid + Moringa leaf extract with the dekoxy method at a dose of 500 mg/kgBW (P2). Termination of the experimental animals was carried out on the 15th day and the rat pulmonary organs were taken to assess the microscopic structure of the rat lung. Results: The results of the Kruskal-Wallis test and continued with the Mann-Whitney test showed a significant difference (p < 0.05), however, there was no significant difference in the degree of pulmonary damage in the P1 to P2 groups. Conclusion: There is an effect of Moringa leaf extract (Moringa oleifera) on the microscopic structure of the lungs of male Wistar rats given inhalation of liquid vapor of electric cigarettes.

Effects of Electronic Cigarette Aerosol Exposure on Kidney Health in Diabetic/Obese Mice

Effects of Electronic Cigarette Aerosol Exposure on Kidney Health in Diabetic/Obese Mice

Mechanisms of E-Cigarette Vape-Induced Epithelial Cell Damage.

E-cigarette use has been reported to affect cell viability, induce DNA damage, and modulate an inflammatory response resulting in negative health consequences. Most studies focus on oral and lung disease associated with e-cigarette use. However, tissue damage can be found in the cardio-vascular system and even the bladder. While the levels of carcinogenic compounds found in e-cigarette aerosols are lower than those in conventional cigarette smoke, the toxicants generated by the heat of the vaping device may include probable human carcinogens. Furthermore, nicotine, although not a carcinogen, can be metabolized to nitrosamines. Nitrosamines are known carcinogens and have been shown to be present in the saliva of e-cig users, demonstrating the health risk of e-cigarette vaping. E-cig vape can induce DNA adducts, promoting oxidative stress and DNA damage and NF-kB-driven inflammation. Together, these processes increase the transcription of pro-inflammatory cytokines. This creates a microenvironment thought to play a key role in tumorigenesis, although it is too early to know the long-term effects of vaping. This review considers different aspects of e-cigarette-induced cellular changes, including the generation of reactive oxygen species, DNA damage, DNA repair, inflammation, and the possible tumorigenic effects.

Cytotoxicity, mutagenicity and genotoxicity of electronic cigarettes emission aerosols compared to cigarette smoke: the REPLICA project

Concerns have recently increased that the integrity of some scientific research is questionable due to the inability to reproduce the claimed results of some experiments and thereby confirm that the original researcher's conclusions were justified. This phenomenon has been described as 'reproducibility crisis' and affects various fields from medicine to basic applied sciences. In this context, the REPLICA project aims to replicate previously conducted in vitro studies on the toxicity of cigarette smoke and e-cigarette aerosol, sometimes adding experiments or conditions where necessary, in order to verify the robustness and replicability of the data. In this work the REPLICA Team replicated biological and toxicological assessment published by Rudd and colleagues in 2020. As in the original paper, we performed Neutral Red Uptake (NRU) assay for the evaluation of cytotoxicity, Ames test for the evaluation of mutagenesis and In Vitro Micronuclei (IVMN) assay for the evaluation of genotoxicity on cells treated with cigarette smoke or e-cigarette aerosol. The results showed high cytotoxicity, mutagenicity and genotoxicity induced by cigarette smoke, but slight or no cytotoxic, mutagenic and genotoxic effects induced by the e-cigarette aerosol. Although the two studies presented some methodological differences, the findings supported those previously presented by Rudd and colleagues.

A rapid semi-quantitative screening method to assess chemicals present in heated e-liquids and e-cigarette aerosols

Abstract. ​​​​​​​Electronic cigarettes (e-cigarettes) lack regulatory status as therapeutic products in all jurisdictions worldwide. They are potentially unsafe consumer products, with significant evidence they pose a risk to human health. Therefore, developing rapid, economical test methods to assess the chemical composition of e-liquids in heated and unheated forms and the aerosols produced by e-cigarettes is crucial. Four different e-liquids were heated using two different methods: (1) “typical” vaping using an e-cigarette device, by cycling “on” for 3 s every minute for 2 h (e-liquid obtained from remainder in the tank and aerosol collected in an impinger), and (2) “accelerated” heating, using an e-cigarette coil submerged in e-liquid and heating in short 20 s bursts on then 20 s off for 2 min only (liquid traps aerosol produced). All e-liquids were then analysed to test for the presence and quantity of 13 chemicals by gas chromatography–mass spectrometry and compared to an unheated sample. E-liquids heated with the accelerated method showed a comparable trend to the typical heating method, i.e. increase or decrease in chemical compound quantity, for more than two-thirds of the detected compounds analysed over all e-liquids. Six chemicals were detected as aerosol from the impinger fluid with the typical heating method at negligible levels. We propose that this accelerated version of the typical vaping method could form the basis of a standardized screening tool to test heated e-liquids (and e-cigarette aerosols) for harmful or banned substances. This will ensure that only approved products reach the consumer and reduce potential e-cigarette harm.

Utilizing primary human airway mucociliary tissue cultures to model ramifications of chronic E-cigarette usage

Electronic cigarettes are battery powered devices that use a vape-liquid to produce a vapor that is inhaled. A consequence of the rise in e-cigarette usage was the 2019 emergence of a vaping-induced respiratory disease denoted as ‘e-cigarette or vaping use-associated lung injury’ (EVALI). One of the suspected causes of EVALI is Vitamin E Acetate (VEA), which was found to be a diluent in certain illicit vape-pens, whereas nicotine is commonly diluted in equal parts propylene glycol and vegetable glycerin (PG:VG). The prevalent use of e-cigarettes and the emergence of a novel illness has made understanding how e-cigarette vapors affect our respiratory tissues a public health concern. We have designed and produced a simple device that can operate e-cigarettes and deliver the vapor to a chamber containing a standard cell culture multi-well plate. Here we utilize our device to model the response of human airway mucociliary tissue after chronic exposure to vapors produced from either PG:VG or VEA. We note several differences between how PG:VG and VEA vapors interact with and alter airway tissue cultures and suggest potential mechanisms for how VEA-vapors can exacerbate EVALI symptoms. Our device combined with primary human airway tissue cultures make an economical and compact model system that allows for animal-free investigations into the acute and chronic consequences of e-cigarette vapors on primary respiratory cells.

Particle size matters: Discrepancies in the health risks posed by traditional cigarettes and e-cigarettes in mice and humans

Electronic cigarettes (ECs), considered a healthier alternative to traditional cigarettes (TCs), vaporize e-liquid, which may produce harmful by-products due to thermal decomposition and metal transfer. These by-products' deposition in the respiratory tract is largely determined by particle size distribution (PSD). We employ the Multiple-Path Particle Dosimetry (MPPD) model to assess particle deposition within the human and mouse respiratory tracts. Leveraging the known connection between TC smoke inhalation and atherosclerosis, we used human aortic endothelial cells (HAECs) and ApoE-/- mice to explore the potential effects of EC aerosol inhalation on atherosclerosis. Our findings reveal that TCs exhibit a highly variable PSD, with mean diameters of approximately 300 nm for mainstream (MS) smoke and 120 nm for side stream (SS) smoke. Conversely, ECs demonstrate a more stable PSD. Combined with MPPD, the deposition fraction in the human respiratory system and mice is mainly deposited in the pulmonary region and head airway. For the Apoe-/- mice exposure experiment, preliminary findings suggest a potential impact on atherosclerosis, although not statistically significant, likely due to the limited sample size and exposure duration. This study highlights the importance of considering PSD, exposure dosage, and species-specific differences in risk assessments of EC aerosols.

Adverse Biophysical Impact of e-Cigarette Flavors on Pulmonary Surfactant.

The attractiveness and abundance of flavors are primary factors eliciting youth to use e-cigarettes. Emerging studies in recent years revealed the adverse health impact of e-cigarette flavoring chemicals, including disruption of the biophysical function of pulmonary surfactants in the lung. Nevertheless, a comprehensive understanding of the biophysical impact of various flavoring chemicals is still lacking. We used constrained drop surfactometry as a new alternative method to study the biophysical impact of flavored e-cigarette aerosols on an animal-derived natural pulmonary surfactant. The dose of exposure to e-cigarette aerosols was quantified with a quartz crystal microbalance, and alterations to the ultrastructure of the surfactant film were visualized using atomic force microscopy. We have systematically studied eight representative flavoring chemicals (benzyl alcohol, menthol, maltol, ethyl maltol, vanillin, ethyl vanillin, ethyl acetate, and ethyl butyrate) and six popular recombinant flavors (coffee, vanilla, tobacco, cotton candy, menthol/mint, and chocolate). Our results suggested a flavor-dependent inhibitory effect of e-cigarette aerosols on the biophysical properties of the pulmonary surfactant. A qualitative phase diagram was proposed to predict the hazardous potential of various flavoring chemicals. These results provide novel implications in understanding the environmental, health, and safety impacts of e-cigarette aerosols and may contribute to better regulation of e-cigarette products.

Accelerated epigenetic age, inflammation, and gene expression in lung: comparisons of smokers and vapers with non-smokers

BackgroundCigarette smoking and aging are the main risk factors for pulmonary diseases, including cancer. Epigenetic aging may explain the relationship between smoking, electronic cigarette vaping, and pulmonary health. No study has examined smoking and vaping-related epigenetic aging in relation to lung biomarkers.MethodsLung epigenetic aging measured by DNA methylation (mAge) and its acceleration (mAA) was assessed in young (age 21–30) electronic cigarette vapers (EC, n = 14, including 3 never-smoking EC), smokers (SM, n = 16), and non-EC/non-SM (NS, n = 39). We investigated relationships of mAge estimates with chronological age (Horvath-mAge), lifespan/mortality (Grim-mAge), telomere length (TL-mAge), smoking/EC history, urinary biomarkers, lung cytokines, and transcriptome.ResultsCompared to NS, EC and SM had significantly older Grim-mAge, shorter TL-mAge, significantly accelerated Grim-mAge and decelerated TL-mAge. Among SM, Grim-mAA was associated with nicotine intake and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). For EC, Horvath-mAA was significantly correlated with puffs per day. Overall, cytokines (IL-1β, IL-6, and IL-8) and 759 transcripts (651 unique genes) were significantly associated with Grim-mAA. Grim-mAA-associated genes were highly enriched in immune-related pathways and genes that play a role in the morphology and structures of cells/tissues.ConclusionsFaster lung mAge for SM is consistent with prior studies of blood. Faster lung mAge for EC compared to NS indicates possible adverse pulmonary effects of EC on biological aging. Our findings support further research, particularly on epigenetic markers, on effects of smoking and vaping on pulmonary health. Given that most EC are former smokers, further study is needed to understand unique effects of electronic cigarettes on biological aging.

A Single 10-Minute E-cigarette Vapor Exposure Reduces Tidal Volume and Minute Ventilation in Normoxia and Normobaric Hypoxia in Adult Rats.

The present study investigated the effects of a single 10-minute exposure to e-cigarette vapor on ventilation in adult male Long-Evans rats. Ventilation was recorded using awake, unrestrained whole-body plethysmography. Baseline recordings were taken the day before full-body exposure to either room air (n = 9; air control group) or e-cigarette vapor (n = 9; treatment group). Post-exposure recordings were taken immediately after the 10-minute room air or vapor exposure. As part of the ventilation protocol, in addition to recording the subject's ventilation in room air, the subjects were also exposed to 10% oxygen (balanced with nitrogen) to assess the effects of e-cigarette vapor on an increased drive to breathe. Ventilation data were analyzed using a 2x2x2 mixed-model ANOVA measuring treatment (vape vs. air) x time (baseline vs. post-treatment) x condition (normoxia vs. hypoxia) for breathing frequency, tidal volume, and minute ventilation. Breathing frequency increased in both treatment groups (air and vape) with exposure to normobaric hypoxia (p < 0.001), with no effect of time (baseline vs. post-treatment) for either group. Tidal volume increased in both treatment groups (air and vape) with exposure to normobaric hypoxia (p < 0.001), and an effect of time (baseline vs. post-treatment) was observed (p = 0.010) for the vape group. Minute ventilation increased in both treatment groups (air and vape) with exposure to normobaric hypoxia (p < 0.001), and an effect of time (baseline vs. post-treatment) was observed (p < 0.001) for the vape group. In conclusion, immediately following a single 10-minute e-cigarette vapor exposure, both tidal volume and minute ventilation were reduced during normoxia and normobaric hypoxia, indicating a decrease in ventilation after a single 10-minute e-cigarette vapor exposure. Furthermore, this exposure also blunted the physiological response to acute hypoxia exposure. Subjects in the vape group, while breathing more rapidly as expected, experienced shallower breathing than the air group during hypoxia. The findings in this study confirm that vaping could result in reduced lung function.

What is the impact of e-cigarettes on periodontal stem cells as revealed by transcriptomic analyses?

The research used an in vitro cell exposure model and multi-omics integration of transcriptome and epigenome profiling to compare the molecular effects of e-cigarettes and tobacco smoke on dental stem cells. The study aimed to compare the effects of e-cigarette and tobacco smoke on periodontal stem cells using a multi-omics approach to understand gene regulation. This research studied primary human gingival mesenchymal stem cells (GMSCs) and periodontal ligament stem cells (PDLSCs) obtained from healthy donors. The cells were subjected to tobacco smoke, e-cigarette aerosol (both tobacco and menthol flavors), e-cigarette liquid (both tobacco and menthol flavors), or untreated conditions using an in vitro exposure system. RNA sequencing and bioinformatics analysis were used to profile the transcriptome and identify differential gene expression. Additionally, chromatin immunoprecipitation sequencing (ChIP-seq) was used to conduct genome-wide histone modification mapping for H3K27me3. Transcriptome profiling was combined with histone modification characterization to understand gene regulatory mechanisms. The study compared the effects of smoke versus e-cigarette, aerosol versus liquid exposure, and tobacco versus menthol flavor on gene expression and epigenetic landscapes in the two oral stem cell populations. The use of tobacco smoke caused damage to the DNA and nucleus in GMSCs, as well as mitochondrial dysfunction in PDLSCs. Regarding e-cigarettes, the aerosol and liquid affected non-coding RNA expression differently. The chemokine CXCL2 was found to be downregulated by aerosol but upregulated by liquid in GMSCs. An integrative analysis revealed that the upregulation of CXCL2 caused by e-liquid involved reduced H3K27me3 and activation of distal enhancers. On the other hand, aerosol exposure maintained H3K27me3 levels, while direct e-liquid exposure resulted in genome-wide reductions in H3K27me3, particularly in enhancer regions. Overall, the specific delivery methods and components of e-cigarettes caused unique changes in the transcriptome and epigenome of oral stem cells. E-cigarettes affect oral stem cells differently than tobacco smoke. Their aerosol and liquid have varying impacts on gene expression and regulatory landscapes in oral cells. Multi-omics approaches are important to understanding the molecular changes caused by e-cigarette components. This can help with toxicological assessments and determine their impact on periodontal health. Transcriptome and epigenome profiling are powerful tools to examine the unique molecular mechanisms involved in cellular responses to e-cigarettes.

Investigating Behavioral and Neuronal Changes in Adolescent Mice Following Prenatal Exposure to Electronic Cigarette (E-Cigarette) Vapor Containing Nicotine.

A substantial percentage of pregnant smokers stop using traditional cigarettes and switch to alternative nicotine-related products such as e-cigarettes. Prenatal exposure to tobacco increases the risk of psychiatric disorders in children. Adolescence is a complex phase in which higher cognitive and emotional processes undergo maturation and refinement. In this study, we examined the behavioral and molecular effects of first-trimester prenatal exposure to e-cigarettes. Adult female mice were divided into normal air, vehicle, and 2.5%-nicotine-exposed groups. Our analyses indicated that the adolescents in the 2.5%-nicotine-exposed group exhibited a significant lack of normal digging behavior, elevated initial sucrose intake, and reduced recognition memory. Importantly, we identified a substantial level of nicotine self-administration in the 2.5%-nicotine-exposed group. At a molecular level, the mRNAs of metabotropic glutamate receptors and transporters in the nucleus accumbens were not altered. This previously undescribed work indicates that prenatal exposure to e-cigarettes might increase the risk of nicotine addiction during adolescence, reduce cognitive capacity, and alter normal adolescent behavior. The outcome will aid in translating research and assist healthcare practitioners in tackling addiction and mental issues caused by toxicological exposure. Further, it will inform relevant policymaking, such as recommended taxation, labeling e-cigarette devices with more detailed neurotoxic effects, and preventing their sale to pregnant women and adolescents.

Impairment of Endothelial Function by Cigarette Smoke and e-Cigarette Aerosol Requires RAGE.

Impairment of Endothelial Function by Cigarette Smoke and e-Cigarette Aerosol Requires RAGE.

Effects of E-Cigarette Vapor Smoke on Pulmonary Alveoli in Rattus norvegicus Lungs

Introduction: Vapor is considered a safer alternative to tobacco cigarettes because the high nicotine content is less. However, vapor still contains substances that are classified as toxic to humans. Short-term exposure to vapors from liquids can induce an inflammatory response in the lungs and cause oxidative stress. This study aimed to determine the effects of e-cigarette vapor smoke on pulmonary alveoli in Rattus norvegicus lungs. Methods: This was an experimental study on 32 adult male Rattus norvegicus rats. They were divided into two groups exposed to nicotine-containing vapor smoke two times a day for one and three months, respectively, and one group as control. After vapor exposure, the lung tissues of the rats were taken and then subjected to histopathological examination under a microscope. Results: After exposure for one month, epithelial and endothelial cells degenerated, characterized by a decrease in collagen and elastin fibers in the extracellular matrix. For three months, there were changes, the alveolar membrane had no nucleus, the surrounding endothelial cells were not visible due to damage to the extracellular matrix, the alveolar lumen had widened, causing edema in the lumen of the alveoli, and the alveoli wall was destroyed. Therefore, the connection between the alveoli was stretched. Conclusion: This study found that short-term exposure to nicotine vapor causes damage to the alveoli membrane.

Pharmacological effects of nicotine salts on dopamine release in the nucleus accumbens.

With the growing number of individuals regularly using e-cigarettes, it has become increasingly important to understand the psychobiological effects of nicotine salts. Nicotine increases the release of dopamine (DA) into the nucleus accumbens (NAc), causing feelings of satisfaction. However, the differences in the DA-increasing effects of different nicotine salts have not been reported. In this study, we used a G protein-coupled receptor-activated DA fluorescent probe (GRABDA1m) and optical fiber photometric recording equipment to monitor the dynamic changes and kinetics of DA release in the NAc of mice exposed to different e-cigarette aerosols, including nicotine, nicotine benzoate, nicotine tartrate, nicotine lactate, nicotine levulinic acid, nicotine malate, and nicotine citrate. The results of this study were as follows: 1) Different types of nicotine salts could increase the release of DA in the NAc. 2) The slopes and half-effective concentrations of the fitted curves were different, suggesting that each nicotine salt had a difference in the efficiency of increasing DA release with concentration changes. 3) The absorption rates of different nicotine salts containing the same original nicotine concentration were significantly different by measuring the blood nicotine content. The effect of nicotine salts on increasing DA was directly proportional to the blood nicotine level. In conclusion, by observing the effects of nicotine salts on DA release in real time in vivo, differences in the pharmacological effects of nicotine salts are revealed to better understand the mechanism underlying the regulatory effects of nicotine salts on the brain.

Carcinogenic and non-carcinogenic health risk assessment of organic compounds and heavy metals in electronic cigarettes

E-cigarettes are now very popular in the world. Compared to traditional cigarettes, e-cigarettes are often considered safer and healthier. However, their safety remains controversial and requires further research and regulation. In this study, we aimed to understand the possible hazards to humans of four compounds (formaldehyde, acetaldehyde, acrolein, and acetone) and seven heavy metals (arsenic, cadmium, manganese, lead, copper, nickel, and chromium) contained in e-cigarette liquids and aerosols and perform a health risk assessment. We searched PubMed, CNKI, and other databases for relevant literature to obtain data on organic compounds and heavy metals in e-cigarette liquids and aerosols, and conducted acute, chronic, and carcinogenic risk assessments of various chemicals by different exposure routes. This study showed that exposure to four organic compounds and seven heavy metals in e-cigarette aerosols and e-liquids can cause varying levels of health risks in humans through different routes, with the inhalation route posing a higher overall risk than dermal exposure and oral intake. Various chemicals at high exposure doses can produce health risks beyond the acceptable range. E-cigarette designers must improve their products by changing the composition of the e-liquid and controlling the power of the device to reduce the health effects on humans.