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Background: Smoking and alcohol are the main risk factors for head and neck cancer. Despite the significant psychological impact, many patients continue to smoke and drink alcohol after diagnosis of cancer. This study aims to analyze the patients' behavior post diagnosis and treatment of head and neck cancer., Methods: An observational retrospective study was conducted on patients suffering from head and neck cancer. Their smoking and alcohol habits before and after diagnosis of cancer were studied., Results: A total of 85 patients were recruited: 80 % males, mean age 61.77±9.30 years. Among smokers, 35.80 % continued smoking post-diagnosis. A statistically significant correlation was found between smoking habit after diagnosis of cancer and type of treatment and tracheostomy. Among drinkers, 65.52 % continued to consume alcohol after diagnosis of cancer. A statistically significant correlation was found between alcohol consumption post-diagnosis and sex., Conclusions: Patients undergoing more invasive treatments are more likely to quit smoking and/or drinking alcohol, suggesting the strong psychological impact of cancer and its therapy. Many patients continue smoking and consuming alcohol due to unawareness, depression, or addiction. However, most patients reduced cigarette smoking and alcohol consumption. Comprehensive care, including psychological support, is essential for these patients., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Purpose: The objective of this study is to assess the impact of smoking on stroke prevalence and to delineate the relationship between smoking-related factors and the risk of stroke, incorporating an analysis of demographic variations influencing this association., Methods: Our analysis encompassed 9,176 participants, evaluating clinical attributes alongside smoking-related characteristics such as duration of cigarette consumption, and levels of nicotine, tar, and carbon monoxide. We employed weighted univariate logistic regression and restricted cubic splines to examine the association between smoking indicators and stroke risk, complemented by subgroup analyses for demographic differentiation., Results: The overall prevalence of stroke in our cohort was 3.4%. Statistically significant associations were found between stroke incidence and factors such as age, gender, education, and marital status (p < 0.05). Adjusted logistic regression models showed increased odds ratios (ORs) for stroke with higher nicotine and carbon monoxide levels across progressively adjusted models: Model 1 (unadjusted), Model 2 (adjusted for age, gender), Model 3 (further adjusted for education, marital status, BMI, PIR), and Model 4 (fully adjusted for additional factors including hypertension, hyperlipidemia, diabetes, and drinking). Specifically, ORs for nicotine increased from 2.39 in Model 1 to 2.64 in Model 4; for carbon monoxide, from 1.10 to 1.11 over the same models.​The threshold analysis using restricted cubic splines revealed critical points for stroke risk increase at smoke exposure levels of 410 units, tar 12 mg, nicotine 1.1 mg, and carbon monoxide 12 ppm. Above these thresholds, stroke risk escalates significantly. Additionally, the presence of family smoking history was associated with higher stroke risks compared to those without such history., Conclusion: This study confirms that smoking significantly contributes to increased stroke risk, particularly through exposure to nicotine and carbon monoxide. The findings emphasize the necessity for tailored stroke prevention strategies that specifically address smoking behaviors and consider demographic susceptibilities. Incorporating smoking-related indicators into risk assessment models could enhance the precision of stroke prevention efforts., (© 2024. The Author(s).)

Purpose: Stressors brought on by the pandemic may have further encouraged lesbian, gay, bisexual, transgender, queer, and intersex plus (LGBTQI +) cancer survivors to smoke. The purpose of this study is to examine factors associated with smoking among LGBTQI + cancer survivors during the pandemic., Methods: We used a secondary data analysis of OUT: The National Cancer Survey. We conducted logistic regression analysis to examine the associations between psychological distress, binge drinking, and socio-demographic factors with ever use and current use of cigarettes, other tobacco, and nicotine products., Results: Of the 1629 participants in our sample, 53% used in their lifetime and 13% reported current use. Correlates of increased ever use included being of older age (AOR = 1.02; 95% CI: 1.01, 1.03) and binge drinking (AOR = 2.47; 95% CI: 1.17, 5.20) while correlates of decreased ever use were among those with a graduate or professional degree (AOR = 0.40; 95% CI: 0.23, 0.71). Correlates of increased current use included being of Latine descent (AOR = 1.89; 95% CI: 1.07, 3.36), binge drinking (AOR = 3.18; 95% CI: 1.56, 6.48), without health insurance (AOR = 2.37; 95% CI: 1.10, 5.10), and being disabled (AOR = 1.64; 95% CI: 1.19, 2.26) while correlates of decreased current use were among cisgender women (AOR = 0.30; 95% CI: 0.12, 0.77), being of younger age (AOR = 0.98; 95% CI: 0.96, 0.99), and having a graduate or professional degree (AOR = 0.33; 95% CI: 0.15, 0.70)., Conclusions: Our findings demonstrate that a proportion of LGBTQI + cancer survivors continue to smoke during the pandemic despite the increased risk involved with smoking. Furthermore, individuals with intersecting marginalized identities experience additional stressors that may have been further exacerbated by the conditions of the pandemic that encourage them to smoke., Implications for Cancer Survivors: Quitting smoking after a cancer diagnosis can decrease the chances of recurrence and a new primary malignancy. In addition, practitioners and researchers should advocate towards examining and addressing systemic forms of oppression in institutions that LGBTQI + cancer survivors navigate during the pandemic., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The factors influencing the development and maintenance of nicotine dependence are numerous and complex. Recent studies indicate that smokers exhibit distinct genetic predispositions to nicotine dependence. We aimed to analyse (1) the association between rs2551038 and cigarette smoking, (2) the association of between the rs3864236-rs2526303-rs2551038 haplotype and cigarette smoking, and (3) the personality traits measured by the NEO Five-Factor Inventory in cigarette users and never-smokers. No significant differences were present in the frequency of rs2551038 genotypes and alleles in the studied cigarette users compared to the control group. Cigarette users, compared to the control group, had higher scores on the NEO-FFI Extraversion scale ( p = 0.0011), and lower scores were obtained by the cigarette users for the NEO-FFI Openness ( p = 0.0060), Agreeability ( p ≤ 0.000), and Conscientiousness ( p ≤ 0.000) scales. There was a significant positive Pearson's linear correlation between the age and the Fagestrom test (r = 0.346; p < 0.0001) and the NEO-FFI Openness scale (r = 0.180; p < 0.0001) in the group of cigarette users. We observed significant linkage disequilibrium between rs2526303 and rs3864236 (D' = 0.3581; p < 2.2204 × 10 -16 ) and between rs2526303 and rs2551038 (D' = 0.9993; p < 2.2204 × 10 -16 ) in the tested sample. The sex-stratified haplotype analysis revealed that in the group of male never-smokers, the GTC haplotype was significantly more frequent than in the group of cigarette users (38% vs. 22%; p = 0.0039). The presented study reveals significant differences in personality trait scores between cases and controls. Moreover, the sex-stratified analysis showed significant differences in haplotype distribution. These results underscore the interplay between genetic predisposition, sex, and personality in nicotine-using individuals.

Background: Despite high smoking rate in people with depressive symptoms, there is ongoing debate about relationship between smoking and depressive symptoms., Methods: Study participants were 57,441 Korean men. We collected their baseline data between 2011 and 2012, and conducted follow-up from 2013 to 2019. They were categorized by smoking status (never: < 100 cigarettes smoking in life time, former: currently quitting smoking, and current smoker: currently smoking), smoking amount (pack/day and pack-year) and urine cotinine excretion. The development of depressive symptoms was determined in CES-D score ≥ 16. Cox proportional hazards model was used to analyze the multivariable-adjusted hazard ratio (HR) and 95% confidence intervals (CI) for depressive symptoms in relation to smoking status, smoking amount, and urine cotinine excretion., Results: During 6.7 years of median follow-up, the risk of depressive symptoms increased in order of never (reference), former (HR = 1.08, 95% CI: 1.01-1.15) and current smoker (HR = 1.24, 95% CI: 1.16-1.32). Among current smoker, the risk of depressive symptoms increased proportionally to daily smoking amount (< 1 pack; HR = 1.21, 95% CI: 1.13-1.29, and ≥ 1 pack; HR = 1.34, 95% CI: 1.23 - 1.45). This pattern of relationship was consistently observed for pack-year in former smoker and current smoker. Additionally, urine cotinine excretion was proportionally associated with the risk of depressive symptoms., Conclusion: Exposure to smoking was associated with the increased risk of depressive symptoms. Dose dependent relationship was observed between smoking amount and the risk of depressive symptoms., (© 2024. The Author(s).)

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., (© 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.)

Cues associated with smoking can induce relapse, which is likely driven by cue-induced neurobiological and physiological mechanisms. For instance, greater relapse vulnerability is associated with increases in cue-induced insula activation and heightened cortisol concentrations. Determining if there is a link between such cue-induced responses is critical given the need for biomarkers that can be easily measured in clinical settings and used to drive targeted treatment. Further, comprehensively characterising biological reactions to cues promises to aid in the development of therapies that address this specific relapse risk factor. To determine whether brain and cortisol responses to smoking cues are linked, this study recruited 27 nicotine-dependent tobacco-smoking individuals and acquired whole-brain functional activation during a cue reactivity task; salivary cortisol was measured before and after scanning. The results showed that increases in blood-oxygen-level-dependent activation in the right anterior insula and right dorsolateral prefrontal cortex (DLPFC) when viewing smoking versus neutral cues were positively correlated with a post-scan rise in salivary cortisol concentrations. These brain regions have been previously implicated in substance use disorders for their role in salience, interoception and executive processes. These findings show that those who have a rise in cortisol following smoking cue exposure also have a related rise in cue-induced brain reactivity, in brain regions previously linked with heightened relapse vulnerability. This is clinically relevant as measuring cue-induced cortisol responses is a more accessible proxy for assessing the engagement of cue-induced neurobiological processes associated with the maintenance of nicotine dependence., (© 2023 The Authors. Addiction Biology published by John Wiley & Sons Ltd on behalf of Society for the Study of Addiction.)

The effect of smoking and nicotine exposure during pregnancy on fetal nephrogenesis is a growing area of research. The objective of this systematic review is to summarise the current evidence in this research field. Our literature search identified a total of 415 articles from PubMed, Embase, Scopus, and Cochrane. After electronic sorting and manual screening, 18 eligible articles were found, 6 being human studies and 12 being animal studies. Articles that did not study nicotine or smoking, did not focus on fetal kidney development, or did not include nicotine or smoking exposure during pregnancy were excluded from the systematic review. The main outcomes of the studies were kidney weight, volume and size, kidney histopathology and morphology, and kidney function. Evidence from human studies identified a reduction in fetal kidney size, volume, and weight in offspring exposed to smoking during pregnancy; and the greatest impact was seen in offspring exposed to >5-10 cigarettes per day. Animal studies investigated kidney histopathology and highlighted kidney injury and microscopic changes in response to nicotine exposure during pregnancy. Further research is required to determine the impact on kidney function. Recreational nicotine use is evolving, and with the increasing use of urine cotinine in the evaluation of nicotine exposure, further research is needed.

Background: Variability in decision-making capacity and reward responsiveness may underlie differences in the ability to abstain from smoking. Computational modeling of choice behavior, as with the Hierarchical Drift Diffusion Model (HDDM), can help dissociate reward responsiveness from underlying components of decision-making. Here we used the HDDM to identify which decision-making or reward-related parameters, extracted from data acquired in a reward processing task, contributed to the ability of people who smoke that are not seeking treatment to abstain from cigarettes during a laboratory task., Methods: 80 adults who smoke cigarettes completed the Probabilistic Reward Task (PRT) - a signal detection task with a differential reinforcement schedule - following smoking as usual, and the Relapse Analogue Task (RAT) - a task in which participants could earn money for delaying smoking up to 50min - after a period of overnight abstinence. Two cohorts were defined by the RAT; those who waited either 0-min (n=36) or the full 50-min (n=44) before smoking., Results: PRT signal detection metrics indicated all subjects learned the task contingencies, with no differences in response bias or discriminability between the two groups. However, HDDM analyses indicated faster drift rates in 50-min vs. 0-min waiters., Conclusions: Relative to those who did not abstain, computational modeling indicated that people who abstained from smoking for 50min showed faster evidence accumulation during reward-based decision-making. These results highlight the importance of decision-making mechanisms to smoking abstinence, and suggest that focusing on the evidence accumulation process may yield new targets for treatment., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier B.V.)

Introduction/objective: E-cigarette use poses an additional risk for individuals who are not cigarette smokers, especially adolescents. The marketing tactics of the industry have substantially increased the prevalence of e-cigarettes, use among adolescents. India banned e-cigarette in September 2019 that has been criticized by interested groups.  We investigated that among adults and adolescents, who are more aware and using e-cigarette more?, Methods: The data were taken from a population-based representative household survey conducted in Mumbai and Kolkata in the year 2019-2020.  A household was enrolled if it had a 12-14 year old adolescent living in it and both adolescent and adult caregivers agreed to participate in the survey. The data from 944 adolescents out of 15,436 enumerated in Mumbai and 1038 out of 24,284 enumerated in Kolkata and their caregivers were analyzed for awareness and ever use of e-cigarettes.  Result: The awareness of e-cigarettes among 12-14 year olds in Mumbai was 15.5%, almost identical among boys and girls whereas is in Kolkata it was 11.2%. In contrast, among the adolescents' adult caregivers in Mumbai, the awareness was low, 3.9% and in Kolkata, 4.6%. Overall awareness was significantly higher among adolescents than among caregivers, especially among adolescent girls than among female caregivers in both cities., Conclusion: The awareness and the use of e-cigarette were very little and the messages from the e-cigarette industry seem to be targeted more towards adolescents than adults.  The ban on an e-cigarette in India has helped in prevented the marketing of ENDS to adolescents.

Smoking is a risk factor for respiratory diseases, and it worsens sleep quality due to nicotine stimulation and sudden nicotine withdrawal during sleep. This can increase the severity of OSA through alterations upper airway inflammation and neuromuscular function, arousal mechanisms, and sleep architecture. Therefore, it may lead to sleep-disrupted breathing, particularly obstructive sleep apnea (OSA). Herein, this study aims to research the association between smoking and OSA through the STOP-Bang index. In this study, total sample of 3442 participants (1465 men and 1977 women) were analyzed. We used data from the Korea National Health and Nutrition Examination Survey in 2020 by classifying adults into current, ex-, and non-smokers. A multiple logistic regression analysis was used to investigate the association between smoking and OSA. Furthermore, multinomial regression analysis was used to investigate the effect of smoking cessation. For males, compared to the non-smokers, the odds ratios (OR) for the OSA were significantly higher in the ex-smokers (OR: 1.53, 95% confidence interval(CI) 1.01-2.32) and current smokers (OR: 1.79, 95% CI 1.10-2.89). In females, higher ORs were observed for OSA risk, similar to the non-smokers, smoking cessation, and pack-years. Among men, OSA was significantly associated with a moderate risk for ex-smokers (OR: 1.61, 95% CI 1.05-2.48) and a severe risk for current smokers (OR: 1.88, 95% CI 1.07-3.29). This study observed that smoking might contribute to OSA risk among adults. Smoking cessation can help to manage sleep quality properly., (© 2023. The Author(s).)

Introduction: Smoking behaviors are partly heritable, yet the genetic and environmental mechanisms underlying smoking phenotypes are not fully understood. Developmental nicotine exposure (DNE) is a significant risk factor for smoking and leads to gene expression changes in mouse models; however, it is unknown whether the same genes whose expression is impacted by DNE are also those underlying smoking genetic liability. We examined whether genes whose expression in D1-type striatal medium spiny neurons due to DNE in the mouse are also associated with human smoking behaviors., Methods: Specifically, we assessed whether human orthologs of mouse-identified genes, either individually or as a set, were genetically associated with five human smoking traits using MAGMA and S-LDSC while implementing a novel expression-based gene-SNP annotation methodology., Results: We found no strong evidence that these genes sets were more strongly associated with smoking behaviors than the rest of the genome, but ten of these individual genes were significantly associated with three of the five human smoking traits examined (p < 2.5e-6). Three of these genes have not been reported previously and were discovered only when implementing the expression-based annotation., Conclusions: These results suggest the genes whose expression is impacted by DNE in mice are largely distinct from those contributing to smoking genetic liability in humans. However, examining a single mouse neuronal cell type may be too fine a resolution for comparison, suggesting that experimental manipulation of nicotine consumption, reward, or withdrawal in mice may better capture genes related to the complex genetics of human tobacco use., Implications: Genes whose expression is impacted by DNE in mouse D1-type striatal medium spiny neurons were not found to be, as a whole, more strongly associated with human smoking behaviors than the rest of the genome, though ten individual mouse-identified genes were associated with human smoking traits. This suggests little overlap between the genetic mechanisms impacted by DNE and those influencing heritable liability to smoking phenotypes in humans. Further research is warranted to characterize how developmental nicotine exposure paradigms in mice can be translated to understand nicotine use in humans and their heritable effects on smoking., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Childhood experiences are linked to myriad indices of health and wellbeing in adulthood, including substance use behaviors. Increasingly, there has been a paradigm shift in prevention science focused on healthy outcomes of positive experiences. The current study examined associations between retrospective reports of positive childhood experiences and patterns of smoking and alcohol use in adulthood. Data were from the 2019 Montana Behavioral Risk Factor Surveillance System survey (N = 6,495; M age  = 55.9 years; 49% male as assigned at birth). Outcomes examined with regard to positive childhood experiences included lifetime smoking (> 100 cigarettes), current smoking status, and past-month alcohol use indices (i.e., total drinks, typical quantity, heavy episodic drinking, and peak drinking occasion). Positive childhood experience scores were inversely associated with both smoking outcomes (AORs = 0.66 and 0.61). Curiously, positive childhood experiences were positively associated with any past-month alcohol use (AOR = 1.12), but among respondents who did use alcohol in the past month, positive childhood experiences were inversely associated with all indices of alcohol use patterns: total drinks (CR = 0.94), drinks per occasion (CR = 0.95), heavy episodic occasions (AOR = 0.91), and peak drinking (AOR = 0.95). Findings generally indicated that positive childhood experiences may be protective against cigarette and high-risk alcohol use behaviors in adulthood. Item-by-item analyses identified specific childhood experiences that may be particularly protective, which may inform prevention efforts and policy (prevention recommendations are discussed below)., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Introduction: Trends in knowledge and beliefs about e-cigarette (EC) harm have been changing. Our study examined whether change in risk perception of ECs predicts cigarettes smoked per week (CPW) among Black and Latinx individuals who smoke enrolled in an EC switching randomized clinical trial (RCT)., Methods: We analyzed data from one arm of a 6-week EC RCT of individuals who smoke attempting to switch to nicotine salt pod system ECs (n = 110; Black, n = 57; Latinx, n = 53). Our explanatory variable was change in risk perception of ECs compared to combustible cigarettes (CC) from baseline to week 6. Our outcome was CPW measured by a 7-day timeline follow-back interview. A negative binomial GEE model was conducted to examine the association between risk perception and CPW at baseline and week 6., Results: The mean CPW decreased from 82.8 (SD=49.8) at baseline to 15.8 (SD=29.8) at week 6. A one-level increase in EC risk perception (i.e., EC perceived as riskier than CC from baseline to week 6) was associated with an increase in CPW (IRR: 1.83, 95% CI: 1.03; 3.24). Latinx participants were more likely to have higher CPW as EC risk perception increased compared to Black participants (IRR=1.89, 95% CI: 1.09; 3.26)., Conclusion: We found that CPW at week 6 was significantly higher as change in risk perception of EC relative to CC increased. Given the influence of risk perception on smoking behavior, people who smoke should be educated on the benefits and harms of ECs., Competing Interests: Declaration of Competing Interest Dr. Ahluwalia received sponsored funds for travel expenses as a speaker for the 2021 annual GTNF conference. Dr. Ahluwalia serves as a consultant and has equity in a start-up company Qnovia, formerly known as Respira Technologies., (Copyright © 2023 Elsevier B.V. All rights reserved.)

While the US Food and Drug Administration (FDA)'s proposal to reduce the nicotine content in cigarettes is gaining traction, it is still undetermined whether the policy will also include other combustible tobacco products, such as little cigars and cigarillos (LCCs), and how such a policy should be communicated given the patterns of use and perceptions around LCCs. This study examined perceptions of nicotine and addiction related to LCC use and involved data collection from eight semi-structured virtual focus groups conducted in Summer 2021 in the US. Participants were adults who reported past-30-day use of LCCs, consisting of African American males ( n = 9), African American females ( n = 9), white males ( n = 14), and white females ( n = 11). Participants discussed their perceptions of nicotine and addiction in general and in relation to LCC use. Inductive thematic analysis of transcripts was conducted. Differences across race and sex groups were examined. Participants did not consider nicotine to be a characterizing feature of LCCs; rather, they generally associated nicotine with cigarettes. Participants' views of nicotine and addiction related to LCCs were discussed along four dimensions: context of use, frequency of use, the presence of cravings, and whether a product is modified (e.g., by adding marijuana). Social and infrequent use, a lack of cravings, and the use of LCCs for marijuana were considered indicative of a lack of addiction and reasons not to be concerned about nicotine in LCCs. Because perceptions of nicotine and addiction related to LCCs differ from those of cigarettes, communications about a reduced nicotine policy that includes LCCs should consider these differences to ensure the policy is understood by people who currently use LCCs and to prevent people who use cigarettes from switching to LCCs.

Purpose: To examine the effects of chronic smoking on vascular density in superficial and deep retinal vascular plexuses and choroidal thicknesses., Method: Superficial and deep vessel densities and choroidal thicknesses of smoking volunteers and healthy non-smoking volunteers were measured with the Topcon DRI OCT-1 Tritron® device and compared with each other., Results: This study included 108 eyes of 54 smoking volunteers and 108 eyes of 54 healthy volunteers as a control group. The average superficial vascular density index and deep vascular density indexes of smokers were found to be 39.81 ± 1.5% and 42.53 ± 1.9%, respectively (P = 0.53), while the non-smoking control group was 40.09 ± 1.3% and 41.57 ± 1.6%, respectively (P = 0.006). Average choroidal thicknesses were 284.22 ± 59 in smokers and 270.72 ± 61 in the control group (P = 0.247). Also, smoking quantity per day x years was found to be significantly negatively correlated with average choroidal thicknesses. (P = 0,011)., Discussion: In this study, it was determined that chronic smoking increases deep retinal vascular densities on retinal vascular plexus. However, the cumulative effect of smoking was found to be negatively correlated with choroidal thicknesses. Smoking has microvascular effects on vessels such as vasodilatation, vasoconstriction, increased platelet aggregation, endothelial dysfunction. However, studies in the literature are in dispute with the effects of smoking on choroidal and retinal vessels. This study may show that chronic smoking may have different vascular effects on the superficial and deep plexuses and choroidal vessels, as well as different effects from acute use.

Nicotine exposure in pregnant rats and sheep has shown a more than 50% increase in female fetal testosterone (FFT) levels. Increased testosterone levels have also been linked to infertility, increased anogenital distance (AGD), and reduced second to fourth digit (2D:4D) finger length ratios (FLR). In humans, we hypothesized that maternal total testosterone (MTT) levels would increase in smoking mothers and would cause increased FFT levels, increased AGD, and decreased 2D:4D FLR. This prospective study separated women expecting a female fetus into nonsmoking and smoking cohorts. Maternal cotinine (MC) was tested at 3rd trimester and delivery to assess nicotine exposure. MTT levels were drawn at delivery, and FFT levels were collected from cord blood. The AGD and 2D:4D FLRs were measured at birth. Data were analyzed using parametric and nonparametric tests. The data of 36 smokers and 28 nonsmokers were analyzed. Smoking mothers had higher parity, drug abuse history and were more likely white race. No statistical differences were seen among the primary outcomes of MTT and FFT. MTT was higher among nonsmokers versus smokers (144 versus 107 ng/dL). No correlations were noted between MC levels at delivery, MTT, and FFT levels. No statistical differences were noted among secondary outcomes of AGD and FLR. Although animal studies showed increased FFT levels after nicotine exposure, this was not seen in our human study. Placental differences in animals and humans may be at work. Our pilot study reveals a need for research on the effects of smoking in pregnancy on fetal hormones., (© 2022. Society for Reproductive Investigation.)

Tobacco smoking is an important public health issue recognized by the world health organization as one of the most serious, preventable risk factors for developing a series of pregnancy pathologies. Maternal smoking is positively associated with intrauterine growth restriction (IUGR) and gestational diabetes (GDM), but negatively associated with preeclampsia (PE). In this review, we examine epidemiological, clinical and laboratory studies of smoking effects on immunoregulation during pregnancy, trophoblast function, and placental vasculature development and metabolism. We aim to identify effects of tobacco smoke components on specific placental compartments or cells, which may contribute to the understanding of the influences of maternal smoking on placenta function in normal and pathological pregnancies. Data corroborates that in any trimester, smoking is unsafe for pregnancy and that its detrimental effects outweigh questionable benefits. The effects of maternal smoking on the maternal immune regulation throughout pregnancy and the impact of different tobacco products on fetal growth have not yet been fully understood. Smoking cessation rather than treatment with replacement therapies is recommended for future mothers because also single components of tobacco and its smoke may have detrimental effects on placental function., (Copyright © 2021. Published by Elsevier Ltd.)

Background: Chronic obstructive pulmonary disease (COPD) is a respiratory disease that causes a wide range of cognitive impairments. Although COPD-Smoking comorbidity is common, the relationship between smoking and cognitive function in COPD-Smoking comorbidity remains unclear. This study aimed to investigate the effect of smoking on cognitive function like attention in COPD-Smoking patients., Methods: In this study, we used the Montreal Cognitive Assessment (MoCA) scale and resting-state functional magnetic resonance imaging (fMRI) to explore the effect of smoking on attention in patients with COPD., Results: Behavioral analysis revealed that among patients with COPD the smokers had a shorter course of COPD and showed a worse attention performance than the non-smokers. Resting-state fMRI analysis revealed that among patients with COPD smokers showed lower regional homogeneity (ReHo) value of the fusiform gyrus than non-smokers. Importantly, the ReHo of the fusiform gyrus is positively associated with attention and mediates the effect of smoking on attention in COPD., Conclusions: In summary, our study provides behavioral and neurobiological evidence supporting the positive effect of smoking on attention in COPD. This may be helpful for understanding and treating COPD and even other diseases comorbid with smoking., (© 2022. The Author(s).)

The routine techniques currently applied for the determination of nicotine and its major metabolites, cotinine, and trans -3'-hydroxycotinine, in biological fluids, include spectrophotometric, immunoassays, and chromatographic techniques. The aim of this study was to develop, and compare two new chromatographic methods high-performance liquid chromatography coupled to triple quadrupole mass spectrometry (HPLC-QQQ-MS/MS), and RP-HPLC enriched with chaotropic additives, which would allow reliable confirmation of tobacco smoke exposure in toxicological and epidemiological studies. The concentrations of analytes were determined in human plasma as the sample matrix. The methods were compared in terms of the linearity, accuracy, repeatability, detection and quantification limits (LOD and LOQ), and recovery. The obtained validation parameters met the ICH requirements for both proposed procedures. However, the limits of detection (LOD) were much better for HPLC-QQQ-MS/MS (0.07 ng mL -1 for trans -3'-hydroxcotinine; 0.02 ng mL -1 for cotinine; 0.04 ng mL -1 for nicotine) in comparison to the RP-HPLC-DAD enriched with chaotropic additives (1.47 ng mL -1 for trans -3'-hydroxcotinine; 1.59 ng mL -1 for cotinine; 1.50 ng mL -1 for nicotine). The extraction efficiency (%) was concentration-dependent and ranged between 96.66% and 99.39% for RP-HPLC-DAD and 76.8% to 96.4% for HPLC-QQQ-MS/MS. The usefulness of the elaborated analytical methods was checked on the example of the analysis of a blood sample taken from a tobacco smoker. The nicotine, cotinine, and trans -3'-hydroxycotinine contents in the smoker's plasma quantified by the RP-HPLC-DAD method differed from the values measured by the HPLC-QQQ-MS/MS. However, the relative errors of measurements were smaller than 10% (6.80%, 6.72%, 2.04% respectively).

Background: Maternal smoking during pregnancy (MSDP) affects development of multiple organ systems including the placenta, lung, brain, and vasculature. In particular, children exposed to MSDP show lifelong deficits in pulmonary function and increased risk of asthma and wheeze. Our laboratory has previously shown that vitamin C supplementation during pregnancy prevents some of the adverse effects of MSDP on offspring respiratory outcomes. Epigenetic modifications, including DNA methylation (DNAm), are a likely link between in utero exposures and adverse health outcomes, and MSDP has previously been associated with DNAm changes in blood, placenta, and buccal epithelium. Analysis of placental DNAm may reveal critical targets of MSDP and vitamin C relevant to respiratory health outcomes., Results: DNAm was measured in placentas obtained from 72 smokers enrolled in the VCSIP RCT: NCT03203603 (37 supplemented with vitamin C, 35 with placebo) and 24 never-smokers for reference. Methylation at one CpG, cg20790161, reached Bonferroni significance and was hypomethylated in vitamin C supplemented smokers versus placebo. Analysis of spatially related CpGs identified 93 candidate differentially methylated regions (DMRs) between treatment groups, including loci known to be associated with lung function, oxidative stress, fetal development and growth, and angiogenesis. Overlap of nominally significant differentially methylated CpGs (DMCs) in never-smokers versus placebo with nominally significant DMCs in vitamin C versus placebo identified 9059 candidate "restored CpGs" for association with placental transcript expression and respiratory outcomes. Methylation at 274 restored candidate CpG sites was associated with expression of 259 genes (FDR < 0.05). We further identified candidate CpGs associated with infant lung function (34 CpGs) and composite wheeze (1 CpG) at 12 months of age (FDR < 0.05). Increased methylation in the DIP2C, APOH/PRKCA, and additional candidate gene regions was associated with improved lung function and decreased wheeze in offspring of vitamin C-treated smokers., Conclusions: Vitamin C supplementation to pregnant smokers ameliorates changes associated with maternal smoking in placental DNA methylation and gene expression in pathways potentially linked to improved placental function and offspring respiratory health. Further work is necessary to validate candidate loci and elucidate the causal pathway between placental methylation changes and outcomes of offspring exposed to MSDP. Clinical trial registration ClinicalTrials.gov, NCT01723696. Registered November 6, 2012. https://clinicaltrials.gov/ct2/show/record/NCT01723696 ., (© 2021. The Author(s).)

Maternal smoking during pregnancy is associated with an ensemble of neurodevelopmental consequences in children and therefore constitutes a pressing public health concern. Adding to this burden, contemporary epidemiological and especially animal model research suggests that grandmaternal smoking is similarly associated with neurodevelopmental abnormalities in grandchildren, indicative of intergenerational transmission of the neurodevelopmental impacts of maternal smoking. Probing the mechanistic bases of neurodevelopmental anomalies in the children of maternal smokers and the intergenerational transmission thereof, emerging research intimates that epigenetic changes, namely DNA methylome perturbations, are key factors. Altogether, these findings warrant future research to fully elucidate the etiology of neurodevelopmental impairments in the children and grandchildren of maternal smokers and underscore the clear potential thereof to benefit public health by informing the development and implementation of preventative measures, prophylactics, and treatments. To this end, the present review aims to encapsulate the burgeoning evidence linking maternal smoking to intergenerational epigenetic inheritance of neurodevelopmental abnormalities, to identify the strengths and weaknesses thereof, and to highlight areas of emphasis for future human and animal model research therein., (© The Author(s) 2021. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: The evidence on the effects of chronic tobacco smoking on neuropsychological functions is conflicting. The literature remains limited by inconsistent accounting for potentially confounding biomedical and psychiatric conditions. This study aimed to assess the neuropsychological functions of adult chronic tobacco smokers in comparison to group-matched non-smokers., Method: The study included 73 smokers and 84 group-matched non-smokers. The data was collected during the year 2019. After an initial interview to collect demographics and smoking profile, the subjects undertook neuropsychological assessments that targeted a wide range of cognitive domains., Results: The performance of smokers was poorer on almost all neuropsychological domains, namely selective attention (p ≤ .001, p = .044), alternating attention (p = .002) working memory (p ≤ .001), Short-term memory (p = .006 and .003), Long-term memory (p ≤ .001), processing accuracy (p ≤ .001), and executive function (p = .011 and .026). Smokers were intact on processing speed. Smoking accumulation and lower age onset of regular smoking were correlated with lower neuropsychological function., Conclusion: Our findings add to the growing body of evidence suggesting that chronic tobacco smoking impacts cognition negatively.

[Figure: see text].

Background: Over one-quarter of all smokers in the United States identify as non-daily smokers and this number is projected to rise. Unlike daily smokers who typically maintain consistent levels of nicotine exposure with regular smoking, non-daily smokers have variable patterns of smoking that likely result in high intraindividual variability in nicotine intake. The current study aimed to characterize the weekly intraindividual variability in cotinine and identify smoking-related predictors in nondaily smokers., Methods: An ecological momentary assessment of 60 non-daily smokers ages 24-57 years was conducted over a consecutive 7-day at-home protocol to log each smoking session, assessments of mood and social activity during smoking, and collection of daily saliva samples in a convenience sample from Pennsylvania, USA. Hierarchical linear regression analyses were conducted to determine the effects of smoking characteristics on total cotinine exposure measured by pharmacokinetic area under the curve and the range, maximum, and minimum cotinine values during the week controlling for demographic variables., Results: The mean daily cotinine level was 119.2 ng/ml (SD = 168.9) with individual values that ranged from nondetectable to 949.6 ng/ml. Menthol predicted increased total cotinine levels (P < 0.05). Shorter time to the first cigarette of the day predicted significantly higher minimum (P < 0.05), maximum (P < 0.05), and total cotinine values (P < 0.05) after controlling for covariates. Negative emotions and social interactions with others were also significantly associated with higher cotinine metrics. There was no significant effect of the nicotine metabolite ratio., Conclusions: Our findings highlight the variability in nicotine exposure across days among non-daily smokers and point to the role of smoking context in nicotine exposure. The findings suggest the need to develop better assessment methods to determine health and dependence risk and personalized cessation interventions for this heterogeneous and growing group of smokers.

Rationale: There is strong evidence that nicotine can enhance cognitive functions and growing evidence that this effect may be larger in young healthy APOE ε4 carriers. However, the moderating effects of the APOE ε4 allele on cognitive impairments caused by nicotine deprivation in chronic smokers have not yet been studied with brain indices., Objective: We sought to determine whether young female carriers of the APOE ε4 allele, relative to noncarriers, would exhibit larger abstinence-induced decreases in P3b amplitude during a two-stimulus auditory oddball task., Methods: We compared parietal P3bs in female chronic smokers with either APOE ε3/ε3 (n = 54) or ε3/ε4 (n = 20) genotype under nicotine-sated conditions and after 12-17-h nicotine deprivation., Results: Nicotine deprivation significantly reduced P3b amplitudes in APOE ε4 carriers, but not in APOE-ε3/ε3 individuals, such that the difference seen prior to nicotine deprivation was eliminated., Conclusions: The results suggest that subjects with the APOE ε4 allele are more sensitive to nicotine, which could influence smoking patterns, the risk for nicotine dependence, and the cognitive effects of nicotine use in these individuals.

Adolescence represents a highly sensitive period of mammalian neurodevelopment wherein critical synaptic and structural changes are taking place in brain regions involved in cognition, self-regulation and emotional processing. Importantly, neural circuits such as the mesocorticolimbic pathway, comprising the prefrontal cortex, sub-cortical mesolimbic dopamine system and their associated input/output centres, are particularly vulnerable to drug-related insults. Human adolescence represents a life-period wherein many individuals first begin to experiment with recreational drugs such as nicotine and cannabis, both of which are known to profoundly modulate neurochemical signalling within the mesocorticolimbic pathway and to influence both long-term and acute neuropsychiatric symptoms. While a vast body of epidemiological clinical research has highlighted the effects of adolescent exposure to drugs such as nicotine and cannabis on the developing adolescent brain, many of these studies are limited to correlative analyses and rely on retrospective self-reports from subjects, making causal interpretations difficult to discern. The use of pre-clinical animal studies can avoid these issues by allowing for precise temporal and dose-related experimental control over drug exposure during adolescence. In addition, such animal-based research has the added advantage of allowing for in-depth molecular, pharmacological, genetic and neuronal analyses of how recreational drug exposure may set up the brain for neuropsychiatric risk. This review will explore some of the advantages and disadvantages of these models, with a focus on the common, divergent and synergistic effects of adolescent nicotine and cannabis exposure on neuropsychiatric risk.

Diabetic nephropathy (DN) is the leading cause of end-stage kidney disease. Besides glycemic and blood pressure control, environmental factors such as cigarette smoking (CS) adversely affect the progression of DN. The effects of CS on DN progression have been attributed to combustion-generated molecules without consideration to the role of nicotine (NIC), responsible for the addictive properties of both CS and electronic cigarettes (ECs). Podocytes are essential to preserve the structure and function of the glomerular filtration barrier, and strong evidence indicates that early podocyte loss promotes DN progression. We performed experiments in human podocytes and in a mouse model of diabetes that develops nephropathy resembling human DN. We determined that NIC binding to podocytes in concentrations achieved with CS and ECs activated NADPH oxidase, which sets in motion a dysfunctional molecular network integrated by cyclooxygenase 2, known to induce podocyte injury; downregulation of AMP-activated protein kinase, important for maintaining cellular energy stores and antioxidation; and upregulation of CD36, which increased lipid uptake and promoted apoptosis. In diabetic mice, NIC increased proteinuria, a recognized marker of chronic kidney disease progression, accompanied by reduced glomerular podocyte synaptopodin, a crucial stabilizer of the podocyte cytoskeleton, and increased fibronectin expression. This novel study critically implicates NIC itself as a contributor to DN progression in CS and EC users. NEW & NOTEWORTHY In this study, we demonstrate that nicotine increases the production of reactive oxygen species, increases cyclooxygenase-2 expression, and upregulates Cd36 while inducing downregulation of AMP-activated protein kinase. In vivo nicotine increases proteinuria and fibronectin expression in diabetic mice. This study demonstrates that effects of nicotine on podocytes are responsible, at least in part, for the deleterious effects of smoking in the progression of chronic kidney disease, including diabetic nephropathy.

Rationale: The degree to which the EU version of Juul with 20 mg/ml nicotine (Juul EU) delivers nicotine to users is likely to determine its treatment potential., Objectives: To compare the pharmacokinetic profile and user ratings of Juul EU, Juul US (59 mg/ml nicotine), cigarettes and other e-cigarette (EC) products., Methods: In a within-subjects crossover design, 18 vapers used, at separate sessions, their own brand cigarette (OBC), Juul US and Juul EU for 5 min ad libitum, after overnight abstinence. Seven of the participants also tested eight other EC previously. Blood samples were taken at baseline and 2, 4, 6, 8, 10 and 30 min after initiating product use. Products were rated on a range of characteristics., Results: Juul EU delivered less nicotine than OBC (t(13) = -4.64 p < .001) and than Juul US (t(13) = -6.40, p < .001): AUC 0 ≥ 30 77.3, 324.8 and 355.9, respectively. Maximum nicotine concentration (C max ) was also much lower for Juul EU than Juul US (z = -3.59, p < .001): C max 3.8 ng/ml vs 21.1 ng/ml, respectively. Juul EU was perceived to relieve urges to smoke less than Juul US (z = -2.29, p = .022) and to provide less nicotine (z = -2.57. p = 0.010). Juul EU delivered less nicotine than refillable EC (C max : t(6) = 3.02, p = 0.023; AUC 0 ≥ 30 : z = -2.20, p = 0.028) and also less than cig-a-like EC, though the difference did not reach significance (C max : t(6) = 2.49, p = 0.047; AUC 0 ≥ 30 : z = -1.99, p = 0.046). Subjective ratings of Juul EU and other EC products were similar., Conclusions: Juul EU delivers much less nicotine to users than Juul US, and also less than refillable EC products. It may thus have more limited potential to help smokers quit.

Co-administration of tobacco/nicotine and marijuana (e.g., using both products on the same occasion by mixing them in the same delivery device) is a risky, yet common, form of co-use among young adults. Understanding motivations for co-administration co-use, and how these are associated with subsequent use and related problems, is needed to inform policy, prevention, and intervention efforts. We conducted a latent class analysis on 342 young adults with past-year co-administration of tobacco/nicotine and marijuana to determine how emergent classes of 16 co-use motives were associated with use and co-administration co-use of tobacco/nicotine and marijuana one year later. Four classes emerged: (1) a high all class that reported high endorsement of all motives, (2) a high coping class that reported high endorsement of co-use due to coping with stress and bad moods, (3) a high social/physiological reinforcement class that reported low endorsement of coping but high probability of social and relaxation motives and motives to even out effects of each substance, and (4) a low all class that reported low endorsement of all motives. The high all and high coping classes reported greater frequency and quantity of single substance use and co-administration. The high coping class reported more marijuana consequences than the low all class. The high all and high coping classes reported younger age of initiation of each individual substance and co-administration. Considering co-use motives may be useful in identifying those at highest risk for future use and consequences and tailoring interventions to the distinct needs of co-use subgroups. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Nicotine intake and cortical activity are closely related, as they can influence each other. Nicotine is implicated in the induction and modification of cortical plasticity and excitability, whereas a change on cortical plasticity and excitability can also lead to a modification of the smoking behaviour of an individual. The aim of this systematic review was, on the one hand, to evaluate the effects of nicotinergic modulation on cortical excitability and plasticity, and, on the other hand, to assess if modifying the brain's excitability and plasticity could influence one's smoking behaviour. Two systematic literature searches in the PubMed/MEDLINE and PsycINFO databases were conducted. Studies focusing either on the impact of nicotinergic modulation on cortical activity or the treatment effect of non-invasive brain stimulation techniques (NIBS) on smoking behaviour were included. A total of 22 studies for the first systematic search and 35 studies for the second one were included after full-text screening. Nicotine's effect on cortical activity appeared to depend on smoking status of the individual. While deprived smokers seem to generally profit from nicotine consumption in terms of cortical excitability and plasticity, the contrary was true for non-smokers. Regarding the questions of how changes in cortical excitability can influence smoking behaviour, a trend points towards NIBS being a potential intervention technique for smoking cessation.

Aims: To compare success rates and characteristics of smokers treated a second time by a smokers' clinic with success rates of their first treatment., Design: Retrospective cohort study., Setting: Tobacco Dependence Treatment clinic in Prague, Czech Republic, between 2005 and 2017., Participants: A total of 5225 smokers treated either once (n = 5006, single treatment sample, SS) or also second time (n = 219, re-treated sample, RS), on average 4.47 years after the first visit., Intervention: Smokers received intensive treatment of tobacco dependence with pharmacotherapy options. Outcomes were evaluated after 1 year. In case of failure or relapse, participants could undergo re-treatment in the same setting at least 1 year after the start of the first treatment., Measurements: Twelve-month self-reported continuous abstinence; CO-validated (≤ 6 parts per million); number of visits; type of pharmacotherapy; mental health history; Fagerström Test for Cigarette Dependence; time between first and second treatment., Results: The abstinence rate in the SS was 34.8% [95% confidence interval (CI) = 33.4%, 36.1%] and in the RS was 37% (95% CI = 30.6%, 43.8%) and 39.7% (95% CI = 33.2%, 45.5%) for their first and second treatments, respectively. The samples were comparable on smoking and socio-demographic characteristics and pharmacotherapy used, but the RS in the second treatment had a higher prevalence of diagnosed mental health disorder at 39.3% (95% CI = 32.8%; 46.1%) compared with 23.7% (95% CI = 22.5%; 24.9%) in the SS. Participants who initiated their second quit attempt 1 to 2 years after the first one were less successful than those who initiated their second quit attempt later (25 versus 43%; P < 0.05). The results of the first treatment cycle were not found to be a reliable predictor for outcomes of the second cycle of treatment in univariate or multivariate logistic regression (odds ratio = 1.35, 95% CI = 0.70-2.63, P = 0.373)., Conclusion: In Prague, Czech Republic, smokers re-attending stop-smoking treatment more than 2 years after their previous quit attempt appear to achieve similar success rates to those being treated for the first time., (© 2020 Society for the Study of Addiction.)

Aim of the Study: The study aims to present the current state of knowledge on the impact of traditional cigarettes and the nicotine contained in them on the incidence and course of SARS-CoV-2 infection. Moreover, we decided to exhibit the possibility of using this substance to treat COVID-19 infections., Material and Methods: The latest available scientific publications were reviewed until November 14, 2020, from the PubMed platform., Results: Nicotine is a cholinergic agonist and pro-inflammatory cytokines inhibitor. Some authors present that smoking and nicotine reduce the amount of the ACE2 receptors which are used by the novel coronavirus to enter cells, while others claim that ACE2 receptors are upregulated in smokers. Moreover, the interaction of SARS-CoV-2 with nAChR is suspected of dysregulation of the nicotinic cholinergic system, which is associated with the pathophysiology of COVID-19. Due to the harmfulness of cigarettes, a high frequency of smokers is suspected among people suffering from COVID-19. However, some studies report that the number of current smokers hospitalized for SARS-CoV-2 infection is lower than expected, considering the prevalence of smoking in individual countries. Nicotine could restore the impaired function of the nicotine cholinergic system and possibly mitigate the cytokine storm., Conclusions: There is no clear attitude regarding the impact of smoking on the new coronavirus infection now. Researchers do not recommend smoking as a tool to combat the pandemic and show the importance of fighting addiction to reduce the adverse health effects of smoking. Both the relationship between cigarettes and the morbidity and severity of COVID-19, as well as the possibility of using nicotine in the treatment of the disease, require further analysis., (© National Institute of Public Health – National Institute of Hygiene / Narodowy Instytut Zdrowia Publicznego – Państwowy Zakład Higieny.)

Purpose: Evidence for the complete nicotine cessation is inadequate among electronic cigarettes (ECs) single users (SUs, use only ECs), and dual users (DUs, use both ECs and conventional cigarettes (CCs). The primary aim of this study was to evaluate the nicotine cessation among SUs and DUs who used ECs over one year., Methods: We observed 70 SUs and 148 DUs for 52 weeks and tested their exhaled carbon monoxide and saliva cotinine to confirm their complete nicotine cessation status through cotinine in saliva. Safety issues were to be identified through self-report. Smoking cessation, CCs reduction of ≥ 50%, and relapsed to CCs smoking and safety issues were also documented., Results: The nicotine cessation rate was higher in SUs then DUs (15.9% vs. 6.8%; P = 0.048; 95% CI (2.328-0.902). A similar result for smoking cessation (34.8% SUs vs. 17.1% DUs; P = 0.005; 95% CI: 2.031-0.787), whereas CCs ≥ 50% reduction was 23.3% DUs vs 21.7% SUs (P = 0.863; 95% CI :1.020-0.964). Relapse to CC smoking was 47.3% in DUs versus 30.4% in SUs (P = 0.026; 95% CI: 1.555-0.757). The adverse effects reported were coughing and breathing problems, whereas craving smoking was documented as a major withdrawal symptom. Smoking-related diseases were also identified, five in DUs and two in SUs, during the one-year study period., Conclusions: Study showed SUs achieved higher complete nicotine and smoking cessation rates as compared to DUs. However, the rates of reduced CC use were not different between both the groups. No serious adverse effects related to the sole use of ECs were detected. However, the safety of the sole use of ECs in absolute terms needs to be further validated in different populations.

Objectives: This study aimed to identify relapse patterns in smokers who participated in an inpatient treatment program and to investigate factors related to relapse., Methods: The participants comprised 463 smokers who participated in an inpatient treatment operated by the Daejeon Tobacco Control Center from 2015 to 2018. Participants received high-intensity smoking cessation intervention for 5 consecutive days, including pharmacotherapy and behavioral support, and continued with follow-up for 1 year to determine whether they maintained smoking cessation after discharge from inpatient treatment. Kaplan-Meier and Cox proportional hazard models were used in the analysis., Results: Participants' relapse rate within 1 year was 72.8%, and 59.8% of participants smoked again within 6 months after participation. A higher number of counseling sessions was significantly associated with a lower risk of relapse (hazard ratio [HR], 0.23; 95% confidence interval [CI], 0.17 to 0.32 for ≥9 vs. ≤5 counseling sessions). Conversely, higher relapse rates were significantly associated with the use of nicotine replacement therapy (NRT) (HR, 1.91; 95% CI, 1.43 to 2.55 for use vs. no use), and higher levels of baseline expired carbon monoxide (CO) (HR, 1.58; 95% CI, 1.21 to 2.06 for expired CO concentrations of 10-19 ppm vs. expired CO concentrations <10 ppm)., Conclusions: High-intensity smoking cessation interventions in hospital settings can be effective for smoking cessation in smokers with high nicotine dependence. In addition, the results suggest that for quitters to maintain long-term abstinence, they should receive regular follow-up counseling for 1 year after completing a high-intensity smoking cessation intervention.

Nicotine is a major constituent of cigarette smoke. Its primary metabolite in maternal and cord sera, cotinine, is considered a biomarker of prenatal smoking. Nicotine and cotinine half-lives are decreased in pregnancy due to their increased rate of metabolism and conversion to downstream metabolites such as norcotinine and 3-hydroxycotinine. Hence, downstream metabolites of nicotine may provide informative biomarkers of prenatal smoking. In this study of three generations (F0-mothers, F1-offspring who became mothers, and F2-offspring), we present a biochemical assessment of prenatal smoking exposure based on maternal and cord sera levels of nicotine, cotinine, norcotinine, and 3-hydroxycotinine. As potential markers of early effects of prenatal smoking, associations with differential DNA methylation (DNAm) in the F1- and F2-offspring were assessed. All metabolites in maternal and cord sera were associated with self-reported prenatal smoking, except for nicotine. We compared maternal self-report of smoking in pregnancy to biochemical evidence of prenatal smoking exposure. Self-report of F0-mothers of F1 in 1989-1990 had more accuracy identifying prenatal smoking related to maternal metabolites in maternal serum (sensitivity = 94.6%, specificity = 86.9%) compared to self-reports of F1-mothers of F2 (2010-2016) associated with cord serum markers (sensitivity = 66.7%, specificity = 78.8%). Nicotine levels in sera showed no significant association with any DNAm site previously linked to maternal smoking. Its downstream metabolites, however, were associated with DNAm sites located on the MYO1G , AHRR , and GFI1 genes. In conclusion, cotinine, norcotinine, and 3-hydroxycotinine in maternal and cord sera provide informative biomarkers and should be considered when assessing prenatal smoking. The observed association of offspring DNAm with metabolites, except for nicotine, may imply that the toxic effects of prenatal nicotine exposure are exerted by downstream metabolites, rather than nicotine. If differential DNA methylation on the MYO1G , AHRR , and GFI1 genes transmit adverse effects of prenatal nicotine exposure to the child, there is a need to investigate whether preventing changes in DNA methylation by reducing the metabolic rate of nicotine and conversion to harmful metabolites may protect exposed children.

Nicotine dependence is one of the main reasons for the continuation of smoking among adolescents. Loss of autonomy (LOA) is a measure of dependence. This study is the first to investigate LOA and its determinants among Greek adolescents. In 2013, 13-to-15-year-old middle-school students were selected by multi-stage clustered sampling. LOA was evaluated with the Hooked-on-Nicotine Checklist (HONC). Multiple univariate analysis was used to assess the association between adolescent demographics, smoking habits, and loss of autonomy. Three-hundred thirty-nine current smokers responded to the questionnaire (response rate: 82.3%). Of these respondents, 51.2% were male and 88.8% reported at least one LOA symptom. The mean HONC score was 4.13/10 (95% CI: 3.82-4.45). Higher scores were negatively associated with lower smoking frequency (cumulative odds ratio (cOR): 0.240, 95% CI: 0.144-0.400) and positively associated with lower age at first cigarette (cOR: 2.29, 95% CI: 1.38-3.82). Female gender was significantly associated with the prevalence but not the degree of LOA. Overall, the prevalence and the degree of nicotine dependence among adolescent smokers in Greece is similar to other countries. Frequent smoking and initiation of smoking at a younger age are linked to nicotine dependence, although it was not possible to make causal inferences. The relationship between nicotine dependence and gender remains unclear.

Burn patients admitted to the hospital with concurrent intoxication are believed to be at an increased risk of poor outcomes and the development of complications, however data varies within the literature and remains controversial. This systematic review and meta-analysis compared outcomes and complications between nicotine/smoking, alcohol, and/or substance use in 26,512 burn patients admitted to the hospital to 299,543 burn patients admitted without these characteristics. The PubMed, EMBASE, Cochrane Library, and Web of Science databases were systematically and independently searched. PRISMA and Cochrane guidelines were strictly followed. Clinical characteristics, nicotine/smoking use, alcohol use, substance use, outcomes and complications were recorded. Seventeen of the 27 studies included in the study, were eligible for meta-analysis, with results from 39 of the possible 84 outcomes and complications. In conclusion, this systematic review and meta-analysis found that compared to non-nicotine/smoking, non-alcohol, non-substance use burn patients, patients using nicotine/smoking, alcohol, and/or substances were associated with more burn related operations, higher rates of graft loss/failure, longer hospital LOS (length of stay), higher rates of intubation, longer ICU (intensive care unit) LOS, increased mortality, and increased wound/local skin infections. Patients using nicotine/smoking were associated with higher rates of intubation and wound/local skin infections. Patients consuming alcohol were associated with more days on a ventilator, had higher rates of intubation, higher rates of inhalation injury, longer ICU LOS, and increased mortality. Patients taking substances were associated with higher %TBSA (percent total body surface area) of burns, longer hospital LOS, higher rates of intubation, higher rates of inhalation injury, longer ICU LOS, and increased wound/local skin infections., (Copyright © 2019 Elsevier Ltd and ISBI. All rights reserved.)

Introduction: Greater use of nicotine replacement therapy (NRT) is related to smoking cessation success, but the causal direction is unclear. This study characterized the relationship between NRT use and smoking lapse and relapse., Methods: Participants (N = 416 smokers; 57% female, 85% White) were recruited from primary care for a smoking cessation factorial experiment and analyzed if abstaining ≥1 day in the first 2 weeks post-target quit day (TQD). Participants were randomized to counseling and 8 versus 26 weeks of nicotine patch plus nicotine gum post-TQD. Participants carried electronic dispensers that timestamped each gum use. Participants who lapsed (smoked after abstaining) within 6 weeks post-TQD were matched with nonlapsers (n = 146 pairs) on multiple variables. We compared lapsers' versus matched nonlapsers' gum use in the 5 days before and after the lapsers' first lapse., Results: By week 6 post-TQD, 63% of participants lapsed. Compared with nonlapsers, lapsers used less gum 1 and 2 days pre-"lapse" and on the 5 days post-lapse. Lapsers used less gum during the 5 days post-lapse than the 5 days pre-lapse. Univariate survival analyses with lapsers showed greater gum use during both pre- and post-lapse periods predicted longer latency to relapse in the first 6 weeks., Conclusions: In a smoking cessation attempt using nicotine patch plus gum, lapsers versus matched nonlapsers used less gum immediately preceding and following their first lapse. Lower mean gum use before and after lapses predicted a more rapid escalation to relapse. Decreased nicotine gum use both precedes and follows returns to smoking during cessation attempts., Implications: This research examined electronically monitored nicotine gum use collected in real time and found that among smokers engaged in a quit attempt, lapsers (vs. matched nonlapsers) tended to decrease their gum use 1-2 days prior to lapsing and to further decrease their gum use from pre- to post-lapse. Decreased gum use pre-lapse may signal heightened lapse risk in 1-2 days, with lower level of gum use predicting a more precipitous course of relapse. These results encourage further exploration of objective measures of smoking medication use patterns to examine their signaling properties and to inform understanding of cessation failure., Clinical Trial Registration: ClinicalTrials.gov NCT01120704., (© The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved.For permissions, please e-mail: journals.permissions@oup.com.)

This study (a) examined changes in marijuana and cigarette initiation sequencing and (b) considered implications of such changes for prevention efforts by examining associations between initiation sequencing and current adolescent substance use. Analyses used 2000-2019 cross-sectional data from the national Monitoring the Future (MTF) study (78,252 U.S. 12th grade students). Models examined trends in six distinct patterns of initiation order, and multivariable associations between order of initiation and 30-day cigarette and marijuana use prevalence, cigarette and marijuana use frequency among users, and nicotine and marijuana vaping prevalence. While the percentage of students initiating neither cigarettes nor marijuana increased, increases also were observed in marijuana-only initiation (the fastest-growing pattern) and initiation of marijuana before cigarettes; these increases were accompanied by a significant decrease in cigarette-only initiation. Cigarette use prevalence and frequency were highest among students initiating cigarettes before marijuana; marijuana use prevalence and frequency were highest among students initiating marijuana before cigarettes. Cigarette and marijuana prevalence, as well as marijuana frequency, were lowest among students initiating only a single substance. Nicotine vaping was less prevalent among students initiating a single substance versus both substances, but no significant differences were observed in nicotine vaping prevalence between those initiating only cigarettes versus only marijuana. Implications of these findings for prevention efforts are discussed in the frameworks of both the common liability model and route of administration model.

There is an urgent need to address the devastating pandemic, COVID-19, caused by SARS-CoV-2. The efforts to understand the details of this disease in hope of providing effective treatments are commendable. It is clear now that the virus can cause far more damage in patients with comorbid conditions-particularly in those with respiratory, cardiovascular, or immune-compromised system-than in patients without such comorbidities. Drug use can further exacerbate the condition. In this regard, the ill effects of smoking are amply documented, and no doubt can be a confounding factor in COVID-19 progression. Although conflicting hypotheses on the potential role of nicotine in COVID-19 pathology have recently been offered, we believe that nicotine itself, through its interaction with the nicotinic cholinergic system, as well as ACE2, may not only be of use in a variety of neuropsychiatric and neurodegenerative diseases, but may also be of potential use in COVID-19. Thus, on one hand, while we strongly support smoking cessation as a means of harm reduction associated with COVID-19, on the other hand, we support a potential therapeutic role for nicotine, nicotinic agonists, or positive allosteric modulators of nicotinic cholinergic receptors in COVID-19, owing to their varied effects including mood regulation, anti-inflammatory, and purported interference with SARS-CoV-2 entry and/or replication., (© 2020 Federation of European Biochemical Societies.)

Background: The relationship between self-reported and urinary cotinine-verified smoking status and atrial arrhythmia (AA) is unclear. The aim of this study was to evaluate the association of self-reported and urine cotinine-verified smoking status with AA., Method: A total of 201,788 participants (106,375 men, mean age 37 years) who had both a urinary cotinine measurement and electrocardiogram were included. Cotinine-verified current smoking was defined as a urinary cotinine level above 50 ng/mL. Individuals were divided into three groups based on self-reported smoking and two groups based on cotinine-verified smoking status., Results: Among overall subjects, 505 had documented AA (0.3%) and 135 had atrial fibrillation (AF) (0.1%). Self-reported current smoking was associated with an increased risk of AA (odds ratio [OR], 1.42; 95% confidence interval [CI], 1.06-1.91; P = 0.019) and AF (OR, 2.20; 95% CI, 1.24-3.90; P = 0.007), whereas self-reported former smoking had no significant association with AA (OR, 1.30; 95% CI, 0.97-1.73; P = 0.078) and AF (OR, 1.74; 95% CI, 1.00-3.04; P = 0.051). Cotinine-verified current smoking showed no significant association with AA (OR, 1.24; 95% CI, 0.98-1.58; P = 0.080) and AF (OR, 1.20; 95% CI, 0.79-1.83; P = 0.391)., Conclusion: Self-reported current smoking was associated with AA and AF, while self-reported former smoking and cotinine-verified current smoking showed no significant association with AA and AF., Competing Interests: The authors have no potential conflicts of interest to disclose., (© 2020 The Korean Academy of Medical Sciences.)

The effects of smoking on Corona Virus Disease 2019 (COVID-19) are currently unknown. The purpose of this study was to systematically examine the prevalence of current smoking among hospitalized patients with COVID-19 in China, considering the high-population smoking prevalence in China (26.6%). A systematic review of the literature (PubMed) was performed on April 1. Thirteen studies examining the clinical characteristics of hospitalized COVID-19 patients in China and presenting data on the smoking status were found. The pooled prevalence of current smoking from all studies was calculated by random-effect meta-analysis. To address the possibility that some smokers had quit shortly before hospitalization and were classified as former smokers on admission to the hospital, we performed a secondary analysis in which all former smokers were classified as current smokers. A total of 5960 patients were included in the studies identified. The current smoking prevalence ranged from 1.4% (95% CI 0.0-3.4%) to 12.6% (95% CI 10.6-14.6%). An unusually low prevalence of current smoking was observed from the pooled analysis (6.5%, 95% CI 4.9-8.2%) as compared to population smoking prevalence in China. The secondary analysis, classifying former smokers as current smokers, found a pooled estimate of 7.3% (95% CI 5.7-8.9%). In conclusion, an unexpectedly low prevalence of current smoking was observed among patients with COVID-19 in China, which was approximately 1/4th the population smoking prevalence. Although the generalized advice to quit smoking as a measure to reduce health risk remains valid, the findings, together with the well-established immunomodulatory effects of nicotine, suggest that pharmaceutical nicotine should be considered as a potential treatment option in COVID-19.

Background: Smokers with cardiovascular disease have been reported to have decreased mortality compared to non-smokers. Rib fractures are associated with significant underlying injuries such as lung contusions, lacerations, and/or pneumothoraces. We hypothesized that blunt trauma patients with rib fractures who are smokers have decreased ventilator days and risk of in-hospital mortality compared to non-smokers., Study Design: The Trauma Quality Improvement Program (2010-2016) was queried for patients presenting with a blunt rib fracture. Patients that died within 24 h of admission were excluded. A multivariable logistic regression model was performed., Results: From 282,986 patients with rib fractures, 57,619 (20.4%) were smokers. Compared to non-smokers with rib fractures, smokers had a higher median injury severity score (17 vs. 16, p < 0.001). Smokers had a higher rate of pneumonia (7.5% vs. 6.6%, p < 0.001), however, less ventilator days (5 vs. 6, p = 0.04), and lower in-hospital mortality rate (2.3% vs. 4.6%, p < 0.001), compared to non-smokers. After controlling for covariates, smokers with rib fractures were associated with a decreased risk for in-hospital mortality compared to non-smokers with rib fractures (OR 0.64, 0.56-0.73, p < 0.001)., Conclusion: Despite having more severe injuries and increased rates of pneumonia, smokers with rib fractures were associated with nearly a 40% decreased risk of in-hospital mortality and one less ventilator day compared to non-smokers. The long-term detrimental effects of smoking have been widely established. However, the biologic and pathophysiologic adaptations that smokers have may confer a survival benefit when recovering in the hospital from chest wall trauma. This study was limited by the database missing the number of pack-years smoked. Future prospective studies are needed to confirm this association and elucidate the physiologic mechanisms that may explain these findings.

This study examined airborne emissions from cigarette butts for styrene, 2-methyl-2-cyclopenten-1-one, naphthalene, triacetin, and nicotine. Ten experiments were conducted by placing butts in a stainless steel chamber and measuring the chemical concentrations in chamber air. Emission rates were determined from the concentrations. Triacetin and nicotine concentrations were roughly 50% of initial concentrations after 100 hours, while concentrations of other chemicals decayed to less than 10% of initial concentrations within 24 hours. Initial emission rates per cigarette butt ranged from 200 to 3500 ng h -1 . Triacetin and nicotine emission rates at 25°C were 1.6 to 2.2 times higher than the rates at 20°C, while the emission rates of other chemicals at 25°C were 1.1 to 1.3 times higher than the rates at 20°C only during the first sampling period. The chemical concentrations and emission rates at 30°C were comparable or lower than the values at 25°C, possibly due to different batches of cigarettes used. The 24-hours emitted mass of nicotine from a cigarette butt at 25°C could be up to 14% of the literature reported nicotine masses emitted from a burning cigarette., (Published 2020. This article is a U.S. Government work and is in the public domain in the USA.)