On the Influence of Moisture Content in Cigarettes on Combustion Temperature and Transferred Amount of Nicotine into Cigarettes Smoke

The effects of moisture content of cigarettes on both combustion temperature and the amount of nicotine transferred into the smoke were studied under different smoking conditions. The combustion temperatures of domestic commercial blended cigarettes were not affected by smoking procedures or amount of moisture in the cigarette. No significant differences in the amount of nicotine transferred into smoke were observed between the cigarettes with medium (10.9%) and high (15.4%) moisture contents, while the values obtained from the low moisture content (6.6%) cigarettes were always slightly higher than those obtained from medium or high moisture content cigarette.     

The Influence of Inorganic Salts on the Combustion of Cigarette and on the Transfer of Nicotine on to Smoke

The effects of several inorganic salts on the combustion of cigarette and the transfer of nicotine into cigarette smoke have been investigated. Ferric, ferrous, ammonium, magnesium salts and chlorides or sulfates depress the combustibility. Contrary to this, potassium, calcium salts, nitrates and carbonates promote it. The combustion-zone temperatures of cigarettes are within the range from 815°C to 857°C, they are not significantly affected by an addition of inorganic salts. Magnesium nitrate, zinc nitrate and potassium phosphate improve the whiteness of cigarette ash, but the other salts rather darken it. Any relations, however, are not recognized between the whiteness of ash and combustibility of cigarettes. The amounts of nicotine transferred into smoke can be reduced by an addition of inorganic salts, among which magnesium is the most effective.     

Genetic Variants and Early Cigarette Smoking and Nicotine Dependence Phenotypes in Adolescents

Background

While the heritability of cigarette smoking and nicotine dependence (ND) is well-documented, the contribution of specific genetic variants to specific phenotypes has not been closely examined. The objectives of this study were to test the associations between 321 tagging single-nucleotide polymorphisms (SNPs) that capture common genetic variation in 24 genes, and early smoking and ND phenotypes in novice adolescent smokers, and to assess if genetic predictors differ across these phenotypes.

Methods

In a prospective study of 1294 adolescents aged 12–13 years recruited from ten Montreal-area secondary schools, 544 participants who had smoked at least once during the 7–8 year follow-up provided DNA. 321 single-nucleotide polymorphisms (SNPs) in 24 candidate genes were tested for an association with number of cigarettes smoked in the past 3 months, and with five ND phenotypes (a modified version of the Fagerstrom Tolerance Questionnaire, the ICD-10 and three clusters of ND symptoms representing withdrawal symptoms, use of nicotine for self-medication, and a general ND/craving symptom indicator).

Results

The pattern of SNP-gene associations differed across phenotypes. Sixteen SNPs in seven genes (ANKK1, CHRNA7, DDC, DRD2, COMT, OPRM1, SLC6A3 (also known as DAT1)) were associated with at least one phenotype with a p-value <0.01 using linear mixed models. After permutation and FDR adjustment, none of the associations remained statistically significant, although the p-values for the association between rs557748 in OPRM1 and the ND/craving and self-medication phenotypes were both 0.076.

Conclusions

Because the genetic predictors differ, specific cigarette smoking and ND phenotypes should be distinguished in genetic studies in adolescents. Fifteen of the 16 top-ranked SNPs identified in this study were from loci involved in dopaminergic pathways (ANKK1/DRD2, DDC, COMT, OPRM1, and SLC6A3).

Impact

Dopaminergic pathways may be salient during early smoking and the development of ND.     

The Experimental Autoimmune Encephalomyelitis Disease Course Is Modulated by Nicotine and Other Cigarette Smoke Components

Epidemiological studies have reported that cigarette smoking increases the risk of developing multiple sclerosis (MS) and accelerates its progression. However, the molecular mechanisms underlying these effects remain unsettled. We have investigated here the effects of the nicotine and the non-nicotine components in cigarette smoke on MS using the experimental autoimmune encephalomyelitis (EAE) model, and have explored their underlying mechanism of action. Our results show that nicotine ameliorates the severity of EAE, as shown by reduced demyelination, increased body weight, and attenuated microglial activation. Nicotine administration after the development of EAE symptoms prevented further disease exacerbation, suggesting that it might be useful as an EAE/MS therapeutic. In contrast, the remaining components of cigarette smoke, delivered as cigarette smoke condensate (CSC), accelerated and increased adverse clinical symptoms during the early stages of EAE, and we identify a particular cigarette smoke compound, acrolein, as one of the potential mediators. We also show that the mechanisms underlying the opposing effects of nicotine and CSC on EAE are likely due to distinct effects on microglial viability, activation, and function.     

Cigarette Smoking in Pregnancy: Its Influence on Birth Weight and Perinatal Mortality

In a British population cigarette smoking during pregnancy increased the late fetal plus neonatal mortality rate by 28% and reduced birth weight by 170 g, and these differences persist even after allowing for a number of “mediating” maternal and social variables. A change in smoking habit by the end of the fourth month of pregnancy places a mother in the risk category appropriate to her changed habit. This evidence should have important implications for health education aimed at getting pregnant mothers to give up smoking.     

Protobacco Media Exposure and Youth Susceptibility to Smoking Cigarettes,Cigarette Experimentation,and Current Tobacco Use among US Youth

Purpose

Youth are exposed to many types of protobacco influences, including smoking in movies, which has been shown to cause initiation. This study investigates associations between different channels of protobacco media and susceptibility to smoking cigarettes, cigarette experimentation, and current tobacco use among US middle and high school students.

Methods

By using data from the 2012 National Youth Tobacco Survey, structural equation modeling was performed in 2013. The analyses examined exposure to tobacco use in different channels of protobacco media on smoking susceptibility, experimentation, and current tobacco use, accounting for perceived peer tobacco use.

Results

In 2012, 27.9% of respondents were never-smokers who reported being susceptible to trying cigarette smoking. Cigarette experimentation increased from 6.3% in 6th grade to 37.1% in 12th grade. Likewise, current tobacco use increased from 5.2% in 6th grade to 33.2% in 12th grade. Structural equation modeling supported a model in which current tobacco use is associated with exposure to static advertising through perception of peer use, and by exposure to tobacco use depicted on TV and in movies, both directly and through perception of peer use. Exposure to static advertising appears to directly increase smoking susceptibility but indirectly (through increased perceptions of peer use) to increase cigarette experimentation. Models that explicitly incorporate peer use as a mediator can better discern the direct and indirect effects of exposure to static advertising on youth tobacco use initiation.

Conclusions

These findings underscore the importance of reducing youth exposure to smoking in TV, movies, and static advertising.     

Effect of Electric Aversion on Cigarette Smoking

Electric aversion was administered to 14 cigarette smokers. Six of the nine who completed the treatment were still abstinent at one-year follow-up. Three cases relapsed (at one, three, and four months) and five dropped out of treatment. Depression was a troublesome side-effect and was responsible for two of the drop-outs. The overall average of 21·5 cigarettes on the day before treatment dropped to an average of 1·4 cigarettes per day after the third aversion session, and though individual response varied widely most patients stopped smoking within five sessions. It is concluded that electric aversion is a powerful suppressor of cigarette smoking, but more experience is needed to ensure its best use as a measure to achieve permanent abstinence. Its use is limited to a small group of well-motivated smokers.     

The Effects of Chronic Cigarette Smoking on Gray Matter Volume: Influence of Sex

Cigarette smoke contains nicotine and toxic chemicals and may cause significant neurochemical and anatomical brain changes. Voxel-based morphometry studies have examined the effects of smoking on the brain by comparing gray matter volume (GMV) in nicotine dependent individuals (NDs) to nonsmoking individuals with inconsistent results. Although sex differences in neural and behavioral features of nicotine dependence are reported, sex differences in regional GMV remain unknown. The current study examined sex differences in GMV in a large sample of 80 NDs (41 males) and 80 healthy controls (41 males) using voxel-based morphometry. Within NDs, we explored whether GMV was correlated with measures of cigarette use and nicotine dependence. High-resolution T1 structural scans were obtained from all participants. Segmentation and registration were performed in SPM8 using the optimized DARTEL approach. Covariates included age and an estimate of total global GMV. Differences were considered significant at p≤0.001, with a whole brain FWE-corrected cluster probability of p<0.025. Among NDs compared to Controls less GMV was observed in the thalamus and bilateral cerebellum and greater GMV was observed in the bilateral putamen and right parahippocampus. Lower thalamic GMV was observed in both female and male NDs compared to Controls. Female NDs also had lower GMV in the left cerebellum and in the ventral medial and orbitofrontal cortices with no areas of greater GMV. Male NDs had lower GMV in bilateral cerebellum and greater GMV in bilateral parahippocampus and left putamen. Within male NDs, GMV in the left putamen was correlated with number of pack years. This study, conducted in a large cohort, contributes to our knowledge of brain morphology in nicotine addiction and provides additional evidence of sex-specific effects on GMV in NDs. Identifying brain vulnerabilities with respect to sex provides a methodological framework for personalized therapies to improve relapse rates for both sexes.     

Puffing Topography and Nicotine Intake of Electronic Cigarette Users

BackgroundPrior electronic cigarette (EC) topography data are based on two video analyses with limited parameters. Alternate methods for measuring topography are needed to understand EC use and nicotine intake.ObjectivesThis study evaluated EC topography with a CReSS Pocket device and quantified nicotine intake.MethodsValidation tests on pressure drop, flow rate, and volume confirmed reliable performance of the CReSS Pocket device. Twenty participants used Blu Cigs and V2 Cigs for 10 minute intervals with a 10–15 minute break between brands. Brand order was reversed and repeated within 7 days Data were analyzed to determine puff duration, puff count, volume, flow rate, peak flow, and inter-puff interval. Nicotine intake was estimated from cartomizer fluid consumption and topography data.ResultsNine patterns of EC use were identified. The average puff count and inter-puff interval were 32 puffs and 17.9 seconds. All participants, except one, took more than 20 puffs/10 minutes. The averages for puff duration (2.65 seconds/puff), volume/puff (51ml/puff), total puff volume (1,579 ml), EC fluid consumption (79.6 mg), flow rate (20 ml/s), and peak flow rate (27 ml/s) were determined for 10-minute sessions. All parameters except total puff count were significantly different for Blu versus V2 EC. Total volume for Blu versus V2 was four-times higher than for conventional cigarettes. Average nicotine intake for Blu and V2 across both sessions was 1.2 ± 0.5 mg and 1.4 ± 0.7 mg, respectively, which is similar to conventional smokers.ConclusionsEC puffing topography was variable among participants in the study, but often similar within an individual between brands or days. Puff duration, inter-puff interval, and puff volume varied from conventional cigarette standards. Data on total puff volume and nicotine intake are consistent with compensatory usage of EC. These data can contribute to the development of a standard protocol for laboratory testing of EC products.     

Fractionation and Phenol Composition of Cellulose Cigarette Smoke Condensate

Fractionation of smoke condensate and a detailed analysis of phenols in the cellulose cigarette smoke were performed during the course of systematic compositional studies of the smoke. Nearly equal yields of phenolic, acidic and neutral fractions were obtained in fractionation of cellulose cigarette smoke condensate. Thirtyseven phenols were newly identified in the smoke of cellulose cigarette in addition to six phenols ever found in pyrolysis products of cellulose. Semi-quantitative determination of some of these phenols revealed that dihydric phenols, such as catechol, hydroquinone, resorcinol and their alkyl derivatives were the main phenols and monohydric phenols were the minor phenols.     

Mechanisms of Cigarette Smoke Effects on Human Airway Smooth Muscle

Cigarette smoke contributes to or exacerbates airway diseases such as asthma and COPD, where airway hyperresponsiveness and airway smooth muscle (ASM) proliferation are key features. While factors such as inflammation contribute to asthma in part by enhancing agonist-induced intracellular Ca²⁺ ([Ca²⁺]i) responses of ASM, the mechanisms by which cigarette smoke affect ASM are still under investigation. In the present study, we tested the hypothesis that cigarette smoke enhances the expression and function of Ca²⁺ regulatory proteins leading to increased store operated Ca²⁺ entry (SOCE) and cell proliferation. Using isolated human ASM (hASM) cells, incubated in the presence and absence cigarette smoke extract (CSE) we determined ([Ca²⁺]i) responses and expression of relevant proteins as well as ASM proliferation, reactive oxidant species (ROS) and cytokine generation. CSE enhanced [Ca²⁺]i responses to agonist and SOCE: effects mediated by increased expression of TRPC3, CD38, STIM1, and/or Orai1, evident by attenuation of CSE effects when siRNAs against these proteins were used, particularly Orai1. CSE also increased hASM ROS generation and cytokine secretion. In addition, we found in the airways of patients with long-term smoking history, TRPC3 and CD38 expression were significantly increased compared to life-long never-smokers, supporting the role of these proteins in smoking effects. Finally, CSE enhanced hASM proliferation, an effect confirmed by upregulation of PCNA and Cyclin E. These results support a critical role for Ca²⁺ regulatory proteins and enhanced SOCE to alter airway structure and function in smoking-related airway disease.     

Composition of the Water-soluble Portion of Cellulose Cigarette Smoke Condensate

Water-soluble portion of the smoke condensate of cellulose cigarette was studied and 42 compounds—10 lactones, 6 cyclopentanones (or cyclopentenones), 5 pyrans and other compounds—were either positively or tentatively identified. Of these 42 compounds, 12, such as succinaldehyde, 5-hydroxy-2-pentenone, etc., were identified for the first time in cellulose pyrolyzate. Semi-quantitative estimation of some of the major components in water-soluble portion revealed that 1,6-anhydroglucopyranose (levoglucosan) was the most abundant, followed by 2-hydroxy-3-methyl-2-cyclopentenone (cyclotene), acetol, 2-hydroxy-5-pentanolide, etc. Glycolaldehyde which seems to be more abundant than cyclotene on chxomatogram could not be estimated because of peak tailing. Of these water-soluble components, succinaldehyde has very pungent and irritating effect and seems to be a cause of the pungent and irritating odor of cellulose cigarette smoke.     

Cigarette Smoke Decreases the Maturation of Lung Myeloid Dendritic Cells

BackgroundConflicting data exist on the role of pulmonary dendritic cells (DCs) and their maturation in patients with chronic obstructive pulmonary disease (COPD). Herein, we investigated whether disease severity and smoking status could affect the distribution and maturation of DCs in lung tissues of patients undergoing elective pneumectomy or lobectomy for suspected primary lung cancer.ResultsCOPD was diagnosed in 43 patients (16 current smokers and 27 former smokers), whereas the remaining 32 subjects were classified as non-COPD (11 current smokers, 13 former smokers, and 8 never smokers). The number and maturation of DCs did not differ significantly between COPD and non-COPD patients. However, the results of flow cytometry indicated that maturation markers CD40 and CD83 of BDCA1-positive mDCs were significantly decreased in smokers than in non-smokers (P = 0.023 and 0.013, respectively). Immunohistochemistry also revealed a lower number of LDCs in COPD patients than in non-COPD subjects.ConclusionsCigarette smoke, rather than airflow limitation, is the main determinant of impaired DCs maturation in the lung.     

Effect of Cigarette Smoking on Competence of the Pylorus: Preliminary Study

The competence of the pylorus was studied in 13 normal volunteers and nine dyspeptic patients by means of a radiological technique involving intubation of the duodenum. The pylorus was found to be competent in most normal individuals and in fewer than half of the dyspeptic patients. However, on smoking a cigarette, appreciable increase in duodenogastric reflux was seen in nine out of the 13 normal volunteers and in seven out of the nine dyspeptic patients. Such induced pyloric incompetence and the resultant regurgitation of duodenal juices may explain the increased incidence of gastritis and gastric ulceration in heavy smokers.     

The Effect of a Perforated Mouthpiece Tube on Cigarette Smoke Reduction

Cigarette smoke reduction due to a perforated mouthpiece tube was measured, and its results were compared with the reduction caused by conventionally vented acetate filters. The reduction of nicotine and tar increased with the ventilation rate through the perforated tube. In the absence of a filter material, the difference between the reduction of tar and nicotine was found to be greater than that observed for conventionally vented filters, and the concentration of nicotine in tar was enhanced. The reduction of carbon monoxide, carbon dioxide, acetaldehyde, isoprene and acetone were all proportional to the ventilation rate through the perforated tube. The presence of a filter material had no effect on the gas and vapor phase components.     

Effects of Cigarette Smoke Extracts on the Growth and Senescence of Skin Fibroblasts In Vitro

Epidemiological studies have shown that cigarette smoke (CS), a very common environmental factor, plays an important role in skin aging. Although some in vivo studies have suggested that CS affects skin aging, the detailed effects of CS on skin cells in vitro remain largely unknown. In this study, we investigated the effects of cigarette smoke extract (CSE) on the growth, proliferation, and senescene of skin fibroblasts and the possible mechanism underlying these effects. Primary cultured human fibroblasts were exposed to a range of concentrations of CSE. Cell viability and cell proliferation after CSE exposure were analyzed with the methyl thiazolyl tetrazolium (MTT) assay and bromodeoxyuridine incorporation assay, respectively. Growth curves of fibroblasts exposed to different concentrations of CSE were developed and prolonged CSE-exposed cells were observed. Morphological and ultrastructural changes in fibroblasts were assessed by inverted light microscopy and transmission electron microscopy (TEM). Dying cells were stained with senescence-associated β-galactosidase (SA β-gal). Intracellular reactive oxygen species (ROS) levels, superoxide dismutase (SOD) activity, and glutathione peroxidase (GSH-Px) activity were determined by a colorimetric method. We found that proliferative capacity and growth were inhibited by CSE exposure in a dose- and time-dependent manner. Fibroblasts exposed to even low concentrations of CSE for a long period of time (5 passages) showed significantly increased SA β-gal activity and typical features of aging cells. Meanwhile, CSE inhibited superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and augmented ROS levels. Our observations suggest that CSE exposure impairs fibroblast growth and proliferation and leads to features similar to those seen in senescent cells. Oxidative stress injury and inhibition of antioxidant defense activity may be involved in CSE-induced fibroblast senescence.