Cigarette butt waste is a widespread form of tobacco-related litter and an increasingly recognized source of environmental contamination. This systematic review synthesized evidence on the environmental impacts of cigarette butts and other tobacco and nicotine product waste, including contaminant release, plastic-derived particle generation, affected environmental matrices, ecotoxicological effects, dose-effect relationships, and ecological and human health risk assessment within a One Health framework. Following PRISMA guidelines and PROSPERO registration, PubMed, Scopus, and Web of Science were systematically searched. Forty-seven studies were included. Cigarette butts and related waste were found to release diverse contaminants, including metals, nicotine, PAHs, VOCs, BTEX, pesticides, phenolic compounds, aromatic amines, and cellulose-acetate-derived micro- and nanoplastics. Nicotine emerged as a prominent contaminant, with rapid release and high modelled ecological risk reported in some studies. Freshwater and marine environments were most frequently investigated, while soils, urban environments, stormwater systems, landfills, and waste-management pathways were also represented. Experimental studies reported mortality, growth inhibition, oxidative stress, reproductive and developmental impairment, genotoxicity, metabolic and behavioral alterations, and community-level effects. Evidence on emerging nicotine product waste remained limited and was constrained by differences in product design, terminology, characterization, and experimental scenarios. Overall, these wastes represent hybrid chemical-particulate environmental stressors, although their substantial heterogeneity limits broader generalization.

Background: Multiple effects of flavored E-liquids or E-liquid aerosols on various cell lines have been reported. However, concentrations of E-liquids and aerosols are not usually equivalent, making it difficult to determine the relative effect heating and aerosolization plays on the cells tested. To match concentrations of E-liquids with their aerosols, the mass and the concentration of the E-liquid nicotine dissolved in culture media must be compared to that of the aerosol bubbled into the culture media. The aim of this study is to compare the effects of equivalent amounts of E-liquids and their aerosols ± flavors (tobacco, menthol, cinnamon, strawberry and blueberry) on the morphology and viability of OKF6/TERT-2 oral epithelial cells. Methods: HPLC-UV was used to measure nicotine concentrations in culture media containing E-liquids or aerosols. Morphology and viability of OKF6/TERT-2 cells exposed to equivalent amounts of E-liquids or aerosols over a 24 h period were subsequently assessed using light microscopy, LDH cytotoxicity assays, flow cytometry and DAPI staining. Results: One hundred puffs of aerosol bubbled into 50 mL of media is equivalent to 0.17% E-liquid. As indicated by altered morphology, increased LDH activity, flow cytometry and DAPI fluorescent staining, OKF6/TERT-2 cells are negatively impacted by 100 puffs of aerosols flavored with strawberry resulting in reduced cell viability, while the same amount of E-liquids directly administered have minimal to no effect. Conclusions: The data suggests that heating and aerosolization enhance the cytotoxic effect of strawberry flavored E-liquid.

Background/Objectives. Electronic cigarettes allow smokers to consume nicotine, a highly addictive substance, without burning tobacco. Since their commercialization in early 2004, electronic cigarettes have become popular in the Asian market and then worldwide. Initially conceived as an alternative to combustible smoking, they have gradually established themselves as a mass consumption product, raising both hopes for the reduction of the risks caused by burned cigarettes and concerns about their use among non-smokers, especially young people. Currently, because of their availability, accessibility to non-smokers, including young people, and their manageability, electronic cigarettes are causing more concern than hope among health professionals. This narrative review aimed to synthesize current evidence on the different chemical components generated by electronic cigarette devices and their effects on oral health. We specifically sought to (i) compile and discuss the available evidence regarding the effects of each chemical component in the e-cigarette aerosols on oral health outcomes, and (ii) feature the risks associated with e-cigarette use and how to ovoid/prevent them. Methods: We reviewed relevant English-language literature on electronic cigarette design, use, chemical generation, and adverse effects on oral health through targeted searches of PubMed, Elsevier, Oxford Academic, BioMed Central, MDPI, Scopus, and Google Scholar from 2008 to 2026. Evidence was narratively synthesized to shed light on different oral health concerns reported following electronic cigarette use. Results: This narrative review highlights several adverse effects of electronic cigarettes on oral health, including functional deregulation of the soft (tongue, gums, salivary glands) tissues, hard tissues (teeth, dental restorative materials), and the oral microbiota. These effects were attributed to the different chemicals generated when electronic cigarettes heat-vape e-liquids. These chemicals damage oral tissues/cells, leading to apoptosis, oxidative stress, and DNA damage that may lead to oral cancer. These effects may reduce oral cell growth and increase tissue inflammation, which may delay wound healing. The reviewed studies identified several limitations, including the need for additional investigations involving electronic cigarette use and long-term follow-up. Conclusions: The available in vitro and in vivo studies clearly show the potential harm of vaping on oral health. This review offers a good overview to electronic cigarette users, oral health professionals, and scientists about the potential oral harm effects of electronic cigarettes. The available studies suggest the need for oral health professionals' support in providing information and awareness about the harmful effects of electronic cigarettes. Thus, the health system and professional orders should develop information and awareness tools to help oral health professionals in their interventions with e-cigarette users.

Background/Objective: The increasing use of electronic cigarettes (e-cigarettes) has raised concerns about their possible effects on oral immune responses. Neutrophils are essential for host defense against cariogenic bacteria such as Streptococcus mutans (S. mutans), and impaired neutrophil function may facilitate the progression of oral diseases. This study aims to investigate whether exposure to vaping aerosols alters neutrophil viability, oxidative responses, and proinflammatory cytokine production in response to the cariogenic bacterium S. mutans. Methods: Human neutrophils isolated from healthy donors were exposed to e-cigarette aerosol extracts produced from flavored and unflavored e-liquids, with and without nicotine. Cytotoxicity was determined by measuring lactate dehydrogenase (LDH) release. Intracellular reactive oxygen species (ROS) generation following S. mutans exposure was used as an indirect measure of neutrophil phagocytic activity. Pro-inflammatory cytokines (interleukin-1 beta (IL-1β) and interleukin-8 (IL-8)) were measured using an enzyme-linked immunosorbent assay (ELISA). Results: Under the tested conditions, e-cigarette aerosol extracts did not cause significant cytotoxicity. However, in neutrophils stimulated with S. mutans, certain flavorings (particularly tobacco and dessert-related flavors) significantly reduced ROS generation, suggesting impaired antimicrobial responses. In contrast, fruit and mint flavors had little impact. Minor flavor-dependent differences were observed for IL-1β and IL-8. The presence of nicotine did not significantly affect the levels of these cytokines. Conclusions: Aerosol extracts from e-cigarettes altered neutrophil oxidative responses in a flavor-dependent manner but did not cause significant cytotoxicity. These findings suggest mild immunological modulation rather than a direct inflammation effect and indicate that e-cigarette aerosols may alter antimicrobial responses despite having minimal effects on IL-1β and IL-8.

Background/Objectives: Alternative nicotine-containing products have gained popularity in recent years. Our aim is to compare clinical periodontal outcomes following non-surgical periodontal therapy (NSPT) among patients with periodontitis according to nicotine exposure status: cigarette smokers (CS), former smokers (FS), quitters (Q), users of electronic cigarettes (EC), smokeless tobacco users (ST), and non-smokers (NS). Methods: A systematic search of four electronic databases (PubMed, EMBASE, Web of Science, CENTRAL) was performed until January 2025. Sixty-seven studies were included in the qualitative synthesis, of which 56 studies were included in a frequentist network meta-analysis. Two researchers independently collected data on probing pocket depth (PPD), clinical attachment loss, bleeding on probing, plaque index, full mouth plaque score, gingival index, and gingival crevicular fluid volume. Results: NS had significantly higher change in PPD compared with CS (MD: 0.25; CI: 0.13, 0.37; 50 studies; 1359 patients; moderate certainty), EC (MD: 0.98; CI: 0.47, 1.49; 2 studies; 56 patients; very low certainty), and ST (MD: 0.99; CI: 0.49, 1.49; 2 studies; 82 patients; low certainty). Q (MD: 0.02; CI: -0.56, 0.60; 2 studies; 52 patients; low certainty) and FS (MD: 0.03; CI: -0.62, 0.69; 4 studies; 267 patients; low certainty) did not differ significantly from NS. In secondary outcomes, NS, FS, or Q were ranked first. Conclusions: FS and Q showed no statistically significant differences from NS; EC and ST generally had less favorable treatment rankings than CS. The certainty of evidence varied across exposure groups and outcomes. Further studies are needed to support firm clinical recommendations.

A single nucleotide polymorphism (SNP) of the alpha5 subunit of nicotinic acetylcholine receptors (nAChRs) increases human risk for nicotine dependence, alcohol use disorders (AUDs), and schizophrenia. Here, we used transgenic mice carrying either this SNP (rs16969968; α5SNP/α5KI) or a Chrna5 knockout (α5KO) to examine the role of α5-containing nAChRs in affective state discrimination and prosocial, rescuing-like behaviors. α5KO mice failed to recognize a negative affective state in a familiar peer and displayed severely altered prosocial, empathy-related behaviors, at times assaulting distressed peers. In contrast, α5KI mice discriminated affective states normally and showed increased rescuing-like behavior. Effects of α5 mutations on affective state discrimination were sex stratified. These findings demonstrate the critical implication of α5∗nAChRs in affective state discrimination and prosocial-like behaviors, revealing sex-stratified patterns of these social-emotional deficits in α5KI and α5KO mice, which are reminiscent of the behavioral features of two characterized subtypes of AUD in humans.

Introduction : Disposable e-cigarette devices are popular among youth with fruit and candy flavored products dominating the market. While the addition of novel sweeteners and synthetic coolants has been quantified in the e-liquid of such devices, the relative amount of these compounds transferred into the aerosol and inhaled by users remains unknown. In this study, popular US disposable e-cigarette devices were analyzed for coolant, sweetener, and nicotine concentration, and subsequent carryover to aerosol was determined using an established protocol with cold-finger traps to collect aerosol. Methods 12 popular disposable e-cigarettes were identified and purchased between 2023-26, and 3 Sensa devices labeled as "0-nicotine" and 2 SpreeBar devices labeled to contain "Metatine" (6-methylnicotine) were also included to probe for the effect of nicotine on carryover. Menthol, nicotine, 6-methylnicotine (6MN), the synthetic coolants WS-23 and WS-3, and the artificial sweeteners neotame and sucralose were quantified in the liquids and the generated aerosol (20 puffs in triplicate) of 17 disposable e-cigarettes using GC-FID and LC-MS-MS. Results Neotame and WS-23 were present in all 17 devices at concentrations ranging from 0.05-2.73 mg/g and 3.52-35.0 mg/g, respectively. Nicotine was found in 11/17 devices, menthol in 9/17, WS-3 in 4/17, sucralose in 2/17, and 6MN in 2/17. Mean carryover rates to aerosol were: Neotame 40 ± 13%, WS-23 84 ± 9%, nicotine 88 ± 12%, menthol 81 ± 8%, WS-3 88 ± 10%, and sucralose and 6MN carryover ranged from 26-54% and 72-77%, respectively. Conclusions Although carryover rates to aerosol were lower for sweeteners compared to nicotine and coolants, users of these devices can be expected to be exposed to substantial amounts of the quantified 6 compounds. It is unclear whether neotame is thermally stable or breaks down during the aerosolization process. This study aims to provide a foundation for future toxicological and pharmacological studies that are needed to better understand the implications of chronic inhalation of neotame, WS-23 and the other tested compounds.

Purpose Targeted therapies for breast cancer, including CDK4/6, PARP, mTOR, and PI3K inhibitors, have raised concerns regarding thrombosis risk, but real-world data comparing these agents remain limited. We investigated thrombosis incidence and risk factors in a large national cohort of breast cancer patients. Methods In this retrospective cohort study using the TriNetX national database, we evaluated the thrombotic risk and associated factors among patients with breast cancer treated with these therapies. The primary outcome was any arterial or venous thrombotic event. Results Among 4,165 patients on targeted therapy, treatment with CDK4/6i was associated with increased risk of any thrombosis (HR 3.36, 95% CI 2.89-3.92) and venous thrombosis (HR 4.45, 95% CI 3.68-5.39). PARPi (HR 3.78, 95% CI 1.82-7.85; venous HR 5.79, 95% CI 2.52-13.3) and everolimus (HR 6.59, 95% CI 3.82-11.4; venous HR 9.67, 95% CI 5.29-17.7) showed similar associations. Within CDK4/6i, palbociclib carried the highest hazard for any thrombosis (HR 3.64, 95% CI 3.02-4.39) and venous thrombosis (HR 5.11, 95% CI 4.05-6.45). Nicotine dependence (HR 2.01, 95% CI 1.91-2.12), brain metastases (HR 4.20, 95% CI 2.98-5.93), and higher BMI (HR 1.03, 95% CI 1.03-1.03) were independent risk factors. Conclusion This real-world analysis demonstrates that CDK4/6i and everolimus were associated with increased risk of both arterial and venous thrombosis, while PARPi was specifically associated with venous thrombosis. Similar risk was seen across CDK4/6 inhibitor agents. These results support risk stratification tools incorporating both agent and patient-level factors to better inform clinical management.