Search Results (590)

Background: Immigrant adolescents experience distinct risk and protective factors related to substance use; however, cross-national differences between immigrant and native-born youth remain insufficiently understood. This study examines differences in the prevalence of psychoactive substance use between immigrant and non-immigrant 15-year-old adolescents and assesses the protective role of family support across Europe, Central Asia, and North America. Materials and Methods: Data were drawn from nationally representative samples of the 2021/2022 WHO Health Behaviour in School-aged Children (HBSC) survey, including 15-year-olds from 32 countries, representing Belgium by two separate regions (n = 66,400). Outcomes included cigarette smoking, electronic cigarette use, alcohol consumption, drunkenness, and cannabis use in the past 30 days. Key predictors were immigrant status and family support. Multilevel analyses incorporated country-level indicators, including the proportion of immigrant youth and the Inclusiveness Index, and were adjusted for sex and family affluence. Results: Substantial cross-national variation in substance use prevalence was observed. Immigrant adolescents were more likely to smoke cigarettes, use electronic cigarettes, and use cannabis, whereas alcohol consumption was more common among non-immigrant adolescents. However, in countries with a low proportion of immigrant youth (<5%), immigrant adolescents showed an elevated likelihood of engaging in all forms of psychoactive substance use, including alcohol consumption. Low family support emerged as the strongest and most consistent predictor of substance use across all outcomes. Conclusions: Immigrant adolescents living in countries with low immigration rates constitute a particularly vulnerable group facing increased risk of substance use. Family support is protective against adolescent substance use for both immigrant and non-immigrant youth, with the strongest effect for alcohol use in low-immigration contexts. Full article

Extracellular vesicles (EVs) are lipid-enclosed particles secreted from a wide variety of cells, with the ability to transfer biologically active content from parent to recipient cells. Lung epithelial-derived EVs (LE-EVs) play an important role in the progression of pulmonary disease, but there is limited evidence regarding the impact of cigarette smoke (CS) and electronic cigarette aerosol (ECA) on epithelial-derived EVs. The aim of this systematic review was to evaluate the current published literature on the impact of cigarette smoke and electronic cigarette aerosol on LE-EVs. Original research studies and clinical data were included, but research involving microparticles or non-epithelial-derived EVs was excluded. A total of 29 articles were identified from three databases (EMBASE, Web of Science and PubMed), of which nine demonstrated that CS exposure leads to molecular changes in epithelial-derived EVs, whereas 21 reported that CS-induced LE-EVs can deliver their cargo to neighbouring cells. The results highlighted that LE-EVs secreted in response to cigarette or e-cigarette exposure presented altered EV cargo, associated with increased cellular damage, inflammation and disease development. The current literature suggests that conventional and electronic cigarettes can influence the secretion of EVs from lung epithelial cells, with these EVs potentially playing a role in the development of lung inflammation. Nonetheless, there is limited research studying the impact of ECA on LE-EVS. Further research examining the impact of electronic cigarettes on lung epithelial-derived EVs, using robust human in vitro models coupled with clinical studies, is required. Full article

Background: The increasing use of electronic cigarettes (ECIGs), especially among youth, has raised concerns about the impact of vaping on oral health. While ECIGs are often marketed as a safer alternative, the existing literature suggests that their use may have detrimental effects on the pulmonary and cardiovascular systems. The oral cavity is the first point of contact for ECIG aerosol, and new reports link vaping to the onset of periodontal disease. It is critical to understand the potential effects of vaping on the oral microbiome, which affects systemic health. This study investigates how flavored E-liquids and commensal bacteria influence the growth of Porphyromonas gingivalis, a periodontal pathobiont, under planktonic and biofilm conditions. Methods: P. gingivalis was grown planktonically in the presence of the supernatants of four streptococcal species (Streptococcus gordonii, Streptococcus intermedius, Streptococcus mitis, and Streptococcus oralis) and flavored E-liquids (tobacco, menthol, cinnamon, strawberry, and blueberry) under anaerobic conditions. Multispecies biofilms, including all the species mentioned above and Fusobacterium nucleatum, were also grown anaerobically and quantified by crystal violet assays, qPCR, and CFU counts. Results: Although E-liquids inhibit P. gingivalis growth under planktonic conditions, the presence of commensal supernatants partially mitigates this effect. However, P. gingivalis growth in multispecies biofilms is increased by E-liquid treatments. Conclusions: This study highlights the enhanced growth of P. gingivalis as part of an oral microbial community in the presence of E-liquids. These results suggest that E-liquid-induced alterations in multispecies biofilms may contribute to the observed dysbiosis in vapers and the associated risk of oral diseases. Full article

Background/Objectives: Lung cancer remains a major global health burden, largely driven by cigarette use. Although electronic cigarettes (e-cigarettes) are viewed as safer alternatives due to their reduced chemical load, growing evidence shows their vapor can disrupt cellular transcriptomes, including long noncoding RNAs (lncRNAs). In this study, we examined the regulation and function of vape-associated lncRNA transcript 1 (VALT1), a novel transcript upregulated in the oral transcriptomes of e-cigarette users and similarly elevated in non-small-cell lung cancer (NSCLC) tumors. Methods: Publicly available RNA-seq datasets were analyzed, and VALT1 was identified as an e-cigarette-responsive lncRNA. Its dose-dependent induction by e-cigarette smoke extract (eCSE) and cytoplasmic localization were confirmed via RT-qPCR. Its effects on cancer-associated phenotypes including proliferation, ROS detoxification, resistance to apoptosis, migration, cytoskeletal disorganization, and nuclear remodeling were assessed through overexpression and siRNA-mediated knockdown in A549 and BEAS-2B cells. Results: Acute eCSE exposure induced a biphasic, dose-dependent increase in VALT1 expression, accompanied by enhanced proliferation, ROS detoxification, apoptosis resistance, migration, cytoskeletal disorganization, and nuclear remodeling in A549 cells. VALT1 overexpression reproduced these phenotypes in both cell lines without eCSE treatment, whereas knockdown attenuated them. VALT1 promoted survival under cytotoxic stress in A549 but not BEAS-2B cells. Conclusions: These findings support an active role for VALT1 as an e-cigarette vapor-upregulated transcript that contributes to its phenotypic readout and enhances cellular survival under extracellular chemical stress—thereby aggravating tumorigenic phenotypes even in the absence of mutations that contribute to malignant transformation. Full article

The growing popularity of electronic cigarettes (e-cigarettes) necessitates a better understanding of their biological effects. In this study, we aimed to evaluate the effects of e-cigarette aerosol condensates generated from either e-cigarette carrier liquid alone or with e-cigarette liquid with nicotine and flavor on bronchial epithelial cells. BEAS-2B cells were exposed to e-cigarettes for 24 h, and transcriptional and proteomic profiling, including assessment of protein modifications, was performed. Additionally, cell-based assays were used to evaluate mitochondrial function, rate of protein synthesis, lysosomal signal, lipid droplet quantity and actin formation. Our findings reveal that short-term exposure to both types of aerosol condensates altered transcriptome and proteome profiles, disrupting cellular homeostasis in BEAS-2B cells through impaired proteostasis and mitochondrial function in response to both types of condensates. Changes in lipid and lysosome content, as well as a reduction in polymerized actin, were observed with nicotine- and flavor-containing condensate. E-cigarette exposure also induced irreversible protein modifications, including different chemical derivatives (25 out of 49 in nicotine/flavor condensate; 20 out of 48 in nicotine/flavor-free condensate; 4 out of 35 in control), suggesting their particularly harmful effect. Together, these findings point to early-onset cellular stress and impaired lung epithelial fitness caused by acute e-cigarette exposure. Full article

The electronic cigarette has divided the medical community. While promoted as a tool for smoking cessation, its use has opened a Pandora’s box. Evidence from studies on both cardiovascular and pulmonary health demonstrates that e-cigarettes are associated with multiple adverse effects. In this review, we specifically examine their consequences and associations with coronary artery disease, myocardial infarction, arrhythmias, arterial hypertension, and related conditions. Finally, we highlight approaches to counter the spread of these so-called harm-reduction alternatives, drawing on data from the European Respiratory Society, the European Society of Cardiology, and the Cochrane Collaboration. Full article

Electronic cigarette (ECIG) liquids are marketed with labeled nicotine concentrations and propylene glycol (PG) to vegetable glycerin (VG) ratios, yet quality control inconsistencies may alter vaping emissions. We quantified discrepancies between labeled and measured chemical content and evaluated how these differences affect emissions of particulate matter with an aerodynamic diameter of 2.5 µm or smaller (PM_2.5). Flavor-free liquids (n = 20) spanning nicotine labels of 0, 9, 18, and 48 mg/mL and PG content from 0% to 80% were purchased. Nuclear magnetic resonance spectroscopy measured nicotine, PG, and VG. Aerosols were generated using a standardized device in a controlled exposure chamber. PM_2.5 was measured using a pDR-1500 and SMPS/APS, with gravimetric correction factors calculated. Labeling inaccuracies were widespread: “nicotine-free” liquids contained 0.1 to 0.4 mg/mL nicotine, and labeled nicotine deviated by up to ±30%. PG/VG ratios were frequently incorrect; 70% of samples contained higher VG than labeled, including “100% VG” products with about 10% PG. Higher VG consistently increased PM_2.5 mass, while nicotine had a minimal effect. The pDR overestimated mass, whereas SMPS/APS underestimated due to volatilization losses. Overall, inaccurate ECIG liquid labeling can alter measured PM_2.5 emissions under controlled conditions. Full article

Electronic cigarettes (ECs) are promoted as a safer alternative to traditional cigarettes, yet their impact on immune cells remains incompletely understood. This study investigates the activation of human primary adherent and non-adherent monocytes exposed ex vivo to aerosols from four flavored ECs (classic tobacco, menthol, watermelon, and strawberry) compared to cigarette smoke (CS) and nicotine alone. EC aerosols (ECEs) induced modest cytotoxicity, oxidative stress, and superoxide dismutase activity compared to CS, with high cell response heterogeneity indicating subpopulation-specific effects. Adherent monocytes showed elevated integrin expression (CD11a, CD11b), ICAM-1 (CD54), TNFα, and oxidative stress versus non-adherent cells, amplified by ECE. Dual fluorescence flow cytometry (green DCF for ROS and red for anti-TNFα Ab) revealed shifts toward pro-inflammatory/oxidative quadrants, particularly upper-right high-intensity relatively small subsets with macrophage M1-like CD68 expression in adherent cells. ECEs reduced phagocytosis in adherent monocytes, mimicking CS effects, probably driven by non-nicotine components. Strawberry flavor (ECE 4) elicited the strongest TNFα induction. These findings demonstrate EC-induced subclinical inflammation via selective monocyte activation, potentially contributing to chronic cardiopulmonary risks despite significantly lower overall toxicity than CS. Full article

Diacetyl has been a known key volatile compound for almost one century, a metabolite naturally produced by different microorganisms during fermentation processes, with traditional applications in food products preparations. Since its discovery, diacetyl has been recognized and actively explored regarding its buttery aroma, which is beneficial for a variety of fermented dairy foods. It is primarily synthesized by lactic acid bacteria (LAB) and other microbial groups through citrate metabolism, a pathway that is strain-dependent and strongly influenced by environmental conditions. Moreover, beyond its sensory relevance, diacetyl has attracted increasing scientific attention because of its antimicrobial activity, including synergistic interactions with bacteriocins and other microbial metabolites, which may enhance food preservation and biotechnological strategies. In contrast, its presence merits attention and needs to be carefully monitored in alcoholic beverages such as beer and wine, where excessive accumulation may compromise product quality. Some studies suggested that diacetyl may have negative health influences and presents safety concerns, as inhalation exposure was associated with pulmonary toxicity and occupational diseases, and was even suggested as one of the risk factors in electronic cigarettes. Emerging studies suggest that diacetyl may exhibit pharmacological potential, including antioxidant, antifungal, and even neuroprotective properties, although research is still in early stages and merits deeper scientific evaluation. Considering its dual nature, beneficial and harmful, this review provides an overview of diacetyl’s properties, safety considerations, and promising applications in biotechnology, biomedicine, and fermented food systems, but with a focus on potential industrial and health hazards. In the current review, we have presented evidence for diacetyl’s beneficial properties and discussed its hazards. Full article

Electronic cigarettes (e-cigarettes) have emerged as a prevalent substitute for conventional cigarettes, garnering perceptions of being a safer option for health. Nicotine addicts use e-cigarettes to cease smoking. These products have also become common among young people because of their taste, smell, and attractive appearance. However, accumulating experimental and clinical evidence indicates that e-cigarette use is not risk-free. The inhalation of e-cigarette aerosols exposes users and their non-using peers to a complex mixture of chemical compounds, including aldehydes, heavy metals, and flavoring agents, many of which possess pro-oxidative and pro-inflammatory properties. This review summarizes and critically analyzes current evidence on the molecular and cellular mechanisms underlying the biological effects of e-cigarette aerosols. Particular attention is given to excessive production of reactive oxygen species, mitochondrial dysfunction, DNA damage, and the activation of redox-sensitive signaling pathways, including NF-κB and NRF2. These molecular alterations may trigger acute and, with prolonged exposure, chronic oxidative stress and inflammation, which in turn can affect gene expression, protein function, and metabolic pathways. While molecular and experimental studies often demonstrate adverse biological responses to e-cigarette aerosols, the translation of these findings into long-term clinical outcomes remains an area of ongoing investigation. Full article

Background/Objectives: Cigarette smoking is a well-established risk factor for periodontal tissue damage caused by oxidative stress and increased proteolytic activity. Electronic cigarettes (e-cigarettes), marketed as less harmful alternatives, deliver nicotine and reactive compounds that may similarly disrupt periodontal health. However, their molecular effects on clinically healthy periodontal tissues remain unclear. This study aimed to compare oxidative stress-related and matrix-degradative biomarkers in the gingival crevicular fluid (GCF) of cigarette smokers (CS), e-cigarette (EC) users, and non-smokers (NS), and to examine the relationships among these markers. Methods: Sixty individuals, who were systemically and periodontally healthy (20 CS, 20 EC, and 20 NS), were examined. Clinical parameters, including probing depth (PD), clinical attachment level (CAL), plaque index (PI), and bleeding on probing (BOP), were recorded. GCF samples were analyzed for reactive oxygen species (ROS), matrix metalloproteinase-9 (MMP-9), and forkhead box protein O-1 (FOXO-1) using ELISA. Initial group comparisons were descriptive, followed by analysis of covariance (ANCOVA) to adjust for age; PI and PD were included as covariates in separate models. Correlations were assessed using Spearman’s analysis. Results: PD was significantly higher in both EC users and CS compared with NS (p = 0.022). MMP-9 levels were significantly higher in CS than in EC users and NS (p < 0.05), while FOXO-1 concentrations were significantly lower in CS compared with NS (p = 0.0227). ROS levels did not differ significantly among groups (p > 0.05). After adjustment for age, PI, or PD, group differences in MMP-9 and FOXO-1 remained statistically significant, whereas ROS levels remained comparable. FOXO-1 demonstrated positive correlations with ROS and MMP-9 within exposure groups; these associations were considered exploratory. Conclusions: In this cross-sectional study, CS and EC use were associated with altered matrix-regulatory biomarker profiles in clinically healthy periodontal tissues, independent of age and periodontal indices. Causal or temporal inferences cannot be drawn, and longitudinal studies are needed to clarify the long-term periodontal implications of these findings. Full article

Conventional cigarette smoke and electronic cigarette vapor contain toxic compounds that may impair immune function, particularly in the spleen. This study evaluated histopathological changes in the spleen in male white rats (Rattus norvegicus, n = 32) divided into four groups: control, conventional-cigarette smoke (CCS), electronic cigarette vapor (ECS), and transitional cigarette smoke (TCS). The TCS group was sequentially exposed to CCS for 15 days followed by ECS for 15 days, with twice-daily exposure. Spleen tissues were analyzed semi-quantitatively using ImageJ and statistically using the Kruskal–Wallis test after Shapiro–Wilk normality testing. Comparisons among the four groups showed significant differences in necrosis (p = 0.025) and vascular degeneration (p = 0.027). In contrast, hemosiderin, congestion, stretching, and vacuolization parameters did not show statistically significant differences among groups (p > 0.05). These findings suggest that switching from conventional cigarettes to e-cigarettes does not protect against splenic damage and may exacerbate immune dysfunction due to cumulative toxic exposure. Full article

Background/Objectives: Coupled with the already-problematic background rates of traditional cigarette consumption during pregnancy, the surging epidemic of electronic cigarette usage among pregnant women redoubles the importance of understanding the impacts of nicotine exposure during critical periods of development. To date, a burgeoning body of human epidemiological and animal model research indicates that not only the children but also the grandchildren of maternal smokers are at higher risk for neurodevelopmental disorders such as ADHD, autism, and schizophrenia and are predisposed to neurodevelopmental abnormalities which transcend these diagnoses. However, the roles of discrete cellular sub-populations in these and other intergenerational consequences of smoking during pregnancy remain indeterminate. Methods: Toward the resolution of this void in the literature, the present study characterized alterations in the gene expression profiles of dopamine receptor D1-expressing striatal cells from the first- and second-generation male progeny of female mice that were continuously exposed to nicotine beginning prior to conception, continuing throughout pregnancy, and concluding upon weaning of offspring. Results: Dopamine receptor D1-expressing striatal cells from our mouse models of the children and grandchildren of maternal smokers exhibit differential expression patterns for a multitude of genes that are (1) individually associated with neurodevelopmental disorders, (2) collectively overrepresented in gene set annotations related to brain, behavioral, neurobiological, and epigenomic phenotypes shared among neurodevelopmental disorders, and (3) orthologous to human genes that exhibit differential DNA methylation signatures in the newborns of maternal smokers. Conclusions: Together with our and others’ previous findings, the results of this study support the emerging theory that, by inducing extensive alterations in gene expression that in turn elicit cascading neurobiological changes which ultimately confer widespread neurobehavioral abnormalities, nicotine-induced epigenomic dysregulation may be a primary driver of neurodevelopmental deficits and disorders in the children and grandchildren of maternal smokers. Full article

Background: Nicotine use among the youth has been on the rise, especially with the introduction of E-cigarettes. This has sparked concerns regarding E-cigarettes and traditional cigarettes in terms of patterns, dependence, and perceptions within the youth population, which are issues this study aimed to investigate. Methods: A cross-sectional survey was conducted among university students at Ajman University, which is in the Middle East and North Africa (MENA) region. Using the Cigarette Dependence Scale (CDS-12) and Penn State Electronic Cigarette Dependence Index (PS-ECDI), dependence on both cigarettes and E-cigarettes was quantified. Results: Out of 1713 respondents, 18.9% were currently using nicotine products, including E-cigarettes (12.7%) and traditional cigarettes (5.1%). Nicotine use was significantly associated more with males than females with an odds ratio of 4.14. However, there was no difference between genders in the dependence scores. In addition, dual nicotine use and an earlier onset of nicotine consumption were associated with significantly higher dependence scores than single users and a late onset of smoking. Participants overall attributed cigarettes and E-cigarettes as equally harmful. Conclusions: Both cigarette and e-cigarette use were prevalent and associated with notable dependence. Although E-cigarettes are often promoted as cessation aids, their use in our sample did not appear to facilitate quitting and may instead sustain nicotine dependence. Targeted youth-focused cessation programs and stricter marketing and sales regulations are essential to prevent further normalization. Longitudinal studies are needed to track evolving patterns and health impacts in the MENA region. Full article