Tobacco Cigarette Smoking Research Articles

Tobacco and Cannabis Use During and After Pregnancy in California.

ObjectivesAs the social and legal acceptance of cannabis use grows, health professionals must understand and mitigate the impact of cannabis use in the perinatal period. Here we compare the prevalence of tobacco and cannabis use during and after pregnancy in California, a state that recently legalized cannabis use.MethodsMeasures of tobacco and cannabis use during and after pregnancy were obtained from California’s Maternal and Infant Health Assessment, an annual population-based survey of California resident women with a live birth. To allow analysis of county-level variation, we pooled data from the 35 counties with the largest numbers of births from 2017 to 2019.ResultsCannabis use was more than twice as common as cigarette smoking among pregnant women (4.9% vs. 2.1%) in California. This difference was even more pronounced in some counties; for example, in Los Angeles, cannabis use was four times more prevalent than cigarette use. Either during or soon after birth, 7.3% of women in California reported cannabis use. Of those who smoked tobacco cigarettes prior to pregnancy, 73% quit before their third trimester of pregnancy, though 33.0% of these women reported a post-partum relapse in cigarette use.ConclusionsStates that have legalized cannabis must attend to the increasing prevalence of perinatal cannabis use, as well as concurrent use with tobacco and other substances. Efforts to support cannabis cessation should draw from successful public health approaches in tobacco control.

Cytotoxic and genotoxic effects of cigarette and waterpipe tobacco smoking on buccal mucosa: A systematic review and meta-analysis.

Waterpipe tobacco smoking (WTS) is an issue all over the world, although it is particularly prevalent in the Middle East, and Southeast Asia. The genotoxic effects of smoking were reported to be associated with nucleus abnormalities such as micronuclei (MN), karyorrhexis (KR), karyolysis, pyknosis, binucleates, broken eggs, condensed chromatin in exfoliated buccal mucosal cells, and was believed to be associated with apoptosis of cells and was not correlated to the exposure time. The aim of this study was to evaluate and compare the cytotoxic and genotoxic effects of cigarette and WTS on buccal mucosa. The pertinent search was done through the computerized literature on MEDLINE, EMBASE, and PUBMED databases, which included case-control, clinical and observational studies regarding the mutagenic effects of cigarettes and WTS in oral tissues. The retraction of data in this study was undertaken from May 2010 to May 2022. A total of 60 articles from the search data were retrieved. This investigation was registered with the research center of Riyadh Elm University for institution review board approval (IRB) and obtained the IRB number "FRP/2021/448/733/707 and the systematic review registration number with respect to PROSPERO is 345417. After the removal of duplicates, 32 were evaluated for the inclusion and exclusion criteria. Out of 32 articles, twenty studies were evaluated for cytogenetic abnormalities in buccal mucosal cells of waterpipe tobacco smokers (WTS) and cigarette smokers, and 12 were excluded. The mean MN levels in the oral tissues of WTS were more (1.94 ± 0.39) than in non-smokers (1.68 ± 0.35). Therefore, we conclude that the MN count can be employed as a biomarker and preliminary signal for the identification of changes in oral mucosa among smokers, which develop towards cancer formation.

Editorial: Vaping and Cardiovascular health � An opportunity or a risk?

The history of smoking dates back to the ancient times and mankind has been smoking different plant materials for the leisure and addiction. One of its kind, tobacco cigarette smoking was introduced in the 19th century and its use increased exponentially by the mid of 20th century. Initially it was thought that the tobacco cigarette smoking had some medicinal properties but as the rate of tobacco smoking increased, the adverse effects started appearing and by the end of 20th century it was a well-known fact that tobacco cigarette smoking was a health hazard and a major risk factor for the fatal diseases like cancer and cardiovascular diseases1. With the emergent side effects and health hazards tobacco cigarette smoking was discouraged on a larger scale in the society and the search for the alternative to it led to the creation of E-cigarettes in the early 21st century.
 Since the introduction of vaping i.e., use of E-cigarettes, E-hookahs, vape pens or Electronic Nicotine Delivery Systems (ENDS), it is taken as a safe alternative of tobacco cigarettes smoking and a way to help in smoking cessation2. The perception of less harmful tobacco smoking substitute, extensive marketing and a vogue of vaping have resulted in an explosive increase in the use of vaping devices among the former smokers, current smokers and even in never smoker adolescents and young adults in the past two decades. According to the National Health Interview Survey (NIHS), the number of E-cigarette users increased to 8.1 million in United States in 20183 and according to National Youth Tobacco Survey in US 19.6% of high school students and 4.7% of middle school students are regular users of E-cigarettes4.
 Most vaping devices are made up of four components, including: a cartridge or pod containing e-liquid, a metallic heating coil, a battery and a mouthpiece. The e-liquid contains chemicals like propylene glycol, vegetable glycerin, flavoring substance and varying amount of nicotine. Propylene glycol and vegetable glycerin act as solvent carriers. When a person puffs/inhales, it activates the heating coil that causes the e-liquid to vaporize that is inhaled by the person. The vapors or aerosols that are inhaled deliver certain chemicals into the body that are mainly:
 
 Nicotine
 Organic volatile compounds generated by heating of solvent carriers such as glycols, glycerin, toluene that cause irritation to the eyes, oral and laryngeal mucosa.
 Carbonyls such as acetaldehyde, formaldehyde, acrolein and glyoxal which are carcinogenic and cause extensive damage to the lungs.
 Chemical present in flavoring agents like Diacetyl, acetyl propionyl and acetoin cause severe asthma and bronchiolitis obliterans
 The contaminants that may be the tobacco derived alkaloids and nitrosamines
 Metal particles from the heating coils like chromium, cadmium, nickel, lead; and particles of copper, nickel, and silver
 
 These chemicals are responsible for the injuries to the respiratory mucosa, skin and are considered as carcinogens.
 The cardiovascular effects of vaping are mediated by:
 
 Nicotine, it has been demonstrated that activation of nicotinic Ach receptors causes release of catecholamines and promotes hemodynamic alterations, endothelial dysfunction, insulin resistance, dyslipidemia and arrhythmogenesis5.
 Increased oxidative stress that is produced due to aerosolized chemicals, metals, particulates and acrolein. It causes generation of oxygen derived free radical species causing inflammation and damage to the endothelial cells, reduced bioavailability of NO, plaque destabilization, platelet activation and thrombus formation causing myocardial infarction, stroke and cardiovascular events5.
 
 Though tobacco cigarette smoking is 3 times more harmful than vaping6 the studies have shown that the vaping is associated with increased risk of cardiovascular events as compared to non-users and the use of tobacco cigarette smoking along with vaping cause the highest number of cardiovascular events as compared to non-users, vaping or tobacco cigarette smoking alone7.
 The vaping epidemic and its potential hazards can be controlled by certain measures:
 
 Regulating the advertisements of e-cigarettes
 Reducing the access of adolescents and young adults to the vaping products
 Public awareness campaigns to educate children and adults about the harmful effects of vaping
 Reducing the second-hand exposure to vaping aerosols by precluding its use in the indoors and public spaces.
 
 The studies so far have not proved vaping to be an effective tool for smoking cessation, instead the user who start vaping for smoking cessation often end up using both and the use of vaping among adolescents increases the propensity of them to become tobacco cigarette smoker. In the author�s opinion the use of vaping should not be recommended, and its use should be discouraged owing to its adverse effects on health.

Cytotoxic, genotoxic, and toxicogenomic effects of heated tobacco products and cigarette smoke in human primary keratinocytes.

INTRODUCTIONHeated tobacco products (HTPs) appear to be less harmful to health than conventional cigarettes (CCs). However, limited analytical data are available to support this claim. This study aimed to compare the cytotoxic, genotoxic, and toxicogenomic effects of HTPs and CCs in carcinogenesis via multistep gene mutations in the oral mucosal cells.METHODSCigarette smoke extract (CSE) was obtained from HTPs and CCs. Primary human oral keratinocytes (HOKs) were treated with 5% and 20% CSE from HTPs and CCs. Cell survival rate assays were performed after 6, 12, and 24 h. After 6 h, DNA double-strand breaks (DSBs) were evaluated using anti-γH2AX antibodies with immunohistochemistry. mRNAs expressions of mediator of DNA damage checkpoint 1 (MDC1) and ataxia telangiectasia and Rad3-related protein (ATR), were analyzed. Expressions of miR-22 and miR-185 were analyzed because miR-22 targets MDC1 and miR-185, ATR.RESULTSThe HOKs had equivalent survival rates after exposure to the same concentrations of CSE from CCs and HTPs. HTPs increased foci formation of γH2AX in HOKs, as did CCs (without CSE vs 20% HTP, p<0.05; without CSE vs 20% CC, p<0.05). Expressions of MDC1 and ATR decreased in cells exposed to CSE from CCs and HTPs (MDC1: without CSE vs 20% HTP, p<0.05; without CSE vs 20% CC, p<0.05; ATR: without CSE vs 20% HTP, p<0.05; without CSE vs 20% CC, p<0.05). Expressions of miR-22 and miR-185 were not significantly increased when exposed to CSE from CCs or HTPs.CONCLUSIONSHTPs and CCs had similar cytotoxic effects. HTPs are genotoxic, can cause DSBs, and have toxicogenomic damage because they inhibit the MDC1 and ATR-CHK1 DNA repair pathways in the oral mucosa. The miRNA-mRNA axis was not related to these inhibitions.

Tobacco and electronic cigarette smoking among in-school adolescents in Vietnam between 2013 and 2019: prevalence and associated factors

ABSTRACT Background Smoking among adolescents in schools is a major global public health concern. There is limited evidence regarding prevalence and associated factors in Vietnam. Objective To compare the prevalence of smoking and associated factors among in-school adolescents aged 13–17 years in Vietnam between 2013 and 2019. Methods Data were collected from two rounds of the national representative Vietnam Global School-based Student Health Survey (GSHS) conducted in 2013 (n = 3,331) and 2019 (n = 7,690). Logistic regression was used to identify the factors associated with tobacco and electronic cigarette smoking among in-school adolescents. Results There was a significant reduction in the prevalence of current smoking (water pipes and cigarettes) from 5.4% (95% CI: 4.0–7.2) in 2013 to 2.8% (95% CI: 2.2–3.6) in 2019. In 2019, 2.6% of the in-school adolescents reported having used electronic cigarette products 30 days prior to the survey. Factors associated with a significantly higher likelihood of current smoking status included gender, loneliness, suicidal ideation, sexual activity, truancy, and alcohol consumption. Similar patterns were observed for e-cigarettes. Conclusion Smoking among in-school adolescents in Vietnam decreased between 2013 and 2019. Follow-up studies are needed to further investigate causal factors so that future policies and communication programmes can be more effectively targeted to reduce smoking in adolescents.

Associations Between E-cigarettes and Subsequent Cocaine Use in Adolescence: An Analysis of the UK Millennium Cohort Study.

Nicotine exposure via early combustible cigarette smoking can prime the adolescent brain for subsequent cocaine use. However, there is limited evidence whether e-cigarette use, a nicotine delivery system that is increasingly popular among youth, is associated with later cocaine use. We examine the association between e-cigarette use by the age of 14 years and cocaine use by the age of 17 years. The Millennium Cohort Study is a nationally representative sample of 18 552 9-month-old children born between September 2000 and January 2002 in the United Kingdom. Follow-up interviews and surveys were collected from children and their caregivers at modal ages 3, 5, 7, 9, 11, 14, and 17 years. Our analytic sample included 340 youth who had used e-cigarettes by age 14 years (exposure variable), matched using coarsened exact matching, to 4867 nicotine naïve youth on childhood common liability confounders and demographics measured from infancy to age 11. The outcome was cocaine use by the modal age of 17 years. Of the 5207 successfully matched youth, 7.6% of adolescent e-cigarette users by age 14 years used cocaine by age 17 years versus 3.1% of non-e-cigarette users. Multivariable logistic regression in the matched sample indicated that e-cigarette use by age 14 years was associated with 2.7 times higher odds of cocaine use by age 17 years (95% CI, 1.75 to 4.28). These findings in a UK sample showed that e-cigarette use in early adolescence is associated with higher odds of cocaine use later in adolescence, similar to risks posed by tobacco cigarette smoking. In this large-scale prospective cohort study (n = 5207), youth who had used e-cigarettes by the age of 14 years were matched to nicotine naïve youth on childhood common liability confounders and demographics measured from infancy to age 11 years (e.g. school engagement, risk-taking propensity, delinquency, peer and parental smoking, parental educational attainment). After matching, 7.6% of age 14 years e-cigarette users had subsequently used cocaine by the age of 17 years versus 3.1% of non-e-cigarette users. Although e-cigarettes are promoted as a strategy for nicotine-dependent users to reduce the harms of combustible cigarettes, the evidence here suggests that for nicotine naïve youth, they may increase the risk of subsequent cocaine use.

Prefrontal cortex and putamen grey matter alterations in cannabis and tobacco users.

Previous magnetic resonance imaging studies in regular cannabis users report altered grey matter volume (GMV) in brain regions, including the prefrontal cortex (PFC), putamen and hippocampus. However, most studies have tended to recruit recreational users with high levels of cannabis use, and have not controlled for the possible confounding effects of tobacco use. We attempt to address these limitations in the present study. We acquired volumetric images in sex, age and IQ-matched groups of (1) regular Cannabis users who also smoke Tobacco cigarettes ('CT'; n = 33), (2) non-cannabis-using Tobacco cigarette smokers ('T'; n = 19) and (3) non-cannabis/tobacco-using Controls ('C'; n = 35). GMV in bilateral PFC, putamen and hippocampal regions was compared across groups. We also examined the associations between GMV differences and levels of cannabis and tobacco use, measures of intellectual function, and of depression, anxiety and stress. Relative to controls, both CT and T groups showed lower GMV in the left inferior frontal gyrus, and greater GMV in the putamen. In addition, lower GMV in the right frontal pole in the CT group (but not the T group) was associated with lifetime cannabis use, but not with cigarette use. Regular cannabis users who also smoked tobacco cigarettes showed altered GMV patterns relative to controls. However, a similar pattern of GMV differences was also seen between regular tobacco users that did not use cannabis. Further research is needed to disentangle the effects of cannabis and tobacco use on brain structure.

The Impact of Tobacco Cigarettes, Vaping Products and Tobacco Heating Products on Oxidative Stress.

Cells constantly produce oxidizing species because of their metabolic activity, which is counteracted by the continuous production of antioxidant species to maintain the homeostasis of the redox balance. A deviation from the metabolic steady state leads to a condition of oxidative stress. The source of oxidative species can be endogenous or exogenous. A major exogenous source of these species is tobacco smoking. Oxidative damage can be induced in cells by chemical species contained in smoke through the generation of pro-inflammatory compounds and the modulation of intracellular pro-inflammatory pathways, resulting in a pathological condition. Cessation of smoking reduces the morbidity and mortality associated with cigarette use. Next-generation products (NGPs), as alternatives to combustible cigarettes, such as electronic cigarettes (e-cig) and tobacco heating products (THPs), have been proposed as a harm reduction strategy to reduce the deleterious impacts of cigarette smoking. In this review, we examine the impact of tobacco smoke and MRPs on oxidative stress in different pathologies, including respiratory and cardiovascular diseases and tumors. The impact of tobacco cigarette smoke on oxidative stress signaling in human health is well established, whereas the safety profile of MRPs seems to be higher than tobacco cigarettes, but further, well-conceived, studies are needed to better understand the oxidative effects of these products with long-term exposure.

Longitudinal bidirectional association between youth electronic cigarette use and tobacco cigarette smoking initiation in Thailand

IntroductionThis study quantifies the longitudinal association between e-cigarette use and subsequent conventional cigarette initiation and vice versa among Thai youths.MethodsData from a longitudinal survey of 6045 Thai seventh grade students...

Differences in risk indicators associated with electronic cigarette use and tobacco smoking among adolescents and young people in Nigeria

IntroductionThe study determined the proportion of adolescents and young persons (AYP) in Nigeria who use e-cigarettes and smoke tobacco; and identified factors associated with the use of e-cigarettes and tobacco...

Drugs of Misuse: Focus on Vascular Dysfunction.

Common drugs of misuse, including cannabis, opioids, stimulants, alcohol, and anabolic steroids, have strikingly disparate acute and chronic vascular effects, leading to a wide range of clinical cardiovascular presentations. Acute cannabis smoking has been associated with increased risk for myocardial infarction and ischemic stroke in otherwise healthy young people. However, it remains uncertain if people who exclusively smoke cannabis have increased risk for accelerated atherosclerosis similar to that found in people who exclusively smoke tobacco cigarettes. Cocaine and methamphetamines, both stimulants, increase risk for stroke, myocardial infarction, aortic dissection, and accelerated atherosclerosis, but only methamphetamine use is strongly linked to pulmonary hypertension. Chronic alcohol use is strongly associated with chronic hypertension and hemorrhagic stroke, but perhaps confers a lower risk for myocardial infarction. Finally, anabolic steroid use, presumably through adverse effects on circulating lipids and the hematopoietic system, is associated with increased risk for accelerated atherosclerosis and myocardial infarction. Physicians, especially cardiologists, emergency medicine, and internal medicine physicians, should be familiar with the short- and long-term vascular consequences of use of these substances, thereby ensuring appropriate, specific, and informed counselling and treatment.

Toxicity risk assessment in tobacco chewers, cigarette smokers and alcohol consumers using urinary DNA adduct and exfoliated buccal cells micronuclei as non-invasive biomarkers

To assess the toxicity amongst alcohol consumers, tobacco chewers and cigarette smokers using non invasive biomarkers such as urinary DNA adduct and buccal cell micronuclei. Fifty subjects aged between (20-40 years) of different social habits (alcoholics, tobacco chewers and cigarette smokers) of Meerut City (India), were registered for this study. Similarly non-alcoholics, non-tobacco chewers and non-smokers were also selected. Each volunteer completed a health and occupational questionnaire that included information on food habit, smoking habit and consumption of alcohol. Samples were collected in white sterilized plastic bottles and transported in an ice box to the laboratory and stored at −20 0 C (Remi, India) for further analyses of specific gravity of urine, creatinine (Toro and Ackerman, 1975), urinary DNA adduct (8-OHdG) and exfoliated buccal cell micronuclei. ELISA kit was used to determine 8–OHdG in the urine samples of selected subjects. The results showed that minimum amount of 8–OHdG was present in the urine samples of control subjects, whereas maximum value of 8–OHdG was found in tobacco. Alcoholics showed lower values than smokers. Subjects with all the three habits showed further lower value for 8–OHdG. Microscopical examination of the buccal epithelium showed the presence of MN. The least number of cells with micronuclei was recorded in control subjects. Whereas, maximum number of cells with MN was found in tobacco chewers followed by smokers and alcoholics. It is concluded that intake of alcohol, cigarette smoke and tobacco promote generation of reactive oxygen species in the buccal epithelium exposing their DNA to continuous oxidative stress which finally leads to DNA damage and MN formation. Additionally, DNA adducts and micronuclei formation in human tissue can be use as a simple tool and non invasive toxicity biomarkers.

Prevalence of electronic and tobacco cigarette smoking among health sciences students in Saudi Arabia

Prevalence of electronic and tobacco cigarette smoking among health sciences students in Saudi Arabia

The Prevalence and 5-Year Incidence Rate of Cigarette Smoking and Water-Pipe Tobacco Smoking and Their Associated Factors among 15 to 80 Years Old Urban Population in Southeast Iran: Results from KERCADR Study.

Cigarette and tobacco smoking are closely associated with chronic cardiovascular disease and lung cancer. We aimed to assess the prevalence and 5-year incidence rate (IR) of these two risk factors for cardiovascular diseases in Kerman, southeastern of Iran. 10015 individuals aged 15-80 were recruited to the study between 2014 and 2018 (Kerman coronary artery disease (CAD) risk factors study, KERCADRS) of which 2820 had also participated in the first phase (5 years earlier). We took fasting blood samples and collected demographic information and data on cigarette and water-pipe tobacco smoking (WPTS) through interviews. The overall prevalence of cigarette smoking increased from 8.1% in phase1 to 8.8% in phase 2. During the same period, the prevalence of WPTS increased from 10% to 14%, especially in the age groups of 15-45 years. The prevalence of opium dependance was higher among cigarette smokers compared to WPT users. The overall 5-year IR of cigarette and WPTS was 3.6 and 4.65 per 1000 person-years respectively. The highest IRs of cigarette smoking and WPTS were reported in the age group of 15-39 years, and IR of WPTS was higher among women. Obesity, diabetes, and hypertension associated with a reduced IRs of cigarette and WPTS. Over the past five years, the prevalence of cigarette smoking has increased slightly, but WPTS has increased more rapidly, especially among women. The highest prevalence of cigarette and WPT smoking was in the age groups of 15-39 years. Smoking is shifting from cigarette smoking to WPTS. Age- and gender-oriented interventions would help correct the unhealthy life style in the community and prevent further smoking-related morbidities and mortalities.

Transcriptomic Evidence That Switching from Tobacco to Electronic Cigarettes Does Not Reverse Damage to the Respiratory Epithelium.

The health benefits of switching from tobacco to electronic cigarettes (ECs) are neither confirmed nor well characterized. To address this problem, we used RNA-seq analysis to compare the nasal epithelium transcriptome from the following groups (n = 3 for each group): (1) former smokers who completely switched to second generation ECs for at least 6 months, (2) current tobacco cigarette smokers (CS), and (3) non-smokers (NS). Group three included one former cigarette smoker. The nasal epithelial biopsies from the EC users vs. NS had a higher number of differentially expressed genes (DEGs) than biopsies from the CS vs. NS and CS vs. EC sets (1817 DEGs total for the EC vs. NS, 407 DEGs for the CS vs. NS, and 116 DEGs for the CS vs. EC comparison). In the EC vs. NS comparison, enriched gene ontology terms for the downregulated DEGs included cilium assembly and organization, whereas gene ontologies for upregulated DEGs included immune response, keratinization, and NADPH oxidase. Similarly, ontologies for cilium movement were enriched in the downregulated DEGs for the CS vs. NS group. Reactome pathway analysis gave similar results and also identified keratinization and cornified envelope in the upregulated DEGs in the EC vs. NS comparison. In the CS vs. NS comparison, the enriched Reactome pathways for upregulated DEGs included biological oxidations and several metabolic processes. Regulator effects identified for the EC vs. NS comparison were inflammatory response, cell movement of phagocytes and degranulation of phagocytes. Disease Ontology Sematic Enrichment analysis identified lung disease, mouth disease, periodontal disease and pulmonary fibrosis in the EC vs. NS comparison. Squamous metaplasia associated markers, keratin 10, keratin 13 and involucrin, were increased in the EC vs. NS comparison. Our transcriptomic analysis showed that gene expression profiles associated with EC use are not equivalent to those from non-smokers. EC use may interfere with airway epithelium recovery by promoting increased oxidative stress, inhibition of ciliogenesis, and maintaining an inflammatory response. These transcriptomic alterations may contribute to the progression of diseases with chronic EC use.

210Po and 210Pb content in the smoke of Heated Tobacco Products versus Conventional Cigarette smoking

210Po is a radioactive component of conventional cigarette tobacco smoke and is a recognized carcinogen. Despite the expanding market of heated tobacco products, no data are available on the activity of 210Po in the smoke of IQOS Heets cigarette. We determined the 210Po activity in the mainstream smoke of thirteen cigarette brands available on the Swiss market using a smoking machine and compared the results to the 210Po activity measured in the mainstream smoke of the IQOS system. In addition, we measured the 210Po and 210Pb loss on heating after uniform heating from 50 to 600 °C for several cigarette brands and the Heets cigarettes. 13.6 ± 4.1% of 210Po activity was found in the mainstream smoke in conventional cigarette smoking (7% for 210Pb). This dropped to 1.8 ± 0.3% in the mainstream smoke of IQOS Heets. Conversely, when the tobacco was heated uniformly at 330 °C, a loss of 210Po of more than 80% was observed for all type of cigarettes. Apparently, IQOS significantly reduced the 210Po and 210Pb activities in the mainstream smoke. However, our results show that only 15% of the Heets tobacco reaches 330 °C with IQOS. While IQOS reduces the 210Po and 210Pb activities in the mainstream smoke compared to conventional cigarettes, it only heats a marginal fraction of the tobacco present in the Heets cigarette. Because smoking is an addiction (mostly due to nicotine), IQOS could possibly deliver an unsatisfactory dose of nicotine to a Heets cigarette smoker, as most of the tobacco is left unaltered.

Tobacco cigarette smokers who endorse greater intolerance for nicotine withdrawal also report more severe insomnia symptoms.

It has been suggested that nighttime nicotine withdrawal may help to explain why tobacco cigarette smokers are more likely than nonsmokers to experience clinically significant insomnia. There is also reason to believe that intolerance for withdrawal symptoms could play a role in withdrawal-related sleep disturbance. However, we are not aware of any previous research that examined whether smokers who endorse greater intolerance for smoking abstinence also report greater difficulty initiating and/or maintaining sleep. To address this question, 224 adult cigarette smokers (42.9% female, Mcigarettes per day = 21.3) completed the baseline portion of an experimental study that included assessment of current/historical smoking behavior, perceived intolerance for smoking abstinence, and insomnia severity and impact on functioning. The results indicated that, after accounting for general distress intolerance and sociodemographic factors, smokers who endorsed greater intolerance for nicotine withdrawal also reported greater insomnia severity and impact. Logistic regression further revealed that, for every 1-point increase in nicotine withdrawal intolerance scores, smokers were nearly twice as likely to score above threshold for clinically significant insomnia (p = .001). Collectively, these initial findings suggest that intolerance for nicotine withdrawal may warrant consideration as a potentially modifiable mechanistic factor in comorbid insomnia and nicotine/tobacco dependence. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

How do heated tobacco products (HTPs) and cigarette smoking compare in terms of safety?

How do heated tobacco products (HTPs) and cigarette smoking compare in terms of safety?

Chronic Exposure to Electronic Cigarettes Induces Lung Oxidative Stress, Inflammation, Fibrosis, and Impaired DNA Repair

BackgroundElectronic cigarettes (e‐cig) have been marketed as a safer alternative to tobacco cigarette smoking (TCS). While there are far less toxic compounds in e‐cig vape (ECV) than in tobacco cigarette smoke, detectable levels of toxicants are still present. Multiple in vitro and short‐term in vivo studies on e‐cig‐induced lung cell damage have been reported; however, questions remain regarding the health effects of chronic e‐cig use on the lungs. Therefore, studies were performed in a chronic mouse exposure model to investigate the deleterious effects of long‐term ECV exposure on the lungs.MethodsC57/BL6 male mice were exposed for 2 hours/day, 5 days/week to either air (control group; 25 mice) or ECV generated from e‐cig liquid containing 24 mg/ml nicotine (e‐cig group; 25 mice) for 16 weeks. At the end of the exposure, animals were euthanized, lungs were lavaged, then the recovered bronchoalveolar lavage fluid (BALF) was prepared to assess the percentages of inflammatory cells in BALF. Fixed lung sections were also prepared and stained with hematoxylin and eosin (H &amp; E) or Masson’s trichrome stain to assess the degree of lung inflammation and fibrosis; respectively. Superoxide radical generation was measured in frozen lung sections using DHE. Western blotting (WB) and immunofluorescence (IF) in lung tissue were used to detect the levels of nitrotyrosine, and the expression of the DNA repair enzymes XPC and OGG1.ResultsThe number of inflammatory cells present in the BALF, including neutrophils, macrophages, and eosinophils, was significantly higher in ECV‐exposed mice compared to that with air exposure. In the ECV‐exposed mice, H &amp; E stained lung sections showed clear inflammatory infiltrates with lymphoid aggregates of lymphocytes, plasma cells and macrophages that stretch from the perivascular and peribronchiolar areas into adjacent septal adipose tissue. Masson’s trichrome stained slides showed increase in connective tissue around airways and bronchioles in e‐cig exposed mice, indicating the presence of pulmonary fibrosis. Using the fluorescence‐based superoxide probe DHE, significantly increased superoxide generation was observed in the lungs of ECV exposed mice, compared to control. This DHE‐derived fluorescence was largely quenched by preincubation with the SOD mimetic MnTBAP, confirming that the observed fluorescence was largely derived from superoxide. WB and IF showed elevated levels of nitrotyrosine. Reduced expression of the DNA damage repair proteins XPC and OGG1 were seen in lung tissue of the ECV exposed mice compared to the controls.ConclusionChronic ECV exposure induced lung inflammation, pulmonary fibrosis, and increased superoxide generation. ECV exposure increased oxidative stress and inflammation in the lungs while decreasing the levels of DNA damage repair proteins. These findings suggest that chronic e‐cig use can trigger oxidative stress with inflammatory lung damage and impaired DNA repair that together may predispose to neoplastic transformation and cancer onset.

Role of Human Aldehyde Oxidase in the Generation of Reactive Oxygen Species during the Metabolism of Nicotine

Nicotine is the major addictive constituent of tobacco and alternative tobacco products including electronic cigarettes (e‐cigs). While e‐cig vaping has been proposed as safer than traditional tobacco smoking, recent studies has demonstrated that these products can also trigger oxidant stress and inflammation with resultant pulmonary and cardiovascular disease. E‐cig liquids contain high levels of nicotine typically of 12 to 24 mg/ml or more and with the use of high power delivery devices high, poorly controlled levels of nicotine can be delivered. When inhaling tobacco cigarette smoke or e‐cig vape, nicotine is rapidly absorbed through the lungs. The major pathway of nicotine metabolism in humans consists of the C‐oxidation of nicotine to produce cotinine involving a two‐step process: the first step is CYP2A6‐catalyzed 5′‐oxidation to nicotine‐Δ1′(5′)‐iminium ion (NI), which is in equilibrium with 5′‐hydroxynicotine; and the second step is aldehyde oxidase (AO) catalyzed oxidation of NI to cotinine.Using both cytochrome‐c reduction and EPR spin trapping techniques, we show for the first time that the oxidation of NI by human AO produces superoxide radical anion (O2• −) with high flux rates. Purified recombinant human AO (hAO) was prepared and characterized by SDS gel electrophoresis and optical absorption spectroscopy. hAO, 40 nM was incubated in the presence of NI concentrations from 1‒50 µM. The kinetic parameters, Km and Vmax values, for superoxide generation from NI were determined to be 2.7 ± 0.4 μM and 694 ± 24 nmol min−1 mg−1 of protein, respectively. From quantitation of the measured superoxide and the amount of NI consumed, we estimate that ~60% of the oxygen consumed in this process is converted to superoxide with ~40% hydrogen peroxide. Superoxide generation was almost completely quenched by either 0.5 μM raloxifene, a potent inhibitor of AO, or 0.1 μM Copper‐Zinc‐superoxide dismutase (SOD1) with no superoxide generation detected either in the absence of either AO or nicotine‐Δ1′(5′)‐iminium ion.Therefore, human AO efficiently catalyzes the oxidation of NI to cotinine with concomitant production of reactive oxygen species. Due to the high expression levels of AO in lung tissue as well as its rapid rate of NI metabolism with low Km, AO rapidly and efficiently converts NI to cotinine with the formation of superoxide and hydrogen peroxide. Thus, nicotine metabolism will be associated with the formation of superoxide, hydrogen peroxide and secondary reactive oxygen species that can in turn cause lung oxidative stress and inflammation.