Effects Of Electronic Cigarettes Research Articles

The paradox of the safer cigarette: understanding the pulmonary effects of electronic cigarettes.

Electronic cigarette (e-cigarette) use continues to rise globally. E-cigarettes have been presented as safer alternatives to combustion cigarettes that can mitigate the harm associated with tobacco products; however, the degree to which e-cigarette use itself can lead to morbidity and mortality is not fully defined. Herein we describe how e-cigarettes function; discuss the current knowledge of the effects of e-cigarette aerosol on lung cell cytotoxicity, inflammation, anti-pathogen immune response, mucociliary clearance, oxidative stress, DNA damage, carcinogenesis, matrix remodeling, and airway hyperresponsiveness; and summarize the impact on lung diseases, including COPD, respiratory infection, lung cancer, and asthma. We highlight how the inclusion of nicotine or flavoring compounds in e-liquids can impact lung toxicity. Finally, we consider the paradox of the safer cigarette - the toxicities of e-cigarettes that can mitigate their potential to serve as a harm reduction tool in the fight against traditional cigarettes, and we summarize the research needed in this under-investigated area.

Multidimensional assessment of the biological effects of electronic cigarettes on lung bronchial epithelial cells

Cigarette smoke (CS) exposure is known to cause injury to respiratory tract epithelial cells and is a contributing factor in the development of chronic obstructive pulmonary disease and lung cancer. Electronic cigarettes (e-cigarettes) are gaining popularity as a potential substitute for conventional cigarettes due to their potential for aiding smoking cessation. However, the safety of e-cigarettes remains uncertain, and scientific evidence on this topic is still limited. In this study, we aimed to investigate the effects of CS and e-cigarette smoke (ECS) of different flavors on human lung bronchial epithelial cells. Real-time smoke exposure was carried out using an air–liquid interface system, and cell viability was assessed. RNA-Seq transcriptome analysis was performed to compare the differences between CS and ECS. The transcriptome analysis revealed a significantly higher number of differentially expressed genes in CS than in ECS. Moreover, the impact of mint-flavored e-cigarettes on cells was found to be greater than that of tobacco-flavored e-cigarettes, as evidenced by the greater number of differentially expressed genes. These findings provide a reference for future safety research on traditional cigarettes and e-cigarettes, particularly those of different flavors. The use of omics-scale methodologies has improved our ability to understand the biological effects of CS and ECS on human respiratory tract epithelial cells, which can aid in the development of novel approaches for smoking cessation and lung disease prevention.

The Toxicological Effects of e-Cigarette Use in the Upper Airway: A Scoping Review.

While evidence continues to emerge on the negative health effects of electronic cigarettes (e-cigarettes) on the lungs, little is known regarding their deleterious effects on the upper airway. The purpose of this review is to summarize the toxicological effects of e-cigarettes, and their components, on the upper airway. PubMed, SCOPUS, EMBASE databases. Systematic searches were performed in accordance with Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines from 2003 to 2023. Studies were included if they investigated the toxicological effects of e-cigarette exposure on human or animal upper airway tissue. Two authors independently screened, reviewed, and appraised all included articles. A total of 822 unique articles were identified, of which 53 met inclusion criteria and spanned subsites including the oral cavity (22/53 studies), nasal cavity/nasopharynx (13/53), multiple sites (10/53), larynx (5/53), trachea (2/53), and oropharynx (1/53). The most commonly observed consequences of e-cigarette use on the upper airway included: proinflammatory (15/53 studies), histological (13/53), cytotoxicity (11/53), genotoxicity (11/53), and procarcinogenic (6/53). E-cigarette humectants independently induced toxicity at multiple upper airway subsites, however, effects were generally amplified when flavoring(s) and/or nicotine were added. Across almost all studies, exposure to cigarette smoke exhibited increased toxicity in the upper airway compared with exposure to e-cigarette vapor. Current data suggestthat while e-cigarettes are generally less harmful than traditional cigarettes, they possess a distinct toxicological profile that is enhanced upon the addition of flavoring(s) and/or nicotine. Future investigations into underexamined subsites, such as the oropharynx and hypopharynx, are needed to comprehensively understand the effects of e-cigarettes on the upper airway.

Abstract 105: Sex Difference in Brain Energy Metabolism After Electronic Cigarette Vape Exposure May Contribute to Worsened Stroke Injury in Rats

Introduction: Electronic cigarettes (EC) are battery-powered nicotine delivery devices that have gained popularity as alternatives to tobacco cigarettes for young smokers and smokers trying to cease. Because of its relative novelty, our understanding about the effects of EC vaping on stroke outcome is limited. Here we aim to investigate the effects of EC on energy metabolism in the brain and on stroke outcome in animals of both sexes. Methods: Female and male Sprague-Dawley rats (2-3 months old; n=8) were randomly assigned to either air or EC vapor (5% nicotine Juul pods) exposure for 16 nights using the EcigAero-TM Aerosol Exposure Apparatus. After the exposure period, the rats were divided into two cohorts. The brains were collected from the first cohort of rats for unbiased metabolomic (Metabolon Inc.) or Western blot analysis. The second cohort underwent transient middle cerebral artery occlusion (tMCAO; 90 min) or sham surgery and was survived for 21 days. During the post-tMCAO/sham survival, cognition was assessed using the Morris water maze followed by brain collection for histopathological analysis. Results: Metabolomic analysis showed substantial changes in glycolytic metabolites in EC-exposed female rats in relation to air controls, implying altered brain energetics. In EC-exposed female animals, a significant increase (p<0.05) in glucose, glucose 6-phosphate, fructose-6-phosphate, and fructose 1-6 diphosphate was noted compared to air controls. However, such changes were not seen in EC-exposed male rats. Quantification of infarct volume demonstrated that, compared to air rats, EC-exposed rats displayed a significantly increased infarct volume in female rats while showing a trend of increase in male rats. In female rats, infarct volumes were 86 ± 19 mm 3 and 151 ± 25 mm 3 for air and EC groups, respectively, a significant difference (p<0.05). In the male rat air group, tMCAO resulted in an infarct volume of 80 ± 37 mm 3 , while EC yielded 130 ± 38 mm 3 . Behavioral testing showed worsened post-stroke cognitive outcome in EC groups compared to air groups in rats of both sexes. Conclusion: EC vape exposure, even for as short as two weeks, impacts glucose metabolism and worsens post-stroke cognitive deficits in female more than male rats.

Vaping and the Brain: Effects of Electronic Cigarettes and E-Liquid Substances.

Vaping and the Brain: Effects of Electronic Cigarettes and E-Liquid Substances.

Effectiveness of Electronic Cigarettes in Smoking Cessation

Background: Numerous investigations have been carried out to evaluate the effectiveness of electronic cigarettes in aiding individuals to quit smoking and to ascertain the security and feasibility of utilizing them as an alternative to traditional tobacco cigarettes. Research expenditures must be allocated significantly to the product's evaluation in order to perform an exhaustive examination of its usage prevalence, which includes its use as a smoking cessation tool as well as its adoption as a regular smoking behavior. Methods: The current cross-sectional study was conducted at King Abdulaziz University's Faculty of Medicine in the first few months of 2022. There were 263 students that participated in the study in total. In the previous study, the researchers used an anonymous, standardized questionnaire, which they confirmed and put into practice. The concept was assessed and put to the test using statistical analysis using "IBM SPSS Statistics version 20.0." Results: The study included a sample of 263 students, of whom 39.1% were classified as female and 60.9% as male. 49 of the 133 pupils in total were determined to have smoked in the past, while the remaining 86 were smokers currently. Regarding the sort of smoking habit used, it was discovered that 23 people (17.3%) used tobacco cigarettes, whereas 90 people (67.7%) used e-cigarettes or vapes. Furthermore, twenty people (15%) disclosed using other tobacco products. Of those who smoke, 36.1% use electronic cigarettes, or e-cigarettes, to cut back on tobacco use. There was a statistically significant link (P<0.05) found between the individuals' marital status and academic year and their regular use of e-cigarettes or vape. Conclusion: The current study found that among a cohort of medical students who successfully quit smoking through its implementation, the use of electronic cigarettes (e-cigarettes) or vaping is a contributing factor in their success. Moreover, it is considered a transitional strategy for individuals who want to cut back on their total tobacco consumption.

Does vaping increase the likelihood of SARS-CoV-2 infection? Paradoxically yes and no.

Data on the relationship between electronic cigarettes (ECs) and SARS-CoV-2 infection are limited and contradictory. Our objectives were to investigate the impact of EC aerosols on SARS-CoV-2 infection of human bronchial epithelial cells and identify the causative chemical(s). Fully differentiated human bronchial epithelial tissues (hBETs) were exposed at the air-liquid interface (ALI) to aerosols produced from JUUL "Virginia Tobacco" and BLU ECs, as well as nicotine, propylene glycol (PG), vegetable glycerin (VG), and benzoic acid, and infection was then evaluated with SARS-CoV-2 pseudoparticles. Pseudoparticle infection of hBETs increased with aerosols produced from PG/VG, PG/VG plus nicotine, or BLU ECs; however, JUUL EC aerosols did not increase infection compared with controls. Increased infection in PG/VG alone was due to enhanced endocytosis, whereas increased infection in PG/VG plus nicotine or in BLU ECs was caused by nicotine-induced elevation of the aerosol's pH, which correlated with increased transmembrane protease, serine 2 (TMPRSS2) activity. Notably, benzoic acid in JUUL aerosols mitigated the enhanced infection caused by PG/VG or nicotine, offering protection that lasted for at least 48 h after exposure. In conclusion, the study demonstrates that EC aerosols can impact susceptibility to SARS-CoV-2 infection depending on their specific ingredients. PG/VG alone or PG/VG plus nicotine enhanced infection through different mechanisms, whereas benzoic acid in JUUL aerosols mitigated the increased infection caused by certain ingredients. These findings highlight the complex relationship between ECs and SARS-CoV-2 susceptibility, emphasizing the importance of considering the specific aerosol ingredients when evaluating the potential effects of ECs on infection risk.NEW & NOTEWORTHY Data on the relationship between electronic cigarettes (ECs) and SARS-CoV-2 infection are limited and contradictory. We investigated the impact of EC aerosols and their ingredients on SARS-CoV-2 infection of human bronchial epithelial cells. Our data show that specific ingredients in EC aerosols impact the susceptibility to SARS-CoV-2 infection. Propylene glycol (PG)/vegetable glycerin (VG) alone or PG/VG plus nicotine enhanced infection through different mechanisms, whereas benzoic acid in JUUL aerosols mitigated the increased infection caused by these ingredients.

Electronic cigarette use and respiratory symptoms in the French population-based Constances cohort

BackgroundKnowledge about the consequences of electronic cigarette (EC) use on respiratory health is still limited. We aimed to assess whether EC use is associated with the occurrence of asthma symptoms and chronic bronchitis among the French adult population, with a specific focus on never combustible cigarettes (CC) smokers. We further investigated whether the association differed in men and women. MethodsConstances is a population-based cohort of adults aged 18–69 years at inception. We analyzed baseline data collected in 136,276 participants recruited in 2015–2019. Associations of current and former EC use with respiratory symptoms (asthma symptom score and chronic bronchitis) were assessed, controlling for CC smoking, cannabis use, demographics, education and body mass index (BMI). ResultsIncreased frequencies of respiratory symptoms were observed in both current and former EC users (for the asthma symptom score, adjusted mean score ratio (aMSR): 1.34 [95 % confidence interval: 1.28−1.41] and 1.39 [1.33−1.45], respectively; for chronic bronchitis, adjusted prevalence ratio (aPR): 1.27 [1.19−1.36] and 1.40 [1.32−1.48], respectively). Among never CC smokers, ever EC use was associated with an increased asthma symptom score in both men and women (aMSR = 1.44 [1.09−1.90] and 1.36 [1.01−1.83], respectively), and with a higher prevalence of chronic bronchitis only in women (aPR = 1.97 [1.27−3.05]). ConclusionEC use is associated with symptoms of asthma and chronic bronchitis, independently of CC smoking and cannabis use. The fact that these associations are observed among individuals who have never smoked tobacco adds further evidence of the deleterious effects of EC on respiratory health.

Electronic cigarette vapor disrupts key metabolic pathways in human lung epithelial cells

The steady increase in the use of electronic cigarettes (ECs) has reached an epidemic level, increasing mortality and morbidity, mainly due to pulmonary toxicity. Several mechanisms are involved in EC-induced toxicity, including oxidative stress and increased inflammation. Concurrently, the integrity of cellular metabolism is essential for cellular homeostasis and mitigation of toxic insults. However, the effects of EC on cellular metabolism remain largely unknown. In this study, we investigated the metabolic changes induced by EC in human lung epithelial cells (A549) using an untargeted metabolomics approach. A549 cells were exposed to increasing EC vapor extract concentrations, and cell viability, oxidative stress, and metabolomic changes were assessed. Our findings show that ECs induce cell death and increase oxidative stress in a concentration-dependent manner. Metabolomic studies demonstrated that ECs induce unique metabolic changes in key cellular metabolic pathways. Our results revealed that exposure to ECs induced clear segregation in metabolic responses which is driven significantly by number of essential metabolites such as aminoacids, fatty acids, glutathione, and pyruvate. Interstingly, our metabolomics results showed that each concentration of ECs induced unqiues pattern of metabolic changes, suggesting the complexity of ECs induced cytotoxcity. Disrupted metabolites were linked to essential cellular pathways, such as fatty acid biosynthesis, as well as glutathione, pyruvate, nicotinate and nicotinamide, and amino acid metabolisms. These results highlight the potential adverse effects of ECs on cellular metabolism and emphasize the need for further research to fully understand the long-term consequences of EC use. Overall, this study demonstrates that ECs not only induce cell death and oxidative stress but also disrupt cellular metabolism in A549 lung epithelial cells.

Electronic Cigarettes on Sperm Quality: Review in Animal and Human Study

Electronic cigarettes that are currently popular are used as nicotine replacement therapy. There are several substances contained in electronic cigarette liquid that have carcinogenic effects. These substances can also increase free radicals which in turn can cause oxidative stress. Nicotine, propylene glycol, and glycerin can cause disturbances in male reproductive function. Infertility can occur due to lifestyle factors, one of which is smoking. Nicotine found in cigarettes can reduce sperm quality, including concentration, mobility, viability, and sperm morphology. The purpose of this study was to determine the effect of electronic cigarettes on sperm quality. The research method uses a literature review system. The twelve studies that are in accordance with the topic of discussion are experimental studies on mice and rats, two studies on human, and one study on both human and rats. Five journals showed a significant decrease in sperm count and testosterone serum level, three other journals showed a significant decrease in sperm morphology and viability, six journals showed a decrease in sperm motility, seven journals showed a significant impairment of testis histological structure, four journals showed a decrease of steroidogenesis enzymes, and one journal showed a significant increase of DNA fragmentation due to the use of electronic cigarettes. Electronic cigarettes had an effect on sperm quality.

The Relationship between Knowledge of the Effects of Electronic Cigarettes on Oral Health and the Use of Electronic Cigarettes among Students at the University of Jember

Electronic cigarettes, commonly known as Vapes, are electronic devices that resemble conventional cigarettes and can produce vapor as a result of liquid vaporization. The use of electronic cigarettes can have adverse effects on health, especially on oral and dental health, even though the vapor from electronic cigarettes does not leave stains on the tooth surface. Electronic cigarettes have a more significant impact on soft tissue damage, such as ulcers in the buccal, gingival, and palatal mucosa or damage to periodontal tissue. The purpose of this study is to determine the relationship between knowledge about the effects of electronic cigarettes on oral and dental health and the use of electronic cigarettes among students at the University of Jember. This study is analytical observational research with a cross-sectional approach using purposive sampling. There is a significant relationship between knowledge about electronic cigarettes' impact on oral and dental health and the use of electronic cigarettes among University of Jember students. This can be attributed to the presence of Propylene Glycol in electronic cigarettes, which has detrimental effects on enamel and soft oral cavity tissues. Hence, there is a connection between knowledge about the impact of electronic cigarettes on oral and dental health and the use of electronic cigarettes among University of Jember students. Keywords: dental and oral health, electric cigarettes, knowledge

The effects of e-cigarette use on the oral microbiome.

To investigate the effects of electronic cigarette (EC) use on the oral microbiome and gingival inflammation. Saliva and gingival crevicular fluid samples were collected from 150 adult humans between 18 and 34 years in age (50% EC users). Exclusion criteria included professional dental cleaning, antibiotic, or corticosteroid therapy in the last 3 months. Convenience sampling occurred between June 2017 and October 2018. Clinical gingival inflammation was recorded by a single operator using a novel 4-point scale. RNA sequencing was used to determine microbial composition of samples (16S rRNA amplicon sequencing). Statistical analysis included synthesizing alpha and beta diversity using various indices, taxonomic differential abundance analysis, functional differential abundance analysis and mediation analysis. Taxonomic annotation was performed using QIIME2 with functional annotations generated using PICRUSt2. Age, sex, and frequency of tooth brushed were adjusted for. EC users exhibited significantly greater alpha diversity in microbial species and greater differences between EC users and users in beta diversity. Saliva samples were typically more diverse than subgingival samples. EC users demonstrated greater gingival inflammation when adjusted for age, sex and toothbrushing frequency. EC use may increase oral dysbiosis. Further clinical studies on the effects of EC use on the oral microbiome and oral diseases are recommended.

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.

Effects of Short-term Electronic(e)-Cigarette Aerosol Exposure in the Mouse Larynx.

The effects of electronic cigarettes (e-cigarettes) on the larynx are relatively unknown. This study examined the short-term effects of e-cigarette inhalation on cellular and inflammatory responses within the mouse laryngeal glottic and subglottic regions after exposure to pod-based devices (JUUL). Male C57BL6/J mice (8-9 weeks) were assigned to control (n = 9), JUUL flavors Mint (JMi; n = 10) or Mango (JMa; n = 10). JUUL mice were exposed to 2 h/day for 1, 5, and 10 days using the inExpose inhalation system. Control mice were in room air. Vocal fold (VF) epithelial thickness, cell proliferation, subglandular area and composition, inflammatory cell infiltration, and surface topography were evaluated in the harvested larynges. Mouse body weight and urinary nicotine biomarkers were also measured. Chemical analysis of JUUL aerosols was conducted using selective ion flow tube mass spectrometry. JUUL-exposed mice had reduced body weight after day 5. Urinary nicotine biomarker levels indicated successful JUUL exposure and metabolism. Quantitative analysis of JUUL aerosol indicated that chemical constituents differ between JMi and JMa flavors. VF epithelial thickness, cellular proliferation, glandular area, and surface topography remained unchanged after JUUL exposures. Acidic mucus content increased after 1 day of JMi exposure. VF macrophage and T-cell levels slightly increased after 10 days of JMi exposures. Short-term e-cigarette exposures cause minimal flavor- and region-specific cellular and inflammatory changes in the mouse larynx. This work provides a foundation for long-term studies to determine if these responses are altered with multiple e-cigarette components and concentrations. N/A Laryngoscope, 134:1316-1326, 2024.

Harmful effects of electronic cigarette on oral soft tissues mediated by dysbiosis: State of the art.

Harmful effects of electronic cigarette on oral soft tissues mediated by dysbiosis: State of the art.

The Role of Electronic Cigarettes in Dental Caries: A Scoping Review.

Dental caries, a predominant childhood and adolescence affliction, has numerous factors implicated in its pathogenesis. Electronic cigarettes (ECs) have recently gained popularity among the younger population. Various factors, such as the EC liquid composition and aerosols, are associated with the development of dental caries. This review explains numerous EC-related factors which may lead to dental caries. An electronic search was conducted in Medline (Pubmed), Scopus, and Embase databases to evaluate the original research investigating the role of ECs in developing dental caries. About 12 included studies in the review indicated that factors such as the composition of e-liquids and aerosols are significant in the progression of dental caries. Specifically, cariogenic sugars such as sucrose, fructose, glucose, aldehydes, and flavors such as menthol, cinnamon, and strawberry in the e-liquids contribute to dental caries. They are toxic to oral commensals such as Streptococcus gordonii, Streptococcus mitis, Streptococcus intermedius, and Streptococcus oralis and promote the proliferation of cariogenic pathogens such as Streptococcus mutans (S. mutans) which causes dental caries. However, further validation of the effects of ECs on the development of dental caries is warranted through clinical trials.

Comparative analyses of transcriptome sequencing and carcinogenic exposure toxicity of nicotine and 6-methyl nicotine in human bronchial epithelial cells

Electronic cigarettes have become a purported safer alternative to the conventional cigarettes in recent years. Nicotine is the main component of electronic cigarettes, and other nicotinic compounds are synthesized as alternatives to nicotine. However, scientific data on the potential health effects of electronic cigarettes are scarce. Herein, we evaluated the cytotoxicity of nicotine and its analog 6-methyl nicotine (6-MN) on human bronchial epithelial cells (BEAS-2B cells) in vitro. Furthermore, we performed transcriptome sequencing to systematically assess the effects of nicotine and 6-MN on BEAS-2B cells. The cytotoxicity assay revealed that BEAS-2B cells were more sensitive to 6-MN than to nicotine. Transcriptome sequencing revealed 1208 differentially expressed cancer-related proteins (CRP) in the 6-MN groups relative to that with CRP in the control group. In addition, 6-MN had a greater negative effect on the CRP expression than nicotine. Bioinformatic analysis revealed that the differentially expressed genes and proteins in the 6-MN group were significantly enriched in the cancer-related pathways, unlike those in the nicotine group. Further validations of some lung cancer-related proteins, such as NF-κB p65, EGFR, and MET, were conducted by immunoblotting and real-time PCR, which revealed that 6-MN may have a greater negative effect on tumor development and metastasis than nicotine. Taken together, our findings suggest that new electronic cigarettes with 6-MN might offer some advantages over conventional electronic cigarettes containing nicotine.

A Comparative Study of the Effects of Electronic Cigarette and Traditional Cigarette on the Pulmonary Functions of C57BL/6 Male Mice.

Electronic cigarettes (E-cigs) are in a controversial state. Although E-cig aerosol generally contains fewer harmful substances than smoke from burned traditional cigarettes, aerosol along with other compounds of the E-cigs may also affect lung functions and promote the development of lung-related diseases. We investigated the effects of E-cig on the pulmonary functions of male C57BL/6 mice and reveal the potential underlying mechanisms. A total of 60 male C57BL/6 mice were randomly divided into four groups. They were exposed to fresh-air, traditional cigarette smoke, E-cig vapor with 12 mg/mL of nicotine, and E-cig with no nicotine for 8 weeks. Lung functions were evaluated by using quantitative analysis of the whole body plethysmograph, FlexiVent system, lung tissue histological and morphometric analysis, and RT-PCR analysis of mRNA expression of inflammation-related genes. In addition, the effects of nicotine and acrolein on the survival rate and DNA damage were investigated using cultured human alveolar basal epithelial cells. Exposure to E-cig vapor led to significant changes in lung functions and structures including the rupture of the alveolar cavity and enlarged alveolar space. The pathological changes were also accompanied by increased expression of interleukin-6 and tumor necrosis factor-α. The findings of the present study indicate that the safety of E-cig should be further evaluated. Some people currently believe that using nicotine-free E-cigs is a safe way to smoke. However, our research shows that E-cigs can cause lung damage regardless of whether they contain nicotine.

Electronic cigarettes can damage lingual papillae and taste buds. Can vitamins C and E supplementation reverse this damage?

AimsThis histological study focuses on the impact of electronic cigarette liquid (EC) on lingual papillae, especially taste buds, compare it to nicotine, and investigates the potential of vitamins in reversing these unwanted changes. Main methods40 adult male rats were allocated into 5 groups. Control injected saline intraperitoneally, electronic cigarettes group injected EC-liquid containing nicotine of dose (0.75 mg/kg), electronic cigarette group injected EC-liquid then supplemented orally with vitamins C and E, nicotine group injected pure nicotine of dose (0.75 mg/kg) and lastly nicotine group injected with pure nicotine of dose (0.75 mg/kg) then supplemented orally with vitamins C and E. Keratin surface area and the ratio between taste buds and its epithelial covering surface areas in fungiform papillae were measured. Key findingsHistological examination of EC group revealed abnormal epithelial stratification and mitotic figs. EC plus V group showed intact basal cell layer. N group showed better histological stratification than EC group. Fungiform and circumvallate papillae in EC and N groups showed distorted appearance of taste buds. Histomorphometry analysis showed a significant decrease in taste buds to epithelium surface areas in EC, nicotine, and EC plus V groups, p-value (<0.05). There was no significant difference between control and N plus V groups. SignificanceAdministration of vitamins C and E showed preservation of normal histological features of the lingual mucous membrane. EC caused striking damage to taste buds even after the administration of vitamins. The negative effects of electronic cigarettes are not confined only to the presence of nicotine.

Long-Term Impact of Daily E-cigarette Exposure on the Lungs of Asthmatic Mice.

Although the greater popularity of electronic cigarettes (EC) among asthmatics is alarming, there is limited knowledge of the long-term consequences of EC exposure in asthmatics. Mild asthmatic C57/BL6J adult male and female mice were established by intranasal insufflation with three combined allergens. The asthmatic and age and sex-matched' naïve mice were exposed to air, nicotine-free (propylene glycol [PG]/vegetable glycerin [VG]-only), or PG/VG+Nicotine, 4 hours daily for 3 months. The effects of EC exposure were accessed by measuring cytokines in bronchoalveolar lavage, periodic acid-schiff (PAS) staining, mitochondrial DNA copy numbers (mtCN), and the transcriptome in the lung. Significance was false discovery rate <0.2 for transcriptome and 0.05 for the others. In asthmatic mice, PG/VG+Nicotine increased PAS-positive cells and IL-13 compared to mice exposed to air and PG/VG-only. In naïve mice exposed to PG/VG+Nicotine and PG/VG-only, higher INF-γ was observed compared to mice exposed only to air. PG/VG-only and PG/VG+Nicotine had significantly higher mtCN compared to air exposure in asthmatic mice, while the opposite pattern was observed in non-asthmatic naïve mice. Different gene expression patterns were profoundly found for asthmatic mice exposed to PG/VG+Nicotine compared to PG/VG-only, including genes involved in mitochondrial dysfunction, oxidative phosphorylation, and p21-activated kinase (PAK) signaling. This study provides experimental evidence of the potential impact of nicotine enhancement on the long-term effects of EC in asthmatics compared to non-asthmatics. The findings from this study indicate the potential impact of EC in asthmatics by addressing multiple biological markers. The long-term health outcomes of EC in the susceptible group can be instrumental in supporting policymaking and educational campaigns and informing the public, healthcare providers, and EC users about the underlying risks of EC use.