Explore the vast range of titles available.

E-cigarettes with cooling flavours have diversified in ways that complicate tobacco control with the emergence of: (1) Ice-hybrid flavours (eg, ‘Raspberry Ice’) that combine cooling and fruity/sweet properties; and (2) Products containing non-menthol synthetic cooling agents (eg, Wilkinson Sword (WS), WS-3, WS-23 (termed ‘koolada’)). This paper reviews the background, chemistry, toxicology, marketing, user perceptions, use prevalence and policy implications of e-cigarette products with ice-hybrid flavours or non-menthol coolants. Scientific literature search supplemented with industry-generated and user-generated information found: (a) The tobacco industry has developed products containing synthetic coolants since 1974, (b) WS-3 and WS-23 are detected in mass-manufactured e-cigarettes (eg, PuffBar); (c) While safe for limited oral ingestion, inhalational toxicology and health effects from daily synthetic coolant exposure are unknown and merit scientific inquiry and attention from regulatory agencies; (d) Ice-hybrid flavours are marketed with themes incorporating fruitiness and/or coolness (eg, snow-covered raspberries); (e) WS-23/WS-3 concentrates also are sold as do-it-yourself additives, (f) Pharmacology research and user-generated and industry-generated information provide a premise to hypothesise that e-cigarette products with ice flavours or non-menthol cooling agents generate pleasant cooling sensations that mask nicotine’s harshness while lacking certain aversive features of menthol-only products, (g) Adolescent and young adult use of e-cigarettes with ice-hybrid or other cooling flavours may be common and cross-sectionally associated with more frequent vaping and nicotine dependence in convenience samples. Evidence gaps in the epidemiology, toxicology, health effects and smoking cessation-promoting potential of using these products exist. E-cigarettes with ice flavours or synthetic coolants merit scientific and regulatory attention.

In the context of tobacco harm-reduction strategy, the potential reduced impact of electronic cigarette (EC) exposure should be evaluated relative to the impact of cigarette smoke exposure. We conducted a series of in vitro studies to compare the biological impact of an acute exposure to aerosols of “test mix” (flavors, nicotine, and humectants), “base” (nicotine and humectants), and “carrier” (humectants) formulations using MarkTen® EC devices with the impact of exposure to smoke of 3R4F reference cigarettes, at a matching puff number, using human organotypic air–liquid interface buccal and small airway cultures. We measured the concentrations of nicotine and carbonyls deposited in the exposure chamber after each exposure experiment. The deposited carbonyl concentrations were used as representative measures to assess the reduced exposure to potentially toxic volatile substances. We followed a systems toxicology approach whereby functional biological endpoints, such as histopathology and ciliary beating frequency, were complemented by multiplex and omics assays to measure secreted inflammatory proteins and whole-genome transcriptomes, respectively. Among the endpoints analyzed, the only parameters that showed a significant response to EC exposure were secretion of proteins and whole-genome transcriptomes. Based on the multiplex and omics analyzes, the cellular responses to EC aerosol exposure were tissue type-specific; however, those alterations were much smaller than those following cigarette smoke exposure, even when the EC aerosol exposure under the testing conditions resulted in a deposited nicotine concentration approximately 200 times that in saliva of EC users.

Rates of adolescent electronic (e-) cigarette use are increasing, but there has been little study of the chronic effects of use. Components of e-cigarette aerosol have known pulmonary toxicity. To investigate the associations of e-cigarette use with chronic bronchitis symptoms and wheeze in an adolescent population. Associations of self-reported use of e-cigarettes with chronic bronchitic symptoms (chronic cough, phlegm, or bronchitis) and of wheeze in the previous 12 months were examined in 2,086 Southern California Children's Health Study participants completing questionnaires in 11th and 12th grade in 2014. Ever e-cigarette use was reported by 502 (24.0%), of whom 201 (9.6%) used e-cigarettes during the last 30 days (current users). Risk of bronchitic symptoms was increased by almost twofold among past users (odds ratio [OR], 1.85; 95% confidence interval [CI], 1.37-2.49), compared with never-users, and by 2.02-fold (95% CI, 1.42-2.88) among current users. Risk increased with frequency of current use (OR, 1.66; 95% CI, 1.02-2.68) for 1-2 days and 2.52 (95% CI, 1.56-4.08) for 3 or more days in past 30 days compared with never-users. Associations were attenuated by adjustment for lifetime number of cigarettes smoked and secondhand smoke exposure. However, risk of bronchitic symptoms among past e-cigarette users remained elevated after adjustment for relevant potential confounders and was also observed among never-cigarette users (OR, 1.70; 95% CI, 1.11-2.59). There were no statistically significant associations of e-cigarette use with wheeze after adjustment for cigarette use. Adolescent e-cigarette users had increased rates of chronic bronchitic symptoms. Further investigation is needed to determine the long-term effects of e-cigarettes on respiratory health.

National data suggest that non-Hispanic, White youth engage in electronic cigarette (e-cigarette) use at the highest rates. These results are not likely to be mirrored across regional contexts. State-representative data from Utah in 2019 (N = 58,689) were used to estimate the odds of lifetime and past 30-day vaping across seven racial/ethnic categories. Youth in grades 8, 10, and 12 (mean age 15.2; 52% female) self-reported race/ethnicity and vaping product use history, including e-cigarettes, vape pens, or mods. A Cox proportional hazards model estimated the cumulative probabilities for initiating vaping product use. The results indicated that American Indian or Alaskan Native, Black or African American, Hispanic/Latino, Multiracial, and Native Hawaiian or other Pacific Islander youth had significantly higher odds of both lifetime and past 30-day vaping compared to non-Hispanic White youth. The results showed significant variation in the cumulative probability of initiation by race/ethnicity, with Hispanic/Latino youth reporting the highest odds of initiation at each age. The regional patterns of vaping across racial/ethnic groups may not mirror national trends. State- and community-level data should be used to inform efforts to reduce e-cigarette use and promote health equity among youth.

Recently, there has been an outbreak associated with the use of e-cigarette or vaping products, associated lung injury (EVALI). The primary components of vaping products, vitamin E acetate (VEA) and medium-chain triglycerides (MCT), may be responsible for acute lung toxicity. Currently, little information is available on the physiological and biological effects of exposure to these products. We hypothesized that these e-cig vape cartridges and their constituents (VEA and MCT) induce pulmonary toxicity, mediated by oxidative damage and inflammatory responses, leading to acute lung injury. We studied the potential mechanisms of e-cig vape cartridge aerosol induced inflammatory response by evaluating the generation of reactive oxygen species by MCT, VEA, and cartridges and their effects on the inflammatory state of pulmonary epithelium and immune cells both in vitro and in vivo. Cells exposed to these aerosols generated reactive oxygen species, caused cytotoxicity, induced epithelial barrier dysfunction, and elicited an inflammatory response. Using a murine model, the parameters of acute toxicity to aerosol inhalation were assessed. Infiltration of neutrophils and lymphocytes was accompanied by significant increases in IL-6, eotaxin, and G-CSF in the bronchoalveolar lavage fluid (BALF). In mouse plasma, eicosanoid inflammatory mediators, leukotrienes, were significantly increased. Plasma from e-cig users also showed increased levels of hydroxyeicosatetraenoic acid (HETEs) and various eicosanoids. Exposure to e-cig vape cartridge aerosols showed the most significant effects and toxicity compared to MCT and VEA. In addition, we determined SARS-CoV-2 related proteins and found no impact associated with aerosol exposures from these tested cartridges. Overall, this study demonstrates acute exposure to specific e-cig vape cartridges induces in vitro cytotoxicity, barrier dysfunction, and inflammation and in vivo mouse exposure induces acute inflammation with elevated proinflammatory markers in the pathogenesis of EVALI.Recently, there has been an outbreak associated with the use of e-cigarette or vaping products, associated lung injury (EVALI). The primary components of vaping products, vitamin E acetate (VEA) and medium-chain triglycerides (MCT), may be responsible for acute lung toxicity. Currently, little information is available on the physiological and biological effects of exposure to these products. We hypothesized that these e-cig vape cartridges and their constituents (VEA and MCT) induce pulmonary toxicity, mediated by oxidative damage and inflammatory responses, leading to acute lung injury. We studied the potential mechanisms of e-cig vape cartridge aerosol induced inflammatory response by evaluating the generation of reactive oxygen species by MCT, VEA, and cartridges and their effects on the inflammatory state of pulmonary epithelium and immune cells both in vitro and in vivo. Cells exposed to these aerosols generated reactive oxygen species, caused cytotoxicity, induced epithelial barrier dysfunction, and elicited an inflammatory response. Using a murine model, the parameters of acute toxicity to aerosol inhalation were assessed. Infiltration of neutrophils and lymphocytes was accompanied by significant increases in IL-6, eotaxin, and G-CSF in the bronchoalveolar lavage fluid (BALF). In mouse plasma, eicosanoid inflammatory mediators, leukotrienes, were significantly increased. Plasma from e-cig users also showed increased levels of hydroxyeicosatetraenoic acid (HETEs) and various eicosanoids. Exposure to e-cig vape cartridge aerosols showed the most significant effects and toxicity compared to MCT and VEA. In addition, we determined SARS-CoV-2 related proteins and found no impact associated with aerosol exposures from these tested cartridges. Overall, this study demonstrates acute exposure to specific e-cig vape cartridges induces in vitro cytotoxicity, barrier dysfunction, and inflammation and in vivo mouse exposure induces acute inflammation with elevated proinflammatory markers in the pathogenesis of EVALI.

To investigate smoking and vaping in secondary school students (aged 13–18 years) in New Zealand (NZ) following the introduction of ‘pod’ e‐cigarettes, which have been associated with the rapid escalation of youth vaping elsewhere. Data on smoking and vaping were collected in 2019 as part of a comprehensive youth health survey (N=7,721). Vaping was 2–3 times more prevalent than smoking, with 10% of students vaping regularly (monthly or more often), and 6% weekly or more often, compared with 4% and 2%, respectively, for tobacco smoking. Nicotine‐containing e‐cigarettes were sometimes or always used by 80% of regular and 90% of weekly vapers. Regular and weekly smoking was rare in low deprivation (affluent) areas, whereas regular and weekly vaping prevalence was similar across the socioeconomic spectrum. More than 80% of ever‐vapers (N=2732) reported they were non‐smokers when they first vaped, and 49% of regular vapers (N=718) had never smoked. A significant proportion of New Zealand adolescents, many of whom have never smoked, use nicotine‐containing e‐cigarettes regularly. Vaping is less harmful than smoking, but it is not harmless. Public health action is needed to support young non‐smokers to remain smokefree and vape‐free.

To monitor patterns of use of e‐cigarettes to understand their potential impact on the New South Wales (NSW) population in Australia. A cross‐sectional online survey was carried out with a sample of adults in NSW in February 2016. Ever and past 30‐day use of e‐cigarettes, reasons for use, place of purchase and use within outdoor and enclosed public places were assessed along with sociodemographic characteristics. Ever and past 30‐day use was reported by 13% and 4% of the sample, respectively. More than one‐third of participants did not purchase their own e‐cigarette (36.3%). The most frequently reported reason for using an e‐cigarette for smokers and ex‐smokers was to help quit smoking (45.3% and 44.7%, respectively) while for non‐smokers it was novelty (40%). E‐cigarettes were most commonly used at home (59.4%), in outdoor dining areas (36.8%) and in the workplace (27.8%). E‐cigarettes are being used by a small percentage of the NSW population. Reasons for e‐cigarette use varied with smoking status. Different sociodemographic characteristics were associated with ever and past 30‐day use of e‐cigarettes. E‐cigarettes are being used in areas that are covered by smoke‐free legislation. Given e‐cigarettes are being used in smoke‐free areas, policy‐makers could take a precautionary approach by including e‐cigarette use under smoke‐free legislation.

Induced pluripotent stem cells (iPSCs) are a powerful modeling system for medical discovery and translational research. To date, most studies have focused on the potential for iPSCs for regenerative medicine, drug discovery, and disease modeling. However, iPSCs are also a powerful modeling system to investigate the effects of environmental exposure on the cardiovascular system. With the emergence of e‐cigarettes, air pollution, marijuana use, opioids, and microplastics as novel cardiovascular risk factors, iPSCs have the potential for elucidating the effects of these toxins on the body using conventional two‐dimensional (2D) arrays and more advanced tissue engineering approaches with organoid and other three‐dimensional (3D) models. The effects of these environmental factors may be enhanced by genetic polymorphisms that make some individuals more susceptible to the effects of toxins. iPSC disease modeling may reveal important gene–environment interactions that exacerbate cardiovascular disease and predispose some individuals to adverse outcomes. Thus, iPSCs and gene‐editing techniques could play a pivotal role in elucidating the mechanisms of gene–environment interactions and understanding individual variability in susceptibility to environmental effects. Graphical Abstract In this review, J Wu and colleagues discuss the potential of human iPSC as a modeling system to investigate the toxic effects of environmental exposure on human health.

Background/Objectives: Nicotine-free electronic cigarettes (NFECs) are becoming increasingly popular, especially among youth and non-smokers, yet their effects on the gastrointestinal tract (GIT) remain poorly understood. This systematic review synthesizes available in vitro, in vivo, and limited human evidence on NFEC-associated changes in gastrointestinal health and function. Methods: Literature searches were conducted in Medline, Web of Science, Cochrane, and Scopus in July 2025, following PRISMA guidelines. Eligible studies examined NFEC effects on any GIT segment, including the oral cavity, liver, intestines, and microbiome. Data on study design, exposure characteristics, and main outcomes were extracted and narratively synthesized. Results: Of 111 identified records, 94 full-text articles were retrieved, and 21 studies met the inclusion criteria. Most were preclinical, with only one human pilot study. Evidence from oral cell and microbial models suggests that NFEC aerosols can induce pro-inflammatory cytokine production, impair cell viability, and disrupt microbial metabolism through their base constituents (propylene glycol, vegetable glycerine, and flavourings). Animal studies indicate possible hepatic oxidative stress, altered lipid metabolism, and gut barrier dysfunction, with some data suggesting more pronounced steatosis in nicotine-free exposures compared to nicotine-containing counterparts. Microbiome studies report reduced tight junction expression and altered neutrophil function. Conclusions: Current evidence is limited and predominantly preclinical but indicates that NFEC exposure can affect multiple aspects of gastrointestinal health. Robust longitudinal and interventional human studies are urgently needed to determine the clinical relevance of these findings and to inform regulation and public health policy.

Objectives: The aim of this report is to describe the lung biopsy findings in vaping-associated pulmonary illness. Methods: Lung biopsies from eight patients with vaping-associated pulmonary illness were reviewed. Results: The biopsies were from eight men (aged 19-61 years) with respiratory symptoms following e-cigarette use (vaping). Workup for infection was negative in all cases, and there was no evidence for other etiologies. Imaging showed diffuse bilateral ground-glass opacities in all patients. Most recovered with corticosteroid therapy, while one died. Lung biopsies (seven transbronchial, one surgical) showed acute lung injury, including organizing pneumonia and/or diffuse alveolar damage. Common features were fibroblast plugs, hyaline membranes, fibrinous exudates, type 2 pneumocyte hyperplasia, and interstitial organization. Some cases featured a sparse interstitial chronic inflammatory infiltrate. Although macrophages were present within the airspaces in all cases, this feature was not prominent, and findings typical of exogenous lipoid pneumonia were absent. Conclusions: The histopathology of acute pulmonary illness related to e-cigarette use (vaping) is characterized by acute lung injury patterns, supporting the contention that vaping can cause severe lung damage. Key Words: Vaping; Vaping-associated pulmonary illness; Electronic cigarettes; E-clgarettes; Dabbing; Lung pathology; Lung biopsy; Diffuse alveolar damage; Organizing pneumonia; Acute lung injury