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The use of e‐cigarette or vape devices is a growing concern on an international scale, given the devices' addictive nature and questions regarding their short‐ and long‐term health impacts. Their use is especially an issue in young people, many of whom have little or no previous nicotine use experience. This study tested an integrated dual process model in 363 young Australian undergraduates where prospectively measured e‐cigarette use was predicted by the psychological constructs of the theory of planned behavior, supplemented with risk perception, e‐cigarette dependence, habit, and implicit attitude. Intention to use an e‐cigarette was predicted by affective attitude, subjective norm, and e‐cigarette dependance, but not instrumental attitude, perceived behavioral control, or risk perception. E‐cigarette use was predicted by e‐cigarette dependance, intention, habit, implicit attitude, and previous nicotine use, although perceived behavioral control did not directly predict behavior nor moderate the intention–behavior relationship. Current findings provide evidence for important psychological predictors of e‐cigarette use, signposting potential intervention targets. Specifically, interventions may benefit from using strategies that tap affective or normative beliefs alongside automatic constructs and dependence, while focusing less on beliefs about the health impacts of e‐cigarettes or control over using. [ABSTRACT FROM AUTHOR]

This work aimed to determine the chemical composition of 22 e‐liquids available on the Slovenian market. Four different gas chromatography (GC) sample introduction techniques; headspace‐GC‐mass spectrometry (HS‐GC‐MS), liquid injection‐GC‐MS (LI‐GC‐MS), HS‐solid‐phase microextraction‐GC‐MS (HS‐SPME‐GC‐MS), and direct‐immersion‐SPME‐GC‐MS (DI‐SPME‐GC‐MS) were employed for qualitative analysis. Various experimental parameters were assessed for each GC sample introduction technique to maximize compound identification. Despite e‐liquid packaging reporting a maximum of eight compounds, GC‐MS identified more compounds in most samples, especially in menthol‐flavored (58 identifiable compounds by HS‐SPME‐GC‐MS), followed by nicotine‐containing and fruit‐flavored samples. HS‐SPME‐GC‐MS identified the highest number of compounds, followed by HS‐GC‐MS, DI‐SPME‐GC‐MS, and LI‐GC‐MS. Nicotine quantification in six samples was performed by LI‐GC‐MS with dilution in methanol. Nicotine concentration in samples ranged from 16.5 ± 0.5 to 18.5 ± 0.4 mg/mL, which was below the declared concentration of 20 mg/mL. Additionally, quantitative analysis of metals in e‐liquids was performed by inductively coupled plasma‐MS after microwave‐assisted wet acid digestion. Iron was the most abundant metal, with its content ranging from 0.024 to 0.354 µg/g. Barium, bismuth, copper, and tin were also determined in several e‐liquids. [ABSTRACT FROM AUTHOR]

The use of traditional nicotine delivery products such as tobacco has long been linked to detrimental health effects. However, little work to date has focused on the emerging market of aerosolized nicotine delivery known as electronic nicotine delivery systems (ENDS) or electronic cigarettes, and their potential for new effects on human health. Challenges studying these devices include heterogeneity in the formulation of the common components of most available ENDS, including nicotine and a carrier (commonly composed of propylene glycol and vegetable glycerin, or PG/VG). In the present study, we report on experiments interrogating the effects of major identified components in e‐cigarettes. Specifically, the potential concomitant effects of nicotine and common carrier ingredients in commercial "vape" products are explored in vitro to inform the potential health effects on the craniofacial skeleton through novel vectors as compared to traditional tobacco products. MC3T3‐E1 murine pre‐osteoblast cells were cultured in vitro with clinically relevant liquid concentrations of nicotine, propylene glycol (PG), vegetable glycerin (VG), Nicotine+PG/VG, and the vape liquid of a commercial product (Juul). Cells were treated acutely for 24 h and RNA‐Seq was utilized to determine segregating alteration in mRNA signaling. Influential gene targets identified with sparse partial least squares discriminant analysis (sPLS‐DA) implemented in mixOmics were assessed using the PANTHER Classification system for molecular functions, biological processes, cellular components, and pathways of effect. Additional endpoint functional analyses were used to confirm cell cycle changes. The initial excitatory concentration (EC50) studied defined a target concentration of carrier PG/VG liquid that altered the cell cycle of the calvarial cells. Initial sPLS‐DA analysis demonstrated the segregation of nicotine and non‐nicotine exposures utilized in our in vitro modeling. Pathway analysis suggests a strong influence of nicotine exposures on cellular processes including metabolic processes and response to stimuli including autophagic flux. Further interrogation of the individual treatment conditions demonstrated segregation by treatment modality (Control, Nicotine, Carrier (PG+VG), Nicotine+PG/VG) along three dimensions best characterized by: latent variable 1 (PLSDA‐1) showing strong segregation based on nicotine influence on cellular processes associated with cellular adhesion to collagen, osteoblast differentiation, and calcium binding and metabolism; latent variable 2 (PLSDA‐2) showing strong segregation of influence based on PG+VG and Control influence on cell migration, survival, and cycle regulation; and latent variable 3 (PLSDA‐3) showing strong segregation based on Nicotine and Control exposure influence on cell activity and growth and developmental processes. Further, gene co‐expression network analysis implicates targets of the major pathway genes associated with bone growth and development, particularly craniofacial (FGF, Notch, TGFβ, WNT) and analysis of active subnetwork pathways found these additionally overrepresented in the Juul exposure relative to Nicotine+PG/VG. Finally, experimentation confirmed alterations in cell count, and increased evidence of cell stress (markers of autophagy), but no alteration in apoptosis. These data suggest concomitant treatment with Nicotine+PG/VG drives alterations in pre‐osteoblast cell cycle signaling, specifically transcriptomic targets related to cell cycle and potentially cell stress. Although we suspected cell stress and well as cytotoxic effects of Nicotine+PG/VG, no great influence on apoptotic factors was observed. Further RNA‐Seq analysis allowed for the direct interrogation of molecular targets of major pathways involved in bone and craniofacial development, each demonstrating segregation (altered signaling) due to e‐cigarette‐type exposure. These data have implications directed toward ENDS formulation as synergistic effects of Nicotine+PG/VG are evidenced here. Thus, future research will continue to interrogate how varied formulation of Nicotine+PG/VG affects overall cell functions in multiple vital systems. [ABSTRACT FROM AUTHOR]

This article provides a personal account of the author's career in mass spectrometry, both in the United States and Spain. The author discusses their training in the US and their work with Dr. John Oró at the University of Houston, as well as their experiences with mass spectrometry and gas chromatography. They also mention their involvement in NASA research programs and the social and historic events they witnessed during their time in the US. The article then focuses on the challenges faced by the author in establishing a biomedical mass spectrometry laboratory in Spain, including the lack of support and funding for research. Despite these difficulties, the author and their team managed to publish papers and graduate students. The text also discusses the author's efforts to promote the use of biomedical mass spectrometry in Spain, including organizing international symposiums and meetings. The author reflects on the advancements in mass spectrometry technology during this time period. They also discuss their involvement in the organization of international conferences and the development of biomedical mass spectrometry in Spain. The author served on scientific committees and played a key role in organizing the 15th International Mass Spectrometry Conference in Barcelona in 2000. They also discuss the challenges and successes of their research group, including the creation of a proteomics MS lab. The author reflects on their career in the field of mass spectrometry, particularly in the medical community in Spain. They discuss the challenges they faced in conducting research and the lack of available resources and facilities. [Extracted from the article]

Background and Purpose: Traumatic brain injury (TBI) causes lifelong physical and psychological dysfunction in affected individuals. The current study investigated the effects of chronic nicotine exposure via E‐cigarettes (E‐cig) (vaping) on TBI‐associated behavioural and biochemical changes. Experimental Approach: Adult C57/BL6J male mice were subjected to controlled cortical impact (CCI) followed by daily exposure to E‐cig vapour for 6 weeks. Sensorimotor functions, locomotion, and sociability were subsequently evaluated by nesting, open field, and social approach tests, respectively. Immunoblots were conducted to examine the expression of mature brain‐derived neurotrophic factor (mBDNF) and associated downstream proteins (p‐Erk, p‐Akt). Histological analyses were performed to evaluate neuronal survival and neuroinflammation. Key Results: Post‐injury chronic nicotine exposure significantly improved nesting performance in CCI mice. Histological analysis revealed increased survival of cortical neurons in the perilesion cortex with chronic nicotine exposure. Immunoblots revealed that chronic nicotine exposure significantly up‐regulated mBDNF, p‐Erk and p‐Akt expression in the perilesion cortex of CCI mice. Immunofluorescence microscopy indicated that elevated mBDNF and p‐Akt expression were mainly localized within cortical neurons. Immunolabelling of Iba1 demonstrated that chronic nicotine exposure attenuated microglia‐mediated neuroinflammation. Conclusions and Implications: Post‐injury chronic nicotine exposure via vaping facilitates recovery of sensorimotor function by upregulating neuroprotective mBDNF/TrkB/Akt/Erk signalling. These findings suggest potential neuroprotective properties of nicotine despite its highly addictive nature. Thus, understanding the multifaceted effects of chronic nicotine exposure on TBI‐associated symptoms is crucial for paving the way for informed and properly managed therapeutic interventions. [ABSTRACT FROM AUTHOR]

Background and aims Methods Results Conclusion Cannabis and nicotine (tobacco or e‐cigarettes) use commonly co‐occurs and understanding their relationship can help to inform public health strategies to prevent their harms. We conducted a systematic review and meta‐analysis to estimate the association of cannabis use given prior nicotine use and vice versa.PubMed, Embase, PsycINFO, Google Scholar and a hand‐search were conducted in 2023 for longitudinal studies of the general population with no restrictions in settings (locations). Random‐effects meta‐analysis was conducted to estimate odds ratios between cannabis and nicotine use in both directions. The impact of unmeasured confounding was assessed using E‐values.From 5387 identified records, we included 20 studies. Among cannabis‐naïve youths, baseline use of any nicotine products was positively associated with initiation of any cannabis use at follow‐up [odds ratio (OR) = 5.39, 95% confidence interval (CI) = 3.19, 9.11; adjusted OR (aOR) = 2.59, 95% CI = 2.01, 3.32]. In nicotine‐naïve participants (youths + adults), baseline cannabis use was positively associated with the initiation of any nicotine use at follow‐up (OR = 4.08, 95% CI = 2.05, 8.11; aOR = 2.94, 95% CI =1.54, 5.61). There were no significant associations between baseline cannabis use and subsequent initiation of any nicotine (aOR = 3.29, 95% CI = 0.85, 12.76) or daily nicotine use (aOR = 2.63, 95% CI = 0.41, 16.95) among youths. The median E‐values were 5.5 for nicotine exposure and cannabis use initiation and 4.1 for cannabis exposure and nicotine use initiation, indicating that substantial unmeasured confounding would need to have a strong association with both outcomes to fully explain away the cannabis and nicotine relationship.Although the evidence for associations between cannabis use and tobacco use is mixed, a majority of studies to date have found that cannabis use is associated with prior nicotine use and vice versa. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to determine nicotine's impact on receptor‐mediated cyclic adenosine monophosphate (cAMP) synthesis in vascular smooth muscle (VSM). We hypothesize that nicotine impairs β adrenergic–mediated cAMP signaling in VSM, leading to altered vascular reactivity. Methods: The effects of nicotine on cAMP signaling and vascular function were systematically tested in aortic VSM cells and acutely isolated aortas from mice expressing the cAMP sensor TEpacVV (Camper), specifically in VSM (e.g., CamperSM). Results: Isoproterenol (ISO)‐induced β‐adrenergic production of cAMP in VSM was significantly reduced in cells from second‐hand smoke (SHS)–exposed mice and cultured wild‐type VSM treated with nicotine. The decrease in cAMP synthesis caused by nicotine was verified in freshly isolated arteries from a mouse that had cAMP sensor expression in VSM (e.g., CamperSM mouse). Functionally, the changes in cAMP signaling in response to nicotine hindered ISO‐induced vasodilation, but this was reversed by immediate PDE3 inhibition. Conclusions: These results imply that nicotine alters VSM β adrenergic–mediated cAMP signaling and vasodilation, which may contribute to the dysregulation of vascular reactivity and the development of vascular complications for nicotine‐containing product users. [ABSTRACT FROM AUTHOR]

Objectives: Electronic nicotine delivery systems (e‐cigarette, pod, and vape) are currently among the tobacco consumption of adolescents and young adults. The aim is to show oral mucosa and saliva alterations related to vape. Material and Methods: A vape‐user patient, presenting a white plaque in the posterior region of the hard palate, underwent clinical examination, sialometry, pH evaluation, and excisional biopsy of the white lesion. Molecular changes in saliva and vape liquid were analyzed by vibrational spectroscopy. Results: The histopathological analyses showed hyperparakeratosis without dysplasia. Formaldehyde, ketones, and aromatic hydrocarbon species were identified in e‐cig liquid by the FTIR. Conclusions: The use of vape may be related to the development of hyperkeratotic lesions in the oral mucosa as well as significantly modify the patient's salivary patterns as the vape liquid presents carcinogenic and cytotoxic components in its composition. [ABSTRACT FROM AUTHOR]

Background and aims Design, setting and participants Measurements Findings Conclusion Disposable electronic cigarette (e‐cigarette) use is becoming more popular among US youth, given the shifting landscape in product marketing, availability and regulation. This study aimed to estimate the prevalence of and test factors associated with the most used e‐cigarette product (disposable versus other) among US youth aged 9–18 years who currently use e‐cigarettes.This was an observational study using cross‐sectional data from the US‐based 2021 and 2022 National Youth Tobacco Surveys (n = 48 704). We restricted our analytical sample to youth who currently use e‐cigarettes (n = 4137). The sample ranged from 9 to 18 years old and was 53.0% female.We dichotomized e‐cigarette device type to disposable versus all other types (e.g. refillable pods/cartridges). We conducted logistic regression to estimate whether age, sex, race/ethnicity, sexual orientation, frequency of e‐cigarette use, nicotine vaping, flavored e‐cigarette use and current combustible/non‐combustible tobacco use were associated with disposable e‐cigarette use, compared with other e‐cigarette use.Among youth who currently use e‐cigarettes, 54.5% used disposable e‐cigarettes. Older age (17–18 years), relative to younger age (9–14 years) [odds ratio (OR) = 1.43, 95% confidence interval (CI) = 1.07–1.91], non‐Hispanic Black (versus non‐Hispanic White) race/ethnicity (OR = 1.47, 95% CI = 1.01–2.15), any nicotine (versus non‐nicotine) vaping (OR = 2.51, 95% CI = 1.96–3.23) and flavored (versus non‐flavored) e‐cigarette use (OR = 1.93, 95% CI = 1.46–2.56) were associated with increased odds of mainly using disposable e‐cigarettes, compared with using other e‐cigarette products, whereas current combustible tobacco use (versus non‐current) (OR = 0.65, 95% CI = 0.53–0.80) and current non‐combustible tobacco use (versus non‐current) (OR = 0.58, 95% CI = 0.43–0.78) were associated with lower odds.Disposable e‐cigarettes appear to be the most used type of e‐cigarette product among US youth. Older age, non‐Hispanic Black race/ethnicity, nicotine vaping and flavored e‐cigarette use are associated with mainly using disposable e‐cigarettes, relative to other e‐cigarette products. [ABSTRACT FROM AUTHOR]

The leading cause of death in people living with HIV (PLWH) is cardiovascular disease, and the high prevalence of tobacco cigarette (TC) smoking is a major contributor. Switching to electronic cigarettes (ECs) has been promoted as a harm reduction strategy. We sought to determine if acute EC compared to TC smoking had less harmful effects on arrhythmogenic risk factors including acute changes in hemodynamics, heart rate variability (HRV), and ventricular repolarization (VR). In PLWH who smoke, changes in hemodynamics, HRV, and VR were compared pre/post acutely using an EC, TC, or puffing on an empty straw on different days in random order, in a crossover study. Thirty‐seven PLWH (36 males, mean age 40.5 ± 9.1 years) participated. Plasma nicotine was greater after TC versus EC use (10.12 ± 0.96 vs. 6.18 ± 0.99 ng/mL, respectively, p = 0.004). HR increased significantly, and similarly, after acute EC and TC smoking compared to control. Changes in HRV that confer increased cardiac risk (LF/HF ratio) were significantly smaller after acute EC versus TC use, consistent with a harm reduction effect. In a post‐hoc analysis of PLWH with and without positive concurrent recreational drug use as indicated by point of care urine toxicology testing, this differential effect was only seen in PLWH not currently using recreational drugs. Changes in VR were not different among the three exposures. In PLWH who smoke, EC compared to TC smoking resulted in smaller adverse changes in HRV. This differential effect was accompanied by a smaller increase in plasma nicotine, and was negated by concurrent recreational drug use. Additional studies are warranted in this vulnerable population disproportionately affected by tobacco‐related health disparities. [ABSTRACT FROM AUTHOR]

An accurate, disposable and cost‐effective determination, and monitoring of nicotine in human bodily fluids such as serum and saliva is significant due to the deleterious effects on humankind. In this paper, it was reported an electrocatalytic sensing platform for nicotine determination with poly azorubin s film modified pencil graphite electrode qualified by electroanalytical techniques such as cyclic voltammetry and electrochemical impedance spectroscopy, electron beam based technique of scanning electron microscopy, and X‐ray based techniques including photoelectron spectroscopy and energy dispersive spectroscopy. The developed platform exhibited a 410 % signal increase compared to the bare pencil graphite electrode (280 % increase in current density over aPGE) for nicotine detection due to the improved charge transfer and conductivity characteristics of the polymer film. The oxidation peak at 700 mV was employed for nicotine detection with a good detection sensitivity of 4.120μAμM-1cm-2 ${4.120\hskip0.17em\hskip0.17em{\rm \mu }{\rm A}\hskip0.17em{{\rm \mu }{\rm M}}^{-1}\hskip0.17em{{\rm c}{\rm m}}^{-2}}$ , a remarkable detection limit of 89 nM, and wide linear ranges of 0.25–3 μM and 5–100 μM. Furthermore, the electrochemical sensor showcases superb stability, selectivity and accuracy for the determination of nicotine in real samples of human serum and saliva. [ABSTRACT FROM AUTHOR]

Aim: To investigate the associations of individual and combined healthy lifestyle factors (HLS) with the risk of stroke in individuals with diabetes in China. Methods: This prospective analysis included 41 314 individuals with diabetes [15 191 from the Comprehensive Research on the Prevention and Control of the Diabetes (CRPCD) project and 26 123 from the China Kadoorie Biobank (CKB) study]. Associations of lifestyle factors, including cigarette smoking, alcohol consumption, physical activity, diet, body shape and sleep duration, with the risk of stroke, intracerebral haemorrhage (ICH) and ischaemic stroke (IS) were assessed using Cox proportional hazard models. Results: During median follow‐up periods of 8.02 and 9.05 years, 2499 and 4578 cases of stroke, 2147 and 4024 of IS, and 160 and 728 of ICH were documented in individuals with diabetes in the CRPCD and CKB cohorts, respectively. In the CRPCD cohort, patients with ≥5 HLS had a 14% lower risk of stroke (hazard ratio (HR): 0.86, 95% confidence interval (CI): 0.75‐0.98) than those with ≤2 HLS. In the CKB cohort, the adjusted HR (95% CI) for patients with ≥5 HLS were 0.74 (0.66‐0.83) for stroke, 0.74 (0.66‐0.83) for IS, and 0.57 (0.42‐0.78) for ICH compared with those with ≤2 HLS. The pooled adjusted HR (95% CI) comparing patients with ≥5 HLS versus ≤2 HLS was 0.79 (0.69‐0.92) for stroke, 0.80 (0.68‐0.93) for IS, and 0.60 (0.46‐0.78) for ICH. Conclusions: Maintaining a healthy lifestyle was associated with a lower risk of stroke, IS and ICH among individuals with diabetes. [ABSTRACT FROM AUTHOR]

Insect neuronal nicotinic acetylcholine receptors (nAChRs) are transmembrane receptors that play a key role in the development and synaptic plasticity of both vertebrates and invertebrates and are considered to be major targets of neonicotinoid insecticides. We used dorsal unpaired median (DUM) neurons, which are insect neurosecretory cells, in order to explore the intracellular mechanisms leading to the regulation of insect neuronal nAChRs in more detail. Using whole‐cell patch‐clamp and fura‐2AM calcium imaging techniques, we found that a novel CaMKK/AMPK pathway could be involved in the intracellular regulation of DUM neuron nAChRs. The CaMKK selective inhibitor, STO, reduced nicotinic current amplitudes, and strongly when co‐applied with α‐Bgt. Interestingly, intracellular application of the AMPK activator, A‐76, prevented the reduction in nicotine‐induced currents observed in the presence of the AMPK inhibitor, dorsomorphin. STO prevented the increase in intracellular calcium induced by nicotine, which was not dependent on α‐Bgt. Currents induced by 1 mM LMA, a selective activator of nAChR2, were reduced under bath application of STO, and mecamylamine, which blocked nAChR2 subtype, inhibited the increase in intracellular calcium induced by LMA. These findings provide insight into potential complex mechanisms linked to the modulation of the DUM neuron nAChRs and CaMKK pathway. [ABSTRACT FROM AUTHOR]

The addictive use of nicotine contained in tobacco is associated with stressor‐like emotional and cognitive effects such as anxiety and working memory impairment, and the involvement of epigenetic mechanisms such as histone acetylation has recently been reported. Although the precise nature of behavioural plasticity remains unclear, both anxiogenic‐ and working memory impairment‐like effects were observed in the present experimental model of mice treated with repeated subcutaneous nicotine and/or immobilization stress, and these effects were commonly attenuated by the histone deacetylase (HDAC) inhibitors that induce histone acetylation. Such HDAC inhibitor‐induced resilience was mimicked by ligands for the endocannabinoid (ECB) system, a neurotransmitter system that is closely associated with nicotine‐induced addiction‐related behaviours: the anxiogenic‐like effects were mitigated by the cannabinoid type 1 (CB1) agonist arachidonylcyclopropylamide (ACPA), whereas the working memory impairment‐like effects were mitigated by the CB1 antagonist SR 141716A. Moreover, the effects of the HDAC inhibitors were also mimicked by ligands for the endovanilloid (transient receptor potential vanilloid 1 [TRPV1]) system, a system that shares common characteristics with the ECB system: the anxiogenic‐like effects were mitigated by the TRPV1 antagonist capsazepine, whereas the working memory impairment‐like effects were mitigated by the TRPV1 agonist olvanil. Notably, the HDAC inhibitor‐induced anxiolytic‐like effects were attenuated by SR 141716A, which were further counteracted by capsazepine, whereas the working memory improvement‐like effects were attenuated by capsazepine, which were further counteracted by SR 141716A. These results suggest the contribution of interrelated control of the ECB/TRPV1 systems and epigenetic processes such as histone acetylation to novel therapeutic approaches. [ABSTRACT FROM AUTHOR]

Objectives: The present study utilized an intersectional framework to examine if two forms of gendered racism, psychological emasculation and messages about Asian American men being undesirable partners, were associated with Asian American men's nicotine use. We also examined the potential mediating roles of two racial identity statuses, racial conformity and racial immersion. Methods: A sample of 356 Asian American men living in the United States of America (USA) completed a cross‐sectional survey via Qualtrics containing measures assessing the aforementioned constructs of interest. The primary analysis examined separate parallel mediation models, situating psychological emasculation and undesirable partner as separate independent variables, racial conformity and racial immersion as parallel mediators, nicotine use as the outcome, and age and employment as covariates. Results: In separate parallel mediation models, the links between psychological emasculation and undesirable partner on one hand, and nicotine use on the other, were completely mediated only by racial conformity, and not significantly mediated by racial immersion. Specifically, greater endorsement of gendered racism was associated with greater conformity with (and internalization of) these gendered racist beliefs, which in turn were associated with greater nicotine use. Conclusion: Researchers and practitioners may consider racial conformity as an interventional target to ameliorate Asian American men's nicotine use. Future studies should continue to examine other culturally relevant and/or potentially protective constructs (e.g., on the basis of gender, race, and its intersection) that may mitigate Asian American men's nicotine use. [ABSTRACT FROM AUTHOR]

The quantitative measurement of urinary biomarkers in wastewater has emerged as a robust tool for estimating alcohol and tobacco consumption in populations. In this study, we applied the wastewater‐based epidemiology (WBE) approach to compare alcohol and tobacco use between university students and urban inhabitants in Ho Chi Minh City, Vietnam. Ethyl sulfate and cotinine serve as markers for alcohol and tobacco use, respectively. Our findings reveal that urban inhabitants aged 15 and above consume 1.56 ± 0.23 mL of pure ethanol and 2.8 ± 0.33 mg of nicotine per day, while university students consume 0.69 ± 0.13 mL of pure alcohol and 1.2 ± 0.2 mg of nicotine per day. This indicates that, on average, students consume less alcohol and tobacco compared with urban adults. A Monte Carlo simulation indicated that, on average, university students in our study smoke 1.5 cigarettes per day, while urban residents aged 15 and above smoke 4.3 cigarettes per day. Considering the smoking prevalence, a student smoker in this study consumes 6.5 cigarettes per day, a level high enough to establish addiction. On the other hand, alcohol use estimation is significantly lower than previous survey‐based reports, likely due to degradation within on‐site septic tanks. Future research should aim to extend the sampling period to capture seasonal variations and improve the understanding of tobacco and alcohol consumption patterns. The results from this study are crucial for decision‐makers in Ho Chi Minh City to develop effective public health strategies and interventions. Practitioner Points: Wastewater‐based approach is applicable to estimate the tobacco consumption in Ho Chi Minh City.Each current smoker in the urban area of Ho Chi Minh City smokes nearly a package a day.The estimated consumption for student smokers in U‐town is 6.5 cigarettes per day, a level high enough to establish addiction.The existence of septic tanks within Vietnam's drainage systems prevents reliable estimation of alcohol consumption for the entire population. [ABSTRACT FROM AUTHOR]

Introduction: Tobacco smoking is highly prevalent among alcohol and other drugs (AOD) service clients and, despite interest in quitting, abstinence is rarely sustained. Nicotine products may assist after discharge from residential treatment services, but little is known about client receptivity to them. This study examined AOD withdrawal service clients' experiences of two types of nicotine products for smoking cessation post‐discharge, combination nicotine replacement therapy (cNRT) and nicotine vaping products (NVP). Methods: We held semi‐structured telephone interviews with 31 Australian AOD service clients in a clinical trial of a 12‐week smoking cessation intervention using Quitline support plus cNRT or NVP delivered post‐discharge from a smoke‐free residential service. We asked about health and social factors, nicotine cravings, Quitline experience, and barriers and facilitators to cNRT or NVP, then thematically analysed data. Results: cNRT and NVP were described by participants as feasible and acceptable for smoking cessation. For most participants, cost limited cNRT access post study, as did difficulty navigating NVP prescription access. Quitline support was valued, but not consistently used, with participants noting low assistance with NVP‐facilitated cessation. Participants considered both cessation methods acceptable and socially supported, and sought information on decreasing nicotine use via NVP. Discussion and Conclusions: AOD service clients highly valued receiving cNRT or NVP with behavioural support for smoking reduction or abstinence. Both interventions were acceptable to service clients. Findings suggest a potential need to examine both whether NVP use should be permitted in this context, and guidance on the individual suitability of cNRT or NVP. [ABSTRACT FROM AUTHOR]

Background and aims Design and setting Participants Measurements Findings Conclusions In Finland, nicotine pouches entered the national market abruptly in 2023, following a change in April 2023 from medicinal product classification into less regulated tobacco surrogate status. This study aimed to measure adolescent nicotine pouch use and associated characteristics.A cross‐sectional, nationwide school‐based survey among students in comprehensive schools (COMP), general upper secondary schools (GEN) and vocational institutes (VOC) in 2023 in Finland.A total of 151 224 respondents aged 14–20 years (mean age 16.18 years, standard deviation 1.20 years).Nicotine pouch use was used as the outcome variable. Demographics included age, sex, school type and tobacco product use (smoking, snus use and e‐cigarette use). Covariates included parental education and parental smoking. All measures were self‐reported.Unadjusted results showed that current nicotine pouch use was more common among boys (11.3%) than among girls (3.3%), adolescents in VOC (15.4%) compared with COMP (6.8%) and GEN (4.3%), whereas daily use of other tobacco and nicotine products was associated with current nicotine pouch use compared with never using such products and the association was especially strong for snus use. The fully adjusted estimates of current nicotine pouch use remained strong for daily use of other tobacco and nicotine products (snus use: adjusted prevalence ratio [aPR] = 74.95, 95% confidence interval [CI] = 65.65–84.25; smoking: aPR = 1.43, 95% CI = 1.36–1.50; e‐cigarette use: aPR = 2.15, 95% CI = 2.04–2.27) and for sex (boys aPR = 1.53, 95% CI = 1.48–1.57). There was no clear evidence of differences in current nicotine pouch use by school type, age or parental factors in the fully adjusted model.In Finland in 2023, during which the availability of nicotine pouches became less regulated, nicotine pouch use appeared to be more common among boys and adolescents who used other nicotine products. [ABSTRACT FROM AUTHOR]

Background and aims: E‐cigarette and other electronic nicotine delivery systems (ENDS) use has grown considerably over the past decade, with notable increases among young people. US state policy contexts for ENDS and tobacco may shape initiation into ENDS use among adolescents as they age into early adulthood. We aimed to determine whether state‐level comprehensive vaping ban policies reduce the odds of youth initiation into ENDS use, net of additional state‐level ENDS and tobacco policies, as well as the youth's cigarette smoking status. Design: Longitudinal data from the Population Assessment of Tobacco and Health study were merged with a state‐year database on tobacco and ENDS policies. Multivariable discrete‐time event history models of ENDS initiation were estimated. Setting: United States. Participants: Twenty thousand twelve youth assessed over six waves from 2013 to 2019 (n = 53 974 observations). Measurement We examined comprehensive indoor vaping bans (i.e. 100% vape‐free workplaces, restaurants and bars) as a key factor in initiation into ENDS use (i.e. first instance of vaping) from age 13 to 22. Findings Among young people, residing in a state with a comprehensive vaping ban was associated with 18% lower odds of ENDS initiation (odds ratio = 0.82; 95% confidence interval =[0.71, 0.94]), even after controlling for other state ENDS and tobacco policies, the youth's cigarette smoking and socio‐demographic background and state‐level covariates. Conclusions: In the United States, state‐level vaping bans (i.e. 100% vape‐free workplaces, restaurants and bars) are associated with reduced odds of youth initiation into electronic nicotine delivery systems use. [ABSTRACT FROM AUTHOR]

Exposure to cigarette smoke directly damages the lungs and causes lung inflammation. The anti‐inflammatory properties of edible bird's nest (EBN) have been reported. We aimed to determine the effect of EBN on pneumonia in a mouse model exposed to cigarette smoke. Fifty BALB/c mice were randomly divided into control, model, positive drug, low‐dose EBN, and high‐dose EBN groups (n = 10 each). Except for the control group, the mice in each group were exposed to four cigarettes once a day for 8 days. In addition, we validated the effects of EBN on A549 cells and investigated the mechanism by which EBN alleviates lung inflammation. Edible bird's nest (EBN) could alleviate the structural damage of lung tissue and the smoke‐induced inflammatory response in mice. The best effect was observed at the high dose of EBN (0.019 g). The mice treated with EBN had a stronger ability than those in the model group to resist cigarette smoke stimulation, as indicated by a decrease in serum and lung inflammatory markers (interleukin 6 [IL‐6], tumor necrosis factor‐α [TNF‐α], and interleukin 8 [IL‐8]), an increase in serum interleukin 10 (IL‐10) levels, and a decrease in the expression of inflammasome NOD‐like receptor pyrin 3 (NLRP3). In addition, our cell experiments showed that EBN attenuated cigarette smoke‐induced pulmonary inflammation mainly by inhibiting the tumor necrosis factor receptor 1 (TNFR1)/nuclear factor‐kappa B (NF‐κB)/NLRP3 pathway. These findings provide theoretical evidence for the positive nutritional qualities of EBN for the lung by demonstrating that it inhibits the TNFR1/NF‐κB/NLRP3 signaling pathway, which prevents the development of cigarette smoke‐induced pulmonary inflammation. [ABSTRACT FROM AUTHOR]

Background: Controversy persists regarding the causal relationship between Cigarette smoking, alcohol consumption, and Rosacea. This paper employs the Mendelian randomization (MR) method to elucidate the correlation between Cigarette smoking, alcohol consumption, and Rosacea. The aim is to contribute valuable insights to aid in the prevention and early treatment of Rosacea. Method: Summary datasets for cigarette smoking parameters (Cigarettes smoked per day, Smoking status: Previous, smoking status: Current) and alcohol consumption (Alcoholic drinks per week) were selected alongside data for Rosacea from genome‐wide association studies (GWAS). The Two‐sample MR method was employed to analyze the correlation between cigarette smoking, alcohol consumption, and Rosacea. Various MR analysis methods, including inverse variance weighting (IVW), MR‐Egger, Simple Mode, Weighted Mode, and Weighted Median, were chosen. IVW served as the primary analysis method. Results: The results indicate a significant negative association between Cigarettes smoked per day and Rosacea. Moreover, a significant positive correlation was observed between Smoking status: Previous and Rosacea. However, no significant associations were found between Smoking status: Current, Alcoholic drinks per week, and Rosacea. Conclusion: This study provides further clarity on the association between cigarette smoking, drinking, and Rosacea through a two‐sample MR analysis. Notably, the number of cigarettes smoked per day appears to be associated with a reduced incidence of Rosacea, while cigarette smoking cessation may increase the risk. Surprisingly, alcohol consumption does not emerge as a significant risk factor for Rosacea. These findings contribute to a nuanced understanding of the complex relationship between lifestyle factors and the occurrence of Rosacea, offering potential insights for preventive measures and early intervention. [ABSTRACT FROM AUTHOR]

Molecular vibrations and quantum tunneling may link ligand binding to the function of pharmacological receptors. The well‐established lock‐and‐key model explains a ligand's binding and recognition by a receptor; however, a general mechanism by which receptors translate binding into activation, inactivation, or modulation remains elusive. The Vibration Theory of Olfaction was proposed in the 1930s to explain this subset of receptor‐mediated phenomena by correlating odorant molecular vibrations to smell, but a mechanism was lacking. In the 1990s, inelastic electron tunneling was proposed as a plausible mechanism for translating molecular vibration to odorant physiology. More recently, studies of ligands' vibrational spectra and the use of deuterated ligand analogs have provided helpful information to study this admittedly controversial hypothesis in metabotropic receptors other than olfactory receptors. In the present work, based in part on published experiments from our laboratory using planarians as an experimental organism, I will present a rationale and possible experimental approach for extending this idea to ligand‐gated ion channels. [ABSTRACT FROM AUTHOR]

Background and Aims: Nicotine vaping products (NVPs) can potentially help adult tobacco users quit smoking. This study evaluated how adult consumers compare the costs between NVPs and cigarettes. Method: We used data from the US arm of the 2016–2020 International Tobacco Control Four Country Smoking and Vaping (ITC 4CV) surveys to perform a multinomial logit model with two‐way fixed effects to measure how perceived cost comparisons are associated with NVP and cigarette taxes, use patterns, NVP device types and individual sociodemographic factors. Results: Higher cigarette taxes are associated with a greater likelihood of perceiving NVPs and cigarettes as costing the same for the overall population and among people who exclusively smoke, and a lower likelihood of perceiving NVPs as more expensive among people who exclusively vape, compared with lower cigarette taxes. Pre‐filled cartridge and tank users are more likely to perceive NVPs as less expensive than cigarettes, compared with people who use other types of NVPs. The associations between taxes and perceived cost comparison were more pronounced among males, younger and low‐income populations. Conclusions: Higher cigarette taxes are associated with perceived financial incentives for nicotine vaping products (NVPs) over cigarettes, whereas NVP taxes are not associated with perceived cost comparison between NVPs and cigarettes. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to examine the safety of e‐cigarettes (EC) and nicotine patches (NRT) when used to help pregnant smokers quit. Design: A recent trial of EC versus NRT reported safety outcomes in the randomized arms. We conducted a further analysis based on product use. Setting: Twenty‐three hospitals in England and a stop‐smoking service in Scotland took part. Participants: The participants comprised 1140 pregnant smokers. Interventions: We compared women using and not using EC and NRT regularly during pregnancy. Measurements Measurements included nicotine intake compared with baseline, birth weight, other pregnancy outcomes, adverse events, maternal respiratory symptoms and relapse in early abstainers. Findings Use of EC was more common than use of NRT (47.3% vs 21.6%, P < 0.001). Women who stopped smoking (abstainers) and used EC at the end‐of‐pregnancy (EOP) reduced their salivary cotinine by 45% [49.3 ng/ml, 95% confidence interval (CI) = −79.8 to −10]. Only one abstainer used NRT at EOP. In dual users, cotinine increased by 19% (24 ng/ml, 95% CI = 3.5–68). In women reporting a reduction of at least 50% in cigarette consumption, cotinine levels increased by 10% in those using nicotine products and by 9% in those who did not. Birth weights in dual users and exclusive smokers were the same (3.1 kg). Birth weight in abstainers using either nicotine product was higher than in smokers [3.3 kg, standard deviation (SD) = 0.7] versus 3.1 kg, SD = 0.6; difference = 0.15 kg, 95% CI = 0.05–0.25) and not different from abstainers not using nicotine products (3.1 kg, SD = 0.8). Abstainers and smokers using nicotine products had no worse pregnancy outcomes or more adverse events than abstainers and smokers not using them. EC users reported more improvements than non‐users in cough [adjusted relative risk (aRR) = 0.59, 95% CI = 0.37–0.93] and phlegm (aRR = 0.53, 95% CI = 0.31–0.92), controlling for smoking status. EC or NRT use had no association with relapse. Conclusions: Regular use of e‐cigarettes or nicotine patches by pregnant smokers does not appear to be associated with any adverse outcomes. [ABSTRACT FROM AUTHOR]

Background: The psychological well‐being of lung cancer patients is critical in‐patient care but frequently overlooked. Methods: This study, employing a cross‐sectional, questionnaire‐based design, aimed to elucidate the prevalence of depressive and anxiety symptoms among lung cancer patients and identify associated risk factors. Participants' demographic, medical history, disease stage, and pathology were systematically collected. Psychological assessment was conducted using the general anxiety disorder‐7 (GAD‐7), patient health questionnaire‐9 (PHQ‐9), and hospital anxiety and depression scale (HADS). Statistical analyses were performed using SPSS software (version 25.0). Results: Out of 294 distributed questionnaires, 247 lung cancer patients were included in the final analysis, with an average completion time of 9.08 min. Notably, 32.4% exhibited depressive symptoms, while 30% displayed signs of anxiety. A significant correlation was found between both depressive and anxiety symptoms and a history of tobacco and alcohol consumption. Specifically, increased nicotine dependence and greater cumulative tobacco use were linked to higher rates of depressive symptoms, whereas cumulative alcohol consumption was associated with increased risks of anxiety symptoms. Conclusion: The study affirms the feasibility of GAD‐7, PHQ‐9, and HADS as screening tools for depressive and anxiety symptoms in lung cancer patients. It further highlights tobacco and alcohol consumption as significant risk factors for poor psychological health in this population. [ABSTRACT FROM AUTHOR]

Functional MRI (fMRI) and MRS (fMRS) can be used to noninvasively map cerebral activation and metabolism. Recently, hyperpolarized 13C spectroscopy and metabolic imaging have provided an alternative approach to assess metabolism. In this study, we combined 1H fMRI and hyperpolarized [1‐13C]pyruvate MRS to compare cerebral blood oxygenation level‐dependent (BOLD) response and real‐time cerebral metabolism, as assessed with lactate and bicarbonate labelling, during nicotine stimulation. Simultaneous 1H fMRI (multislice gradient echo echo‐planar imaging) and 13C spectroscopic (single slice pulse‐acquire) data were collected in urethane‐anaesthetized female Sprague–Dawley rats (n = 12) at 9.4 T. Animals received an intravenous (i.v.) injection of either nicotine (stimulus; 88 μg/kg, n = 7, or 300 μg/kg, n = 5) or 0.9% saline (matching volume), followed by hyperpolarized [1‐13C]pyruvate injection 60 s later. Three hours later, a second injection was administered: the animals that had previously received saline were injected with nicotine and vice versa, both followed by another hyperpolarized [1‐13C]pyruvate i.v. injection 60 s later. The low‐dose (88 μg/kg) nicotine injection led to a 12% ± 4% (n = 7, t‐test, p ~ 0.0006 (t‐value −5.8, degrees of freedom 6), Wilcoxon p ~ 0.0078 (test statistic 0)) increase in BOLD signal. At the same time, an increase in 13C‐bicarbonate signal was seen in four out of six animals. Bicarbonate‐to‐total carbon ratios were 0.010 ± 0.004 and 0.018 ± 0.010 (n = 6, t‐test, p ~ 0.03 (t‐value −2.3, degrees of freedom 5), Wilcoxon p ~ 0.08 (test statistic 3)) for saline and nicotine experiments, respectively. No increase in the lactate signal was seen; lactate‐to‐total carbon was 0.16 ± 0.02 after both injections. The high (300 μg/kg) nicotine dose (n = 5) caused highly variable BOLD and metabolic responses, possibly due to the apparent respiratory distress. Simultaneous detection of 1H fMRI and hyperpolarized 13C‐MRS is feasible. A comparison of metabolic response between control and stimulated states showed differences in bicarbonate signal, implying that the hyperpolarization technique could offer complimentary information on brain activation. [ABSTRACT FROM AUTHOR]

Objective: 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. Data Sources: PubMed, SCOPUS, EMBASE databases. Review Methods: 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. Results: 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. Conclusion: Current data suggest that 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 FROM AUTHOR]

Background Methods Results Conclusions Why do potentially traumatic events (PTEs) and substance use (SU) so commonly co‐occur during adolescence? Causal hypotheses developed from the study of posttraumatic stress disorder (PTSD) and substance use disorder (SUD) among adults have not yet been subject to rigorous theoretical analysis or empirical tests among adolescents with the precursors to these disorders: PTEs and SU. Establishing causality demands accounting for various factors (e.g. genetics, parent education, race/ethnicity) that distinguish youth endorsing PTEs and SU from those who do not, a step often overlooked in previous research.We leveraged nationwide data from a sociodemographically diverse sample of youth (N = 11,468) in the Adolescent Brain and Cognitive Development Study. PTEs and substance use prevalence were assessed annually. To account for the many pre‐existing differences between youth with and without PTE/SU (i.e. confounding bias) and provide rigorous tests of causal hypotheses, we linked within‐person changes in PTEs and SU (alcohol, cannabis, nicotine) across repeated measurements and adjusted for time‐varying factors (e.g. age, internalizing symptoms, externalizing symptoms, and friends' use of substances).Before adjusting for confounding using within‐person modeling, PTEs and SU exhibited significant concurrent associations (βs = .46–1.26, ps < .05) and PTEs prospectively predicted greater SU (βs = .55–1.43, ps < .05) but not vice versa. After adjustment for confounding, the PTEs exhibited significant concurrent associations for alcohol (βs = .14–.23, ps < .05) and nicotine (βs = .16, ps < .05) but not cannabis (βs = ‐.01, ps > .05) and PTEs prospectively predicted greater SU (βs = .28–.55, ps > .05) but not vice versa.When tested rigorously in a nationwide sample of adolescents, we find support for a model in which PTEs are followed by SU but not for a model in which SU is followed by PTEs. Explanations for why PTSD and SUD co‐occur in adults may need further theoretical analysis and adaptation before extension to adolescents. [ABSTRACT FROM AUTHOR]

Aedes albopictus, the main vector of dengue, yellow fever, chikungunya, and Zika, has caused significant public health concerns, but there are still few effective insecticides. Nicotine and nornicotine‐typed compounds are well‐known for their potential as an insecticide, which has potential activity against Ae. albopictus. Here we report the effects of nornicotine‐typed insecticide against larvae of Ae. albopictus. We developed a novel synthetic strategy for nicotine and nornicotine‐typed compounds. Novel compounds A1‐A8 and B1‐B26 were synthesized by the synthesized nornicotine. And bioassays indicated that most of these compounds exhibited good effects against larvae of Ae. albopictus, and compounds A3, B4, B20, and B26 had excellent activity against Ae. albopictus, and they were not toxic to humans according to other reports. After considering the cost, compounds B4, B20, and B26 could be potential lead compounds against Ae. albopictus and other Aedes mosquitoes. [ABSTRACT FROM AUTHOR]

Polysubstance use (PSU), the use of two or more substances proximally, is highly prevalent and has amplified the risk for morbidity and mortality. However, PSU patterns and associated risk factors are not well characterized. This may be especially relevant to women who are known to be vulnerable to stress/trauma, craving, pain, and anxious and depressive symptoms as associated risk factors for PSU. A cross‐sectional observational study was conducted to characterize substance use patterns in women who regularly used cocaine, opioids, marijuana, alcohol, benzodiazepines and/or nicotine and were being assessed for a placebo‐controlled study of guanfacine treatment (n = 94; ages 19–65). Data on stress/traumatic life events, drug cravings for each substance, pain ratings, and anxiety and depressive symptoms were also obtained using standardized well‐validated surveys. High use per day of two or more drugs was observed (72.7% ± 33.3%) and opioid amounts were high relative to other drug amounts (p's < 0.001). Notably, higher stress/trauma events and higher cravings are each associated with cumulative PSU days, amounts and probability of an individual PSU day (p's < 0.02). This remained when PSU versus single substance use was compared. Pain, anxiety and depressive symptoms were not associated with PSU metrics. These findings characterize specific patterns of PSU in women and show that average drug craving and stress/trauma events are associated with PSU. Interventions that focus on stress/trauma and craving management could be of benefit in reducing PSU risk in women. [ABSTRACT FROM AUTHOR]

Aims: Exposure to crystalline silica (CS) in occupational settings induces chronic inflammation in the respiratory system and, potentially, the brain. Some workers are frequently concurrently exposed to both CS and nicotine. Here, we explored the impact of nicotine on CS‐induced neuroinflammation in the mouse hippocampus. Methods: In this study, we established double‐exposed models of CS and nicotine in C57BL/6 mice. To assess depression‐like behavior, experiments were conducted at 3, 6, and 9 weeks. Serum inflammatory factors were analyzed by ELISA. Hippocampus was collected for RNA sequencing analysis and examining the gene expression patterns linked to inflammation and cell death. Microglia and astrocyte activation and hippocampal neuronal death were assessed using immunohistochemistry and immunofluorescence staining. Western blotting was used to analyze the NF‐κB expression level. Results: Mice exposed to CS for 3 weeks showed signs of depression. This was accompanied by elevated IL‐6 in blood, destruction of the blood–brain barrier, and activation of astrocytes caused by an increased NF‐κB expression in the CA1 area of the hippocampus. The elevated levels of astrocyte‐derived Lcn2 and upregulated genes related to inflammation led to higher neuronal mortality. Moreover, nicotine mitigated the NF‐κB expression, astrocyte activation, and neuronal death, thereby ameliorating the associated symptoms. Conclusion: Silica exposure induces neuroinflammation and neuronal death in the mouse hippocampal CA1 region and depressive behavior. However, nicotine inhibits CS‐induced neuroinflammation and neuronal apoptosis, alleviating depressive‐like behaviors in mice. [ABSTRACT FROM AUTHOR]

The article discusses the impact of Australia's prescription-only model for e-cigarettes on reducing nicotine vaping among young people. The author argues that while preventing youth uptake of e-cigarettes is important, regulations should also support access to e-cigarettes for adults who want to quit smoking. The current prescription-only model has not effectively prevented youth and young adults from vaping, as many have obtained e-cigarettes through illegal means. The article highlights the need for a balanced approach to e-cigarette regulation that considers accessibility for adult smokers while reducing appeal and availability to non-smokers. [Extracted from the article]

A sustainable future world consistently attributes to the development of eco‐friendly methods and materials for detection and elimination of toxic substances from the environment. While addressing the issues, pyrazole carbonitrile derived Schiff base PYR−TZ has been designed and employed for colorimetric and turn on fluorometric cyanide ion sensing. PYR−TZ demonstrated high cyanide ion (CN−) sensitivity with a 1 : 1 binding stoichiometry in aqueous solution. By preventing intramolecular charge transfer, the PYR−TZ sensor demonstrated excellent selectivity towards CN, which caused a color transition from colorless to yellow and impressive "turn‐on" fluorescence emission. The detection thresholds for CN− are 6.5 nm for absorbance spectra and 0.396 nm emission spectra, respectively. Under typical ecological and physiological settings (pH 1–12), the PYR−TZ sensor can function as an effective chemical sensor for detecting the CN− ions. Additionally, the sensor can find CN in tobacco commercial products like cigarettes and cigars. PYR−TZ is a great cyanide sensor probe that has a number of benefits, which includes simple synthesis, distinct color and emission change, a high degree of selectivity, lesser limit of detection, reversibility, and good anti‐interference ability to analyze solution and tobacco commercial things, together with fluorescence imaging. The theoretical optimized structure and electronic transitions were confirmed by DFT and TDDFT studies. On the basis of theoretical and experimental calculations (DFT), the mechanism of the metal ion complex is postulated. [ABSTRACT FROM AUTHOR]

The majority of adenocarcinoma lung cancer is found in nonsmokers. A history of tobacco use is more common in squamous cell carcinoma of the lung. The aim of this study is to identify the cisplatin (CDDP)‐resistance that promotes lung squamous carcinoma cell growth through nicotine‐mediated HDAC1/7nAchR/E2F/pRb cell cycle activation. Squamous cell carcinoma (NCI‐H520 and NCI‐H157) cells were examined after cisplatin and nicotine treatment by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H‐tetrazolium bromide assay, cell migration assay, immunofluorescence staining, western blot analysis, and immunoprecipitation analysis. Consequently, CDDP is released from DNA and Rb phosphorylated pRb as a result of nicotine‐induced cancer cell proliferation through 7nAchR, which then triggers the opening of the HDAC1 cell cycle. The cell cycle is stopped when CDDP adducts are present. Nicotine exerts cancer cytoprotective effects by allowing HDAC1 repair mechanisms to re‐establish E2F promoting DNA stimulation cell cycle integrity in the cytosol and preventing potential CDDP and HDAC1 suppressed in the nuclear. Concentration expression of nicotine causes squamous carcinoma cell carcinogens to emerge from inflammation. COX2, NF‐KB, and NOS2 increase as a result of nicotine‐induced squamous carcinoma cell inflammation. Nicotine enhanced the cell growth‐related proteins such as α7nAchR, EGFR, HDAC1, Cyclin D, Cyclin E, E2F, Rb, and pRb by western blot analysis. It also induced cancer cell inflammation and growth. As a result, we suggest that nicotine will increase the therapeutic resistance effects of CDDP. This has the potential to interact with nicotine through α7nAchR receptors and HDAC1/Cyclin D/E2F/pRb potentially resulting in CDDP therapy resistance, as well as cell cycle‐induced cancer cell growth. Significance statement: Nicotine is active in highly cisplatin (CDDP)‐resistant cancer cells. The mechanisms of the nicotine treatment of CDDP‐resistant lung cancer for histone deacetylase 1 (HDAC1) activity. HDAC1 transfected cells were directly binding between cytosol and nucleus distribution. Here, in cell viability and migration methods, we first found nicotine‐regulated cisplatin‐resistant cell growth by targeting HDAC1. Expression of cisplatin was negatively correlated with HDAC1. HDAC1 inhibitor, VPA, in the cancer cells, was predicted. Besides, CDDP inhibited cell growth and reduced the expression of E2F proteins. However, nicotine increases the detoxification of CDDP and induces CDDP resistance to induce lung cancer cell growth through α7nAchR and EGFR receptors. On the other hand, nicotine regulates HDAC1 by α7nAchR receptors in nuclear, but EGFR receptors in the cell cytosol. [ABSTRACT FROM AUTHOR]

Background and aims: Oral nicotine pouches (ONPs) probably offer reduced harm compared with cigarettes, but independent data concerning their misuse liability are lacking. We compared nicotine delivery and craving relief from ONPs with different nicotine concentrations to cigarettes. Design: This was a single‐blind, three‐visit (≥ 48‐hour washout), randomized‐cross‐over study. Participants were encouraged to complete all study visits in less than 1 month. Setting: The study took place in Rural/Appalachian Ohio. Participants: Participants comprised 30 adults who smoke cigarettes. Participants (meanage = 34.5) were 60% men and 90% White. Intervention: Participants who were ≥ 12‐hour tobacco‐abstinent used: (1) a 3‐mg nicotine concentration ONP, (2) a 6‐mg nicotine concentration ONP and (3) usual brand cigarette in separate visits. ONPs (wintergreen Zyn) were used for 30 minutes; cigarettes were puffed every 30 sec for 5 minutes. Measurements Plasma nicotine and self‐reported craving were assessed at t = 0, 5, 15, 30, 60 and 90 minutes. The primary outcome was plasma nicotine concentration at t = 30 minutes. A secondary outcome was craving relief at t = 5 minutes. Findings At t = 30, mean [95% confidence interval (CI)] plasma nicotine was 9.5 ng/ml (95% CI = 7.1, 11.9 ng/ml) for the 3 mg nicotine ONP, 17.5 ng/ml (95% CI = 13.7, 21.3) for the 6 mg nicotine ONP and 11.4 ng/ml (95% CI = 9.2, 13.6 ng/ml) for the cigarette. Mean plasma nicotine at t = 30 minutes differed between the 3‐ and 6‐mg nicotine ONPs (P = 0.001) and between the 6‐mg nicotine ONP and cigarette (P = 0.002). Mean (95% CI) craving at t = 5 minutes was lower for the cigarette (mean = 1.00, 95% CI = 0.61, 1.39) than either the 3 mg (mean = 2.25, 95% CI = 1.68, 2.82; P < 0.0001) or 6 mg nicotine (mean = 2.19, 95% CI = 1.60, 2.79; P < 0.0001) ONP. Conclusions: Among adult smokers, using 6‐mg nicotine concentration oral nicotine pouches (ONPs) was associated with greater plasma nicotine delivery at 30 minutes than 3‐mg ONPs or cigarettes, but neither ONP relieved craving symptoms at 5 minutes as strongly as a cigarette. Accelerating the speed of nicotine delivery in ONPs might increase their misuse liability relative to cigarettes. [ABSTRACT FROM AUTHOR]

Epidemiologic surveys have indicated that cigarette smoking is an important risk factor for diabetes, but its mechanisms remain unclear. Andrographolide, an herb traditionally utilized in medicine, provides anti‐inflammatory benefits for various diseases. In the present work, 265 patients with Type 2 diabetes (T2D) were investigated, and male C57BL/6 mice were exposed to cigareete smoke (CS) and/or to intraperitoneally injected andrographolide for 3 months. To elucidate the mechanism of CS‐induced hyperglycemia and the protective mechanism of andrographolide, MIN6 cells were exposed to cigarette smoke extract (CSE) and/or to andrographolide. Our data from 265 patients with T2D showed that urinary creatinine and serum inflammatory cytokines (interleukin 6 (IL‐6), IL‐8, IL‐1β, and tumor necrosis factor α (TNF‐α)) increased with smoking pack‐years. In a mouse model, CS induced hyperglycemia, decreased insulin secretion, and elevated inflammation and pyroptosis in β‐cells of mice. Treatment of mice with andrographolide preserved pancreatic function by reducing the expression of inflammatory cytokines; the expression of TXNIP, NLRP3, cleaved caspase 1, IL‐1β; and the N‐terminal of gasdermin D (GSDMD) protein. For MIN6 cells, CSE caused increasing secretion of the inflammatory cytokines IL‐6 and IL‐1β, and the expression of TXNIP and pyroptosis‐related proteins; however, andrographolide alleviated these changes. Furthermore, silencing of TXNIP showed that the blocking effect of andrographolide may be mediated by TXNIP. In sum, our results indicate that CS induces hyperglycemia through TXNIP‐NLRP3‐GSDMD axis‐mediated inflammation and pyroptosis of islet β‐cells and that andrographolide is a potential therapeutic agent for CS‐induced hyperglycemia. [ABSTRACT FROM AUTHOR]

Harmful components in cigarette smoke, such as nicotine, tar, and organic particulate matter, are the primary culprits behind lung diseases. While conventional filter materials based on cellulose, carbon, and molecular sieves exhibit commendable filtration capabilities, their high cost restricts their widespread applications. Based on this, the authors aim to prepare PET‐based filter materials with good adsorption properties through a simple surface functionalisation strategy. The adsorption performance of the PET‐based non‐woven fabric was enhanced by the introduction of sodium alginate (SA). The gas adsorption experiments results reveal that SA‐modified PET (SA‐PET) exhibits significantly improved filtration efficiency for nicotine, tar, and total particulate matter—increasing by 27.1%, 26.2%, and 21.3%, respectively. Moreover, SA‐PET exhibits more odour control ability than traditional activated carbon‐based filter materials. These results prove that surface‐functionalised SA‐PET has better filtration performance for harmful substances in smoke and provides a new strategy for the design of high‐performance filtration materials. [ABSTRACT FROM AUTHOR]

The link between smoking and a lower risk of Parkinson's disease (PD) is one of the strongest environmental or lifestyle associations in neuroepidemiology. Growing evidence supports the hypothesis that the association is based on a neuroprotective effect of smoking on PD, despite the plausible alternative that smoking serves as a marker for a proximal protective influence without itself conferring benefit. But how smoking could protect against neurodegeneration in PD is not well understood. Of several candidate molecules and mechanisms that have been nominated, nicotine has received the most attention. However, randomized controlled clinical trials of nicotine in PD have failed to demonstrate benefit on motor endpoints, including the NIC‐PD study in which recently diagnosed participants were randomly assigned to placebo or nicotine treatment for 1 year. Given these results, the time is right to evaluate the neuroprotective potential of other molecules and biochemical cascades triggered by smoking. Here, we review the evidence supporting smoking's possible protective effect on PD, compounds in tobacco and smoke that might mediate such benefit, and non‐causal classes of explanation, including reverse causation and the prospect of shared genetic determinants of smoking and PD resistance. The therapeutic potential of non‐nicotine components of smoke is suggested by studies supporting multiple alternative mechanisms ranging from monoamine oxidase inhibitors to gut microbiome disruption to antioxidant response induction by chronic exposure to low levels of carbon monoxide. Rigorous investigation is warranted to evaluate this molecule and others for disease‐preventing and disease‐modifying activity in PD models and, if warranted, in clinical trials. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Tobacco smoking is a serious health problem in society. While smoking rates are declining, smoking remains a serious risk to national health. Currently, there are several medications available to aid in smoking cessation. However, these medications have the disadvantages of low success rates in smoking cessation and various side effects. Therefore, natural‐based smoking cessation aids are being suggested as a good alternative due to their accessibility and minimal side effects. The roots and stems of Acanthopanax koreanum (AK) Nakai, a plant that is native to Jeju Island, South Korea, have traditionally been used as tonic and sedatives. Moreover, eleutheroside B and chlorogenic acid are the main components of AK stem extract. In the present study, we investigated the effect of 70% ethanol AK extract and its components on ameliorating nicotine dependence and withdrawal symptoms by using behavioural tests in mice. In addition, alterations in the dopaminergic and DRD1‐EPAC‐ERK‐CREB pathways were observed using dopamine ELISA and western blotting using mouse brains. Our findings demonstrate that the AK extract and its components effectively mitigated the effects of nicotine treatment in behavioural tests. Furthermore, it normalized the dopamine concentration and the expression level of nicotine acetylcholine receptor α7. Additionally, it was observed that AK extract and its components led to the normalization of DRD1, ERK and CREB expression levels. These results indicate that AK extract exhibits effects in ameliorating nicotine dependence behaviour and alleviating withdrawal symptoms. Moreover, EB and CGA are considered potential marker components of AK extract. [ABSTRACT FROM AUTHOR]

The influence of phosphorus substitution of nitrogen in heterocyclic compounds on the vibrational spectroscopy as well as frontier molecular orbitals are analyzed. Nicotine with two nitrogen atoms in its structure is taken as the sample system to be studied computationally. By replacing the nitrogen atom in one or both rings of this molecule with phosphorus, three nicotine derivatives are created. The vibrational circular dichroism and infrared spectra of these four molecules in their monomer state, as well as the assemblies up to trimers are determined. The aforementioned spectra are calculated using static quantum chemical calculations employing a cluster‐weighted approach. The calculated gas phase spectra of nicotine are compared to their respective experimental spectra. It is observed that the nicotine derivatives with phosphorus in the methylpyrrolidine ring have considerably different gas phase and bulk phase vibrational circular dichroism spectra when compared to nicotine. The phosphorus substitution reduces the energy gap between the highest occupied molecular orbital and the lowest unoccupied molecular orbital as well as altering the polarizability and reactivity of the investigated molecules. [ABSTRACT FROM AUTHOR]

Substance use disorders are heritable disorders characterized by compulsive drug use, the biological mechanisms for which remain largely unknown. Genetic correlations reveal that predisposing drug‐naïve phenotypes, including anxiety, depression, novelty preference and sensation seeking, are predictive of drug‐use phenotypes, thereby implicating shared genetic mechanisms. High‐throughput behavioral screening in knockout (KO) mice allows efficient discovery of the function of genes. We used this strategy in two rounds of candidate prioritization in which we identified 33 drug‐use candidate genes based upon predisposing drug‐naïve phenotypes and ultimately validated the perturbation of 22 genes as causal drivers of substance intake. We selected 19/221 KO strains (8.5%) that had a difference from control on at least one drug‐naïve predictive behavioral phenotype and determined that 15/19 (~80%) affected the consumption or preference for alcohol, methamphetamine or both. No mutant exhibited a difference in nicotine consumption or preference which was possibly confounded with saccharin. In the second round of prioritization, we employed a multivariate approach to identify outliers and performed validation using methamphetamine two‐bottle choice and ethanol drinking‐in‐the‐dark protocols. We identified 15/401 KO strains (3.7%, which included one gene from the first cohort) that differed most from controls for the predisposing phenotypes. 8 of 15 gene deletions (53%) affected intake or preference for alcohol, methamphetamine or both. Using multivariate and bioinformatic analyses, we observed multiple relations between predisposing behaviors and drug intake, revealing many distinct biobehavioral processes underlying these relationships. The set of mouse models identified in this study can be used to characterize these addiction‐related processes further. [ABSTRACT FROM AUTHOR]

Adolescence is a developmental period in which individuals demonstrate increased likelihood of engaging in disordered eating and risk‐taking behaviors, such as substance use. Nicotine use, in particular, (e.g., via vaping, combustible cigarettes, smokeless tobacco) is pervasive among middle and high school students. In 2022, 17.4% of middle school and high school students reported current nicotine vaping. Daily use of nicotine was reported among 27.6% of current users (Cooper et al., 2022). Research posits that eating disorders and nicotine use are highly comorbid. A recent study by Ganson and Nagata (2021) found that nearly 20% of participating adolescents with an eating disorder also used nicotine within the past 30 days. This is problematic, as nicotine use increases the mortality rate for eating disorders, which already has the second highest rate of all mental health disorders. Nicotine use may also exacerbate many of the medical complications associated with eating disorders (e.g., neuroendocrinal, dental, nutritional) and negatively impact eating disorder recovery (Ganson & Nagata, 2021). [ABSTRACT FROM AUTHOR]

Background: Fetal alcohol syndrome (FAS) can have adverse effects on health outcomes throughout the life course. Adults with FAS have an increased risk of chronic and infectious diseases. Although these conditions can affect reproductive health, few have described perinatal outcomes among individuals with an FAS diagnosis. Methods: We analyzed data from the Study of Mothers and Infants, an administrative birth cohort derived from California birth certificates linked with a hospital discharge database. The cohort consisted of 7.3 million singleton, live births between 2005 and 2021. FAS was identified by International Classification of Diseases (ICD) codes in maternal hospital discharge records. Pregnancy and birth outcomes were captured via ICD codes in maternal or infant records. We performed descriptive analyses for pregnancy and birth outcomes by maternal FAS diagnosis. Results: There were 35 babies born to 30 individuals with an FAS diagnosis between 2005 and 2021 (0.5/100,000 live births). The prevalence of births to individuals with an FAS diagnosis increased over the period. Individuals with an FAS diagnosis were more likely to identify as non‐Hispanic White, or "other/multiple" race, and less likely to be Hispanic than those without FAS. They were also more likely to be publicly insured and less than 18 years old. Birthing individuals with FAS were also more likely to use nicotine during pregnancy and to have diagnoses of mental health disorders, epilepsy, substance use disorders, preexisting or gestational hypertension, and sexually transmitted infections or other infections complicating pregnancy. Infants of individuals with FAS were more likely to be born prematurely or small for gestational age and be admitted to the neonatal intensive care unit. Conclusions: These findings highlight the need for improved recognition of FAS among birthing people. The results suggest that individuals with FAS would benefit from early and sustained medical care prior to pregnancy to optimize perinatal outcomes. [ABSTRACT FROM AUTHOR]

Introduction: Consumer preferences should be important factors that are considered when developing health policies and interventions. This paper examines the prevalence of, and factors associated with, consumer preferences regarding smoking behaviour 1 to 2 years in the future. Methods: At least weekly cigarette smokers in the 2020 wave of the International Tobacco Control Four Country Smoking and Vaping Survey (USA, Canada, England and Australia) (N = 8642) were asked if they preferred to continue to smoke or to quit with or without an alternative nicotine product (ANP) over the next 1–2 years. Results: Country‐specific weighted data showed 21.5% preferred to continue smoking and 8.0% were uncertain, leaving 70.6% preferring to quit: 13.7% using an ANP and 56.9% completely quitting nicotine. Apart from interest in quitting, the main predictors of preferring to quit were history of vaping, being aged 55 and over, smoking weekly, worrying about smoking harms, regretting starting and believing vaping is less harmful relative to smoking. Among those preferring to quit, preferring to use ANPs in future was very strongly associated with current vaping (especially daily), being younger, living in England, reporting strong urges to smoke, believing vaping is much less harmful than smoking, and not strongly regretting starting to smoke, and not wanting to quit. Discussion and Conclusions: A significant minority of smokers preferred not to quit, at least in the next year or two. Both interest in quitting and preference for ANPs over complete cessation were associated with similar covariates, including interest in vaping. [ABSTRACT FROM AUTHOR]

Background: Systemic inflammation in which lipopolysaccharide (LPS) is released into circulation can cause cognitive dysfunction and we have previously shown that LPS impaired working memory (WM) which refers to the ability to guide incoming behavior by retrieving recently acquired information. However, the mechanism is not very clear, and currently, there is no approved strategy to improve inflammation‐induced WM deficit. Notably, epidemiological studies have demonstrated a lower occurrence rate of inflammatory‐related diseases in smoking patients, suggesting that inflammation‐induced WM impairment may be improved by nicotine treatment. Here, our object is to investigate the effect and potential mechanisms of acute and chronic nicotine treatment on LPS‐produced WM deficiency. Methods: Delayed alternation T‐maze task (DAT) was applied for evaluating WM which includes both the short‐term information storage and the ability to correct errors in adult male mice. Immunofluorescence staining and immunoblotting were used for assessing the levels and distribution of CREB‐regulated transcription coactivator 1 (CRTC1) and hyperpolarization‐activated cation channels 2 (HCN2) in the medial prefrontal cortex (mPFC) and hippocampus. Quantitative PCR and ELISA were employed for analyzing the mRNA and protein levels of TNF‐α and IL‐1β. Results: Our results revealed that administration of LPS (i.p.) at a dose of 0.5 mg/kg significantly produced WM impairment in the DAT task accompanied by an increase in IL‐1β and TNF‐α expression in the mPFC. Moreover, intra‐mPFC infusion of IL‐1Ra, an IL‐1 antagonist, markedly alleviated LPS‐induced WM deficiency. More important, chronic (2 weeks) but not acute nicotine (0.2 mg/kg, subcutaneous) treatment significantly alleviated LPS‐induced WM deficiency by upregulating CRTC1 and HCN2. Of note, intra‐mPFC infusion of HCN blocker ZD7288 produced significant WM deficiency. Conclusions: In summary, in this study, we show that chronic nicotine treatment ameliorates acute inflammation‐induced working memory deficiency by increasing CRTC1 and HCN2 in adult male mice. [ABSTRACT FROM AUTHOR]

Epigenetics refers to the modification of gene expression rather than alteration of the genetic code itself. The DNA doesn't [ABSTRACT FROM AUTHOR]

Introduction: Kyphoplasty is a minimally invasive treatment for chronic refractory pain secondary to spinal compression fracture. This study investigates racial and socioeconomic disparities in kyphoplasty among the Medicare population. Materials and Methods: This study utilized data from the Medicare Limited Data Sets (LDS), a CMS administrative claims database. Patients aged 18 and older with ICD code consistent with spinal pathology and compression fractures were included. Outcome was defined as kyphoplasty by race and socioeconomic status (SES) with low SES defined by dual enrollment in Medicare/Medicaid. Results: There was a total of 215,502 patients gathered from CMS data, and 717 (0.33%) of these patients underwent kyphoplasty during the study period. Of these patients, 458 (63.8%) were female, the average age was 76.5 years old, 655 (91.3%) were White, 20 (2.7%) were Black, 9 (1.3%) were Hispanic, and 98 (13.7%) were Medicare/Medicaid dual eligible. White patients (32,317/157,177 [20.6%]) were less likely to be dual enrollment eligible in Medicare and Medicaid than Black (5407/13,522 [39.9%]), Hispanic (2833/3675 [77.1%]), Asian (2087/3312 [63.0%]), or North American Native patients (778/1578 [49.1%]). Multivariate regression (MVR) analysis was performed and showed that Blacks were less likely than Whites to have a kyphoplasty performed (OR 0.46 [95% CI: 0.29–0.72], p‐value <0.001). Although Hispanics (OR 0.95 [0.49–1.86]), North American Native (OR 0.82 [0.3–2.19]), and unknown race had a decreased odd of undergoing kyphoplasty, it was not statistically significant. Conclusion: Our study showed after adjustment for pertinent comorbidities, Medicare/Medicaid dual‐eligible patients and Black patients were significantly less likely to receive kyphoplasty than White patients with Medicare. [ABSTRACT FROM AUTHOR]

Increased acceptance of cannabis containing the psychoactive component, Δ9‐tetrahydrocannabinol (THC), raises concerns about the potential for impaired drivers and increased highway accidents. In contrast to the "breathalyzer" test, which is generally accepted for determining the alcohol level in a driver, there is no currently accepted roadside test for THC in a motorist. There is a need for an easily collectible biological sample from a potentially impaired driver coupled with an accurate on‐site test to measure the presence and quantity of THC in a driver. A novel breath collection device is described, which includes three separate sample collectors for collecting identical A, B, and C breath samples from a subject. A simple one‐step ethanol extraction of the "A" breath collector sample can be analyzed by UHPLC/selected ion monitoring (SIM) liquid chromatography/mass spectrometry (LC/MS) to provide qualitative and quantitative determination of THC in breath sample in less than 4 min for samples collected up to 6 h after smoking a cannabis cigarette. SIM LC/MS bioanalyses employed d3‐THC as the stable isotope internal standard fortified in negative control breath samples for quantitation including replicates of six calibrator standards and three quality control (QC) samples. Subsequent confirmation of the same breath sample in the B collectors was then confirmed by a reference lab by LC/MS/MS analysis. Fit‐for‐purpose bioanalytical validation consistent with pharmaceutical regulated bioanalyses produced pharmacokinetic (PK) curves for the two volunteer cannabis smokers. These results produced PK curves, which showed a rapid increase of THC in the breath of the subjects in the first hour followed by reduced THC levels in the later time points. A simpler single‐point calibration curve procedure with calibrators and QC prepared in ethanol provided similar results. Limitations to this approach include the higher cost and operator skill sets for the instrumentation employed and the inability to actually determine driver impairment. [ABSTRACT FROM AUTHOR]

Chronic tobacco use can lead to liver damage and inflammation due to the accumulation of various toxins in the body. This study aimed to investigate the correlation between the molecular mechanisms of nicotine‐induced liver injury, the caspase cascade, and the Akt/NF‐κB signaling pathway, as well as the protective effects of dexpanthenol (DEX). Male rats were subjected to intraperitoneal injections of nicotine at a concentration of 0.5 mg/kg/day and/or DEX at a concentration of 500 mg/kg/day for 8 weeks. After the treatment period, liver function tests were conducted on serum samples, and tissue samples were analyzed for protein levels of Akt, NF‐κB, Bax, Bcl‐xL, Caspase‐3, and Caspase‐9, along with histopathological changes. Additionally, assessments of oxidative stress markers and proinflammatory cytokines were carried out. Nicotine administration led to elevated levels of IL‐6, IL‐1β, MDA, TOS, and oxidative stress index, accompanied by decreased TAS levels. Moreover, nicotine exposure reduced the p‐Akt/Akt ratio, increased NF‐κB, Bax, Caspase‐3, and Caspase‐9 protein levels, and decreased the antiapoptotic protein Bcl‐xL levels. DEX treatment significantly mitigated these effects, restoring the parameters to levels comparable to those of the control group. Nicotine‐induced liver injury resulted in oxidative stress, inflammation, and apoptosis, mediated by Bax/Bcl‐xL, Caspase‐3, Caspase‐9, and Akt/NF‐κB pathways. Conversely, DEX effectively attenuated nicotine‐induced liver injury by modulating apoptosis through NF‐κB, Caspase‐3, Caspase‐9, Bax inhibition, and Bcl‐xL activation. [ABSTRACT FROM AUTHOR]

Rates of cigarette smoking in people with HIV (PWH) are two to three times higher than in people without HIV. Nicotine is metabolized by CYP2A6 and the nicotine metabolite ratio (NMR; 3‐hydroxycotinine/cotinine) is a measure of nicotine clearance. Higher NMR has been observed in PWH and is associated with lower quit rates. Efavirenz, a mainstay antiretroviral therapy (ART) globally, partially upregulates its own metabolism through CYP2A6. We hypothesized that efavirenz also upregulates nicotine metabolism by CYP2A6, resulting in a higher NMR, and switching to non‐efavirenz ART would decrease the NMR, potentially leading to improved quit rates. We compared the NMR during and after efavirenz use among PWH in a longitudinal, multisite cohort. Eligibility criteria included: (i) active cigarette smoking, (ii) ART switched from efavirenz‐based to non‐efavirenz‐based regimen, (iii) plasma available at pre‐ and post‐ART switch, and (iv) viral suppression during study period. Plasma cotinine and 3‐hydroxycotinine were measured by liquid chromatography–tandem mass spectrometry. T‐tests compared the NMR on and off efavirenz. Samples were collected between 2010 and 2019 in 72 PWH. The mean NMR difference after switching to a non‐efavirenz‐based regimen was −0.24 (SD: 0.37, P < 0.001); 44 PWH had at least a 0.1 decrease in NMR. Effect modification by race was present; Black PWH had a larger mean decrease. Our findings suggest that previously observed higher NMR among PWH may be due to direct pharmacologic effects of ART. Assessing the effect of ART on the NMR suggests that avoiding nicotine metabolism inducers could potentially increase quit rates. [ABSTRACT FROM AUTHOR]