Association Between Nicotine-dependent Gene Polymorphism and Smoking Cessation in Patients With Lung Cancer

BackgroundPatients with lung cancer continue to smoke owing to complex factors. Failure to quit smoking (defined as nicotine dependence) is significantly associated with genetic status. This study aimed to investigate the relationship between polymorphisms in nicotine dependence genes and smoking status after the diagnosis of lung cancer.Patients and MethodsA total of 240 patients with lung cancer were included from July 2017 to March 2018. According to the actual smoking condition after lung cancer diagnosis, eligible patients were divided into 3 groups: the never-smoking group, the failure to quit smoking group, and the successful smoking cessation group. Fagerstrom Test for Nicotine Dependence scores were used to evaluate the smoking status of each group. Three nicotine-dependent genes with 6 loci were detected.ResultsAmong the 240 patients, 86 were never-smokers, 51 failed to quit smoking, and 104 successfully quit smoking. The initial age of smoking in the failure to quit smoking group was significantly younger than those in the successful smoking cessation group (P = .001). There was a significant difference in the GG and AG and AA genotype distributions of CHRNA3 (rs578776) among the 3 groups (P = .003). There was also a significant difference in the distribution of CHRNA4 (rs2229959) genotypes among the 3 groups (P = .003). However, there was no significant difference in the genotype distribution of CHRNA5 (rs588765) among the 3 groups (P = .277).ConclusionsGene polymorphisms of CHRNA3 (rs578776) and CHRNA4 (rs1044396 and rs2229959) were associated with the success of smoking cessation after the diagnosis of lung cancer, which should be considered in the management of smoking cessation after patients are diagnosed with lung cancer.     

Young people's perspectives of e-cigarette use in the home

There is concern that the emergence of e-cigarettes could result in an increase in young people's intake of, and exposure to, nicotine. This UK study used friendship group interviews to elicit the perspectives of young people from socioeconomically contrasting backgrounds regarding e-cigarettes. Young people from both advantaged and disadvantaged backgrounds described similar e-cigarette practices in the home environment, and, for both health and sensory reasons, viewed these as preferable to tobacco smoking. Space-related practices of adult e-cigarette use in the home were revealed to be more malleable than those of tobacco use. Results also highlighted that e-cigarettes offered young people new opportunities for nicotine consumption in the home. Methods of storing e-cigarettes in domestic spaces posed safety risks to younger children and easy access to e-cigarettes for others.     

E-cigarettes: Are we renormalizing public smoking? Reversing five decades of tobacco control and revitalizing nicotine dependency in children and youth in Canada

An electronic cigarette (e-cigarette) is a battery attached to a chamber containing liquid that may (or may not) contain nicotine. The battery heats the liquid and converts it into a vapour, which is inhaled, mimicking tobacco smoking. The e-cigarette does not rely on tobacco as a source of nicotine but, rather, vaporizes a liquid for inhalation. E-liquids are often flavoured and may contain nicotine in various concentrations, although actual amounts are seldom accurately reflected in container labelling. The deleterious effects of nicotine on paediatric health are well established. The use of e-cigarettes in the paediatric age group is on the rise in Canada, as are associated nicotine poisonings. E-devices generate substantial amounts of fine particulate matter, toxins and heavy metals at levels that can exceed those observed for conventional cigarettes. Children and youth are particularly susceptible to these atomized products. Action must be taken before these devices become a more established public health hazard. Policies to denormalize tobacco smoking in society and historic reductions in tobacco consumption may be undermined by this new ‘gateway’ product to nicotine dependency.     

Colitis and colorectal tumors should be further explored and differentiated

The original article by Yuichi et al explored whether the Japan Narrow-Band Imaging Expert Team classification and the pit pattern classification are suitable for diagnosing neoplastic lesions in patients with ulcerative colitis. In this letter, we offer some other perspectives. Risk factors for colorectal tumors include type 2 diabetes. Among genetic factors, the deletion or mutation of some genes, such as the p53 gene, can lead to colorectal tumors. There are significant gender differences in the occurrence and development of colorectal tumors. Some non-genetic factors, such as smoking, are also associated with the development of colorectal tumors. These all suggest that colorectal tumors are not only caused by ulcerative colitis, and we suggest further exploration and differentiation between colitis and colorectal tumors.     

Effects of Negative Affect,Urge to Smoke,and Working Memory Performance (n-back) on Nicotine Dependence

Background: Three key domains including negative emotionality, incentive salience, and executive function form the core functional elements of addictive behaviors. Variables related to these broader domains have been studied extensively in relation to one another; however, no studies to date, have examined models including variables from all three domains, in relation to nicotine dependence. Method: Smokers (N = 117), 65.8% female, 78% white, mean age of 44.4 (SD = 10.8), enrolled in a smoking cessation program completed measures of negative affect (a component of negative emotionality), urge to smoke (incentive salience), and working memory (WM; a core executive function), during a baseline assessment period prior to initiating treatment. Results: Negative affect was associated with greater urge to smoke, and this elevated urge to smoke was associated with higher levels of nicotine dependence. Further, a significant moderated mediation indicated that WM moderated the relationship between increased urge to smoke and nicotine dependence. For those with low to average WM, urge to smoke was significantly related to nicotine dependence; however, for those with higher WM (+1 SD), urge to smoke stemming from negative affect was not associated with nicotine dependence. Conclusions: To our knowledge, this is the first reported relationship between negative affect, urge to smoke, WM, and nicotine dependence. Although preliminary, results indicate that WM may moderate the relationship between urge to smoke associated with negative affect and nicotine dependence. Treatments targeting WM may be particularly useful for individuals with average to low WM who experience urge to smoke related to negative affect.     

Black Light Smokers: How Nicotine Intake and Carcinogen Exposure Differ Across Various Biobehavioral Factors

ObjectiveThe study objective was to identify biobehavioral variables associated with greater intake of nicotine and a tobacco carcinogen among Black light smokers who smoke 1 to 10 cigarettes per day (CPD).MethodsWe analyzed baseline data collected from 426 Black light smokers enrolled in Kick It at Swope III (KIS III), a smoking cessation trial for Black smokers. We examined differences in concentrations of tobacco biomarkers, including urinary total nicotine equivalents (TNE) and total 4-(methylnitrosamino)-1-(3)pyridyl-1-butanonol (NNAL; a human carcinogen), across gender, age, plasma nicotine metabolite ratio (NMR), CPD, and measures of tobacco dependence, including time to first cigarette (TFC), using ANOVA.ResultsTobacco biomarker levels were significantly higher among those who smoked more CPD (6–10 vs 1–5 CPD) and those with greater reported physical dependence on tobacco. Concurrently, those who smoked 1–5 CPD smoked each cigarette more intensely than those who smoked 6–10 CPD. While we found no gender differences overall, among those who smoked 1–5 CPD, women had higher NNAL levels compared to men. The rate of nicotine metabolism, measured by the nicotine metabolite ratio, was not significantly related to TNE or NNAL levels.ConclusionAmong Black Light smokers, higher cigarette consumption and greater physical dependence—but not rate of nicotine metabolism, menthol use, or socioeconomic status—were associated with greater toxicant exposure and thus a likely increased risk of tobacco-related diseases. The lack of data on light smokers, and specifically on Blacks, make this observation important given the disproportionate burden of lung cancer in this population.     

Systemic absorption of nicotine following acute secondhand exposure to electronic cigarette aerosol in a realistic social setting

Evidence suggests exposure of nicotine-containing e-cigarette aerosol to nonusers leads to systemic absorption of nicotine. However, no studies have examined acute secondhand exposures that occur in public settings. Here, we measured the serum, saliva and urine of nonusers pre- and post-exposure to nicotine via e-cigarette aerosol. Secondarily, we recorded factors affecting the exposure.Six nonusers of nicotine-containing products were exposed to secondhand aerosol from ad libitum e-cigarette use by three e-cigarette users for 2?h during two separate sessions (disposables, tank-style). Pre-exposure (baseline) and post-exposure peak levels (Cmax) of cotinine were measured in nonusers’ serum, saliva, and urine over a 6-hour follow-up, plus a saliva sample the following morning. We also measured solution consumption, nicotine concentration, and pH, along with use behavior.Baseline cotinine levels were higher than typical for the US population (median serum session one?=?0.089?ng/ml; session two?=?0.052?ng/ml). Systemic absorption of nicotine occurred in nonusers with baselines indicative of no/low tobacco exposure, but not in nonusers with elevated baselines. Median changes in cotinine for disposable exposure were 0.007?ng/ml serum, 0.033?ng/ml saliva, and 0.316?ng/mg creatinine in urine. For tank-style exposure they were 0.041?ng/ml serum, 0.060?ng/ml saliva, and 0.948?ng/mg creatinine in urine. Finally, we measured substantial differences in solution nicotine concentrations, pH, use behavior and consumption.Our data show that although exposures may vary considerably, nonusers can systemically absorb nicotine following acute exposure to secondhand e-cigarette aerosol. This can particularly affect sensitive subpopulations, such as children and women of reproductive age.     

Root surface conditioning with nicotine or cotinine reduces viability and density of fibroblasts in vitro

The purpose of study was to evaluate fibroblast attachment and cellular morphology on root surfaces chemically conditioned with nicotine or cotinine. A secondary objective was to determine if mechanical scaling and root planning of these chemically conditioned surfaces would alter cellular attachment. Root surface dentin specimens were prepared from uniradicular teeth of non-smoking patients. Specimens were randomly assigned to two experimental groups: no treatment (chemical conditioning only) and scaling and root planning after conditioning (SRPC). The concentrations of the tested substances were in the range of 0–1 mg/mL (nicotine) and 0–1 ?g/mL (cotinine). After a 24-h conditioning period, dentin slices were incubated with continuous lineage of fibroblastic cells from rat (McCoy cells) for another 24 h. Specimens were prepared for SEM analysis and microphotographs. The statistical analysis of the data indicated significant alteration of cellular morphology on fibroblasts that were grown on root surface exposed to nicotine concentrations greater than 1 ?g/mL. This effect of nicotine was not reduced by SRPC. On the other hand, in the SRPC group cellular density was greater. For cotinine-conditioned specimens, the greater concentrations also led to alteration on morphology, and these alterations were observed in the SRPC group as well. Cotinine did not induce significant changes on cellular density. The results indicated that fibroblasts are negatively influenced by nicotine present on the dentin substrate and also that scaling may reduce these effects. Cotinine treatment on root surfaces may alter cell morphology and density but these effects were less severe than that promoted by nicotine, and were not affected by scaling.