E-cigarette Aerosol Research Articles

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.

Varied effects of tobacco smoke and e-cigarette vapor suggest that nicotine does not affect endothelium-dependent relaxation and nitric oxide signaling

Chronic smoking causes dysfunction of vascular endothelial cells, evident as a reduction of flow-mediated dilation in smokers, but the role of nicotine is still controversial. Given the increasing use of e-cigarettes and other nicotine products, it appears essential to clarify this issue. We studied extracts from cigarette smoke (CSE) and vapor from e-cigarettes (EVE) and heated tobacco (HTE) for their effects on vascular relaxation, endothelial nitric oxide signaling, and the activity of soluble guanylyl cyclase. The average nicotine concentrations of CSE, EVE, and HTE were 164, 800, and 85 µM, respectively. At a dilution of 1:3, CSE almost entirely inhibited the relaxation of rat aortas and porcine coronary arteries to acetylcholine and bradykinin, respectively, while undiluted EVE, with a 15-fold higher nicotine concentration, had no significant effect. With about 50% inhibition at 1:2 dilution, the effect of HTE was between CSE and EVE. Neither extract affected endothelium-independent relaxation to an NO donor. At the dilutions tested, CSE was not toxic to cultured endothelial cells but, in contrast to EVE, impaired NO signaling and inhibited NO stimulation of soluble guanylyl cyclase. Our results demonstrate that nicotine does not mediate the impaired endothelium-dependent vascular relaxation caused by smoking.

Estimation of Health Risks Caused by Metals Contained in E-cigarette Aerosol through Passive Vaping

Estimation of Health Risks Caused by Metals Contained in E-cigarette Aerosol through Passive Vaping

Sex-specific lung inflammation and mitochondrial damage in a model of electronic cigarette exposure in asthma.

The prevalence of electronic cigarette (EC) use among adult with asthma has continued to increase over time, in part due to the belief of being less harmful than smoking. However, the extent of their toxicity and the involved mechanisms contributing to the deleterious impact of EC exposure on patients with preexisting asthma have not been delineated. In the present project, we tested the hypothesis that EC use contributes to respiratory damage and worsening inflammation in the lungs of patients with asthma. To define the consequences of EC exposure in established asthma, we used a mouse model with/without preexisting asthma for short-term exposure to EC aerosols. C57/BL6J mice were sensitized and challenged with a DRA (dust mite, ragweed, Aspergillus fumigates, 200 µg/mL) mixture and exposed daily to EC with nicotine (2% nicotine in 30:70 propylene glycol: vegetable glycerin) or filtered air for 2 wk. The mice were evaluated at 24 h after the final EC exposure. After EC exposure in asthmatic mice, lung inflammatory cell infiltration and goblet cell hyperplasia were increased, whereas EC alone did not cause airway inflammation. Our data also show that mitochondrial DNA (mtDNA) content and a key mtDNA regulator, mitochondrial transcription factor A (TFAM), are reduced in asthmatic EC-exposed mice in a sex-dependent manner. Together, these results indicate that TFAM loss in lung epithelium following EC contributes to male-predominant sex pathological differences, including mitochondrial damage, inflammation, and remodeling in asthmatic airways.NEW & NOTEWORTHY Respiratory immunity is dysregulated in preexisting asthma, and further perturbations by EC use could exacerbate asthma severity. However, the extent of their toxicity and the involved mechanisms contributing to the deleterious impact of EC exposure on patients with preexisting asthma have not been delineated. We found that EC has unique biological impacts in lungs and potential sex differences with loss of TFAM, a key mtDNA regulator, in lung epithelial region from our animal EC study.

Making Every Single Puff Count-Simple and Sensitive E-Cigarette Aerosol Sampling for GCxIMS and GC-MS Analysis.

The analysis of the aerosol from tobaccoless electronic cigarettes (e-cigarettes) is an important part of understanding their impact on human health, yet sampling aerosol from e-cigarettes is still considered a challenge. It lacks a standard method for research and quality control and there are a variety of methods. However, few are simple and inexpensive, and none have been suggested for the use with gas chromatography coupled ion mobility spectrometry (GCxIMS). This work presents and evaluates such a setup made from standard lab equipment to quickly collect a quantitative sample from the aerosol of a single puff (5 s totaling 125 mL). The aerosol condensates directly in the cooled headspace (HS) vial, which is analyzed in the HS-GCxIMS or mass spectrometer (HS-GC-MS). The combined use of GC-MS and GCxIMS allows the simple and sensitive identification of unknown substances in complex mixtures and the identification of degradation products in the aerosols. A calibration of 26 flavor compounds (0.2-20 µg/g) was created using single puffs of a spiked, flavorless commercial refill solution and 2-alkanones as internal standards. This sensitive but easily reproducible setup enables a wide range of further investigations, even for labs that were previously unable to afford it.

Determination of chemical constituent yields in e-cigarette aerosol using partial and whole pod collections, a comparative analysis.

Literature reports the chemical constituent yields of electronic nicotine delivery systems (ENDS) aerosol collected using a range of aerosol collection strategies. The number of puffs to deplete an ENDS product varies widely, but collections often consist of data from the first 50-100 puffs. However, it is not clear whether these discrete puff blocks are representative of constituent yields over the life of a pod. We aimed to assess the effect of differing aerosol collection strategies on reported yields for select chemical constituents in the aerosol of closed pod-based ENDS products. Constituents analyzed were chosen to reflect important classes of compounds from the Final Premarket Tobacco Product Application Guidance. Yields were normalized to total device mass loss (DML). Collection strategies that consisted of partial pod collection were valid for determining yields of constituents whose DML normalized yields were consistent for the duration of pod life. These included primary aerosol constituents, such as propylene glycol, glycerol, and nicotine, and whole pod yields could be determined from initial puff blocks. However, changes were observed in the yields of some metals, some carbonyl compounds, and glycidol over pod life in a chemical constituent and product dependent manner. These results suggest that collection strategies consisting of initial puff block collections require validation per chemical constituent/product and are not appropriate for chemical constituents with variable yields over pod life. Whole pod collection increased sensitivity and accuracy in determining metal, carbonyl, and glycidol yields compared to puff block-based collection methodologies for all products tested.

Differential Toxicity of Electronic Cigarette Aerosols Generated from Different Generations of Devices In Vitro and In Vivo.

Electronic cigarettes (e-cigs) have become increasingly popular, especially among youth, raising concerns about their potential health risks. JUUL and Tank devices are two common types of e-cigs that deliver aerosols with varying nicotine levels and flavors. However, the differences in the aerosols generated from different devices and their corresponding cytotoxicity and pulmonary injury effects remain poorly understood. This study addresses these knowledge gaps by characterizing the aerosols of JUUL and Tank e-cig devices and testing their toxic effects on THP-1 and BEAS-2B human cell lines as well as the C57BL/6J mouse model. In our study, the lower-voltage device, the 3.7 V JUUL generates 2.72 mg/puff aerosols by using e-liquid containing 3% nicotine salt (i.e., nicotine benzoate), which is less than the 11.06 mg/puff aerosols generated by the 7.5 V Tank using e-liquid containing 2.4% freebase nicotine. Yet, the cytotoxicity results reveal that JUUL aerosols induced higher toxicity and increased production of pro-inflammation cytokines compared to Tank aerosols per puff. Additionally, we observed that JUUL induced more severe pulmonary inflammation and DNA damage compared to Tank after normalizing for cotinine, a nicotine metabolite, in vivo. Our findings suggest that the device design plays a more important role in e-cig aerosol-induced toxicity than the composition of the e-liquid or voltage. These results provide valuable insights into the health risks associated with various electronic-cig devices and offer an approach for evaluating them.

E-cigarette vapor renders neutrophils dysfunctional due to filamentous actin accumulation

Electronic cigarette (e-cigarette) use continues to rise despite concerns of long-term effects, especially the risk of developing lung diseases such as chronic obstructive pulmonary disease. Neutrophils are central to the pathogenesis of chronic obstructive pulmonary disease, with changes in phenotype and function implicated in tissue damage. We sought to measure the impact of direct exposure to nicotine-containing and nicotine-free e-cigarette vapor on human neutrophil function and phenotype. Neutrophils were isolated from the whole blood of self-reported nonsmoking, nonvaping healthy volunteers. Neutrophils were exposed to 40 puffs of e-cigarette vapor generated from e-cigarette devices using flavorless e-cigarette liquids with and without nicotine before functions, deformability, and phenotype were assessed. Neutrophil surface marker expression was altered, with CD62L and CXCR2 expression significantly reduced in neutrophils treated with e-cigarette vapor containing nicotine. Neutrophil migration to IL-8, phagocytosis of Escherichia coli and Staphylococcus aureus pHrodo bioparticles, oxidative burst response, and phorbol 12-myristate 13-acetate-stimulated neutrophil extracellular trap formation were all significantly reduced by e-cigarette vapor treatments, independent of nicotine content. E-cigarette vapor induced increased levels of baseline polymerized filamentous actin levels in the cytoplasm, compared with untreated controls. The significant reduction in effector neutrophil functions after exposure to high-power e-cigarette devices, even in the absence of nicotine, is associated with excessive filamentous actin polymerization. This highlights the potentially damaging impact of vaping on respiratory health and reinforces the urgency of research to uncover the long-term health implications of e-cigarettes.

Inhalation of electronic cigarettes slightly affects lung function and inflammation in mice.

Electronic cigarettes have become increasingly popular, but the results of previous studies on electronic cigarette exposure in animals have been equivocal. This study aimed to evaluate the effects of electronic cigarette smoke (ECS) and cigarette smoke (CS) on lung function and pulmonary inflammation in mice to investigate whether electronic cigarettes are safer when compared to cigarettes. 32 specific pathogen-free BALB/c male mice were randomly grouped and exposed to fresh air (control), mint-flavored ECS (ECS1, 6mg/kg), cheese-flavored ECS (ECS2, 6mg/kg), and CS (6mg/kg). After 3weeks exposure to ECS or CS, we measured lung function (PIF and Penh) and blood oxygen saturation. The levels of TNF-α and IL-6 in the bronchoalveolar lavage fluid (BALF) and serum were measured using ELISA. HE staining was performed to observe the pathological changes in the lung tissues. The levels of IL-6 in BALF and serum, and TNF-α in BALF, were elevated similarly in the ECS and CS groups compared to the control group. Significant elevation was observed in serum TNF-α levels in the CS group. The total count of cells in BALF were increased after ECS1 exposure and CS exposure. PIF and oxygen saturation decreased, and Penh increased markedly in the CS group but not in the ECS groups. Compared with the ECS groups, mice in the CS group had widened lung tissue septa and increased inflammatory cell infiltration. However, we did not detect significant differences between mint-flavored and cheese-flavored e-cigarettes in our study. Overall, our findings suggested that both ECS and CS impair lung function and histopathology while promoting inflammation. In contrast, ECS has a less negative impact than CS.

Third-Hand Exposure to E-Cigarette Vapour Induces Pulmonary Effects in Mice.

In the last decade, e-cigarette usage has increased, with an estimated 82 million e-cigarette users globally. This is, in part, due to the common opinion that they are "healthier" than tobacco cigarettes or simply "water vapour". Third-hand e-vapour exposure is the chemical residue left behind from e-cigarette aerosols, which is of concern due to its invisible nature, especially among young children. However, there is limited information surrounding third-hand e-vapour exposure. This study aimed to investigate the pulmonary effects of sub-chronic third-hand e-vapour exposure in a murine model. BALB/c mice (4 weeks of age) were exposed to a towel containing nicotine free (0 mg) e-vapour, nicotine (18 mg) e-vapour, or no e-vapour (sham) and replaced daily for 4 weeks. At the endpoint, lung function was assessed, and bronchoalveolar lavage fluid and lungs were collected to measure inflammation and fibrosis. Mice exposed to third-hand e-vapour without nicotine had alveolar enlargement compared to sham exposed controls. Mice exposed to third-hand e-vapour with nicotine had reduced bronchial responsiveness to provocation, increased epithelial thickening in large airways, increased epithelial layers in small airways, alveolar enlargement, and increased small airway collagen deposition, compared to sham exposed controls. In conclusion, our study shows that third-hand e-vapour exposure, particularly in the presence of nicotine, negatively affects the lung health of mice and highlights the need for greater public awareness surrounding the dangers of third-hand exposure to e-cigarette vapour.

Gestational dependent responses to second hand smoke (SHS) and e-cigarette vapor in mouse pregnancies

Gestational dependent responses to second hand smoke (SHS) and e-cigarette vapor in mouse pregnancies

Preliminary study on the E-liquid and aerosol on the neurobehavior of C. elegans

E-cigarettes, also known as electronic nicotine delivery systems (ENDS), are mainly used among adolescents and young adults. Similar to traditional cigarettes, different concentrations of nicotine are also added to E-cigarette's liquid (E-liquid), but due to the supplementation of chemicals such as propylene glycol (PG), vegetable glycerin (VG) and flavors, it is difficult to determine the risk after using E-cigarettes. And given to the specificity of the aerosol particle composition and atomization process of E-cigarettes, it is necessary to assess the neurotoxic effects of long-term E-cigarettes use. In this study, two commercial nicotine-containing (5%) and nicotine-free E-liquids were diluted to investigate the neurobehavioral changes and addictive tendencies of developing C. elegans after sub-chronic exposure to E-liquid. The results showed that sub-chronic exposure of E-liquid could lead to impaired growth and development of nematodes, abnormal general neuromotor behavior and advanced learning and memory behavior, and nicotine-containing E-liquid could also lead to increased addiction tendency of nematodes. Although the damage effect of nicotine free E-liquid is smaller than that of the nicotine-containing group, its toxic effect cannot be ignored. Further analysis of the neurotoxicity mechanism found that redox imbalance-mediated mitochondrial stress and aging may be important causes of E-liquid-induced biological damage. The biosafety of e-cigarette aerosols was also included in the assessment. The study found that the heated atomization process did not alter the E-liquid components, and E-cigarette aerosols still have the effect of interfering with the growth and development of nematodes and neurobehavior, and its addictive nature is also of concern. This study can provide new ideas for future studies on the neurotoxic effects and safety assessment of the E-cigarettes, and provide theoretical reference for the study on the injury mechanism of E-cigarettes.