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Sample records for cigarette smoke exposure

  1. Cigarette smoke exposure-associated alterations to noncoding RNA

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    Matthew Alan Maccani

    2012-04-01

    Full Text Available Environmental exposures vary by timing, severity, and frequency and may have a number of deleterious effects throughout the life course. The period of in utero development, for example, is one of the most crucial stages of development during which adverse environmental exposures can both alter the growth and development of the fetus as well as lead to aberrant fetal programming, increasing disease risk. During fetal development and beyond, the plethora of exposures, including nutrients, drugs, stress, and trauma, influence health, development, and survival. Recent research in environmental epigenetics has investigated the roles of environmental exposures in influencing epigenetic modes of gene regulation during pregnancy and at various stages of life. Many relatively common environmental exposures, such as cigarette smoking, alcohol consumption, and drug use, may have consequences for the expression and function of noncoding RNA (ncRNA, important post-transcriptional regulators of gene expression. A number of ncRNA have been discovered, including microRNA (miRNA, Piwi-interacting RNA (piRNA, and long noncoding RNA (long ncRNA. The best-characterized species of ncRNA are miRNA, the mature forms of which are ~22 nucleotides in length and capable of post-transcriptionally regulating target mRNA utilizing mechanisms based largely on the degree of complementarity between miRNA and target mRNA. Because miRNA can still negatively regulate gene expression when imperfectly base-paired with a target mRNA, a single miRNA can have a large number of potential mRNA targets and can regulate many different biological processes critical for health and development. The following review analyzes the current literature detailing links between cigarette smoke exposure and aberrant expression and function of noncoding RNA, assesses how such alterations may have consequences throughout the life course, and proposes future directions for this intriguing field of

  2. Comparison of Nicotine and Carcinogen Exposure with Water pipe and Cigarette Smoking

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    Jacob, Peyton; Abu Raddaha, Ahmad H.; Dempsey, Delia; Havel, Christopher; Peng, Margaret; Yu, Lisa; Benowitz, Neal L.

    2013-01-01

    Background Smoking tobacco preparations in a water pipe (hookah) is widespread in many places of the world and is perceived by many as relatively safe. We investigated biomarkers of toxicant exposure with water pipe compared to cigarette smoking. Methods We conducted a cross-over study to assess daily nicotine and carcinogen exposure with water pipe and cigarette smoking in 13 people who were experienced in using both products. Results While smoking an average of 3 water pipe sessions compared to smoking 11 cigarettes per day, water pipe use was associated with a significantly lower intake of nicotine, greater exposure to carbon monoxide and a different pattern of carcinogen exposure compared to cigarette smoking, with greater exposure to benzene and high molecular weight PAHs, but less exposure to tobacco-specific nitrosamines, 1,3-butadiene and acrolein, acrylonitrile, propylene oxide, ethylene oxide, and low molecular weight PAHs. Conclusions A different pattern of carcinogen exposure might result in a different cancer risk profile between cigarette and water pipe smoking. Of particular concern is the risk of leukemia related to high levels of benzene exposure with water pipe use. Impact Smoking tobacco in water pipes has gained popularity in the United States and around the world. Many believe that water pipe smoking is not addictive and less harmful than cigarette smoking. We provide data on toxicant exposure that will help guide regulation and public education regarding water pipe health risk. PMID:23462922

  3. Digital image analysis of cigarette filter staining to estimate smoke exposure.

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    O'Connor, Richard J; Kozlowski, Lynn T; Hammond, David; Vance, Tammy T; Stitt, Joseph P; Cummings, K Michael

    2007-08-01

    Sufficient variation exists in how people smoke each cigarette that the number of cigarettes smoked daily and the years of smoking represent only crude measures of exposure to the toxins in tobacco smoke. Previous research has shown that spent cigarette filters can provide information about how individuals smoke cigarettes. Digital image analysis has been used to identify filter vent blocking and may also provide an inexpensive, unobtrusive index of overall smoke exposure. A total of 1,124 cigarette butts smoked by 53 participants in a smoking topography study were imaged and analyzed. Imaging showed test-retest reliability of more than 95% among those smoking their own brand. Mean color scores (CIELAB system) showed acceptable stability (>.60) across days, paralleling the basic stability of smoking topography measures across waves. A principal components scoring showed that center tar staining, edge tar staining, and their interaction were significantly related to total smoke volume, accounting for 73% of the variation. Estimated smoke volume was a significant predictor of salivary cotinine when accounting for cigarettes smoked per day. These data suggest that digital image analysis of spent cigarette butts can serve as a reliable proxy measure of total smoke volume.

  4. Pharmacokinetics of nicotine in rats after multiple-cigarette smoke exposure

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    Rotenberg, K.S.; Adir, J.

    1983-06-15

    The pharmacokinetics of nicotine and its major metabolites was evaluated in male rats after multiple-cigarette smoke exposure. A smoke-exposure apparatus was used to deliver cigarette smoke to the exposure chamber. The rats were exposed to smoke from a single cigarette every 8 hr for 14 days and to the smoke of a cigarette spiked with radiolabeled nicotine on the 15th day. Blood and urine samples were collected at timed intervals during the 10-min smoke-exposure period of the last cigarette and up to 48 hr thereafter. Nicotine, cotinine, and other polar metabolites were separated by thin-layer chromatography and quantified by liquid scintillation counting. The data were analyzed by computer fitting, and the derived pharmacokinetic parameters were compared to those observed after a single iv injection of nicotine and after a single-cigarette smoke exposure. The results indicated that the amount of nicotine absorbed from multiple-cigarette smoke was approximately 10-fold greater than that absorbed from a single cigarette. Also, unlike the single-cigarette smoke exposure experiment, nicotine plasma levels did not decay monotonically but increased after the 5th hr, and high plasma concentrations persisted for 30 hr. The rate and extent of the formation of cotinine, the major metabolite of nicotine, were decreased as compared with their values following a single-cigarette smoke exposure. It was concluded that nicotine or a constituent of tobacco smoke inhibits the formation of cotinine and may affect the biotransformation of other metabolites. Urinary excretion tended to support the conclusions that the pharmacokinetic parameters of nicotine and its metabolites were altered upon multiple as compared to single dose exposure.

  5. Scrambled and fried: Cigarette smoke exposure causes antral follicle destruction and oocyte dysfunction through oxidative stress

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    Sobinoff, A.P. [Reproductive Science Group, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW 2308 (Australia); Priority Research Centre for Chemical Biology, University of Newcastle, Callaghan, NSW 2308 (Australia); Beckett, E.L.; Jarnicki, A.G. [Centre for Asthma and Respiratory Disease, The University of Newcastle and Hunter Medical Research Institute, Callaghan, NSW 2308 (Australia); Sutherland, J.M. [Reproductive Science Group, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW 2308 (Australia); Priority Research Centre for Chemical Biology, University of Newcastle, Callaghan, NSW 2308 (Australia); McCluskey, A. [Priority Research Centre for Chemical Biology, University of Newcastle, Callaghan, NSW 2308 (Australia); Hansbro, P.M. [Centre for Asthma and Respiratory Disease, The University of Newcastle and Hunter Medical Research Institute, Callaghan, NSW 2308 (Australia); McLaughlin, E.A., E-mail: eileen.mclaughlin@newcastle.edu.au [Reproductive Science Group, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW 2308 (Australia); Priority Research Centre for Chemical Biology, University of Newcastle, Callaghan, NSW 2308 (Australia)

    2013-09-01

    Cigarette smoke is a reproductive hazard associated with pre-mature reproductive senescence and reduced clinical pregnancy rates in female smokers. Despite an increased awareness of the adverse effects of cigarette smoke exposure on systemic health, many women remain unaware of the adverse effects of cigarette smoke on female fertility. This issue is compounded by our limited understanding of the molecular mechanisms behind cigarette smoke induced infertility. In this study we used a direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease to characterise mechanisms of cigarette-smoke induced ovotoxicity. Cigarette smoke exposure caused increased levels of primordial follicle depletion, antral follicle oocyte apoptosis and oxidative stress in exposed ovaries, resulting in fewer follicles available for ovulation. Evidence of oxidative stress also persisted in ovulated oocytes which escaped destruction, with increased levels of mitochondrial ROS and lipid peroxidation resulting in reduced fertilisation potential. Microarray analysis of ovarian tissue correlated these insults with a complex mechanism of ovotoxicity involving genes associated with detoxification, inflammation, follicular activation, immune cell mediated apoptosis and membrane organisation. In particular, the phase I detoxifying enzyme cyp2e1 was found to be significantly up-regulated in developing oocytes; an enzyme known to cause molecular bioactivation resulting in oxidative stress. Our results provide a preliminary model of cigarette smoke induced sub-fertility through cyp2e1 bioactivation and oxidative stress, resulting in developing follicle depletion and oocyte dysfunction. - Highlights: • Cigarette smoke exposure targets developing follicle oocytes. • The antral follicle oocyte is a primary site of ovarian cigarette smoke metabolism. • Cyp2e1 is a major enzyme involved in ameliorating smoke-induced ovotoxicity. • Cigarette smoke causes oocyte

  6. Evaluation of E-Cigarette Liquid Vapor and Mainstream Cigarette Smoke after Direct Exposure of Primary Human Bronchial Epithelial Cells

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    Stefanie Scheffler

    2015-04-01

    Full Text Available E-cigarettes are emerging products, often described as “reduced-risk” nicotine products or alternatives to combustible cigarettes. Many smokers switch to e-cigarettes to quit or significantly reduce smoking. However, no regulations for e-cigarettes are currently into force, so that the quality and safety of e-liquids is not necessarily guaranteed. We exposed primary human bronchial epithelial cells of two different donors to vapor of e-cigarette liquid with or without nicotine, vapor of the carrier substances propylene glycol and glycerol as well as to mainstream smoke of K3R4F research cigarettes. The exposure was done in a CULTEX® RFS compact  module, allowing the exposure of the cells at the air-liquid interface. 24 h post-exposure, cell viability and oxidative stress levels in the cells were analyzed. We found toxicological effects of e-cigarette vapor and the pure carrier substances, whereas the nicotine concentration did not have an effect on the cell viability. The viability of mainstream smoke cigarette exposed cells was 4.5–8 times lower and the oxidative stress levels 4.5–5 times higher than those of e-cigarette vapor exposed cells, depending on the donor. Our experimental setup delivered reproducible data and thus provides the opportunity for routine testing of e-cigarette liquids to ensure safety and quality for the user.

  7. Creatine kinase isoenzyme patterns upon chronic exposure to cigarette smoke: protective effect of Bacoside A.

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    Anbarasi, K; Vani, G; Balakrishna, K; Devi, C S Shyamala

    2005-01-01

    Cigarette smoking is implicated as a major risk factor in the development of cardiovascular and cerebrovascular diseases. Creatine kinase (CK) and its isoforms (CK-MM, MB, BB) have been advocated as sensitive markers in the assessment of cardiac and cerebral damage. Therefore, in the present study, we report the isoenzyme patterns of CK in rats upon exposure to cigarette smoke and the protective effect of Bacoside A against chronic smoking induced toxicity. Adult male albino rats were exposed to cigarette smoke and simultaneously administered with Bacoside A, the active constituent from the plant Bacopa monniera, for a period of 12 weeks. The activity of CK was assayed in serum, heart and brain, and its isoenzymes in serum were separated electrophoretically. Rats exposed to cigarette smoke showed significant increase in serum CK activity with concomitant decrease in heart and brain. Also cigarette smoke exposure resulted in a marked increase in all the three isoforms in serum. Administration of Bacoside A prevented these alterations induced by cigarette smoking. Cigarette smoking is known to cause free radical mediated lipid peroxidation leading to increased membrane permeability and cellular damage in the heart and brain resulting in the release of CK into the circulation. The protective effect of Bacoside A on the structural and functional integrity of the membrane prevented the leakage of CK from the respective tissues, which could be attributed to its free radical scavenging and anti-lipid peroxidative effect.

  8. Mouse protocadherin-1 gene expression is regulated by cigarette smoke exposure in vivo.

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    Henk Koning

    Full Text Available Protocadherin-1 (PCDH1 is a novel susceptibility gene for airway hyperresponsiveness, first identified in families exposed to cigarette smoke and is expressed in bronchial epithelial cells. Here, we asked how mouse Pcdh1 expression is regulated in lung structural cells in vivo under physiological conditions, and in both short-term cigarette smoke exposure models characterized by airway inflammation and hyperresponsiveness and chronic cigarette smoke exposure models. Pcdh1 gene-structure was investigated by Rapid Amplification of cDNA Ends. Pcdh1 mRNA and protein expression was investigated by qRT-PCR, western blotting using isoform-specific antibodies. We observed 87% conservation of the Pcdh1 nucleotide sequence, and 96% conservation of the Pcdh1 protein sequence between men and mice. We identified a novel Pcdh1 isoform encoding only the intracellular signalling motifs. Cigarette smoke exposure for 4 consecutive days markedly reduced Pcdh1 mRNA expression in lung tissue (3 to 4-fold, while neutrophilia and airway hyperresponsiveness was induced. Moreover, Pcdh1 mRNA expression in lung tissue was reduced already 6 hours after an acute cigarette-smoke exposure in mice. Chronic exposure to cigarette smoke induced loss of Pcdh1 protein in lung tissue after 2 months, while Pcdh1 protein levels were no longer reduced after 9 months of cigarette smoke exposure. We conclude that Pcdh1 is highly homologous to human PCDH1, encodes two transmembrane proteins and one intracellular protein, and is regulated by cigarette smoke exposure in vivo.

  9. A longitudinal study of smokers' exposure to cigarette smoke and the effects of spontaneous product switching.

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    Cunningham, Anthony; Sommarström, Johan; Camacho, Oscar M; Sisodiya, Ajit S; Prasad, Krishna

    2015-06-01

    A challenge in investigating the effect of public health policies on cigarette consumption and exposure arises from variation in a smoker's exposure from cigarette to cigarette and the considerable differences between smokers. In addition, limited data are available on the effects of spontaneous product switching on a smoker's cigarette consumption and exposure to smoke constituents. Over 1000 adult smokers of the same commercial 10mg International Organization for Standardization (ISO) tar yield cigarette were recruited into the non-residential, longitudinal study across 10 cities in Germany. Cigarette consumption, mouth level exposure to tar and nicotine and biomarkers of exposure to nicotine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone were measured every 6months over a 3 and a half year period. Cigarette consumption remained stable through the study period and did not vary significantly when smokers spontaneously switched products. Mouth level exposure decreased for smokers (n=111) who switched to cigarettes of 7mg ISO tar yield or lower. In addition, downward trends in mouth level exposure estimates were observed for smokers who did not switch cigarettes. Data from this study illustrate some of the challenges in measuring smokers' long-term exposure to smoke constituents in their everyday environment.

  10. Transient and persistent metabolomic changes in plasma following chronic cigarette smoke exposure in a mouse model.

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    Cruickshank-Quinn, Charmion I; Mahaffey, Spencer; Justice, Matthew J; Hughes, Grant; Armstrong, Michael; Bowler, Russell P; Reisdorph, Richard; Petrache, Irina; Reisdorph, Nichole

    2014-01-01

    Cigarette smoke exposure is linked to the development of a variety of chronic lung and systemic diseases in susceptible individuals. Metabolomics approaches may aid in defining disease phenotypes, may help predict responses to treatment, and could identify biomarkers of risk for developing disease. Using a mouse model of chronic cigarette smoke exposure sufficient to cause mild emphysema, we investigated whether cigarette smoke induces distinct metabolic profiles and determined their persistence following smoking cessation. Metabolites were extracted from plasma and fractionated based on chemical class using liquid-liquid and solid-phase extraction prior to performing liquid chromatography mass spectrometry-based metabolomics. Metabolites were evaluated for statistically significant differences among group means (p-value≤0.05) and fold change ≥1.5). Cigarette smoke exposure was associated with significant differences in amino acid, purine, lipid, fatty acid, and steroid metabolite levels compared to air exposed animals. Whereas 60% of the metabolite changes were reversible, 40% of metabolites remained persistently altered even following 2 months of smoking cessation, including nicotine metabolites. Validation of metabolite species and translation of these findings to human plasma metabolite signatures induced by cigarette smoking may lead to the discovery of biomarkers or pathogenic pathways of smoking-induced disease.

  11. Transient and persistent metabolomic changes in plasma following chronic cigarette smoke exposure in a mouse model.

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    Charmion I Cruickshank-Quinn

    Full Text Available Cigarette smoke exposure is linked to the development of a variety of chronic lung and systemic diseases in susceptible individuals. Metabolomics approaches may aid in defining disease phenotypes, may help predict responses to treatment, and could identify biomarkers of risk for developing disease. Using a mouse model of chronic cigarette smoke exposure sufficient to cause mild emphysema, we investigated whether cigarette smoke induces distinct metabolic profiles and determined their persistence following smoking cessation. Metabolites were extracted from plasma and fractionated based on chemical class using liquid-liquid and solid-phase extraction prior to performing liquid chromatography mass spectrometry-based metabolomics. Metabolites were evaluated for statistically significant differences among group means (p-value≤0.05 and fold change ≥1.5. Cigarette smoke exposure was associated with significant differences in amino acid, purine, lipid, fatty acid, and steroid metabolite levels compared to air exposed animals. Whereas 60% of the metabolite changes were reversible, 40% of metabolites remained persistently altered even following 2 months of smoking cessation, including nicotine metabolites. Validation of metabolite species and translation of these findings to human plasma metabolite signatures induced by cigarette smoking may lead to the discovery of biomarkers or pathogenic pathways of smoking-induced disease.

  12. Passive cigarette smoke exposure in primary school children in Liverpool

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    A. Delpisheh; Y. Kelly; B.J. Brabin

    2006-01-01

    Objective: To assess environmental tobacco smoke (ETS) exposure amongst primary school children. Methods: A descriptive, community-based, cross-sectional study of self-reported parental smoking patterns and children's salivary cotinine concentrations in 245 children aged 5-11 years attending 10 prim

  13. Lactate dehydrogenase isoenzyme patterns upon chronic exposure to cigarette smoke: Protective effect of bacoside A.

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    Anbarasi, Kothandapani; Sabitha, Kuruvimalai Ekambaram; Devi, Chennam Srinivasulu Shyamala

    2005-09-01

    Despite a strong association between cigarette smoking and alarming increase in mortality rate from smoking-related diseases, around 35-40% of the world's population continues to smoke and many more are being exposed to environmental tobacco smoke. Since the role of free radicals and oxidative damage in the pathogenesis of smoking-related diseases has been suggested, bacoside A, a potent antioxidant was tested for its ability to protect against cigarette smoking-induced toxicity in terms of lactate dehydrogenase (LDH) and its isoenzymes. Rats were exposed to cigarette smoke and simultaneously administered with bacoside A, for a period of 12 weeks. Total LDH activity was assayed in serum, lung, heart, brain, liver and kidney, and serum LDH isoforms were separated electrophoretically. Cigarette smoke exposure resulted in significant increase in serum LDH and its isoenzymes with a concomitant decrease in these organs. These alterations were prevented by administration of bacoside A. Excessive oxidants from cigarette smoke is known to cause peroxidation of membrane lipids leading to cellular damage, thereby resulting in the leakage of LDH into the circulation. Bacoside A could have rendered protection to the organs by stabilizing their cell membranes and prevented the release of LDH, probably through its free radical scavenging and anti-lipid peroxidative effect.

  14. Thirdhand cigarette smoke: factors affecting exposure and remediation.

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    Vasundhra Bahl

    Full Text Available Thirdhand smoke (THS refers to components of secondhand smoke that stick to indoor surfaces and persist in the environment. Little is known about exposure levels and possible remediation measures to reduce potential exposure in contaminated areas. This study deals with the effect of aging on THS components and evaluates possible exposure levels and remediation measures. We investigated the concentration of nicotine, five nicotine related alkaloids, and three tobacco specific nitrosamines (TSNAs in smoke exposed fabrics. Two different extraction methods were used. Cotton terry cloth and polyester fleece were exposed to smoke in controlled laboratory conditions and aged before extraction. Liquid chromatography-tandem mass spectrometry was used for chemical analysis. Fabrics aged for 19 months after smoke exposure retained significant amounts of THS chemicals. During aqueous extraction, cotton cloth released about 41 times as much nicotine and about 78 times the amount of tobacco specific nitrosamines (TSNAs as polyester after one hour of aqueous extraction. Concentrations of nicotine and TSNAs in extracts of terry cloth exposed to smoke were used to estimate infant/toddler oral exposure and adult dermal exposure to THS. Nicotine exposure from THS residue can be 6.8 times higher in toddlers and 24 times higher in adults and TSNA exposure can be 16 times higher in toddlers and 56 times higher in adults than what would be inhaled by a passive smoker. In addition to providing exposure estimates, our data could be useful in developing remediation strategies and in framing public health policies for indoor environments with THS.

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

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    Erika B Fulmer

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

  16. Influence of Machine-Derived Smoke Yields on Biomarker of Exposure (BOE Levels in Cigarette Smokers*

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    Scherer Gerhard

    2015-01-01

    Full Text Available Individual uptake of tobacco smoke constituents by smoking is highly variable in cigarette smokers and cannot be predicted by smoking behaviour variables and machine-derived smoke yields. It is well established that uptake of smoke constituents is best described by a series of bio-markers of exposure (BOEs such as metabolites of nico-tine, tobacco-specific nitrosamines (TSNAs, polycyclic aromatic hydrocarbons (PAHs, aromatic amines, benzene, 1,3-butadiene, acrolein, hydrogen cyanide, 2,5-dimethyl-furan and other smoke constituents.

  17. Glutathione Peroxidase-1 Suppresses the Unfolded Protein Response upon Cigarette Smoke Exposure

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    Patrick Geraghty

    2016-01-01

    Full Text Available Oxidative stress provokes endoplasmic reticulum (ER stress-induced unfolded protein response (UPR in the lungs of chronic obstructive pulmonary (COPD subjects. The antioxidant, glutathione peroxidase-1 (GPx-1, counters oxidative stress induced by cigarette smoke exposure. Here, we investigate whether GPx-1 expression deters the UPR following exposure to cigarette smoke. Expression of ER stress markers was investigated in fully differentiated normal human bronchial epithelial (NHBE cells isolated from nonsmoking, smoking, and COPD donors and redifferentiated at the air liquid interface. NHBE cells from COPD donors expressed heightened ATF4, XBP1, GRP78, GRP94, EDEM1, and CHOP compared to cells from nonsmoking donors. These changes coincided with reduced GPx-1 expression. Reintroduction of GPx-1 into NHBE cells isolated from COPD donors reduced the UPR. To determine whether the loss of GPx-1 expression has a direct impact on these ER stress markers during smoke exposure, Gpx-1−/− mice were exposed to cigarette smoke for 1 year. Loss of Gpx-1 expression enhanced cigarette smoke-induced ER stress and apoptosis. Equally, induction of ER stress with tunicamycin enhanced antioxidant expression in mouse precision-cut lung slices. Smoke inhalation also exacerbated the UPR response during respiratory syncytial virus infection. Therefore, ER stress may be an antioxidant-related pathophysiological event in COPD.

  18. Effects of cigarette smoke exposure on early stage embryos in the rat

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    Tachi, Norihide; Aoyama, Mitsuko (Nagoya City Univ. Medical School (Japan))

    1989-09-01

    It is well recognized that cigarette smoking in pregnant women exerts many deleterious effects on their progenies; intrauterine growth retardation, and increases in perinatal mortality and premature births. The fetal growth retardation also has been reported in animals exposed to cigarette smoke. The authors previously demonstrated that cigarette smoke exposure in pregnant rats retarded the growth of fetuses from mid to late stages of pregnancy. In addition, the weight of uteri containing embryos in animals inhaling the smoke was smaller, although not significant, than that in the control on day 7 of pregnancy. Based on these findings, it was suggested that the growth of embryos in early stage seemed to be harmfully affected as well as during mid and late stages of pregnancy. However, since the uterine weight in early pregnancy was measured in the previous study instead of the direct observation of early stage embryos, it remained unclear whether the early development of embryos was really influenced by cigarette smoke exposure or not. The present study was designed to observe the effects of cigarette smoke inhalation by pregnant rats on early development of embryos from fertilization to implantation.

  19. In vitro toxicity testing of cigarette smoke based on the air-liquid interface exposure: A review.

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    Li, Xiang

    2016-10-01

    Cigarette smoke is a complex aerosol comprising particulate phase and gaseous vapour phase. The air-liquid interface exposure provides a possible technical means to implement whole smoke exposure for the assessment of tobacco products. In this review, the research progress in the in vitro toxicity testing of cigarette smoke based on the air-liquid interface exposure is summarized. The contents presented involve mainly cytotoxicity, genotoxicity, oxidative stress, inflammation, systems toxicology, 3D culture and cigarette smoke dosimetry related to cigarette smoke, as well as the assessment of electronic cigarette aerosol. Prospect of the application of the air-liquid interface exposure method in assessing the biological effects of tobacco smoke is discussed.

  20. Nuclear and Mitochondrial DNA Alterations in Newborns with Prenatal Exposure to Cigarette Smoke

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    Francesca Pirini

    2015-01-01

    Full Text Available Newborns exposed to maternal cigarette smoke (CS in utero have an increased risk of developing chronic diseases, cancer, and acquiring decreased cognitive function in adulthood. Although the literature reports many deleterious effects associated with maternal cigarette smoking on the fetus, the molecular alterations and mechanisms of action are not yet clear. Smoking may act directly on nuclear DNA by inducing mutations or epigenetic modifications. Recent studies also indicate that smoking may act on mitochondrial DNA by inducing a change in the number of copies to make up for the damage caused by smoking on the respiratory chain and lack of energy. In addition, individual genetic susceptibility plays a significant role in determining the effects of smoking during development. Furthermore, prior exposure of paternal and maternal gametes to cigarette smoke may affect the health of the developing individual, not only the in utero exposure. This review examines the genetic and epigenetic alterations in nuclear and mitochondrial DNA associated with smoke exposure during the most sensitive periods of development (prior to conception, prenatal and early postnatal and assesses how such changes may have consequences for both fetal growth and development.

  1. Effects of exposure to cigarette smoke prior to pregnancy in diabetic rats

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    Damasceno Débora C

    2011-08-01

    Full Text Available Abstract Background The purpose of this study was to evaluate the effects of cigarette smoke exposure before pregnancy on diabetic rats and their offspring development. Methods Diabetes was induced by streptozotocin and cigarette smoke exposure was conducted by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Diabetic female Wistar rats were randomly distributed in four experimental groups (n minimum = 13/group: nondiabetic (ND and diabetic rats exposed to filtered air (D, diabetic rats exposed to cigarette smoke prior to and into the pregnancy period (DS and diabetic rats exposed to cigarette smoke prior to pregnancy period (DSPP. At day 21 of pregnancy, rats were killed for maternal biochemical determination and reproductive outcomes. Results The association of diabetes and cigarette smoke in DSPP group caused altered glycemia at term, reduced number of implantation and live fetuses, decreased litter and maternal weight, increased pre and postimplantation loss rates, reduced triglyceride and VLDL-c concentrations, increased levels of thiol groups and MDA. Besides, these dams presented increased SOD and GSH-Px activities. However, the increased antioxidant status was not sufficient to prevent the lipid peroxidation observed in these animals. Conclusion Despite the benefits stemming from smoking interruption during the pregnancy of diabetic rats, such improvement was insufficient to avoid metabolic alterations and provide an adequate intrauterine environment for embryofetal development. Therefore, these results suggest that it is necessary to cease smoking extensive time before planning pregnancy, since stopping smoking only when pregnancy is detected may not contribute effectively to fully adequate embryofetal development.

  2. Influenza virus-induced lung inflammation was modulated by cigarette smoke exposure in mice.

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    Yan Han

    Full Text Available Although smokers have increased susceptibility and severity of seasonal influenza virus infection, there is no report about the risk of 2009 pandemic H1N1 (pdmH1N1 or avian H9N2 (H9N2/G1 virus infection in smokers. In our study, we used mouse model to investigate the effect of cigarette smoke on pdmH1N1 or H9N2 virus infection. Mice were exposed to cigarette smoke for 21 days and then infected with pdmH1N1 or H9N2 virus. Control mice were exposed to air in parallel. We found that cigarette smoke exposure alone significantly upregulated the lung inflammation. Such prior cigarette smoke exposure significantly reduced the disease severity of subsequent pdmH1N1 or H9N2 virus infection. For pdmH1N1 infection, cigarette smoke exposed mice had significantly lower mortality than the control mice, possibly due to the significantly decreased production of inflammatory cytokines and chemokines. Similarly, after H9N2 infection, cigarette smoke exposed mice displayed significantly less weight loss, which might be attributed to lower cytokines and chemokines production, less macrophages, neutrophils, CD4+ and CD8+ T cells infiltration and reduced lung damage compared to the control mice. To further investigate the underlying mechanism, we used nicotine to mimic the effect of cigarette smoke both in vitro and in vivo. Pre-treating the primary human macrophages with nicotine for 72 h significantly decreased their expression of cytokines and chemokines after pdmH1N1 or H9N2 infection. The mice subcutaneously and continuously treated with nicotine displayed significantly less weight loss and lower inflammatory response than the control mice upon pdmH1N1 or H9N2 infection. Moreover, α7 nicotinic acetylcholine receptor knockout mice had more body weight loss than wild-type mice after cigarette smoke exposure and H9N2 infection. Our study provided the first evidence that the pathogenicity of both pdmH1N1 and H9N2 viruses was alleviated in cigarette smoke exposed

  3. Cigarette smoke exposure aggravates air space enlargement and alveolar cell apoptosis in Smad3 knockout mice.

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    Farkas, Laszlo; Farkas, Daniela; Warburton, David; Gauldie, Jack; Shi, Wei; Stampfli, Martin R; Voelkel, Norbert F; Kolb, Martin

    2011-10-01

    The concept of genetic susceptibility factors predisposing cigarette smokers to develop emphysema stems from the clinical observation that only a fraction of smokers develop clinically significant chronic obstructive pulmonary disease. We investigated whether Smad3 knockout mice, which develop spontaneous air space enlargement after birth because of a defect in transforming growth factor-β (TGF-β) signaling, develop enhanced alveolar cell apoptosis and air space enlargement following cigarette smoke exposure. We investigated Smad3(-/-) and Smad3(+/+) mice at different adult ages and determined air space enlargement, alveolar cell proliferation, and apoptosis. Furthermore, laser-capture microdissection and real-time PCR were used to measure compartment-specific gene expression. We then compared the effects of cigarette smoke exposure on Smad3(-/-) and littermate controls. Smad3 knockout resulted in the development of air space enlargement in the adult mouse and was associated with decreased alveolar VEGF levels and activity and increased alveolar cell apoptosis. Cigarette smoke exposure aggravated air space enlargement and alveolar cell apoptosis. We also found increased Smad2 protein expression and phosphorylation, which was enhanced following cigarette smoke exposure, in Smad3-knockout animals. Double immunofluorescence analysis revealed that endothelial apoptosis started before epithelial apoptosis. Our data indicate that balanced TGF-β signaling is not only important for regulation of extracellular matrix turnover, but also for alveolar cell homeostasis. Impaired signaling via the Smad3 pathway results in alveolar cell apoptosis and alveolar destruction, likely via increased Smad2 and reduced VEGF expression and might represent a predisposition for accelerated development of emphysema due to cigarette smoke exposure.

  4. Dose response association of pregnancy cigarette smoke exposure, childhood stature, overweight and obesity

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    G. Koshy; A. Delpisheh; B.J. Brabin

    2011-01-01

    The combined dose response effects of pregnancy cigarette smoke exposure on childhood overweight, obesity and short stature have not been reported. A community based cross-sectional survey of 3038 children aged 5-11 years from 15 primary schools in Merseyside, UK. Self-completed parental questionnai

  5. Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells

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    Hoffmann, Roland F.; Zarrintan, Sina; Brandenburg, Simone M.; Kol, Arjan; de Bruin, Harold G.; Jafari, Shabnam; Dijk, Freark; Kalicharan, Dharamdajal; Kelders, Marco; Gosker, Harry R.; ten Hacken, Nick H. T.; van der Want, Johannes J.; van Oosterhout, Antoon J. M.; Heijink, Irene H.

    2013-01-01

    Background: Cigarette smoking is the major risk factor for COPD, leading to chronic airway inflammation. We hypothesized that cigarette smoke induces structural and functional changes of airway epithelial mitochondria, with important implications for lung inflammation and COPD pathogenesis. Methods:

  6. Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells

    NARCIS (Netherlands)

    Hoffmann, Roland F; Zarrintan, Sina; Brandenburg, Simone M; Kol, Arjan; de Bruin, Harold G; Jafari, Shabnam; Dijk, Freark; Kalicharan, Dharamdajal; Kelders, Marco; Gosker, Harry R; Ten Hacken, Nick Ht; van der Want, Johannes J; van Oosterhout, Antoon Jm; Heijink, Irene H

    2013-01-01

    BACKGROUND: Cigarette smoking is the major risk factor for COPD, leading to chronic airway inflammation. We hypothesized that cigarette smoke induces structural and functional changes of airway epithelial mitochondria, with important implications for lung inflammation and COPD pathogenesis. METHODS:

  7. Oral Gingival Cell Cigarette Smoke Exposure Induces Muscle Cell Metabolic Disruption

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    Andrea C. Baeder

    2016-01-01

    Full Text Available Cigarette smoke exposure compromises health through damaging multiple physiological systems, including disrupting metabolic function. The purpose of this study was to determine the role of oral gingiva in mediating the deleterious metabolic effects of cigarette smoke exposure on skeletal muscle metabolic function. Using an in vitro conditioned medium cell model, skeletal muscle cells were incubated with medium from gingival cells treated with normal medium or medium containing suspended cigarette smoke extract (CSE. Following incubation of muscle cells with gingival cell conditioned medium, muscle cell mitochondrial respiration and insulin signaling and action were determined as an indication of overall muscle metabolic health. Skeletal muscle cells incubated with conditioned medium of CSE-treated gingival cells had a profound reduction in mitochondrial respiration and respiratory control. Furthermore, skeletal muscle cells had a greatly reduced response in insulin-stimulated Akt phosphorylation and glycogen synthesis. Altogether, these results provide a novel perspective on the mechanism whereby cigarette smoke affects systemic metabolic function. In conclusion, we found that oral gingival cells treated with CSE create an altered milieu that is sufficient to both disrupted skeletal muscle cell mitochondrial function and insulin sensitivity.

  8. Assessing the Effect of Simultaneous Exposure to Noise and Cigarette Smoke on Workers’ Blood Pressure

    Science.gov (United States)

    Rahimpour, Farzane; Rafiei Manesh, Ehsan; Jarahi, Lida; Eghbali, Saba

    2016-01-01

    Introduction: Noise, as the most common pollutant in the industrial environment, can lead to hearing loss and negatively affect other organs such as the cardiovascular system. Cigarette smoking is a popular habit among some workers, and can also have a negative effect on the cardiovascular system. This study was aimed to investigate the effect of simultaneous exposure to noise and cigarette smoke on the blood pressure of workers at a manufacturing factory. Materials and Methods: This cross-sectional study enrolled 604 workers at a steel factory. Information relating to workers’ demography, employment, and risk factors were recorded. Based on the level of smoking per day, workers exposed to noise fell into one of the four following groups: 1) Non-smokers exposed to noise <85 DB; 2) Smokers exposed to noise <85 DB; 3) Non-smokers exposed to noise ≥85 DB; 4) Smokers exposed to noise ≥85 DB. A t-test, analysis of variance (ANOVA), and logistic regression were applied for analysis using SPSS v11.5. Results: The prevalence of hypertension, cigarette smoking, and exposure to noise ≥85 DB was 11.6%, 15.3%, and 56.4%, respectively, among the workers. The mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) were 112.3 and 73.9 mmHg, respectively. A significant difference was observed between systolic and diastolic blood pressures in four groups (P=0.001). Posthoc test showed a significant difference between groups 1 and 3 (P=0.001). Regression analysis indicated no significant difference in workers who were simultaneously exposed to noise and cigarette smoke. Conclusion: This study demonstrates that noise is an important factor in terms of hypertension, with no significant differences observed in the prevalence of hypertension between workers who were simultaneously exposed to noise and cigarette smoke. It is suggested that workers’ blood pressure should be regularly monitored in noisy environments. PMID:28008392

  9. Effects of type of smoking (pipe, cigars or cigarettes) on biological indices of tobacco exposure and toxicity.

    Science.gov (United States)

    Funck-Brentano, Christian; Raphaël, Mathilde; Lafontaine, Michel; Arnould, Jean-Pierre; Verstuyft, Céline; Lebot, Martine; Costagliola, Dominique; Roussel, Ronan

    2006-10-01

    Although all forms of smoking are harmful, smoking pipes or cigars is associated with lower exposure to the lethal products of tobacco products and lower levels of morbidity and mortality than smoking cigarettes. Cytochrome P-450-1A (CYP1A) is a major pathway activating carcinogens from tobacco smoke. Our primary aim was to compare CYP1A2 activity in individuals smoking pipes or cigars only, cigarettes only and in non-smokers. We studied 30 smokers of pipes or cigars only, 28 smokers of cigarettes only, and 30 non-smokers male subjects matched for age. CYP1A2 activity was assessed as the caffeine metabolic ratio in plasma. One-day urine collection was used for determining exposure to products of tobacco metabolism. Nitrosamine and benzo[a]pyrene DNA adducts were measured in lymphocytes. CYP1A2 activity was greater (ptobacco metabolism than cigarette smoking and to an absence of CYP1A2 induction. Cigarette smoking was the only independent predictor of CYP1A2 activity in smokers. However, inhalation behaviour, rather than the type of tobacco smoked, may be the key factor linked to the extent of tobacco exposure and CYP1A2 induction. Our results provide a reasonable explanation for the results of epidemiological studies showing pipe or cigar smoking to present fewer health hazards than cigarette smoking.

  10. Acute cigarette smoke exposure causes lung injury in rabbits treated with ibuprofen

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    Witten, M.L.; Lemen, R.J.; Quan, S.F.; Sobonya, R.E.; Magarelli, J.L.; Bruck, D.C.

    1987-01-01

    We studied lung clearance of aerosolized technetium-labeled diethylenetriamine pentaacetic acid (/sup 99m/TcDTPA), plasma concentrations of 6-keto-PGF1 alpha and thromboxane B2, and pulmonary edema as indices of lung injury in rabbits exposed to cigarette smoke (CSE). Forty-six rabbits were randomly assigned to 4 groups: control sham smoke exposure (SS, N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), sham smoke exposure ibuprofen-pretreated (SS-I, N = 10), CSE (N = 9), and CSE ibuprofen-pretreated (CSE-I, N = 19). Ibuprofen (cyclooxygenase eicosanoid inhibitor) was administered as a single daily intramuscular injection (25 mg/kg) for 7 days before the experiment. Cigarette or sham smoke was delivered by syringe in a series of 5, 10, 20, and 30 tidal volume breaths with a 15-min counting period between each subset of breaths to determine /sup 99m/TcDTPA biological half-life (T1/2). In the ibuprofen pretreated group, CSE caused significant decreases in /sup 99m/TcDTPA T1/2 and dynamic lung compliance. Furthermore, these changes in lung function were accompanied by severe injury to type I alveolar cell epithelium, pulmonary edema, and frequently death of the rabbits. These findings suggest that inhibition of the cyclooxygenase pathway before CSE exacerbates lung injury in rabbits.

  11. Cigarette ignition propensity, smoking behavior, and toxicant exposure: A natural experiment in Canada

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    June Kristie M

    2011-12-01

    Full Text Available Abstract Background This study used a 'pre-post' research design to measure the impact of the Canadian reduced ignition propensity law on cigarette toxicity and smoking behavior among Canadian smokers. Method The study was conducted in Ontario, Canada over a ten-month period in 2005-2006, consisting of 4 laboratory visits (baseline N = 61, final N = 42. At Visit 1, questionnaire data and biospecimens were collected. During the following 24 hours, participants smoked 5 cigarettes ad libitum through a topography recording device and collected their cigarette butts. Visit 2 consisted of a questionnaire and smoking one cigarette to measure laboratory topography values. After ten months, these procedures were repeated. Results Generalized estimating equations, with law status (pre and post as a fixed within-subject factor, were used to determine changes in behavior and biomarker exposure. Overall, there were no significant differences in smoking topography, breath carbon monoxide, and saliva cotinine pre-post law (p>0.1. However, analyses revealed a significant increase in the summed concentrations of hydroxyfluorene metabolites (N = 3,, and 1-hydroxypyrene in urine, with at notable increase in hydroxyphenanthrene metabolites (N = 3 (pΣhydroxyfluorene = 0.013, 22% increase; p1-hydroxypyrene = 0.018, 24% increase; pΣhydroxyphenanthrene = 0.061, 17% increase. Conclusion While the results suggest no change in topography variables, data showed increases in exposure to three PAH biomarkers following reduced ignition propensity implementation in Canada. These findings suggest that human studies should be considered to evaluate policy impacts.

  12. Cadmium exposure from smoking cigarettes: variations with time and country where purchased.

    Science.gov (United States)

    Elinder, C G; Kjellström, T; Lind, B; Linnman, L; Piscator, M; Sundstedt, K

    1983-10-01

    Cadmium has been determined in 26 brands of cigarettes purchased in eight different countries throughout the world and in 16 different samples of cigarettes produced in Sweden between 1918 and 1968. In addition the amount of cadmium released from smoking one cigarette to the particulate phase collected from a smoking simulation machine, corresponding to the amount actually inhaled by a smoker, has been determined. The cadmium concentration in different brands of cigarettes ranged from 0.19 to 3.0 micrograms Cd/g dry wt, with a general tendency toward lower values in cigarettes from developing countries. No systematic change in the cadmium concentration of cigarettes with time could be revealed. The amount of cadmium inhaled from smoking one cigarette containing about 1.7 microgram Cd was estimated to be 0.14 to 0.19 microgram, corresponding to about 10% of the total cadmium content in the cigarette.

  13. Cigarette smoke impairs granulosa cell proliferation and oocyte growth after exposure cessation in young Swiss mice: an experimental study

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    Paixão Larissa LO

    2012-09-01

    Full Text Available Abstract Background Cigarette smoke is associated with decreased female fertility, causing damage to ovarian function and disturbing follicle development. However, the effects of cigarette toxicants on ovarian function depend on duration and intensity of exposure. The aim of this study was to assess the effects of brief, intense exposure to tobacco smoke on granulosa cell number, oocyte growth, and follicle size during puberty in female Swiss mice. Methods Ten female Swiss mice aged 35 days were exposed to tobacco smoke from 3R4F reference research cigarettes. They were exposed to an automatic smoking machine 8 h/day, 7 days/week for 15 days. Ten age-matched controls were kept in a different room and exposed to ambient air. At the end of 15 days, five mice in each group were euthanized and the ovaries were analyzed for follicular morphometry and granulosa cell count. The remaining animals were kept for an additional 30 days for further analysis as an ex-smoker group and control group. Comparison between the two groups was evaluated by the Student’s t-test or a two-way ANOVA followed by Bonferroni post-test was applied for multiple comparisons. Results We found that cigarette smoke impaired antral follicular growth even after exposure cessation (p Conclusions The negative effects of cigarette smoking seem to last even after exposure has been interrupted. Moreover, brief exposure during puberty may induce silent oocyte disruption, which could in turn lead to decreased fecundity rates.

  14. Determination of methyl-, 2-hydroxyethyl- and 2-cyanoethylmercapturic acids as biomarkers of exposure to alkylating agents in cigarette smoke.

    Science.gov (United States)

    Scherer, Gerhard; Urban, Michael; Hagedorn, Heinz-Werner; Serafin, Richard; Feng, Shixia; Kapur, Sunil; Muhammad, Raheema; Jin, Yan; Sarkar, Mohamadi; Roethig, Hans-Juergen

    2010-10-01

    Alkylating agents occur in the environment and are formed endogenously. Tobacco smoke contains a variety of alkylating agents or precursors including, among others, N-nitrosodimethylamine (NDMA), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), acrylonitrile and ethylene oxide. We developed and validated a method for the simultaneous determination of methylmercapturic acid (MMA, biomarker for methylating agents such as NDMA and NNK), 2-hydroxyethylmercapturic acid (HEMA, biomarker for ethylene oxide) and 2-cyanoethylmercapturic acid (CEMA, biomarker for acrylonitrile) in human urine using deuterated internal standards of each compound. The method involves liquid/liquid extraction of the urine sample, solid phase extraction on anion exchange cartridges, derivatization with pentafluorobenzyl bromide (PFBBr), liquid/liquid extraction of the reaction mixture and LC-MS/MS analysis with positive electrospray ionization. The method was linear in the ranges of 5.00-600, 1.00-50.0 and 1.50-900 ng/ml for MMA, HEMA and CEMA, respectively. The method was applied to two clinical studies in adult smokers of conventional cigarettes who either continued smoking conventional cigarettes, were switched to test cigarettes consisting of either an electrically heated cigarette smoking system (EHCSS) or having a highly activated carbon granule filter that were shown to have reduced exposure to specific smoke constituents, or stopped smoking. Urinary excretion of MMA was found to be unaffected by switching to the test cigarettes or stop smoking. Urinary HEMA excretion decreased by 46 to 54% after switching to test cigarettes and by approximately 74% when stopping smoking. Urinary CEMA excretion decreased by 74-77% when switching to test cigarettes and by approximately 90% when stopping smoking. This validated method for urinary alkylmercapturic acids is suitable to distinguish differences in exposure not only between smokers and nonsmokers but also between smoking of conventional and

  15. The response of human nasal and bronchial organotypic tissue cultures to repeated whole cigarette smoke exposure.

    Science.gov (United States)

    Talikka, Marja; Kostadinova, Radina; Xiang, Yang; Mathis, Carole; Sewer, Alain; Majeed, Shoaib; Kuehn, Diana; Frentzel, Stefan; Merg, Celine; Geertz, Marcel; Martin, Florian; Ivanov, Nikolai V; Peitsch, Manuel C; Hoeng, Julia

    2014-01-01

    Exposure to cigarette smoke (CS) is linked to the development of respiratory diseases, and there is a need to understand the mechanisms whereby CS causes damage. Although animal models have provided valuable insights into smoking-related respiratory tract damage, modern toxicity testing calls for reliable in vitro models as alternatives for animal experimentation. We report on a repeated whole mainstream CS exposure of nasal and bronchial organotypic tissue cultures that mimic the morphological, physiological, and molecular attributes of the human respiratory tract. Despite the similar cellular staining and cytokine secretion in both tissue types, the transcriptomic analyses in the context of biological network models identified similar and diverse biological processes that were impacted by CS-exposed nasal and bronchial cultures. Our results demonstrate that nasal and bronchial tissue cultures are appropriate in vitro models for the assessment of CS-induced adverse effects in the respiratory system and promising alternative to animal experimentation.

  16. Monitoring low benzene exposure: comparative evaluation of urinary biomarkers, influence of cigarette smoking, and genetic polymorphisms.

    Science.gov (United States)

    Fustinoni, Silvia; Consonni, Dario; Campo, Laura; Buratti, Marina; Colombi, Antonio; Pesatori, Angela C; Bonzini, Matteo; Bertazzi, Pier A; Foà, Vito; Garte, Seymour; Farmer, Peter B; Levy, Leonard S; Pala, Mauro; Valerio, Federico; Fontana, Vincenzo; Desideri, Arianna; Merlo, Domenico F

    2005-09-01

    Benzene is a human carcinogen and an ubiquitous environmental pollutant. Identification of specific and sensitive biological markers is critical for the definition of exposure to low benzene level and the evaluation of the health risk posed by this exposure. This investigation compared urinary trans,trans-muconic acid (t,t-MA), S-phenylmercapturic acid, and benzene (U-benzene) as biomarkers to assess benzene exposure and evaluated the influence of smoking and the genetic polymorphisms CYP2E1 (RsaI and DraI) and NADPH quinone oxidoreductase-1 on these indices. Gas station attendants, urban policemen, bus drivers, and two groups of controls were studied (415 subjects). Median benzene exposure was 61, 22, 21, 9 and 6 microg/m(3), respectively, with higher levels in workers than in controls. U-benzene, but not t,t-MA and S-phenylmercapturic acid, showed an exposure-related increase. All the biomarkers were strongly influenced by cigarette smoking, with values up to 8-fold higher in smokers compared with nonsmokers. Significant correlations of the biomarkers with each other and with urinary cotinine were found. A possible influence of genetic polymorphism of CYP2E1 (RsaI and/or DraI) on t,t-MA and U-benzene in subjects with a variant allele was found. Multiple linear regression analysis correlated the urinary markers with exposure, smoking status, and CYP2E1 (RsaI; R(2) up to 0.55 for U-benzene). In conclusion, in the range of investigated benzene levels (<478 micro/m(3) or <0.15 ppm), smoking may be regarded as the major source of benzene intake; among the study indices, U-benzene is the marker of choice for biomonitoring low-level occupational and environmental benzene exposure.

  17. The health- and addictive effectes due to exposure to aldehydes of cigarette smoke. Part 1; Acetaldehyde, Formaldehyde, Acrolein and Propionaldehyde

    NARCIS (Netherlands)

    Andel I van; Schenk E; Rambali B; Wolterink G; Werken G van de; Stevenson H; Aerts LAGJM van; Vleeming W; LEO; LGM; LOC; CRV

    2003-01-01

    In the desk study presented here, health effects and possible addictive effects of aldehyde exposure due to cigarette smoking are discussed. In the light of currently available literature the health effects of exposure to acetaldehyde, formaldehyde, acrolein and propionaldehyde were assessed. All al

  18. Lung cytotoxicity of combined exposure to refractory ceramic fibres and cigarette smoke.

    Science.gov (United States)

    Cerná, Silvia; Hurbánková, Marta; Kováciková, Zuzana; Beno, Milan; Wimmerová, Sona

    2005-12-01

    Changes in some lung cytotoxic parameters after exposure to refractory ceramic fibres (RCF) or to cigarette smoke (S) and after combined exposure to RCF+S were studied in male Wistar rats in order to evaluate their potential adverse health effects. Four groups of rats were treated as follows : 1) intratracheally instilled by saline solution (0.4 ml); 2) intratracheally instilled by 4 mg of RCF; 3) exposed only to S (85 mg of total particulate matter/m(3) air ) for two hours daily; 4) exposed to RCF+S. After 6 months the animals were exsanguinated and the bronchoalveolar lavage (BAL) was perfomed. Viability and phagocytic activity of alveolar macrophages (AM), activity of lactate dehydrogenase (LDH) in cell-free BAL fluid (cf-BALF), acid phosphatase (ACP) and cathepsin D (CATD) in cfBALF, in BALF cells and in the lung tissue were estimated. Viability of AM was depressed by every type of exposure with RCF+S effect being at least additive. Phagocytic activity of AM increased in the presence of RCF. No significant changes in LDH activity were found. Activities of lysosomal enzymes measured in the lung tissue homogenates were not significantly changed, but those in the cfBALF increased especially after exposure to S with most expressive increase in BALF cells after exposure to S and RCF+S. In the case of CATD the effect of RCF+S was more than additive. The results point out to the persistence of the RCF exposure cytotoxic effects and their amplification by cigarette smoke.

  19. Assessing the mutagenic activities of smoke from different cigarettes in direct exposure experiments using the modified Ames Salmonella assay.

    Science.gov (United States)

    Ishikawa, Shinkichi; Kanemaru, Yuki; Nara, Hidenori; Erami, Kazuo; Nagata, Yasufumi

    2016-06-01

    The Ames assay is useful for evaluating the mutagenic potentials of chemicals, and it has been used to evaluate the mutagenic potential of cigarette smoke (CS). In vitro direct exposure systems have been developed to mimic CS exposure in the human respiratory tract, and the Ames assay has been used with such systems. Ames tests were performed using the Vitrocell(®) direct exposure system in this study. The mutagenic potentials of whole mainstream CS and gas/vapor phase fractions produced by conventional combustible cigarettes under two smoking regimens were compared. Salmonella Typhimurium TA98 and TA100 were used with and without metabolic activation, and the number of revertants induced by exposure to each CS was determined. The amount of smoke particles to which cells were exposed were also determined, and dose-response curves describing the relationships between exposure to smoke particles and the number of revertants induced were plotted. The slopes of linear regressions of the dose-response curves were determined, and the slope for each CS was used as a mutagenic activity index for that CS. A new heated cigarette was also tested and smoke from the heated cigarette had a lower mutagenic activity in TA98 and TA100 with metabolic activation than did the conventional CS. The results indicate that the direct exposure system and the Ames test can be used to determine the mutagenic potentials of CS produced by different cigarettes under different conditions (i.e., using different Salmonella Typhimurium strains with and without metabolic activation, and using different smoking conditions).

  20. Short-term cigarette smoke exposure leads to metabolic alterations in lung alveolar cells.

    Science.gov (United States)

    Agarwal, Amit R; Yin, Fei; Cadenas, Enrique

    2014-08-01

    Cigarette smoke (CS)-induced alveolar destruction and energy metabolism changes are known contributors to the pathophysiology of chronic obstructive pulmonary disease (COPD). This study examines the effect of CS exposure on metabolism in alveolar type II cells. Male A/J mice (8 wk old) were exposed to CS generated from a smoking machine for 4 or 8 weeks, and a recovery group was exposed to CS for 8 weeks and allowed to recover for 2 weeks. Alveolar type II cells were isolated from air- or CS- exposed mice. Acute CS exposure led to a reversible airspace enlargement in A/J mice as measured by the increase in mean linear intercept, indicative of alveolar destruction. The effect of CS exposure on cellular respiration was studied using the XF Extracellular Flux Analyzer. A decrease in respiration while metabolizing glucose was observed in the CS-exposed group, indicating altered glycolysis that was compensated by an increase in palmitate utilization; palmitate utilization was accompanied by an increase in the expression of CD36 and carnitine-palmitoyl transferase 1 in type II alveolar cells for the transport of palmitate into the cells and into mitochondria, respectively. The increase in palmitate use for energy production likely affects the surfactant biosynthesis pathway, as evidenced by the decrease in phosphatidylcholine levels and the increase in phospholipase A2 activity after CS exposure. These findings help our understanding of the mechanism underlying the surfactant deficiency observed in smokers and provide a target to delay the onset of COPD.

  1. Long-term nose-only cigarette smoke exposure induces emphysema and mild skeletal muscle dysfunction in mice

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    Manuela Rinaldi

    2012-05-01

    Mouse models of chronic obstructive pulmonary disease (COPD focus on airway inflammation and lung histology, but their use has been hampered by the lack of pulmonary function data in their assessment. Systemic effects such as muscle dysfunction are also poorly modeled in emphysematous mice. We aimed to develop a cigarette-smoke-induced emphysema mouse model in which serial lung function and muscular dysfunction could be assessed, allowing the disease to be monitored more appropriately. C57Bl6 mice were nose-only exposed to cigarette smoke or filtered air for 3–6 months. Lung function tests were repeated in the same mice after 3 and 6 months of cigarette smoke or air exposure and compared with lung histological changes. Contractile properties of skeletal muscles and muscle histology were also determined at similar time points in separate groups of mice. Serial lung function measurements documented hyperinflation after 3 and 6 months of cigarette smoke exposure, with a significant 31–37% increase in total lung capacity (TLC and a significant 26–35% increase in compliance (Cchord when compared with animals exposed to filtered air only (P<0.001 after 3 and after 6 months. These functional changes preceded the changes in mean linear intercept, which became only significant after 6 months of cigarette smoke exposure and which correlated very well with TLC (r=0.74, P=0.004 and Cchord (r=0.79, P=0.001. After 6 months of cigarette smoke exposure, a significant fiber-type shift from IIa to IIx/b was also observed in the soleus muscle (P<0.05, whereas a 20% reduction of force was present at high stimulation frequencies (80 Hz; P=0.09. The extensor digitorum longus (EDL muscle was not affected by cigarette smoke exposure. These serial pulmonary function variables are sensitive outcomes to detect emphysema progression in a nose-only cigarette-smoke-exposed animal model of COPD. In this model, muscular changes became apparent only after 6 months, particularly in muscles

  2. Exposure to cigarette smoke inhibits the pulmonary T-cell response to influenza virus and Mycobacterium tuberculosis.

    Science.gov (United States)

    Feng, Yan; Kong, Ying; Barnes, Peter F; Huang, Fang-Fang; Klucar, Peter; Wang, Xisheng; Samten, Buka; Sengupta, Mayami; Machona, Bruce; Donis, Ruben; Tvinnereim, Amy R; Shams, Homayoun

    2011-01-01

    Smoking is associated with increased susceptibility to tuberculosis and influenza. However, little information is available on the mechanisms underlying this increased susceptibility. Mice were left unexposed or were exposed to cigarette smoke and then infected with Mycobacterium tuberculosis by aerosol or influenza A by intranasal infection. Some mice were given a DNA vaccine encoding an immunogenic M. tuberculosis protein. Gamma interferon (IFN-γ) production by T cells from the lungs and spleens was measured. Cigarette smoke exposure inhibited the lung T-cell production of IFN-γ during stimulation in vitro with anti-CD3, after vaccination with a construct expressing an immunogenic mycobacterial protein, and during infection with M. tuberculosis and influenza A virus in vivo. Reduced IFN-γ production was mediated through the decreased phosphorylation of transcription factors that positively regulate IFN-γ expression. Cigarette smoke exposure increased the bacterial burden in mice infected with M. tuberculosis and increased weight loss and mortality in mice infected with influenza virus. This study provides the first demonstration that cigarette smoke exposure directly inhibits the pulmonary T-cell response to M. tuberculosis and influenza virus in a physiologically relevant animal model, increasing susceptibility to both pathogens.

  3. Lung injury after cigarette smoking is particle-related

    Science.gov (United States)

    That specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking have yet to be delineated. We propose that 1) injury and disease following cigarette smoking are associated with exposure and retention of particles...

  4. Passive cigarette smoke exposure during various periods of life, genetic variants, and breast cancer risk among never smokers.

    Science.gov (United States)

    Anderson, Laura N; Cotterchio, Michelle; Mirea, Lucia; Ozcelik, Hilmi; Kreiger, Nancy

    2012-02-15

    The association between passive cigarette smoke exposure and breast cancer risk is inconclusive and may be modified by genotype. The authors investigated lifetime passive cigarette smoke exposures, 36 variants in 12 carcinogen-metabolizing genes, and breast cancer risk among Ontario, Canada, women who had never smoked (2003-2004). DNA (saliva) was available for 920 breast cancer cases and 960 controls. Detailed information about passive smoke exposure was collected for multiple age periods (childhood, teenage years, and adulthood) and environments (home, work, and social). Adjusted odds ratios and 95% confidence intervals were estimated by multivariable logistic regression, and statistical interactions were assessed using the likelihood ratio test. Among postmenopausal women, most associations between passive smoke and breast cancer risk were null, whereas among premenopausal women, nonsignificant positive associations were observed. Significant interactions were observed between certain types of passive smoke exposure and genetic variants in CYP2E1, NAT2, and UGT1A7. While these interactions were statistically significant, the magnitudes of the effect estimates were not consistent or easily interpretable, suggesting that they were perhaps due to chance. Although the results of this study were largely null, it is possible that premenopausal women exposed to passive smoke or carrying certain genetic variants may be at higher risk of breast cancer.

  5. Interaction of exposure concentration and duration in determining the apoptosis of testis in rats after cigarette smoke inhalation

    Directory of Open Access Journals (Sweden)

    Lijuan He

    2016-07-01

    Full Text Available The effects of differences in smoke concentration and exposure duration in Sprague Dawley rats to determine variation in type and severity of the testis apoptosis were evaluated. The daily dosages were 10, 20 and 30 non-filter cigarettes for a period of 2, 4, 6, 8 and 12 weeks. Mainstream smoke exposure suppressed body weight gain in all regimens. A dose-related increase in plasma nicotine concentration was observed in smoke-exposed groups for 4, 6, 8 and 12 week regimens. Histopathological examination of the exposed groups showed disturbances in the stages of spermatogenesis, tubules atrophying and these appeared to be dose-related. Cytoplasmic caspase-3 immunostaining was detected both in Sertoli cells and germ cells in smoke-exposure groups. An increase in TUNEL-positive cells of testicular cells was observed after 6 weeks of cigarette exposure. The results indicate that cigarette exposure concentration and duration have interaction effect to induce apoptosis in the rat testes.

  6. Effects of N-acetylcysteine on Clara cells in rats with cigarette smoke exposure

    Institute of Scientific and Technical Information of China (English)

    LIAO Ji-ping; CHI Chun-hua; LI Hai-chao; TANG Xiu-ying

    2010-01-01

    Background The number of Clare cells and the Clara cell 16-kDa protein (CC16) levels of the lung decrease in patients with chronic obstructive pulmonary disease (COPD). N-acetylcysteine (NAC) is a powerful antioxidant and can reduce the frequency of acute exacerbations of COPD. But the exact mechanism is unclear. The present study was designed to investigate the effects of NAC on Clara cells in rats with cigarette smoke exposure.Methods Eighteen adult male Wistar rats were randomly divided into 3 groups, 12 exposed to cigarette smoke (CS) thrice a day, 10 cigarettes for 30 minutes each time for 1 week, without (CS group) or with (CS+NAC group) oral intake of NAC 80 mg·kg~(-1)·d~(-1), and another 6 rats exposed to fresh air (control group). Clara cells were observed by an electron microscope. The Mrna expression of CC16 and CC16 protein in lungs were determined by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry respectively. The glutathion (GSH) level in plasma and lung tissue were tested by fluorimetry assay.Results Compared with the controls, the pathologic score of small airways significantly increased in the CS exposed rats (20.3±14.7 vs. 53.7±11.5, P 0.05). No significant difference was found in the expression of CC16 Mrna among the three groups. Correlation analysis indicated that the percentage of CC16-positive cells in bronchioles negatively correlated with the pathologic score of small airways (r=-0.592, P<0.05), but not with GSH level.Conclusions One-week CS exposure decreased the number of Clara cells and the expression of CC16 in bronchioles in rats. NAC might provide protection of the Clara cells from oxidative damage and possibly through the elevation of the synthesis and secretion of CC16. These data indicate that NAC decreases airway inflammation induced by CS via induction of CC16.

  7. Introspective responses to cues and motivation to reduce cigarette smoking influence state and behavioral responses to cue exposure.

    Science.gov (United States)

    Veilleux, Jennifer C; Skinner, Kayla D

    2016-09-01

    In the current study, we aimed to extend smoking cue-reactivity research by evaluating delay discounting as an outcome of cigarette cue exposure. We also separated introspection in response to cues (e.g., self-reporting craving and affect) from cue exposure alone, to determine if introspection changes behavioral responses to cigarette cues. Finally, we included measures of quit motivation and resistance to smoking to assess motivational influences on cue exposure. Smokers were invited to participate in an online cue-reactivity study. Participants were randomly assigned to view smoking images or neutral images, and were randomized to respond to cues with either craving and affect questions (e.g., introspection) or filler questions. Following cue exposure, participants completed a delay discounting task and then reported state affect, craving, and resistance to smoking, as well as an assessment of quit motivation. We found that after controlling for trait impulsivity, participants who introspected on craving and affect showed higher delay discounting, irrespective of cue type, but we found no effect of response condition on subsequent craving (e.g., craving reactivity). We also found that motivation to quit interacted with experimental conditions to predict state craving and state resistance to smoking. Although asking about craving during cue exposure did not increase later craving, it resulted in greater delaying of discounted rewards. Overall, our findings suggest the need to further assess the implications of introspection and motivation on behavioral outcomes of cue exposure.

  8. Mouse Protocadherin-1 Gene Expression Is Regulated by Cigarette Smoke Exposure In Vivo

    NARCIS (Netherlands)

    Koning, Henk; van Oosterhout, Antoon J. M.; Brouwer, Uilke; den Boef, Lisette E.; Gras, Renee; Reinders-Luinge, Marjan; Brandsma, Corry-Anke; van der Toorn, Marco; Hylkema, Machteld N.; Willemse, Brigitte W. M.; Sayers, Ian; Koppelman, Gerard H.; Nawijn, Martijn C.

    2014-01-01

    Protocadherin-1 (PCDH1) is a novel susceptibility gene for airway hyperresponsiveness, first identified in families exposed to cigarette smoke and is expressed in bronchial epithelial cells. Here, we asked how mouse Pcdh1 expression is regulated in lung structural cells in vivo under physiological c

  9. Cigarette smoking habits among schoolchildren

    NARCIS (Netherlands)

    Branski, D; Knol, K; Kerem, E; Meijer, B.C

    1996-01-01

    Study objective: Cigarette smoking is a major preventable cause of morbidity and mortality worldwide. Most adult smokers start smoking regularly some time before 18 years of age. The aim of this study was to determine the age at which children begin cigarette smoking, to study the environmental fact

  10. Immediate response to cigarette smoke

    Energy Technology Data Exchange (ETDEWEB)

    Rees, P.J.; Chowienczyk, P.J.; Clark, T.J.

    1982-06-01

    Using an automated method of calculating airways resistance in the body plethysmograph, we have investigated changes occurring immediately after inhalation of cigarette smoke. Decreases in specific conductance occurred by the time of the first measurement seven or eight seconds after exposure to single inhalations of cigarette smoke in 12 smokers and 12 non-smokers. Less than half of the initial change was present 40 seconds after the inhalation. Initial responses were greater in the non-smokers. Responses recurred with repeated inhalations in smokers and non-smokers. Prior administration of salbutamol and ipratropium bromide significantly inhibited the response and this inhibition appeared to be greater in non-smokers. Sodium cromoglycate inhaled as a dry powder had no effect on the response.

  11. Expression and significance of myeloid differentiation factor 88 in marrow dendritic cells in asthmatic rats with cigarette smoke exposure

    Institute of Scientific and Technical Information of China (English)

    LI Yi; DU Yong-cheng; XU Jian-ying; HU Xiao-yun

    2012-01-01

    Background Smoking causes frequent asthma attacks,leading to a rapid decline in lung function in patients with asthma,and it can also reduce the therapeutic effect of glucocorticeids in patients with asthma.Therefore,the present study aimed to investigate the effect of cigarette smoke on the expression of myeloid differentiation factor 88 (MyD88) in marrow dendritic cells (DCs) in asthmatic rats,and to explore the molecular mechanism of cigarette smoke exposure on asthma by DCs.Methods Forty Wistar rats were randomly divided into the following groups:control,smoke exposure,asthma,and asthma combined with smoke exposure.The animal model was established,and then rat bone marrow-derived DCs were collected.Additionally,rat spleen lymphocytes and bone marrow-derived DCs were cultured together for mixed lymphocyte responses.Interferon (IFN)-gamma and interleukin (IL)-4,IL-10,and IL-12 expressions were determined by enzyme-linked immunosorbent assay (ELISA).MyD88 expression was determined by Western blotting.The proliferation of lymphocytes was examined with methyl thiazolyl tetrazolium (MTT) colorimetric assay.Results MyD88 expression was decreased in the asthma combined with smoke exposure group compared to the asthma group (P<0.01),and IL-10 and IL-12 expressions were decreased in the asthma combined with smoke exposure group compared to control group (P<0.01).In addition,DCs stimulating activity on allogeneic lymphocytes were significantly decreased in the smoke exposure combined with asthma group compared to the control and asthma groups (P<0.01).After allogeneic mixed lymphocyte responses,IL-4 expression was increased and IFN-gamma was decreased in the asthma group and the asthma combined with smoke exposure group compared to control group (P<0.01).IL-4expression was increased and IFN-gamma was decreased in the asthma combined with smoke exposure group compared to the asthma group (P<0.01).The study also showed that MyD88 expression was positively

  12. Effects of combined exposure of F344 rats to radiation and chronically inhaled cigarette smoke

    Energy Technology Data Exchange (ETDEWEB)

    Finch, G.L.; Nikula, K.J.; Barr, E.B. [and others

    1995-12-01

    Nuclear workers may be exposed to radiation in various forms, such as low-LET {gamma}-irradiation or {alpha}-irradiation from inhaled {sup 239}PuO{sub 2} particles. These workers may then have increased risk for lung cancer compared to the general population. Of additional concern is the possibility that interactions between radiation and other carcinogens may increase the risk of cancer induction, compared to the risks from either type of agent alone. An important and common lung carcinogen is cigarette smoke. The purpose of this project is to better determine the combined effects of chronically inhaled cigarette smoke and either inhaled {sup 239}PuO{sub 2} or external, thoracic X-irradiation on the induction of lung cancer in rats. Histologic and dosimetric evaluations of rats in the CS + {sup 239}PuO{sub 2} study continue, and the study of CS + X rays is beginning.

  13. Cigarette smoking and male infertility

    Directory of Open Access Journals (Sweden)

    Taymour Mostafa

    2010-07-01

    Full Text Available Numerous studies have identified specific body systems affected by the hazardous effects of the cigarette smoking particularly the respiratory and cardiovascular systems. The effect of smoking on male reproduction has also been studied where semen quality was investigated in different cross-sectional studies including infertile patients with conflicting results. This article aimed to assess the relationship between smoking and male infertility. A review of published articles was carried out, using PubMed, medical subject heading (MSH databases and Scopus engine excluding the effects of smoking outside male infertility. Key words used to assess exposure, outcome, and estimates for the concerned associations were: smoking, semen, male infertility, sperm, humans, and fertility. Most of the reports showed that smoking reduces sperm production, sperm motility, sperm normal forms and sperm fertilising capacity through increased seminal oxidative stress and DNA damage. Few papers reported nonsignificant differences in semen parameters between smokers or non-smokers. It is concluded that although some smokers may not experience reduced fertility, men with marginal semen quality can benefit from quitting smoking.

  14. Electronic cigarettes for smoking cessation.

    Science.gov (United States)

    Bullen, Christopher

    2014-11-01

    Electronic cigarettes (e-cigarettes) are novel vaporising devices that, similar to nicotine replacement treatments, deliver nicotine but in lower amounts and less swiftly than tobacco smoking. However, they enjoy far greater popularity than these medications due in part to their behaviour replacement characteristics. Evidence for their efficacy as cessation aids, based on several randomised trials of now obsolete e-cigarettes, suggests a modest effect equivalent to nicotine patch. E-cigarettes are almost certainly far less harmful than tobacco smoking, but the health effects of long-term use are as yet unknown. Dual use is common and almost as harmful as usual smoking unless it leads to quitting. Population effects, such as re-normalising smoking behaviour, are a concern. Clinicians should be knowledgeable about these products. If patients who smoke are unwilling to quit or cannot succeed using evidence-based approaches, e-cigarettes may be an option to be considered after discussing the limitations of current knowledge.

  15. Adolescent Light Cigarette Smoking Patterns and Adult Cigarette Smoking

    Directory of Open Access Journals (Sweden)

    R. Constance Wiener

    2016-01-01

    Full Text Available Purpose. Light cigarette smoking has had limited research. The purpose of this study was to examine the relationship between light smoking in adolescence with smoking in adulthood. Methods. National Longitudinal Study of Adolescent Health data, Waves I and IV, were analyzed. Previous month adolescent smoking of 1–5 cigarettes/day (cpd (light smoking; 6–16 cpd (average smoking; 17 or more cpd (heavy smoking; and nonsmoking were compared with the outcome of adult smoking. Results. At baseline, 15.9% of adolescents were light smokers, 6.8% were average smokers, and 3.6% were heavy smokers. The smoking patterns were significantly related to adult smoking. In logistic regression analyses, adolescent light smokers had an adjusted odds ratio (AOR of 2.45 (95% CI: 2.00, 3.00 of adult smoking; adolescent average or heavy smokers had AOR of 5.57 (95% CI: 4.17, 7.43 and 5.23 (95% CI: 3.29, 8.31, respectively. Conclusion. Individuals who initiate light cigarette smoking during adolescence are more likely to smoke as young adults. Practical Implications. When screening for tobacco use by adolescents, there is a need to verify that the adolescents understand that light smoking constitutes smoking. There is a need for healthcare providers to initiate interventions for adolescent light smoking.

  16. Liver growth factor treatment reverses emphysema previously established in a cigarette smoke exposure mouse model.

    Science.gov (United States)

    Pérez-Rial, Sandra; Del Puerto-Nevado, Laura; Girón-Martínez, Alvaro; Terrón-Expósito, Raúl; Díaz-Gil, Juan J; González-Mangado, Nicolás; Peces-Barba, Germán

    2014-11-01

    Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease largely associated with cigarette smoke exposure (CSE) and characterized by pulmonary and extrapulmonary manifestations, including systemic inflammation. Liver growth factor (LGF) is an albumin-bilirubin complex with demonstrated antifibrotic, antioxidant, and antihypertensive actions even at extrahepatic sites. We aimed to determine whether short LGF treatment (1.7 μg/mouse ip; 2 times, 2 wk), once the lung damage was established through the chronic CSE, contributes to improvement of the regeneration of damaged lung tissue, reducing systemic inflammation. We studied AKR/J mice, divided into three groups: control (air-exposed), CSE (chronic CSE), and CSE + LGF (LGF-treated CSE mice). We assessed pulmonary function, morphometric data, and levels of various systemic inflammatory markers to test the LGF regenerative capacity in this system. Our results revealed that the lungs of the CSE animals showed pulmonary emphysema and inflammation, characterized by increased lung compliance, enlargement of alveolar airspaces, systemic inflammation (circulating leukocytes and serum TNF-α level), and in vivo lung matrix metalloproteinase activity. LGF treatment was able to reverse all these parameters, decreasing total cell count in bronchoalveolar lavage fluid and T-lymphocyte infiltration in peripheral blood observed in emphysematous mice and reversing the decrease in monocytes observed in chronic CSE mice, and tends to reduce the neutrophil population and serum TNF-α level. In conclusion, LGF treatment normalizes the physiological and morphological parameters and levels of various systemic inflammatory biomarkers in a chronic CSE AKR/J model, which may have important pathophysiological and therapeutic implications for subjects with stable COPD.

  17. How does exposure to cigarette advertising contribute to smoking in adolescents? The role of the developing self-concept and identification with advertising models.

    Science.gov (United States)

    Shadel, William G; Tharp-Taylor, Shannah; Fryer, Craig S

    2009-11-01

    Increased exposure to cigarette advertisements is associated with increases in adolescent smoking but the reasons for this association are not well established. This study evaluated whether self-concept development (operationalized as level of self-conflict) and identifying with the models used in cigarette print advertising contributed to smoking intentions among adolescents. Ninety-five adolescents (ages 11-17) participated in this two session study. In session 1, they rated the extent to which they identified with the models used in 10 current cigarette print ads (the models were isolated digitally from the cigarette advertisements) and their level of self-conflict was assessed. In session 2, participants viewed each of the 10 cigarette advertisements from which the models were drawn and rated their intentions to smoke following exposure to each ad. Model identification was associated with similar levels of post ad exposure smoking intentions for both younger and older adolescents when they also exhibited no self-conflict. A contrasting set of findings emerged for younger and older adolescents when they exhibited high levels of self-conflict: Young adolescents who strongly identified with the models used in cigarette advertisements had higher post ad exposure smoking intentions compared to younger adolescents who weakly identified with the models used in the advertisements; in contrast, older adolescents who weakly identified with the models used in cigarette advertisements had stronger post ad exposure smoking intentions compared to older adolescents who strongly identified with the models used in the advertisements. These results point to the importance of examining developmentally-relevant moderators for the effects of cigarette advertising exposure.

  18. The Influence of Second-Hand Cigarette Smoke Exposure during Childhood and Active Cigarette Smoking on Crohn's Disease Phenotype Defined by the Montreal Classification Scheme in a Western Cape Population, South Africa.

    Directory of Open Access Journals (Sweden)

    Tawanda Chivese

    Full Text Available Smoking may worsen the disease outcomes in patients with Crohn's disease (CD, however the effect of exposure to second-hand cigarette smoke during childhood is unclear. In South Africa, no such literature exists. The aim of this study was to investigate whether disease phenotype, at time of diagnosis of CD, was associated with exposure to second-hand cigarette during childhood and active cigarette smoking habits.A cross sectional examination of all consecutive CD patients seen during the period September 2011-January 2013 at 2 large inflammatory bowel disease centers in the Western Cape, South Africa was performed. Data were collected via review of patient case notes, interviewer-administered questionnaire and clinical examination by the attending gastroenterologist. Disease phenotype (behavior and location was evaluated at time of diagnosis, according to the Montreal Classification scheme. In addition, disease behavior was stratified as 'complicated' or 'uncomplicated', using predefined definitions. Passive cigarette smoke exposure was evaluated during 3 age intervals: 0-5, 6-10, and 11-18 years.One hundred and ninety four CD patients were identified. Cigarette smoking during the 6 months prior to, or at time of diagnosis was significantly associated with ileo-colonic (L3 disease (RRR = 3.63; 95% CI, 1.32-9.98, p = 0.012 and ileal (L1 disease (RRR = 3.54; 95% CI, 1.06-11.83, p = 0.040 compared with colonic disease. In smokers, childhood passive cigarette smoke exposure during the 0-5 years age interval was significantly associated with ileo-colonic CD location (RRR = 21.3; 95% CI, 1.16-391.55, p = 0.040. No significant association between smoking habits and disease behavior at diagnosis, whether defined by the Montreal scheme, or stratified as 'complicated' vs 'uncomplicated', was observed.Smoking habits were associated with ileo-colonic (L3 and ileal (L1 disease at time of diagnosis in a South African cohort.

  19. In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells

    Science.gov (United States)

    Jukosky, James; Gosselin, Benoit J.; Foley, Leah; Dechen, Tenzin; Fiering, Steven; Crane-Godreau, Mardi A.

    2016-01-01

    Smokers and individuals exposed to second-hand cigarette smoke have a higher risk of developing chronic sinus and bronchial infections. This suggests that cigarette smoke (CS) has adverse effects on immune defenses against pathogens. Epithelial cells are important in airway innate immunity and are the first line of defense against infection. Airway epithelial cells not only form a physical barrier but also respond to the presence of microbes by secreting antimicrobials, cytokines, and chemokines. These molecules can lyse infectious microorganisms and/or provide signals critical to the initiation of adaptive immune responses. We examined the effects of CS on antimicrobial secretions of primary human nasal epithelial cells (PHNECs). Compared to non-CS-exposed individuals, PHNEC from in vivo CS-exposed individuals secreted less chemokine ligand (C-C motif) 20 (CCL20), Beta-defensin 1 (BD-1), and SLPI apically, less BD-1 and SLPI basolaterally, and more CCL20 basolaterally. Cigarette smoke extract (CSE) exposure in vitro decreased the apical secretion of CCL20 and beta-defensin 1 by PHNEC from non-CS-exposed individuals. Exposing PHNEC from non-CS exposed to CSE also significantly decreased the levels of many mRNA transcripts that are involved in immune signaling. Our results show that in vivo or in vitro exposure to CS alters the secretion of key antimicrobial peptides from PHNEC, but that in vivo CS exposure is a much more important modifier of antimicrobial peptide secretion. Based on the gene expression data, it appears that CSE disrupts multiple immune signaling pathways in PHNEC. Our results provide mechanistic insight into how CS exposure alters the innate immune response and increases an individual’s susceptibility to pathogen infection. PMID:26793127

  20. Effect of restricted food supply to pregnant rats inhaling carbon monoxide on fetal weight, compared with cigarette smoke exposure

    Energy Technology Data Exchange (ETDEWEB)

    Tachi, N.; Aoyama, M.

    1986-12-01

    Although many studies have shown that cigarette smoking during gestation retarded the intrauterine fetal growth, resulting in the decreased birth weight in babies born to smoking mothers, neither causal substance nor mechanism of action to disturb fetal growth has been firmly established yet. Based on the human and animal studies, researchers have implied that fetal hypoxia induced by carbon monoxide (CO) in the cigarette smoke to be responsible for the event. A shortage in energy intake in smoking mothers also has been suspected to cause the retardation in fetal development. In the previous results (Tachi and Aoyama 1983), the weight increment in CO exposed animals was greater than that in the smoke exposed group. The phenomenon seemed to indicate that the reduction in the food intake occurs in animals which inhale the cigarette smoke, and induces the disturbance of fetal development in association with CO. In the present study, so as to evaluate the role of energy intake upon the fetal development in utero, the experiment of paired feeding with pregnant rats exposed to cigarette smoke is designed in animals which inhale the cigarette smoke, CO, or room air, following after the observation of the quantity of food taken by mothers exposed to cigarette smoke, CO, or room air.

  1. Smoked marijuana effects on tobacco cigarette smoking behavior.

    Science.gov (United States)

    Kelly, T H; Foltin, R W; Rose, A J; Fischman, M W; Brady, J V

    1990-03-01

    The effects of marijuana smoke exposure on several measures of tobacco cigarette smoking behavior were examined. Eight healthy adult male volunteers, who smoked both tobacco and marijuana cigarettes, participated in residential studies, lasting 10 to 15 days, designed to measure the effects of marijuana smoke exposure on a range of behavioral variables. Tobacco cigarettes were available throughout the day (9:00 A.M. until midnight). Each day was divided into a private period (9:00 A.M. to 5:00 P.M.), during which subjects were socially isolated, and a social period (5:00 P.M. to midnight), during which subjects could interact. Under blind conditions, subjects smoked placebo and active marijuana cigarettes (0%, 1.3%, 2.3%, or 2.7% delta 9-tetrahydrocannabinol) four times daily (9:45 A.M., 1:30 P.M., 5:00 P.M. and 8:30 P.M.). Each subject was exposed to both placebo and one active dose over 2- to 5-consecutive-day intervals, and dose conditions (i.e., placebo or active) alternated throughout the study. Active marijuana smoking significantly decreased the number of daily tobacco smoking bouts, increased inter-bout intervals and decreased inter-puff intervals. Marijuana decreased the number of tobacco smoking bouts by delaying the initiation of tobacco cigarette smoking immediately after marijuana smoking, whereas decreases in inter-puff intervals were unrelated to the time of marijuana smoking. No consistent interactions between marijuana effects and social or private periods (i.e., time of day) were observed.

  2. Subacute effect of cigarette smoke exposure in rats: protection by pot marigold (Calendula officinalis L.) extract.

    Science.gov (United States)

    Ozkol, Halil; Tülüce, Yasin; Koyuncu, Ismail

    2012-02-01

    This study was carried out to determine the preventive effect of Calendula officinalis L. (pot marigold) on rats exposed to cigarette smoke (CS). Rats were divided into three groups as control, CS and CS + pot marigold (PM). The rats in the CS and CS + PM groups were subjected to CS for 1 h twice a day for 23 days. PM (100 mg/kg body weight) was given to rats in the CS + PM group by gavage, 1 h before each administration period. While malondialdehyde, protein carbonyl contents and reduced glutathione level of the CS group increased, their levels diminished by PM administration. In addition, glutathione peroxidase (GPx), superoxide dismutase activities and β-carotene, vitamins A and C levels decreased in the CS group compared to control, however activities of these enzymes and concentration of vitamins were elevated by PM supplementation. This investigation showed that administration of PM supplied relative protection against subacute CS-induced cell injury.

  3. Differential expression and function of breast regression protein 39 (BRP-39 in murine models of subacute cigarette smoke exposure and allergic airway inflammation

    Directory of Open Access Journals (Sweden)

    Coyle Anthony J

    2011-04-01

    Full Text Available Abstract Background While the presence of the chitinase-like molecule YKL40 has been reported in COPD and asthma, its relevance to inflammatory processes elicited by cigarette smoke and common environmental allergens, such as house dust mite (HDM, is not well understood. The objective of the current study was to assess expression and function of BRP-39, the murine equivalent of YKL40 in a murine model of cigarette smoke-induced inflammation and contrast expression and function to a model of HDM-induced allergic airway inflammation. Methods CD1, C57BL/6, and BALB/c mice were room air- or cigarette smoke-exposed for 4 days in a whole-body exposure system. In separate experiments, BALB/c mice were challenged with HDM extract once a day for 10 days. BRP-39 was assessed by ELISA and immunohistochemistry. IL-13, IL-1R1, IL-18, and BRP-39 knock out (KO mice were utilized to assess the mechanism and relevance of BRP-39 in cigarette smoke- and HDM-induced airway inflammation. Results Cigarette smoke exposure elicited a robust induction of BRP-39 but not the catalytically active chitinase, AMCase, in lung epithelial cells and alveolar macrophages of all mouse strains tested. Both BRP-39 and AMCase were increased in lung tissue after HDM exposure. Examining smoke-exposed IL-1R1, IL-18, and IL-13 deficient mice, BRP-39 induction was found to be IL-1 and not IL-18 or IL-13 dependent, while induction of BRP-39 by HDM was independent of IL-1 and IL-13. Despite the importance of BRP-39 in cellular inflammation in HDM-induced airway inflammation, BRP-39 was found to be redundant for cigarette smoke-induced airway inflammation and the adjuvant properties of cigarette smoke. Conclusions These data highlight the contrast between the importance of BRP-39 in HDM- and cigarette smoke-induced inflammation. While functionally important in HDM-induced inflammation, BRP-39 is a biomarker of cigarette smoke induced inflammation which is the byproduct of an IL-1

  4. Effects of Puerarin on Pulmonary Vascular Remodeling and Protein Kinase C-α in Chronic Cigarette Smoke Exposure Smoke-exposed Rats

    Institute of Scientific and Technical Information of China (English)

    Zhaoxia ZHU; Yongjian XU; Hui ZOU; Zhenxiang ZHANG; Wang NI; Shixin CHEN

    2008-01-01

    In order to investigate the effects of puerarin on pulmonary vascular remodeling and protein kinase C-α (PKC-α) in chronic exposure smoke rats, 54 male Wistar rats were randomly di- vided into 7 groups: control group (C group), smoke exposure groups (S4w group, Saw group), puer- arin groups (P4w group, P8w group), propylene glycol control groups (PC4w group,PC8w group). Rats were exposed to cigarette smoke or air for 4 to 8 weeks. Rats in puerarin groups also received puer- arin. To evaluate vascular remodeling, alpha-smooth muscle actin (α-SM-actin) staining was used to count the percentage of completely muscularised vessels to intraacinar pulmonary arteries (CMA/IAPA) which was determined by morphometric analysis of histological sections. Pulmonary artery smooth muscle cell (PASMC) apoptosis was detected by in situ end labeling technique (TUNEL), and proliferation by proliferating cell nuclear antigen (PCNA) staining. Reverse transcrip- tion-polymerase chain reaction (RT-PCR), immunofluorescence staining and Western blot analysis were done to detect the PKC-α mRNA and protein expression in pulmonary arteries. The results showed that in cigarette smoke-exposed rats the percentage of CMA/IAPA and α-SM-actin expres- sion were increased greatly, PASMC apoptosis was increased and proliferation was markedly in- creased; Apoptosis indices (AI) and proliferation indices (PI) were higher than in C group; AI and PI were correlated with vascular remodeling indices; The expression of PKC-ct mRNA and protein in pulmonary arteries was significantly higher than in C group. In rats treated with puerarin, the per- eentage of CMA/IAPA and cell proliferation was reduced, whereas PASMC apoptosis was increased; The expression levels of PKC-α mRNA and protein were lower than in smoke exposure rats. There was no difference among all these data between S groups and PC groups. These findings suggested that cigarette smoke-induced pulmonary vascular remodeling was most likely an

  5. ACSL6 is associated with the number of cigarettes smoked and its expression is altered by chronic nicotine exposure.

    Directory of Open Access Journals (Sweden)

    Jingchun Chen

    Full Text Available Individuals with schizophrenia tend to be heavy smokers and are at high risk for tobacco dependence. However, the nature of the comorbidity is not entirely clear. We previously reported evidence for association of schizophrenia with SNPs and SNP haplotypes in a region of chromosome 5q containing the SPEC2, PDZ-GEF2 and ACSL6 genes. In this current study, analysis of the control subjects of the Molecular Genetics of Schizophrenia (MGS sample showed similar pattern of association with number of cigarettes smoked per day (numCIG for the same region. To further test if this locus is associated with tobacco smoking as measured by numCIG and FTND, we conducted replication and meta-analysis in 12 independent samples (n>16,000 for two markers in ACSL6 reported in our previous schizophrenia study. In the meta-analysis of the replication samples, we found that rs667437 and rs477084 were significantly associated with numCIG (p = 0.00038 and 0.00136 respectively but not with FTND scores. We then used in vitro and in vivo techniques to test if nicotine exposure influences the expression of ACSL6 in brain. Primary cortical culture studies showed that chronic (5-day exposure to nicotine stimulated ACSL6 mRNA expression. Fourteen days of nicotine administration via osmotic mini pump also increased ACSL6 protein levels in the prefrontal cortex and hippocampus of mice. These increases were suppressed by injection of the nicotinic receptor antagonist mecamylamine, suggesting that elevated expression of ACSL6 requires nicotinic receptor activation. These findings suggest that variations in the ACSL6 gene may contribute to the quantity of cigarettes smoked. The independent associations of this locus with schizophrenia and with numCIG in non-schizophrenic subjects suggest that this locus may be a common liability to both conditions.

  6. Animal models of nicotine exposure: relevance to second-hand smoking, electronic cigarette use and compulsive smoking

    Directory of Open Access Journals (Sweden)

    Ami eCohen

    2013-06-01

    Full Text Available Much evidence indicates that individuals use tobacco primarily to experience the psychopharmacological properties of nicotine and that a large proportion of smokers eventually become dependent on nicotine. In humans, nicotine acutely produces positive reinforcing effects, including mild euphoria, whereas a nicotine abstinence syndrome with both somatic and affective components is observed after chronic nicotine exposure. Animal models of nicotine self-administration and chronic exposure to nicotine have been critical in unveiling the neurobiological substrates that mediate the acute reinforcing effects of nicotine and emergence of a withdrawal syndrome during abstinence. However, important aspects of the transition from nicotine abuse to nicotine dependence, such as the emergence of increased motivation and compulsive nicotine intake following repeated exposure to the drug, have only recently begun to be modeled in animals. Thus, the neurobiological mechanisms that are involved in these important aspects of nicotine addiction remain largely unknown. In this review, we describe the different animal models available to date and discuss recent advances in animal models of nicotine exposure and nicotine dependence. This review demonstrates that novel animal models of nicotine vapor exposure and escalation of nicotine intake provide a unique opportunity to investigate the neurobiological effects of second-hand nicotine exposure, electronic cigarette use and the mechanisms that underlie the transition from nicotine use to compulsive nicotine intake.

  7. Secondhand cigarette smoke exposure causes upregulation of cerebrovascular 5-HT(1) (B) receptors via the Raf/ERK/MAPK pathway in rats

    DEFF Research Database (Denmark)

    Cao, L; Xu, C B; Zhang, Y;

    2013-01-01

    Cigarette smoke exposure increases the risk of stroke. Upregulation of 5-hydroxytryptamine 1B (5-HT(1) (B) ) receptors is associated with the pathogenesis of cerebral ischaemia. This study examined the hypothesis that the expression of 5-HT(1) (B) receptors is altered in brain vessels after...

  8. Plasminogen activator inhibitor-1 in cigarette smoke exposure and influenza A virus infection-induced lung injury.

    Directory of Open Access Journals (Sweden)

    Yashodhar P Bhandary

    Full Text Available Parenchymal lung inflammation and airway and alveolar epithelial cell apoptosis are associated with cigarette smoke exposure (CSE, which contributes to chronic obstructive pulmonary disease (COPD. Epidemiological studies indicate that people exposed to chronic cigarette smoke with or without COPD are more susceptible to influenza A virus (IAV infection. We found increased p53, PAI-1 and apoptosis in AECs, with accumulation of macrophages and neutrophils in the lungs of patients with COPD. In Wild-type (WT mice with passive CSE (PCSE, p53 and PAI-1 expression and apoptosis were increased in AECs as was lung inflammation, while those lacking p53 or PAI-1 resisted AEC apoptosis and lung inflammation. Further, inhibition of p53-mediated induction of PAI-1 by treatment of WT mice with caveolin-1 scaffolding domain peptide (CSP reduced PCSE-induced lung inflammation and reversed PCSE-induced suppression of eosinophil-associated RNase1 (EAR1. Competitive inhibition of the p53-PAI-1 mRNA interaction by expressing p53-binding 3'UTR sequences of PAI-1 mRNA likewise suppressed CS-induced PAI-1 and AEC apoptosis and restored EAR1 expression. Consistent with PCSE-induced lung injury, IAV infection increased p53, PAI-1 and apoptosis in AECs in association with pulmonary inflammation. Lung inflammation induced by PCSE was worsened by subsequent exposure to IAV. Mice lacking PAI-1 that were exposed to IAV showed minimal viral burden based on M2 antigen and hemagglutination analyses, whereas transgenic mice that overexpress PAI-1 without PCSE showed increased M2 antigen and inflammation after IAV infection. These observations indicate that increased PAI-1 expression promotes AEC apoptosis and exacerbates lung inflammation induced by IAV following PCSE.

  9. Cigarette-by-cigarette satisfaction during ad libitum smoking.

    Science.gov (United States)

    Shiffman, Saul; Kirchner, Thomas R

    2009-05-01

    Smoking is thought to produce immediate reinforcement, and subjective satisfaction with smoking is thought to influence subsequent smoking. The authors used ecological momentary assessment (A. A. Stone & S. Shiffman, 1994) to assess cigarette-by-cigarette smoking satisfaction in 394 heavy smokers who subsequently attempted to quit. Across 14,882 cigarettes rated, satisfaction averaged 7.06 (0-10 scale), but with considerable variation across cigarettes and individuals. Women and African American smokers reported higher satisfaction. More satisfied smokers were more likely to lapse after quitting (HR = 1.1, p < .03), whereas less satisfied smokers derived greater benefit from patch treatment to help them achieve abstinence (HR = 1.23, p < .001). Cigarettes smoked in positive moods were more satisfying, correcting for mood at the time of rating. The best predictor of subsequent smoking satisfaction was the intensity of craving prior to smoking. Understanding subjective smoking satisfaction provides insight into sources of reinforcement for smoking.

  10. Effects of Switching to Electronic Cigarettes with and without Concurrent Smoking on Exposure to Nicotine, Carbon Monoxide, and Acrolein.

    Science.gov (United States)

    McRobbie, Hayden; Phillips, Anna; Goniewicz, Maciej L; Smith, Katie Myers; Knight-West, Oliver; Przulj, Dunja; Hajek, Peter

    2015-09-01

    Concern has been raised about the presence of toxicants in electronic cigarette (EC) aerosol, particularly carbonyl compounds (e.g., acrolein) that can be produced by heating glycerol and glycols used in e-liquids. We investigated exposure to carbon monoxide (CO), nicotine (by measuring cotinine in urine), and to acrolein (by measuring its primary metabolite, S-(3-hydroxypropyl)mercapturic acid (3-HPMA) in urine) before and after 4 weeks of EC (green smoke, a "cig-a-like" EC, labeled 2.4% nicotine by volume) use, in 40 smokers. Thirty-three participants were using EC at 4 weeks after quitting, 16 (48%) were abstinent (CO-validated) from smoking during the previous week (EC only users), and 17 (52%) were "dual users." A significant reduction in CO was observed in EC-only users [-12 ppm, 95% confidence interval (CI), -16 to -7, 80% decrease) and dual users (-12 ppm, 95%CI, -19 to -6, 52% decrease). Cotinine levels also declined, but to a lesser extent (EC-only users: -184 ng/mg creatinine; 95% CI, -733 to -365, 17% decrease; and dual users: -976 ng/mg creatinine; 95%CI, -1,682 to -270, 44% decrease). Mean 3-HPMA levels had decreased at 4 weeks by 1,280 ng/mg creatinine (95%CI, -1,699 to -861, 79% decrease) in EC-only users and by 1,474 ng/mg creatinine (95%CI, -2,101 to -847, 60% decrease) in dual users. In dual users, EC use significantly reduced exposure to CO and acrolein because of a reduction in smoke intake. EC may reduce harm even in smokers who continue to smoke, but long-term follow-up studies are needed to confirm this.

  11. Cigarette smoke exposure induced pulmonary artery pressure increase through inhibiting Kv1.5 and Kv2.1 mRNA expression in rat pulmonary artery smooth muscles

    Institute of Scientific and Technical Information of China (English)

    林纯意

    2012-01-01

    Objective To investigate the effect of cigarette smoke exposure on Kv1.5 and Kv2.1 mRNA expression in rat pulmonary arterial smooth muscle cells(PASMCs), and further to clarify the possible mechanism of cigarette smoking induced pulmonary arterial hypertension. Methods Primary

  12. Exposure to Hookah and Cigarette Smoke in Children and Adolescents According to Their Socio-Economic Status: The CASPIAN-IV Study

    Science.gov (United States)

    Kelishadi, Roya; Shahsanai, Armindokht; Qorbani, Mostafa; Ardalan, Gelayol; Poursafa, Parinaz; Heshmat, Ramin; Motlagh, Mohammad Esmaeil

    2016-01-01

    Background Exposure to smoking or passive smoking is one of serious health problems especially in the pediatric age group. Objectives To compare the prevalence and determinants of passive smoking in a nationally representative sample of Iranian children and adolescents according to their socioeconomic status (SES). Materials and Methods This nationwide study was conducted in 2011 - 2012 among 14880 students aged 6 - 18 years, living in 30 provinces in Iran. Exposure to the smoke of hookah or cigarette was documented by using validated questionnaires. Possible influencing factors were determined and the frequency of passive smoking was compared according to the regional and familial SES. Results Participants consisted of 13,486 children and adolescents including 49.2% girls and 75.6% urban inhabitants (90.6% participation rate). The mean age of participants was 12.47 ± 3.36 years. Overall, 43.87% of them (44.07% of boys and 43.66% of girls) were exposed to second hand smoke at home. Exposures to hookah or cigarette smoke at home were respectively reported in 21.46% and 34.49% of participants. The prevalence of passive smoking was lower in children of families with higher SES level, but higher in high SES regions of the country than in low SES ones, and ranged from 39.2% in the region with lowest SES to 49.05% in the highest SES region. Higher education levels of fathers and mothers were significantly associated with lower frequency of passive smoking. Conclusions Exposure to second hand smoke is a major problem among Iranian children and adolescents. Low family SES and low parental education increased the frequency of passive smoking. Appropriate public health education and legislation for smoke free home as well as family-centered counseling should be strengthened. PMID:27781078

  13. Exposure to Hookah and Cigarette Smoke in Children and Adolescents According to Their Socio-Economic Status: The CASPIAN-IV Study

    Directory of Open Access Journals (Sweden)

    Roya Kelishadi

    2016-06-01

    Full Text Available Background Exposure to smoking or passive smoking is one of serious health problems especially in the pediatric age group. Objectives To compare the prevalence and determinants of passive smoking in a nationally representative sample of Iranian children and adolescents according to their socioeconomic status (SES. Materials and Methods This nationwide study was conducted in 2011 - 2012 among 14880 students aged 6 - 18 years, living in 30 provinces in Iran. Exposure to the smoke of hookah or cigarette was documented by using validated questionnaires. Possible influencing factors were determined and the frequency of passive smoking was compared according to the regional and familial SES. Results Participants consisted of 13,486 children and adolescents including 49.2% girls and 75.6% urban inhabitants (90.6% participation rate. The mean age of participants was 12.47 ± 3.36 years. Overall, 43.87% of them (44.07% of boys and 43.66% of girls were exposed to second hand smoke at home. Exposures to hookah or cigarette smoke at home were respectively reported in 21.46% and 34.49% of participants. The prevalence of passive smoking was lower in children of families with higher SES level, but higher in high SES regions of the country than in low SES ones, and ranged from 39.2% in the region with lowest SES to 49.05% in the highest SES region. Higher education levels of fathers and mothers were significantly associated with lower frequency of passive smoking. Conclusions Exposure to second hand smoke is a major problem among Iranian children and adolescents. Low family SES and low parental education increased the frequency of passive smoking. Appropriate public health education and legislation for smoke free home as well as family-centered counseling should be strengthened.

  14. Exposure to Cigarette Smoke Inhibits the Pulmonary T-Cell Response to Influenza Virus and Mycobacterium tuberculosis▿

    OpenAIRE

    2010-01-01

    Smoking is associated with increased susceptibility to tuberculosis and influenza. However, little information is available on the mechanisms underlying this increased susceptibility. Mice were left unexposed or were exposed to cigarette smoke and then infected with Mycobacterium tuberculosis by aerosol or influenza A by intranasal infection. Some mice were given a DNA vaccine encoding an immunogenic M. tuberculosis protein. Gamma interferon (IFN-γ) production by T cells from the lungs and sp...

  15. Electronic cigarette aerosol induces significantly less cytotoxicity than tobacco smoke

    Science.gov (United States)

    Azzopardi, David; Patel, Kharishma; Jaunky, Tomasz; Santopietro, Simone; Camacho, Oscar M.; McAughey, John; Gaça, Marianna

    2016-01-01

    Abstract Electronic cigarettes (E-cigarettes) are a potential means of addressing the harm to public health caused by tobacco smoking by offering smokers a less harmful means of receiving nicotine. As e-cigarettes are a relatively new phenomenon, there are limited scientific data on the longer-term health effects of their use. This study describes a robust in vitro method for assessing the cytotoxic response of e-cigarette aerosols that can be effectively compared with conventional cigarette smoke. This was measured using the regulatory accepted Neutral Red Uptake assay modified for air–liquid interface (ALI) exposures. An exposure system, comprising a smoking machine, traditionally used for in vitro tobacco smoke exposure assessments, was adapted for use with e-cigarettes to expose human lung epithelial cells at the ALI. Dosimetric analysis methods using real-time quartz crystal microbalances for mass, and post-exposure chemical analysis for nicotine, were employed to detect/distinguish aerosol dilutions from a reference Kentucky 3R4F cigarette and two commercially available e-cigarettes (Vype eStick and ePen). ePen aerosol induced 97%, 94% and 70% less cytotoxicity than 3R4F cigarette smoke based on matched EC50 values at different dilutions (1:5 vs. 1:153 vol:vol), mass (52.1 vs. 3.1 μg/cm2) and nicotine (0.89 vs. 0.27 μg/cm2), respectively. Test doses where cigarette smoke and e-cigarette aerosol cytotoxicity were observed are comparable with calculated daily doses in consumers. Such experiments could form the basis of a larger package of work including chemical analyses, in vitro toxicology tests and clinical studies, to help assess the safety of current and next generation nicotine and tobacco products. PMID:27690199

  16. Effect of cigarette smoke on seed germination.

    Science.gov (United States)

    Noble, R E

    2001-02-21

    The effect of cigarette smoke was studied on the germination of radish, kale, lettuce, amaranth, wheat, rice, barley and rye seeds. It was found that such smoke markedly retarded, in all cases, the rate of germination. Furthermore, cigarette smoke caused a retardation of the levels of certain enzymes (alpha-amylase or lysozyme) known to be significant in the germination of these seeds.

  17. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, Henrik; Juel, K

    2000-01-01

    We estimated the mortality from various diseases caused by cigarette smoking using two methods and compared the results. In one method, the "Prevent" model is used to simulate the effect on mortality of the prevalence of cigarette smoking derived retrospectively. The other method, suggested by R......, chronic bronchitis, emphysema, ischemic heart disease, and stroke were caused by cigarette smoking. In the method proposed by Peto et al, 35% of deaths among men and 25% of deaths among women from these causes were estimated to be attributable to cigarette smoking. The differences between the two methods...

  18. Effects of cigarette smoke exposure on nicotinic acetylcholine receptor subunits {alpha}7 and {beta}2 in the sudden infant death syndrome (SIDS) brainstem

    Energy Technology Data Exchange (ETDEWEB)

    Machaalani, Rita, E-mail: rita.machaalani@sydney.edu.au [Department of Medicine, The University of Sydney, NSW 2006 (Australia); Bosch Institute, The University of Sydney, NSW 2006 (Australia); The Children' s Hospital at Westmead, NSW 2145 (Australia); Say, Meichien [Department of Medicine, The University of Sydney, NSW 2006 (Australia); Bosch Institute, The University of Sydney, NSW 2006 (Australia); Waters, Karen A. [Department of Medicine, The University of Sydney, NSW 2006 (Australia); Bosch Institute, The University of Sydney, NSW 2006 (Australia); The Children' s Hospital at Westmead, NSW 2145 (Australia)

    2011-12-15

    It is postulated that nicotine, as the main neurotoxic constituent of cigarette smoke, influences SIDS risk through effects on nicotinic acetylcholine receptors (nAChRs) in brainstem nuclei that control respiration and arousal. This study compared {alpha}7 and {beta}2 nAChR subunit expression in eight nuclei of the caudal and rostral medulla and seven nuclei of the pons between SIDS (n = 46) and non-SIDS infants (n = 14). Evaluation for associations with known SIDS risk factors included comparison according to whether infants had a history of exposure to cigarette smoke in the home, and stratification for sleep position and gender. Compared to non-SIDS infants, SIDS infants had significantly decreased {alpha}7 in the caudal nucleus of the solitary tract (cNTS), gracile and cuneate nuclei, with decreased {beta}2 in the cNTS and increased {beta}2 in the facial. When considering only the SIDS cohort: 1-cigarette smoke exposure was associated with increased {alpha}7 in the vestibular nucleus and increased {beta}2 in the rostral dorsal motor nucleus of the vagus, rNTS and Cuneate, 2-there was a gender interaction for {alpha}7 in the gracile and cuneate, and {beta}2 in the cNTS and rostral arcuate nucleus, and 3-there was no effect of sleep position on {alpha}7, but prone sleep was associated with decreased {beta}2 in three nuclei of the pons. In conclusion, SIDS infants demonstrate differences in expression of {alpha}7 and {beta}2 nAChRs within brainstem nuclei that control respiration and arousal, which is independent on prior history of cigarette smoke exposure, especially for the NTS, with additional differences for smoke exposure ({beta}2), gender ({alpha}7 and {beta}2) and sleep position ({beta}2) evident. -- Highlights: Black-Right-Pointing-Pointer The 'normal' response to smoke exposure is decreased {alpha}7 and {beta}2 in certain nuclei. Black-Right-Pointing-Pointer SIDS infants have decreased {alpha}7 in cNTS, Grac and Cun. Black

  19. Metabonomic study of rats exposed to cigarette sidestream smoke

    Institute of Scientific and Technical Information of China (English)

    LIAN Wen-liu; SHI Xian-zhe; LUO Jia; REN Feng-lian

    2016-01-01

    A metabonomic approach was undertaken in order to detect urinary endogenous and exogenous metabolites and to evaluate the effects of passive exposure to cigarette sidestream smoke on rats. Urinary samples from three groups of rats were determined including control rats, rats treated with blended cigarettes (nonmenthol cigarettes) and rats treated with menthol cigarettes. The total urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), total 1-hydroxypyrene (1-HOP) and 3-hydroxybenzo[a] pyrene (3-HOBaP) were determined for assessing exposure to cigarette sidestream smoke toxins. Urinary endogenous metabolites in the three groups of rats were also analyzed and the data were processed by chemometrics. Eleven endogenous metabolites were found and identified. Their relative levels were compared among the three groups. The results show that cigarette sidestream smoke has complex effect on rats. Blended cigarette group makes difference to menthol cigarette group in the rats' urinary metabolic changes. Menthol adding to cigarettes has positive and negative effects on rats, respectively. The urinary metabolic profiling of menthol cigarette group is closer to that of control group.

  20. INDONESIAN YOUTH AND CIGARETTE SMOKING

    Directory of Open Access Journals (Sweden)

    Dwi Susilowati

    2012-11-01

    Full Text Available Background: The increasing number of children and young adults exposed to tobacco usage in the world is alarming. Indonesia is the third biggest tobacco consumer in the world after China and India. Smoking harms nearly every organ of the body, it reduce quality of life and life expectancy. Smoking causes illnesses, big economic lost and premature death. Tobacco use was the leading cause of preventable death. Smokers began at early age; they became the target of massive tobacco campaigns. Youth were vulnerable to tobacco advertising, once they began to smoke, it was difficult to quit. The Objectives of this paper is to identify tobacco usage among the Indonesian youth, to explore health problems, regulations related to tobacco consumption and efforts to implement the WHO Framework Convention on Tobacco Control. Methods: Method used is by reviewing studies and campaign information provided by researchers and practitioners in tobacco control programs. Result: Data shows that among people aged 10 to 24 years in Indonesia the current smokers were 23.7% daily smokers, 5.5% occasional smokers while the average cigarettes consumed daily were 12.2. Among lndonesian aged 13-15 years, there were 41% boys and 3.5% girls that were current cigarette smoking and 10.3% boys and 3,1% girls that had current tobacco other than cigarette. It is important that this preventable epidemic becomes a top public health issue in all countries. A complete ban on all tobacco advertising, promotion and sponsorship is a powerful tool to protect the world's youth and Indonesia should ratify tobacco ban. Key words: Indonesia, tobacco, youth, advertisement

  1. Cigarette Smoking and Urinary Organic Sulfides 

    Institute of Scientific and Technical Information of China (English)

    JIANLE; CAOWEN-JUN

    2000-01-01

    In order to observe how cigarette smoking influences levels of thio-thiazolidine-4-carboxylic acid(TTCA),high performance liquid chromatography(HPLC) was used to detect TTCA in urine from 18 healthy male volunteers.At the sme time,the total amout of urinary organic sulfides was determined by the iodine azide test(IAT).Nine of the volunteers had smoking higtories(5 to 10 cigarettes per day,as the smoking group),and the rest only occasionally smoke (1 to 2 cigarettes per month,as the control group).Samples were collected in the early morning (limosis)and 90 minutes after smoking a cigarette.Results showed that smoking a single cigaretter could elevate the level of urinary organic sulfides both in the smoking and control groups,while a smoking habit appeared to have no significant influence on the urinary organic sulfide level.No significant cumulative effect of cigarette smoking on urinary organic sulfides was found,The influence of cigarette on uinary organic sulfides was temporary.The results suggest that cigaretter smoking might be a confounding factor in biomontoring the levels of carbon disulfide in exposed workers.

  2. Current Cigarette Smoking Among Adults Infographic

    Data.gov (United States)

    U.S. Department of Health & Human Services — Explore the Current Cigarette Smoking Among Adults Infographic which outlines key facts related to current smoking among adults. For accessibility issues contact...

  3. Short-term cigarette smoke exposure induces reversible changes in energy metabolism and cellular redox status independent of inflammatory responses in mouse lungs.

    Science.gov (United States)

    Agarwal, Amit R; Zhao, Liqin; Sancheti, Harsh; Sundar, Isaac K; Rahman, Irfan; Cadenas, Enrique

    2012-11-15

    Cigarette smoking leads to alteration in cellular redox status, a hallmark in the pathogenesis of chronic obstructive pulmonary disease. This study examines the role of cigarette smoke (CS) exposure in the impairment of energy metabolism and, consequently, mitochondrial dysfunction. Male A/J mice were exposed to CS generated by a smoking machine for 4 or 8 wk. A recovery group was exposed to CS for 8 wk and allowed to recover for 2 wk. Acute CS exposure altered lung glucose metabolism, entailing a decrease in the rate of glycolysis and an increase in the pentose phosphate pathway, as evidenced by altered expression and activity of GAPDH and glucose-6-phosphate dehydrogenase, respectively. Impairment of GAPDH was found to be due to glutathionylation of its catalytic site cysteines. Metabolic changes were associated with changes in cellular and mitochondrial redox status, assessed in terms of pyridine nucleotides and glutathione. CS exposure elicited an upregulation of the expression of complexes II, III, IV, and V and of the activity of complexes II, IV, and V. Microarray analysis of gene expression in mouse lungs after exposure to CS for 8 wk revealed upregulation of a group of genes involved in metabolism, electron transfer chain, oxidative phosphorylation, mitochondrial transport and dynamics, and redox regulation. These changes occurred independently of inflammatory responses. These findings have implications for the early onset of alterations in energy and redox metabolism upon acute lung exposure to CS.

  4. Cigarette smoking and risk of ovarian cancer

    DEFF Research Database (Denmark)

    Faber, Mette T; Kjær, Susanne K; Dehlendorff, Christian;

    2013-01-01

    The majority of previous studies have observed an increased risk of mucinous ovarian tumors associated with cigarette smoking, but the association with other histological types is unclear. In a large pooled analysis, we examined the risk of epithelial ovarian cancer associated with multiple...... measures of cigarette smoking with a focus on characterizing risks according to tumor behavior and histology....

  5. Epigenetic Signatures of Cigarette Smoking

    NARCIS (Netherlands)

    R. Joehanes (Roby); Just, A.C. (Allan C.); R.E. Marioni (Riccardo); L.C. Pilling (Luke); L.M. Reynolds (Lindsay); Mandaviya, P.R. (Pooja R.); W. Guan (Weihua); Xu, T. (Tao); C.E. Elks (Cathy); Aslibekyan, S. (Stella); H. Moreno-Macías (Hortensia); J.A. Smith (Jennifer A); J. Brody (Jennifer); Dhingra, R. (Radhika); P. Yousefi (Paul); J.S. Pankow (James); Kunze, S. (Sonja); Shah, S.H. (Sonia H.); A.F. McRae (Allan F.); K. Lohman (Kurt); Sha, J. (Jin); D. Absher (Devin); L. Ferrucci (Luigi); Zhao, W. (Wei); E.W. Demerath (Ellen); J. Bressler (Jan); M.L. Grove (Megan); T. Huan (Tianxiao); C. Liu (Chunyu); Mendelson, M.M. (Michael M.); C. Yao (Chen); D.P. Kiel (Douglas P.); A. Peters (Annette); R. Wang-Sattler (Rui); P.M. Visscher (Peter); N.R. Wray (Naomi); J.M. Starr (John); Ding, J. (Jingzhong); Rodriguez, C.J. (Carlos J.); N.J. Wareham (Nick); Irvin, M.R. (Marguerite R.); Zhi, D. (Degui); M. Barrdahl (Myrto); P. Vineis (Paolo); Ambatipudi, S. (Srikant); A.G. Uitterlinden (André); A. Hofman (Albert); Schwartz, J. (Joel); Colicino, E. (Elena); Hou, L. (Lifang); Vokonas, P.S. (Pantel S.); D.G. Hernandez (Dena); A. Singleton (Andrew); S. Bandinelli (Stefania); S.T. Turner (Stephen); E.B. Ware (Erin B.); Smith, A.K. (Alicia K.); T. Klengel (Torsten); E.B. Binder (Elisabeth B.); B.M. Psaty (Bruce); K.D. Taylor (Kent); S.A. Gharib (Sina); Swenson, B.R. (Brenton R.); Liang, L. (Liming); D.L. Demeo (Dawn L.); G.T. O'Connor (George); Z. Herceg (Zdenko); Ressler, K.J. (Kerry J.); K.N. Conneely (Karen N.); N. Sotoodehnia (Nona); Kardia, S.L.R. (Sharon L. R.); D. Melzer (David); A.A. Baccarelli (Andrea A.); J.B.J. van Meurs (Joyce); I. Romieu (Isabelle); D.K. Arnett (Donna); Ong, K.K. (Ken K.); Y. Liu (Yongmei); M. Waldenberger (Melanie); I.J. Deary (Ian J.); M. Fornage (Myriam); D. Levy (Daniel); S.J. London (Stephanie J.)

    2016-01-01

    textabstractBackground-DNA methylation leaves a long-term signature of smoking exposure and is one potential mechanism by which tobacco exposure predisposes to adverse health outcomes, such as cancers, osteoporosis, lung, and cardiovascular disorders. Methods and Results-To comprehensively determine

  6. Do electronic cigarettes help with smoking cessation?

    Science.gov (United States)

    2014-11-01

    Smoking causes around 100,000 deaths each year in the UK, and is the leading cause of preventable disease and early mortality. Smoking cessation remains difficult and existing licensed treatments have limited success. Nicotine addiction is thought to be one of the primary reasons that smokers find it so hard to give up, and earlier this year DTB reviewed the effects of nicotine on health. Electronic cigarettes (e-cigarettes) are nicotine delivery devices that aim to mimic the process of smoking but avoid exposing the user to some of the harmful components of traditional cigarettes. However, the increase in the use of e-cigarettes and their potential use as an aid to smoking cessation has been subject to much debate. In this article we consider the regulatory and safety issues associated with the use of e-cigarettes, and their efficacy in smoking cessation and reduction.

  7. Short-Term Effects of Nose-Only Cigarette Smoke Exposure on Glutathione Redox Homeostasis, Cytochrome P450 1A1/2 and Respiratory Enzyme Activities in Mice Tissues

    Directory of Open Access Journals (Sweden)

    Haider Raza

    2013-05-01

    Full Text Available Background/Aims: The components of cigarette smoke (CS have been implicated in the development of cancer as well as in cardiopulmonary diseases. We have previously reported increased oxidative stress in rat tissues induced by tobacco-specific toxins nicotine and 4-(N-methyl-N-nitrosamino-1-(3-pyridyl-1-butanone (NNK. Recently, we have also shown increased oxidative stress and associated inflammatory responses in various tissues after exposure to cigarette smoke. Methods: In this study, we have further investigated the effects of nose-only cigarette smoke exposure on mitochondrial functions and glutathione-dependent redox metabolism in tissues of BALB/C mice. Liver, kidney, heart and lung tissues were analyzed for oxidative stress, glutathione (GSH and cytochrome P450 dependent enzyme activities and mitochondrial functions after exposure to smoke generated by 9 cigarettes/day for 4 days. Control mice were exposed to air only. Results: An increase in oxidative stress as observed by increased production of reactive oxygen species (ROS and altered GSH metabolism was apparent in all the tissues, but lung and heart appeared to be the main targets. Increased expression and activity of CYP450 1A1 and 1A2 were also observed in the tissues after exposure to cigarette smoke. Mitochondrial respiratory dysfunction in the tissues, as observed by alterations in the activities of Complex I and IV enzymes, was also observed after exposure to cigarette smoke. SDS-PAGE and Western blot results also indicate that alterations in the expression of enzyme proteins were in accordance with the changes in their catalytic functions. Conclusion: These results suggest that even short term exposure of cigarette smoke have adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking.

  8. Pressor effects of caffeine and cigarette smoking.

    Science.gov (United States)

    James, J E; Richardson, M

    1991-09-01

    Pressor effects of caffeine and cigarette smoking were examined in 15 normotensive young men and women. A cross-over design was used in which all subjects participated in four separate conditions: placebo alone, caffeine alone, placebo plus smoking, and caffeine plus smoking. Caffeine and smoking produced independent increases in systolic and diastolic blood pressure, and these effects were additive in the caffeine-plus-smoking condition. Heart rate was significantly increased by smoking but was essentially unaffected by caffeine.

  9. Dendritic cells induce Tc1 cell differentiation via the CD40/CD40L pathway in mice after exposure to cigarette smoke.

    Science.gov (United States)

    Kuang, Liang-Jian; Deng, Ting-Ting; Wang, Qin; Qiu, Shi-Lin; Liang, Yi; He, Zhi-Yi; Zhang, Jian-Quan; Bai, Jing; Li, Mei-Hua; Deng, Jing-Min; Liu, Guang-Nan; Liu, Ji-Feng; Zhong, Xiao-Ning

    2016-09-01

    Dendritic cells and CD8(+) T cells participate in the pathology of chronic obstructive pulmonary disease, including emphysema, but little is known of the involvement of the CD40/CD40L pathway. We investigated the role of the CD40/CD40L pathway in Tc1 cell differentiation induced by dendritic cells in a mouse model of emphysema, and in vitro. C57BL/6J wild-type and CD40(-/-) mice were exposed to cigarette smoke (CS) or not (control), for 24 wk. In vitro experiments involved wild-type and CD40(-/-) dendritic cells treated with CS extract (CSE) or not. Compared with the control groups, the CS mice (both wild type and CD40(-/-)) had a greater percentage of lung dendritic cells and higher levels of major histocompatability complex (MHC) class I molecules and costimulatory molecules CD40 and CD80. Relative to the CS CD40(-/-) mice, the CS wild type showed greater signs of lung damage and Tc1 cell differentiation. In vitro, the CSE-treated wild-type cells evidenced more cytokine release (IL-12/p70) and Tc1 cell differentiation than did the CSE-treated CD40(-/-) cells. Exposure to cigarette smoke increases the percentage of lung dendritic cells and promotes Tc1 cell differentiation via the CD40/CD40L pathway. Blocking the CD40/CD40L pathway may suppress development of emphysema in mice exposed to cigarette smoke.

  10. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, H; Juel, K

    2000-01-01

    We estimated the mortality from various diseases caused by cigarette smoking using two methods and compared the results. In one method, the "Prevent" model is used to simulate the effect on mortality of the prevalence of cigarette smoking derived retrospectively. The other method, suggested by R....... Peto et al (Lancet 1992;339:1268-1278), requires data on mortality from lung cancer among people who have never smoked and among smokers, but it does not require data on the prevalence of smoking. In the Prevent model, 33% of deaths among men and 23% of those among women in 1993 from lung cancer......, chronic bronchitis, emphysema, ischemic heart disease, and stroke were caused by cigarette smoking. In the method proposed by Peto et al, 35% of deaths among men and 25% of deaths among women from these causes were estimated to be attributable to cigarette smoking. The differences between the two methods...

  11. Efectos de la exposición a humo de tabaco sobre el asma bronquial en la infancia Effects of cigarette smoke exposure on child asthma

    Directory of Open Access Journals (Sweden)

    PEDRO AGUILAR M

    2008-01-01

    Full Text Available El consumo de tabaco en la población infantil representa un problema de salud pública significativo en diversas partes del mundo. En Sudamérica, Chile ocupa el primer lugar en consumo de tabaco infantil, pese a las campañas sanitarias implementadas para evitarlo. Los efectos dañinos del humo de tabaco, activo y pasivo, afectan al ser humano a lo largo de toda la vida, desde el período intrauterino. El objetivo del presente trabajo es revisar algunos tópicos referentes al efecto del tabaco sobre el asma bronquial en la niñezCigarette smoking in children represents a major public health problem, all over the world. In South America, Chile occupies the first place in cigarette comsuption by children, even though many campaigns exist to avoid it. The devastating effect of tobacco exposure starts in fetal life and continues through lifetime. We present some main features in child asthma related to active and passive exposure to cigarette smoke

  12. Perinatal outcomes following maternal asthma and cigarette smoking during pregnancy.

    Science.gov (United States)

    Hodyl, Nicolette A; Stark, Michael J; Scheil, Wendy; Grzeskowiak, Luke E; Clifton, Vicki L

    2014-03-01

    Does cigarette smoking in pregnancy explain the increased risk of adverse perinatal outcomes that occur with maternal asthma or does it compound the effect? Using population based birth records, a retrospective analysis was conducted of all singleton pregnancies in South Australia over 10 years (1999-2008; n=172 305), examining maternal asthma, cigarette smoking and quantity of smoking to estimate odds ratios. Compared with nonasthmatic females who did not smoke during pregnancy, both asthmatic females who smoked and those who did not smoke during pregnancy had a significantly increased risk of gestational diabetes, antepartum haemorrhage, polyhydramnios, premature rupture of membranes, emergency Caesarean section, and the child being small for gestational age and having congenital abnormalities. These associations suggest that asthma, independently of maternal smoking, increases the risk of these adverse perinatal outcomes. Maternal smoking was itself associated with an increased risk of a number of poor neonatal outcomes, with a dose-response relationship observed. Notably, maternal asthma combined with cigarette smoking significantly increased the risk of preterm birth and urinary tract infections to a greater degree than with either exposure alone. Maternal asthma and cigarette smoking during pregnancy are both independently associated with adverse perinatal outcomes and, combined, compound the risk of preterm birth and urinary tract infections.

  13. Carbon monoxide kinetics following simulated cigarette smoking

    Energy Technology Data Exchange (ETDEWEB)

    Karnik, A.S. (Wayne State Univ., Detroit, MI); Coin, E.J.

    1980-05-01

    Carbon monoxide kinetics were measured in the blood (% carboxyhemoglobin) and alveolar phase (ppM carbon monoxide) after simulated cigarette smoking. Cigarette smoking was siumlated using the same amount of carbon monoxide that 2R1F cigarettes manufactured by the Tobacco Research Institute would contain. Ten boluses of air containing carbon monoxide equivalent to smoking one cigarette were inhaled by six healthy nonsmoker volunteers. Carbon monoxide in the air phase was measured by an Ecolyzer and carboxyhemoglobin was measured by a CO-Oximeter. The mean rise in alveolar carbon monoxide immediately and 20 min after inhaling the last bolus was 3.3 and 3.1 ppM, respectively (p<.005). The mean rise in carboxyhemoglobin immediately and 20 min after inhalation of the last bolus was 0.8 and 0.5% respectively (P<.005). The changes in carboxyhemoglobin were found to be similar to changes that occur when one cigarette is actually smoked.

  14. The p-ERK–p-c-Jun–cyclinD1 pathway is involved in proliferation of smooth muscle cells after exposure to cigarette smoke extract

    Energy Technology Data Exchange (ETDEWEB)

    Li, Tianjia [Department of Vascular surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 5 Dong Dan San Tiao, Beijing 100005 (China); Song, Ting [Nursing Department of Orthopedics 3rd Ward, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 5 Dong Dan San Tiao, Beijing 100005 (China); Ni, Leng; Yang, Genhuan; Song, Xitao; Wu, Lifei [Department of Vascular surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 5 Dong Dan San Tiao, Beijing 100005 (China); Liu, Bao, E-mail: liubao72@yahoo.com.cn [Department of Vascular surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 5 Dong Dan San Tiao, Beijing 100005 (China); Liu, Changwei, E-mail: liucw@vip.sina.com [Department of Vascular surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 5 Dong Dan San Tiao, Beijing 100005 (China)

    2014-10-24

    Highlights: • Smooth muscle cells proliferated after exposure to cigarette smoke extract. • The p-ERK, p-c-Jun, and cyclinD1 expressions increased in the process. • The p-ERK inhibitor, U0126, can reverse these effects. • The p-ERK → p-c-Jun → cyclinD1 pathway is involved in the process. - Abstract: An epidemiological survey has shown that smoking is closely related to atherosclerosis, in which excessive proliferation of vascular smooth muscle cells (SMCs) plays a key role. To investigate the mechanism underlying this unusual smoking-induced proliferation, cigarette smoke extract (CSE), prepared as smoke-bubbled phosphate-buffered saline (PBS), was used to induce effects mimicking those exerted by smoking on SMCs. As assessed by Cell Counting Kit-8 detection (an improved MTT assay), SMC viability increased significantly after exposure to CSE. Western blot analysis demonstrated that p-ERK, p-c-Jun, and cyclinD1 expression increased. When p-ERK was inhibited using U0126 (inhibitor of p-ERK), cell viability decreased and the expression of p-c-Jun and cyclinD1 was reduced accordingly, suggesting that p-ERK functions upstream of p-c-Jun and cyclinD1. When a c-Jun over-expression plasmid was transfected into SMCs, the level of cyclinD1 in these cells increased. Moreover, when c-Jun was knocked down by siRNA, cyclinD1 levels decreased. In conclusion, our findings indicate that the p-ERK–p-c-Jun–cyclinD1 pathway is involved in the excessive proliferation of SMCs exposed to CSE.

  15. Cigarette smoke affects bonding to dentin.

    Science.gov (United States)

    Almeida e Silva, Junio S; de Araujo, Edson Medeiro; Araujo, Elito

    2010-01-01

    This in vitro study evaluated the microtensile bond strength (muTBS) of composite resin bonded to dentin that had been contaminated by cigarette smoke. Ten extracted unerupted human third molars were used: Six molars were prepared for muTBS testing, while the other four molars were assigned to pre- and post-etching scanning electronic microscopy (SEM) analysis. The 20 specimens obtained from the 10 coronal portions were distributed into two experimental groups so that each tooth served as its own control. Group 1 underwent a daily toothbrushing simulation and exposure to a smoking simulation chamber, while Group 2 received only a daily simulated toothbrushing. Student's t-test demonstrated that Group 1 samples demonstrated significantly lower bond strength (49.58 MPa) than Group 2 samples (58.48 MPa). Pre and postetching SEM analysis revealed the presence of contaminants on the dentinal surfaces of the Group 1 specimens. It was concluded that contamination by cigarette smoke decreases the bond strength between dentin and composite resin.

  16. Effects of cigarette smoking on erectile dysfunction.

    Science.gov (United States)

    Kovac, J R; Labbate, C; Ramasamy, R; Tang, D; Lipshultz, L I

    2015-12-01

    Cigarette smoking is a leading cause of preventable morbidity and mortality in the United States. Although public policies have resulted in a decreased number of new smokers, smoking rates remain stubbornly high in certain demographics with 20% of all American middle-aged men smoking. In addition to the well-established harmful effects of smoking (i.e. coronary artery disease and lung cancer), the past three decades have led to a compendium of evidence being compiled into the development of a relationship between cigarette smoking and erectile dysfunction. The main physiologic mechanism that appears to be affected includes the nitric oxide signal transduction pathway. This review details the recent literature linking cigarette smoking to erectile dysfunction, epidemiological associations, dose dependency and the effects of smoking cessation on improving erectile quality.

  17. Bacoside A: Role in Cigarette Smoking Induced Changes in Brain

    Directory of Open Access Journals (Sweden)

    G. Vani

    2015-01-01

    Full Text Available Cigarette smoking (CS is a major health hazard that exerts diverse physiologic and biochemical effects mediated by the components present and generated during smoking. Recent experimental studies have shown predisposition to several biological consequences from both active and passive cigarette smoke exposure. In particular, passive smoking is linked to a number of adverse health effects which are equally harmful as active smoking. A pragmatic approach should be considered for designing a pharmacological intervention to combat the adverse effects of passive smoking. This review describes the results from a controlled experimental condition, testing the effect of bacoside A (BA on the causal role of passive/secondhand smoke exposure that caused pathological and neurological changes in rat brain. Chronic exposure to cigarette smoke induced significant changes in rat brain histologically and at the neurotransmitter level, lipid peroxidation states, mitochondrial functions, membrane alterations, and apoptotic damage in rat brain. Bacoside A is a neuroactive agent isolated from Bacopa monnieri. As a neuroactive agent, BA was effective in combating these changes. Future research should examine the effects of BA at molecular level and assess its functional effects on neurobiological and behavioral processes associated with passive smoke.

  18. Bacoside A: Role in Cigarette Smoking Induced Changes in Brain.

    Science.gov (United States)

    Vani, G; Anbarasi, K; Shyamaladevi, C S

    2015-01-01

    Cigarette smoking (CS) is a major health hazard that exerts diverse physiologic and biochemical effects mediated by the components present and generated during smoking. Recent experimental studies have shown predisposition to several biological consequences from both active and passive cigarette smoke exposure. In particular, passive smoking is linked to a number of adverse health effects which are equally harmful as active smoking. A pragmatic approach should be considered for designing a pharmacological intervention to combat the adverse effects of passive smoking. This review describes the results from a controlled experimental condition, testing the effect of bacoside A (BA) on the causal role of passive/secondhand smoke exposure that caused pathological and neurological changes in rat brain. Chronic exposure to cigarette smoke induced significant changes in rat brain histologically and at the neurotransmitter level, lipid peroxidation states, mitochondrial functions, membrane alterations, and apoptotic damage in rat brain. Bacoside A is a neuroactive agent isolated from Bacopa monnieri. As a neuroactive agent, BA was effective in combating these changes. Future research should examine the effects of BA at molecular level and assess its functional effects on neurobiological and behavioral processes associated with passive smoke.

  19. Tobacco smoking and its consequences on reproductive health: the impact of a lifestyle choices including cigarette smoke exposure on fertility and birth defects.

    Science.gov (United States)

    Merritt, Travis; Mazela, Jan; Merritt, Allen

    2013-01-01

    There are several life style choices which may impact fertility and thus national birth rate. Epidemiological cohort studies indicates that modification of life style habits, among them nicotine consumption can influence reproductive health. Influence of tobacco smoking on reproductive health has to be analyzed within the context of the influence of body mass index, caffeine and alcohol consumption, exercise, maternal and paternal age, and stress. Approximately 27% Polish women and 23% Americans smoke cigarettes during their reproductive years. Cohort studies directly showed the relationship between nicotine consumption and decrease in fertility among smoking women. Besides there is evidence that smoking leads to higher rate of congenital heart defects, limbs abnormalities, central nervous malformations among infants born to smoking mothers. Finally, the relationship between smoking and decreased fertility should be of great concern since Polish fertility rate has dropped from 1989 till 2007 year from 2,1 to 1,27 respectively. Programs focused on improvement in national birth rate should focus also on decrease smoking rates among women.

  20. Women, smoking, cigarette advertising and cancer.

    Science.gov (United States)

    Ernster, V L

    1986-01-01

    Cigarette smoking is a major cause of cancer in women, accounting for about one-fourth of their estimated 219,000 cancer deaths per year. Cigarette smoking specifically increases a woman's risk of developing cancer of the lung, larynx, esophagus, oral cavity, pancreas, kidney, bladder, and possibly uterine cervix. During the past twenty years, concerted efforts have been made by the tobacco industry to increase sales to women. Strategies have included development of "feminine" brands such as Virginia Slims, slick media campaigns portraying smoking as elegant and glamorous, and sponsorship of fashion, women's sports events, and even medical programs. Reversal of these alarming trends requires that women as well as men recognize the role of cigarette smoking in cancer causation, and support programs which promote non-smoking as well as combat the influence of the tobacco industry on women's smoking behavior.

  1. The effect of cigarette smoke and arsenic exposure on urothelial carcinoma risk is modified by glutathione S-transferase M1 gene null genotype

    Energy Technology Data Exchange (ETDEWEB)

    Chung, Chi-Jung [Department of Health Risk Management, College of Public Health, China Medical University, Taichung, Taiwan (China); Department of Medical Research, China Medical University Hospital, Taichung, Taiwan (China); Huang, Chao-Yuan; Pu, Yeong-Shiau [Department of Urology, National Taiwan University Hospital, Taipei, Taiwan (China); Shiue, Horng-Sheng [Department of Chinese Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan (China); Su, Chien-Tien [Department of Family Medicine, Taipei Medical University Hospital, Taipei, Taiwan (China); Hsueh, Yu-Mei, E-mail: ymhsueh@tmu.edu.tw [Department of Public Health, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan (China); School of Public Health, College of Public Health and Nutrition, Taipei Medical University, Taipei, Taiwan (China)

    2013-01-15

    Inter-individual variation in the metabolism of xenobiotics, caused by factors such as cigarette smoking or inorganic arsenic exposure, is hypothesized to be a susceptibility factor for urothelial carcinoma (UC). Therefore, our study aimed to evaluate the role of gene–environment interaction in the carcinogenesis of UC. A hospital-based case–control study was conducted. Urinary arsenic profiles were measured using high-performance liquid chromatography–hydride generator-atomic absorption spectrometry. Genotyping was performed using a polymerase chain reaction-restriction fragment length polymorphism technique. Information about cigarette smoking exposure was acquired from a lifestyle questionnaire. Multivariate logistic regression was applied to estimate the UC risk associated with certain risk factors. We found that UC patients had higher urinary levels of total arsenic, higher percentages of inorganic arsenic (InAs%) and monomethylarsonic acid (MMA%) and lower percentages of dimethylarsinic acid (DMA%) compared to controls. Subjects carrying the GSTM1 null genotype had significantly increased UC risk. However, no association was observed between gene polymorphisms of CYP1A1, EPHX1, SULT1A1 and GSTT1 and UC risk after adjustment for age and sex. Significant gene–environment interactions among urinary arsenic profile, cigarette smoking, and GSTM1 wild/null polymorphism and UC risk were observed after adjustment for potential risk factors. Overall, gene–environment interactions simultaneously played an important role in UC carcinogenesis. In the future, large-scale studies should be conducted using tag-SNPs of xenobiotic-metabolism-related enzymes for gene determination. -- Highlights: ► Subjects with GSTM1 null genotype had significantly increased UC risk. ► UC patients had poor arsenic metabolic ability compared to controls. ► GSTM1 null genotype may modify arsenic related UC risk.

  2. Black tea prevents cigarette smoke-induced apoptosis and lung damage

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    Chattopadhyay Dhrubajyoti

    2007-02-01

    Full Text Available Abstract Background Cigarette smoking is a major cause of lung damage. One prominent deleterious effect of cigarette smoke is oxidative stress. Oxidative stress may lead to apoptosis and lung injury. Since black tea has antioxidant property, we examined the preventive effect of black tea on cigarette smoke-induced oxidative damage, apoptosis and lung injury in a guinea pig model. Methods Guinea pigs were subjected to cigarette smoke exposure from five cigarettes (two puffs/cigarette per guinea pig/day for seven days and given water or black tea to drink. Sham control guinea pigs were exposed to air instead of cigarette smoke. Lung damage, as evidenced by inflammation and increased air space, was assessed by histology and morphometric analysis. Protein oxidation was measured through oxyblot analysis of dinitrophenylhydrazone derivatives of the protein carbonyls of the oxidized proteins. Apoptosis was evidenced by the fragmentation of DNA using TUNEL assay, activation of caspase 3, phosphorylation of p53 as well as over-expression of Bax by immunoblot analyses. Results Cigarette smoke exposure to a guinea pig model caused lung damage. It appeared that oxidative stress was the initial event, which was followed by inflammation, apoptosis and lung injury. All these pathophysiological events were prevented when the cigarette smoke-exposed guinea pigs were given black tea infusion as the drink instead of water. Conclusion Cigarette smoke exposure to a guinea pig model causes oxidative damage, inflammation, apoptosis and lung injury that are prevented by supplementation of black tea.

  3. Menthol Cigarettes, Time to First Cigarette, and Smoking Cessation

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    Sanders Edward

    2017-01-01

    Full Text Available The goal of the present work is to determine if menthol and non-menthol cigarette smokers differ with respect to time to first cigarette (TTFC and successful smoking cessation via a meta-analysis of published results. For 13 independent estimates, menthol smokers were slightly but statistically significantly more likely to exhibit TTFC ≤ 5 min (random-effects odds ratio (OR = 1.12; 95% confidence interval (CI, 1.04–1.21, while 17 independent estimates provided a non-significant difference for TTFC ≤ 30 min (random-effects OR = 1.06; 95% CI, 0.96–1.16. For cessation studies, meta-analysis of 30 published estimates indicated a decreased likelihood for menthol cigarette smokers to quit (random-effects OR = 0.87; 95% CI, 0.80–0.96. There was no difference between cessation rates for Caucasian menthol and non-menthol cigarette smokers, but the results support that African American menthol cigarette smokers find it more difficult to quit. Adjustment of cessation for socioeconomic status eliminated any statistically significant advantage for smoking cessation in non-menthol smokers. In conclusion, these results suggest that the observed differences in cessation rates between menthol and non-menthol cigarette smokers are likely explained by differences in socioeconomic status and also suggest that TTFC may not be a robust predictor of successful smoking cessation.

  4. Cigarette Smoking and Electronic Cigarettes Use: A Meta-Analysis

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    Meng Wang

    2016-01-01

    Full Text Available Increasing evidence indicates that cigarette smoking is a strong predictor of electronic cigarettes (e-cigarettes use, particularly in adolescents, yet the effects has not be systematically reviewed and quantified. Relevant studies were retrieved by searching three databases up to June 2015. The meta-analysis results were presented as pooled odds ratios (ORs with 95% confidence intervals (CIs calculated by a random-effects model. Current smokers were more likely to use e-cigarette currently (OR: 14.89, 95% CI: 7.70–28.78 and the probability was greater in adolescents than in adults (39.13 vs. 7.51. The probability of ever e-cigarettes use was significantly increased in smokers (OR: 14.67, 95% CI: 11.04–19.49. Compared with ever smokers and adults, the probabilities were much greater in current smokers (16.10 vs. 9.47 and adolescents (15.19 vs. 14.30, respectively. Cigarette smoking increases the probability of e-cigarettes use, especially in current smokers and adolescents.

  5. Cigarette Smoking and Electronic Cigarettes Use: A Meta-Analysis.

    Science.gov (United States)

    Wang, Meng; Wang, Jian-Wei; Cao, Shuang-Shuang; Wang, Hui-Qin; Hu, Ru-Ying

    2016-01-12

    Increasing evidence indicates that cigarette smoking is a strong predictor of electronic cigarettes (e-cigarettes) use, particularly in adolescents, yet the effects has not be systematically reviewed and quantified. Relevant studies were retrieved by searching three databases up to June 2015. The meta-analysis results were presented as pooled odds ratios (ORs) with 95% confidence intervals (CIs) calculated by a random-effects model. Current smokers were more likely to use e-cigarette currently (OR: 14.89, 95% CI: 7.70-28.78) and the probability was greater in adolescents than in adults (39.13 vs. 7.51). The probability of ever e-cigarettes use was significantly increased in smokers (OR: 14.67, 95% CI: 11.04-19.49). Compared with ever smokers and adults, the probabilities were much greater in current smokers (16.10 vs. 9.47) and adolescents (15.19 vs. 14.30), respectively. Cigarette smoking increases the probability of e-cigarettes use, especially in current smokers and adolescents.

  6. Effects of maternal inflammation and exposure to cigarette smoke on birth weight and delivery of preterm babies in a cohort of Indigenous Australian women

    Directory of Open Access Journals (Sweden)

    Kirsty ePringle

    2015-03-01

    Full Text Available Sudden Infant Death Syndrome (SIDS, neonatal deaths and deaths from infection are higher among Indigenous Australians. This study aimed to determine the effects of inflammatory responses and exposure to cigarette smoke, two important factors associated with sudden death in infancy, on preterm birth and birth weight in a cohort of Indigenous mothers.Indigenous Australian women (n=131 were recruited as part of a longitudinal study while attending antenatal care clinics during pregnancy; blood samples were collected up to 3 times in pregnancy. Serum cotinine, indicating exposure to smoke, was detected in 50.4% of mothers. Compared with non-Indigenous women, the cohort had 10 times the prevalence of antibodies to Helicobacter pylori (33% v. 3%. Levels of IgG, antibodies to H. pylori and C- reactive protein (CRP were all inversely correlated with gestational age (P < 0.05. CRP levels were positively associated with maternal body mass index (BMI (r = 0.449, P = 0.001.The effects of cigarette smoke (cotinine and inflammation (CRP were assessed in relation to risk factors for SIDS: gestational age at delivery and birth weight. Serum cotinine levels were negatively associated with birth weight (r = -0.37, P < 0.001, this correlation held true for both male (r = -0.39, P = 0.002 and female (r = -0.30, P = 0.017 infants. Cotinine was negatively associated with gestational age at delivery (r = -0.199, P = 0.023. When assessed by fetal sex this was significant only for males (r = -0.327, P = 0.011. CRP was negatively associated with gestational age at delivery for female infants (r = -0.46, P < 0.001. In contrast maternal BMI was significantly correlated with birth weight.These data highlight the importance of putting programs in place to reduce cigarette smoke exposure in pregnancy and to treat women with chronic infections such as H. pylori to improve pregnancy outcomes and decrease risk factors for sudden death in infancy.

  7. Through the smoke: Use of in vivo and in vitro cigarette smoking models to elucidate its effect on female fertility

    Energy Technology Data Exchange (ETDEWEB)

    Camlin, Nicole J. [School of Environment and Life Sciences, University of Newcastle, Callaghan, NSW 2308 (Australia); McLaughlin, Eileen A., E-mail: eileen.mclaughlin@newcastle.edu.au [School of Environment and Life Sciences, University of Newcastle, Callaghan, NSW 2308 (Australia); Holt, Janet E. [School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308 (Australia)

    2014-12-15

    A finite number of oocytes are established within the mammalian ovary prior to birth to form a precious ovarian reserve. Damage to this limited pool of gametes by environmental factors such as cigarette smoke and its constituents therefore represents a significant risk to a woman's reproductive capacity. Although evidence from human studies to date implicates a detrimental effect of cigarette smoking on female fertility, these retrospective studies are limited and present conflicting results. In an effort to more clearly understand the effect of cigarette smoke, and its chemical constituents, on female fertility, a variety of in vivo and in vitro animal models have been developed. This article represents a systematic review of the literature regarding four of experimental model types: 1) direct exposure of ovarian cells and follicles to smoking constituents’ in vitro, 2) direct exposure of whole ovarian tissue with smoking constituents in vitro, 3) whole body exposure of animals to smoking constituents and 4) whole body exposure of animals to cigarette smoke. We summarise key findings and highlight the strengths and weaknesses of each model system, and link these to the molecular mechanisms identified in smoke-induced fertility changes. - Highlights: • In vivo exposure to individual cigarette smoke chemicals alters female fertility. • The use of in vitro models in determining molecular mechanisms • Whole cigarette smoke inhalation animal models negatively affect ovarian function.

  8. Chronic exposure to cigarette smoke during gestation results in altered cholinesterase enzyme activity and behavioral deficits in adult rat offspring: potential relevance to schizophrenia.

    Science.gov (United States)

    Zugno, Alexandra I; Fraga, Daiane B; De Luca, Renata D; Ghedim, Fernando V; Deroza, Pedro F; Cipriano, Andreza L; Oliveira, Mariana B; Heylmann, Alexandra S A; Budni, Josiane; Souza, Renan P; Quevedo, João

    2013-06-01

    Prenatal cigarette smoke exposure (PCSE) has been associated with physiological and developmental changes that may be related to an increased risk for childhood and adult neuropsychiatric diseases. The present study investigated locomotor activity and cholinesterase enzyme activity in rats, following PCSE and/or ketamine treatment in adulthood. Pregnant female Wistar rats were exposed to 12 commercially filtered cigarettes per day for a period of 28 days. We evaluated motor activity and cholinesterase activity in the brain and serum of adult male offspring that were administered acute subanesthetic doses of ketamine (5, 15 and 25 mg/kg), which serves as an animal model of schizophrenia. To determine locomotor activity, we used the open field test. Cholinesterase activity was assessed by hydrolysis monitored spectrophotometrically. Our results show that both PCSE and ketamine treatment in the adult offspring induced increase of locomotor activity. Additionally, it was observed increase of acetylcholinesterase and butyrylcholinesterase activity in the brain and serum, respectively. We demonstrated that animals exposed to cigarettes in the prenatal period had increased the risk for psychotic symptoms in adulthood. This also occurs in a dose-dependent manner. These changes provoke molecular events that are not completely understood and may result in abnormal behavioral responses found in neuropsychiatric disorders, such as schizophrenia.

  9. Menthol attenuates respiratory irritation and elevates blood cotinine in cigarette smoke exposed mice.

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    Michael A Ha

    Full Text Available Addition of menthol to cigarettes may be associated with increased initiation of smoking. The potential mechanisms underlying this association are not known. Menthol, likely due to its effects on cold-sensing peripheral sensory neurons, is known to inhibit the sensation of irritation elicited by respiratory irritants. However, it remains unclear whether menthol modulates cigarette smoke irritancy and nicotine absorption during initial exposures to cigarettes, thereby facilitating smoking initiation. Using plethysmography in a C57Bl/6J mouse model, we examined the effects of L-menthol, the menthol isomer added to cigarettes, on the respiratory sensory irritation response to primary smoke irritants (acrolein and cyclohexanone and smoke of Kentucky reference 2R4 cigarettes. We also studied L-menthol's effect on blood levels of the nicotine metabolite, cotinine, immediately after exposure to cigarette smoke. L-menthol suppressed the irritation response to acrolein with an apparent IC₅₀ of 4 ppm. Suppression was observed even at acrolein levels well above those necessary to produce a maximal response. Cigarette smoke, at exposure levels of 10 mg/m³ or higher, caused an immediate and marked sensory irritation response in mice. This response was significantly suppressed by L-menthol even at smoke concentrations as high as 300 mg/m³. Counterirritation by L-menthol was abolished by treatment with a selective inhibitor of Transient Receptor Potential Melastatin 8 (TRPM8, the neuronal cold/menthol receptor. Inclusion of menthol in the cigarette smoke resulted in roughly a 1.5-fold increase in plasma cotinine levels over those observed in mice exposed to smoke without added menthol. These findings document that, L-menthol, through TRPM8, is a strong suppressor of respiratory irritation responses, even during highly noxious exposures to cigarette smoke or smoke irritants, and increases blood cotinine. Therefore, L-menthol, as a cigarette additive, may

  10. Menthol attenuates respiratory irritation and elevates blood cotinine in cigarette smoke exposed mice.

    Science.gov (United States)

    Ha, Michael A; Smith, Gregory J; Cichocki, Joseph A; Fan, Lu; Liu, Yi-Shiuan; Caceres, Ana I; Jordt, Sven Eric; Morris, John B

    2015-01-01

    Addition of menthol to cigarettes may be associated with increased initiation of smoking. The potential mechanisms underlying this association are not known. Menthol, likely due to its effects on cold-sensing peripheral sensory neurons, is known to inhibit the sensation of irritation elicited by respiratory irritants. However, it remains unclear whether menthol modulates cigarette smoke irritancy and nicotine absorption during initial exposures to cigarettes, thereby facilitating smoking initiation. Using plethysmography in a C57Bl/6J mouse model, we examined the effects of L-menthol, the menthol isomer added to cigarettes, on the respiratory sensory irritation response to primary smoke irritants (acrolein and cyclohexanone) and smoke of Kentucky reference 2R4 cigarettes. We also studied L-menthol's effect on blood levels of the nicotine metabolite, cotinine, immediately after exposure to cigarette smoke. L-menthol suppressed the irritation response to acrolein with an apparent IC₅₀ of 4 ppm. Suppression was observed even at acrolein levels well above those necessary to produce a maximal response. Cigarette smoke, at exposure levels of 10 mg/m³ or higher, caused an immediate and marked sensory irritation response in mice. This response was significantly suppressed by L-menthol even at smoke concentrations as high as 300 mg/m³. Counterirritation by L-menthol was abolished by treatment with a selective inhibitor of Transient Receptor Potential Melastatin 8 (TRPM8), the neuronal cold/menthol receptor. Inclusion of menthol in the cigarette smoke resulted in roughly a 1.5-fold increase in plasma cotinine levels over those observed in mice exposed to smoke without added menthol. These findings document that, L-menthol, through TRPM8, is a strong suppressor of respiratory irritation responses, even during highly noxious exposures to cigarette smoke or smoke irritants, and increases blood cotinine. Therefore, L-menthol, as a cigarette additive, may promote smoking

  11. Development of nitroxide radicals-containing polymer for scavenging reactive oxygen species from cigarette smoke

    Science.gov (United States)

    Yoshitomi, Toru; Kuramochi, Kazuhiro; Binh Vong, Long; Nagasaki, Yukio

    2014-06-01

    We developed a nitroxide radicals-containing polymer (NRP), which is composed of poly(4-methylstyrene) possessing nitroxide radicals as a side chain via amine linkage, to scavenge reactive oxygen species (ROS) from cigarette smoke. In this study, the NRP was coated onto cigarette filters and its ROS-scavenging activity from streaming cigarette smoke was evaluated. The intensity of electron spin resonance signals of the NRP in the filter decreased after exposure to cigarette smoke, indicating consumption of nitroxide radicals. To evaluate the ROS-scavenging activity of the NRP-coated filter, the amount of peroxy radicals in an extract of cigarette smoke was measured using UV-visible spectrophotometry and 1,1-diphenyl-2-picrylhydrazyl (DPPH). The absorbance of DPPH at 517 nm decreased with exposure to cigarette smoke. When NRP-coated filters were used, the decrease in the absorbance of DPPH was prevented. In contrast, both poly[4-(cyclohexylamino)methylstyrene]- and poly(acrylic acid)-coated filters, which have no nitroxide radical, did not show any effect, indicating that the nitroxide radicals in the NRP scavenge the ROS in cigarette smoke. As a result, the extract of cigarette smoke passed through the NRP-coated filter has a lower cellular toxicity than smoke passed through poly[4-(cyclohexylamino)methylstyrene]- and poly(acrylic acid)-coated filters. Accordingly, NRP is a promising material for ROS scavenging from cigarette smoke.

  12. Cigarette smoking and poverty in China.

    Science.gov (United States)

    Liu, Yuanli; Rao, Keqin; Hu, Teh-Wei; Sun, Qi; Mao, Zhenzhong

    2006-12-01

    Drawing on the 1998 China national health services survey data, this study estimated the poverty impact of two smoking-related expenses: excessive medical spending attributable to smoking and direct spending on cigarettes. The excessive medical spending attributable to smoking is estimated using a regression model of medical expenditure with smoking status (current smoker, former smoker, never smoker) as part of the explanatory variables, controlling for people's demographic and socioeconomic characteristics. The poverty impact is measured by the changes in the poverty head count, after smoking-related expenses are subtracted from income. We found that the excessive medical spending attributable to smoking may have caused the poverty rate to increase by 1.5% for the urban population and by 0.7% for the rural population. To a greater magnitude, the poverty headcount in urban and rural areas increased by 6.4% and 1.9%, respectively, due to the direct household spending on cigarettes. Combined, the excessive medical spending attributable to smoking and consumption spending on cigarettes are estimated to be responsible for impoverishing 30.5 million urban residents and 23.7 million rural residents in China. Smoking related expenses pushed a significant proportion of low-income families into poverty in China. Therefore, reducing the smoking rate appears to be not only a public health strategy, but also a poverty reduction strategy.

  13. The Effect of Cigarette Smoke Exposure on the Development of Inflammation in Lungs, Gut and Joints of TNFΔARE Mice.

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    Liesbeth Allais

    Full Text Available The inflammatory cytokine TNF-α is a central mediator in many immune-mediated diseases, such as Crohn's disease (CD, spondyloarthritis (SpA and chronic obstructive pulmonary disease (COPD. Epidemiologic studies have shown that cigarette smoking (CS is a prominent common risk factor in these TNF-dependent diseases. We exposed TNFΔARE mice; in which a systemic TNF-α overexpression leads to the development of inflammation; to 2 or 4 weeks of air or CS. We investigated the effect of deregulated TNF expression on CS-induced pulmonary inflammation and the effect of CS exposure on the initiation and progression of gut and joint inflammation. Upon 2 weeks of CS exposure, inflammation in lungs of TNFΔARE mice was significantly aggravated. However, upon 4 weeks of CS-exposure, this aggravation was no longer observed. TNFΔARE mice have no increases in CD4+ and CD8+ T cells and a diminished neutrophil response in the lungs after 4 weeks of CS exposure. In the gut and joints of TNFΔARE mice, 2 or 4 weeks of CS exposure did not modulate the development of inflammation. In conclusion, CS exposure does not modulate gut and joint inflammation in TNFΔARE mice. The lung responses towards CS in TNFΔARE mice however depend on the duration of CS exposure.

  14. E-Cigarettes Not a Smoking Deterrent for Kids

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_163191.html E-Cigarettes Not a Smoking Deterrent for Kids Study ... 23, 2017 (HealthDay News) -- There's no evidence that e-cigarettes are driving down teen smoking -- and, in ...

  15. Oxidative Stress, Cell Death, and Other Damage to Alveolar Epithelial Cells Induced by Cigarette Smoke

    Directory of Open Access Journals (Sweden)

    Nagai A

    2003-09-01

    Full Text Available Abstract Cigarette smoking is a major risk factor in the development of various lung diseases, including pulmonary emphysema, pulmonary fibrosis, and lung cancer. The mechanisms of these diseases include alterations in alveolar epithelial cells, which are essential in the maintenance of normal alveolar architecture and function. Following cigarette smoking, alterations in alveolar epithelial cells induce an increase in epithelial permeability, a decrease in surfactant production, the inappropriate production of inflammatory cytokines and growth factors, and an increased risk of lung cancer. However, the most deleterious effect of cigarette smoke on alveolar epithelial cells is cell death, i.e., either apoptosis or necrosis depending on the magnitude of cigarette smoke exposure. Cell death induced by cigarette smoke exposure can largely be accounted for by an enhancement in oxidative stress. In fact, cigarette smoke contains and generates many reactive oxygen species that damage alveolar epithelial cells. Whether apoptosis and/or necrosis in alveolar epithelial cells is enhanced in healthy cigarette smokers is presently unclear. However, recent evidence indicates that the apoptosis of alveolar epithelial cells and alveolar endothelial cells is involved in the pathogenesis of pulmonary emphysema, an important cigarette smoke-induced lung disease characterized by the loss of alveolar structures. This review will discuss oxidative stress, cell death, and other damage to alveolar epithelial cells induced by cigarette smoke.

  16. Pathophysiological Impact of Cigarette Smoke Exposure on the Cerebrovascular System with a Focus on the Blood-brain Barrier: Expanding the Awareness of Smoking Toxicity in an Underappreciated Area

    Directory of Open Access Journals (Sweden)

    Luca Cucullo

    2010-11-01

    Full Text Available Recent evidence has indicated that active and passive cigarette smoking are associated, in a dose-dependent manner, with dysfunction of normal endothelial physiology. Tobacco smoke (TS may predispose individuals to atherogenic and thrombotic problems, significantly increasing the risk for ischemic manifestations such as acute coronary syndrome and stroke. Despite the strong evidence for an association between smoking and vascular impairment, the impact of TS exposure on the blood-brain barrier (BBB has only been marginally addressed. This is a major problem given that the BBB is crucial in the maintenance of brain homeostasis. Recent data have also shown that chronic smokers have a higher incidence of small vessel ischemic disease (SVID, a pathological condition characterized by leaky brain microvessels and loss of BBB integrity. In the brain TS increases the risk of silent cerebral infarction (SCI and stroke owing to the pro-coagulant and atherogenic effects of smoking. In this article we provide a detailed review and analysis of current knowledge of the pathophysiology of tobacco smoke toxicity at the cerebrovascular levels. We also discuss the potential toxicity of recently marketed “potential-reduced exposure products”.

  17. Cigarette smoke induced genotoxicity and respiratory tract pathology: evidence to support reduced exposure time and animal numbers in tobacco product testing.

    Science.gov (United States)

    Dalrymple, Annette; Ordoñez, Patricia; Thorne, David; Walker, David; Camacho, Oscar M; Büttner, Ansgar; Dillon, Debbie; Meredith, Clive

    2016-06-01

    Many laboratories are working to develop in vitro models that will replace in vivo tests, but occasionally there remains a regulatory expectation of some in vivo testing. Historically, cigarettes have been tested in vivo for 90 days. Recently, methods to reduce and refine animal use have been explored. This study investigated the potential of reducing animal cigarette smoke (CS) exposure to 3 or 6 weeks, and the feasibility of separate lung lobes for histopathology or the Comet assay. Rats were exposed to sham air or CS (1 or 2 h) for 3 or 6 weeks. Respiratory tissues were processed for histopathological evaluation, and Alveolar type II cells (AEC II) isolated for the Comet assay. Blood was collected for Pig-a and micronucleus quantification. Histopathological analyses demonstrated exposure effects, which were generally dependent on CS dose (1 or 2 h, 5 days/week). Comet analysis identified that DNA damage increased in AEC II following 3 or 6 weeks CS exposure, and the level at 6 weeks was higher than 3 weeks. Pig-a mutation or micronucleus levels were not increased. In conclusion, this study showed that 3 weeks of CS exposure was sufficient to observe respiratory tract pathology and DNA damage in isolated AEC II. Differences between the 3 and 6 week data imply that DNA damage in the lung is cumulative. Reducing exposure time, plus analyzing separate lung lobes for DNA damage or histopathology, supports a strategy to reduce and refine animal use in tobacco product testing and is aligned to the 3Rs (replacement, reduction and refinement).

  18. Cigarette smoking and leukocyte subpopulations in men.

    Science.gov (United States)

    Freedman, D S; Flanders, W D; Barboriak, J J; Malarcher, A M; Gates, L

    1996-07-01

    Because of previously reported associations among the total leukocyte count, cigarette smoking, and risk of cardiovascular disease, we examined the relation of cigarette smoking to various leukocyte subpopulations among 3467 men aged 31 to 45 years. The median total leukocyte count was 36% higher (7840 vs. 5760 cells/mL) among current cigarette smokers than among men who had never smoked, and both stratification and regression analyses were used to examine independent associations with leukocyte subpopulations. At equivalent counts of other subpopulations, CD4+ lymphocytes and neutrophils were the cell types most strongly associated with cigarette smoking; each standard deviation change in counts of these subpopulations increased the odds of current (vs. never) smoking by approximately threefold. Furthermore, whereas 15% of the 238 men with relatively low (men with relatively high counts of both subpopulations were current smokers. Counts of T lymphocytes also tended to be higher among the 32 men with self-reported ischemic heart disease than among other men. These results, along with previous reports of immunologically active T lymphocytes in atherosclerotic plaques, suggest that this subpopulation may be of particular interest in studies examining the relation of leukocytes to cardiovascular disease.

  19. Menthol Cigarettes and the Initiation of Smoking: A White Paper

    OpenAIRE

    2010-01-01

    Publicly available internal tobacco industry documents were analyzed to answer the following questions regarding menthol cigarettes and the uptake of smoking by youth: 1) Does menthol make it easier for young or new/inexperienced smokers to start smoking cigarettes? 2) Do menthol smokers start smoking earlier than non-menthol smokers? Is there a higher use among youth who have been smoking for less than one year? 3) Did current smokers start smoking menthol cigarettes before switching to ...

  20. Effects of Schisandra chinensis extracts on cough and pulmonary inflammation in a cough hypersensitivity guinea pig model induced by cigarette smoke exposure.

    Science.gov (United States)

    Zhong, Shan; Nie, Yi-chu; Gan, Zhen-yong; Liu, Xiao-dong; Fang, Zhang-fu; Zhong, Bo-nian; Tian, Jin; Huang, Chu-qin; Lai, Ke-fang; Zhong, Nan-shan

    2015-05-13

    Schisandra chinensis (S. chinensis) is a traditional Chinese medicine commonly used in prescription medications for the treatment of chronic cough. However, the material basis of S. chinensis in relieving cough has not been completely elucidated yet. This study established a guinea pig model of cough hypersensitivity induced by 14 days of cigarette smoke (CS) exposure, to evaluate the antitussive, antioxidant, and anti-inflammatory effects of three S. chinensis extracts. And then the function of four lignans in reducing expression of TRPV1 and TRPA1 was examined using A549 cells induced by cigarette smoke extract (CSE). The results demonstrated that both ethanol extract (EE) and ethanol-water extract (EWE) of S. chinensis, but not water extract (WE), significantly reduced the cough frequency enhanced by 0.4M citric acid solution in these cough hypersensitivity guinea pigs. Meanwhile, pretreatment with EE and EWE both significantly attenuated the CS-induced increase in infiltration of pulmonary neutrophils and total inflammatory cells, as well as pulmonary MDA, TNF-α, and IL-8, while remarkably increased activities of pulmonary SOD and GSH. According to H&E and immunofluorescence staining assays, airway epithelium hyperplasia, smooth muscle thickening, inflammatory cells infiltration, as well as expression of TRPV1 and TRPA1, were significantly attenuated in animals pretreatment with 1g/kg EE. Moreover, four lignans of EE, including schizandrin, schisantherin A, deoxyschizandrin and γ-schisandrin, significantly inhibited CSE-induced expression of TRPV1, TRPA1 and NOS3, as well as NO release in A549 cells. In conclusion, S. chinensis reduces cough frequency and pulmonary inflammation in the CS-induced cough hypersensitivity guinea pigs. Lignans may be the active components.

  1. In vitro systems toxicology approach to investigate the effects of repeated cigarette smoke exposure on human buccal and gingival organotypic epithelial tissue cultures.

    Science.gov (United States)

    Schlage, Walter K; Iskandar, Anita R; Kostadinova, Radina; Xiang, Yang; Sewer, Alain; Majeed, Shoaib; Kuehn, Diana; Frentzel, Stefan; Talikka, Marja; Geertz, Marcel; Mathis, Carole; Ivanov, Nikolai; Hoeng, Julia; Peitsch, Manuel C

    2014-10-01

    Smoking has been associated with diseases of the lung, pulmonary airways and oral cavity. Cytologic, genomic and transcriptomic changes in oral mucosa correlate with oral pre-neoplasia, cancer and inflammation (e.g. periodontitis). Alteration of smoking-related gene expression changes in oral epithelial cells is similar to that in bronchial and nasal epithelial cells. Using a systems toxicology approach, we have previously assessed the impact of cigarette smoke (CS) seen as perturbations of biological processes in human nasal and bronchial organotypic epithelial culture models. Here, we report our further assessment using in vitro human oral organotypic epithelium models. We exposed the buccal and gingival organotypic epithelial tissue cultures to CS at the air-liquid interface. CS exposure was associated with increased secretion of inflammatory mediators, induction of cytochrome P450s activity and overall weak toxicity in both tissues. Using microarray technology, gene-set analysis and a novel computational modeling approach leveraging causal biological network models, we identified CS impact on xenobiotic metabolism-related pathways accompanied by a more subtle alteration in inflammatory processes. Gene-set analysis further indicated that the CS-induced pathways in the in vitro buccal tissue models resembled those in the in vivo buccal biopsies of smokers from a published dataset. These findings support the translatability of systems responses from in vitro to in vivo and demonstrate the applicability of oral organotypical tissue models for an impact assessment of CS on various tissues exposed during smoking, as well as for impact assessment of reduced-risk products.

  2. Assessing Smoking Behaviour and Tobacco Smoke Exposure: Definitions and Methods

    Directory of Open Access Journals (Sweden)

    Gregg E

    2014-12-01

    Full Text Available In recent years, the increased availability of tobacco products other than conventional cigarettes, the use of puffing topography devices for smoking behaviour studies and the use of biomarkers to study smoke constituents exposure have generated the need for a more comprehensive set of definitions concerning smoking behaviour and exposure to smoke. The definitions offered in this paper are based on many years of practical experience and on consensus within a broad group of scientists working in these areas. It is intended that, with wider and more consistent usage, these definitions should reduce any misunderstandings and facilitate interpretation of future studies.

  3. Depressive Symptoms and Cigarette Smoking in a College Sample

    Science.gov (United States)

    Kenney, Brent A.; Holahan, Charles J.

    2008-01-01

    Objective and Participants: The authors examined (1) the relationship between depressive symptoms and cigarette smoking in a college sample and (2) the role of smoking self-efficacy (one's perceived ability to abstain from smoking) in explaining the relationship between depressive symptoms and cigarette smoking. Methods: Predominantly first-year…

  4. An evaluation of four measures of adolescents' exposure to cigarette marketing in stores.

    Science.gov (United States)

    Feighery, Ellen C; Henriksen, Lisa; Wang, Yun; Schleicher, Nina C; Fortmann, Stephen P

    2006-12-01

    This study evaluates four measures of exposure to retail cigarette marketing in relation to adolescent smoking behavior. The measures are (a) shopping frequency in types of stores known to carry more cigarette advertising than other store types, (b) shopping frequency in specific stores that sell cigarettes in the study community, (c) the amount of exposure to cigarette brand impressions in stores where students shopped, and (d) perceived exposure to cigarette advertising. The study combined data from classroom surveys administered to 6th-, 7th-, and 8th-grade students in three California middle schools, and direct store observations quantifying cigarette marketing materials and product placement in stores where students shopped. Logistic regression models were used to examine how each exposure measure related to the odds of ever smoking and susceptibility to smoke, controlling for grade, gender, ethnicity, school performance, unsupervised time, and exposure to household and friend smoking. Frequent exposure to retail cigarette marketing as defined by each of the four measures was independently associated with a significant increase in the odds of ever smoking. All but the measure of exposure to store types was associated with a significant increase in the odds of susceptibility to smoke. Four measures of exposure to retail cigarette marketing may serve equally well to predict adolescent smoking but may vary in cost, complexity, and meaning. Depending on the outcomes of interest, the most useful measure may be a combination of self-reported exposure to types of stores that contain cigarette marketing and perceived exposure to such messages.

  5. Cigarette Smoking is Associated with Decreased Sperm Density

    Institute of Scientific and Technical Information of China (English)

    2002-01-01

    Objectives To study the association between cigarette smoking and sperm densityin men of reproductive age. Methods We enrolled 224 male employees of a modern petrochemicalplant in Nanjing,China. These men had no prior history of infertility or other reproductive diseases.Epidemiologic data, including information on smoking and other occupational and lifestyle exposures wereobtained by a questionnaire interview. Semen specimens were collected from each participant and analyzedaccording to the WHO guidelines. Regression analyses were performed to estimate the effect of smokingon sperm density. Results Approximately 67% of the subjects had ever smoked cigarettes. Differ-ent measurements of smoking behavior were each associated with decrensed sperm density. There was asignificant dose-response trend between the tertiles of total smoking amount in pack-years and sperm den-sity. As compared to men who never smoked, current smokers had a significant reduction in sperm densi-ty (-13.3×106/ml; 95% CI,-24. 1,-2.5) ,while ex-snokers had only a small decrement inspern density (-2.6× 106/al; 95 % CI,-18. 7 ,13. 5). Starting smoking at less than 20 yearsof age was associated with significant reduction in sperm density (-14.8×106/md; 95% CI ,- 27. 4, - 2.2). Starting smoking at 20 years or older was associated with a slightly snaller de-crease (-10.1×106/ml; 95% CI,-21.7,1.4). Conclusions Cigarette smoking is associ-ated with decreased sperm density ,showing an evident dose-response trend in this population.

  6. [Health consequences of smoking electronic cigarettes are poorly described].

    Science.gov (United States)

    Tøttenborg, Sandra Søgaard; Holm, Astrid Ledgaard; Wibholm, Niels Christoffer; Lange, Peter

    2014-09-01

    Despite increasing popularity, health consequences of vaping (smoking electronic cigarettes, e-cigarettes) are poorly described. Few studies suggest that vaping has less deleterious effects on lung function than smoking conventional cigarettes. One large study found that e-cigarettes were as efficient as nicotine patches in smoking cessation. The long-term consequences of vaping are however unknown and while some experts are open towards e-cigarettes as a safer way of satisfying nicotine addiction, others worry that vaping in addition to presenting a health hazard may lead to an increased number of smokers of conventional cigarettes.

  7. Menthol cigarettes and smoking cessation behavior

    Directory of Open Access Journals (Sweden)

    Hoffman Allison C

    2011-05-01

    Full Text Available Abstract Although much is known about smoking cessation behavior, the vast majority of research has not assessed menthol as an independent factor. The objective of this review is to assess the effects, if any, that use of menthol cigarettes has on smoking cessation success in adults and youth. A total of 20 articles are included in this review. Although some studies have found that menthol smokers have less success in quitting smoking, others fail to find significant differences between menthol and non-menthol smokers. Some clinical trials evaluating the efficacy of various cessation treatments have suggested that menthol smokers have poorer outcomes, however two secondary data analysis studies (which used the same original dataset failed to find any difference in success rate associated with particular treatments. Although there is some suggestion that smoking menthol cigarettes is associated with worse cessation outcomes, differences are not always found. However, if there was a difference, it was always in the direction of worse outcomes for menthol smokers. Given that Black/African American smokers prefer menthol cigarettes more than White smokers, possible interactions with race/ethnicity are discussed.

  8. Could zinc prevent reproductive alterations caused by cigarette smoke in male rats?

    Science.gov (United States)

    Garcia, Patrícia Carvalho; Piffer, Renata Carolina; Gerardin, Daniela Cristina Cecatto; Sankako, Michele Kimie; Alves de Lima, Rodrigo Otávio; Pereira, Oduvaldo Câmara Marques

    2012-01-01

    The aim of the present study was to evaluate the effects of zinc on fertility through semen parameters, testosterone level and oxidative DNA damage to spermatozoa of rats exposed to cigarette smoke. Male Wistar rats (60 days old) were divided into four groups (n = 10 per group): control, cigarette-smoking (20 cigarettes per day), zinc (zinc chloride 20 mg kg⁻¹ day⁻¹) and zinc plus cigarette-smoking (zinc chloride 20 mg kg⁻¹ day⁻¹; 20 cigarettes per day). The treatment was applied for nine weeks and the following parameters were analysed: bodyweight, wet weights of the reproductive organs and the adrenal gland, plasma testosterone concentration, testicular function (seminal analysis and daily sperm production) and sperm DNA oxidative damage. The exposure to cigarette smoke decreased testosterone concentration, the percentage of normal morphology and the motility of spermatozoa. In addition, this exposure increased sperm DNA oxidative damage. Zinc treatment protected against the toxic damage that smoking caused to spermatozoa. This study showed a correlation between smoking and possible male infertility and subfertility, and also that the majority of smoking-induced changes in spermatozoa were prevented by zinc treatment. In conclusion, zinc, an antioxidant and stimulant of cell division, can be indicated as a promising treatment in men with infertility caused by the toxic components of cigarette smoke.

  9. Cigarette smoking and brain regulation of energy homeostasis

    Directory of Open Access Journals (Sweden)

    Hui eChen

    2012-07-01

    Full Text Available Cigarette smoking is an addictive behaviour, and is the primary cause of cardiovascular and pulmonary disease, and cancer (among other diseases. Cigarette smoke contains thousands of components that may affect caloric intake and energy expenditure, although nicotine is the major addictive substance present, and has the best described actions. Nicotine exposure from cigarette smoke can change brain feeding regulation to reduce appetite via both energy homeostatic and reward mechanisms, causing a negative energy state which is characterized by reduced energy intake and increased energy expenditure that are linked to low body weight. These findings have led to the public perception that smoking is associated with weight loss. However, its effects at reducing abdominal fat mass (a predisposing factor for glucose intolerance and insulin resistance are marginal, and its promotion of lean body mass loss in animal studies suggests a limited potential for treatment in obesity. Smoking during pregnancy puts pressure on the mother’s metabolic system and is a significant contributor to adverse pregnancy outcomes. Smoking is a predictor of future risk for respiratory dysfunction, social behavioral problems, cardiovascular disease, obesity and type-2 diabetes. Catch-up growth is normally observed in children exposed to intrauterine smoke, which has been linked to subsequent childhood obesity. Nicotine can have a profound impact on the developing fetal brain, via its ability to rapidly and fully pass the placenta. In animal studies this has been linked with abnormal hypothalamic gene expression of appetite regulators such as downregulation of NPY and POMC in the arcuate nucleus of the hypothalamus. Maternal smoking or nicotine replacement leads to unhealthy eating habits (such as junk food addiction and other behavioral disorders in the offspring.

  10. Another Risk From Cigarette Smoking: Corneal Burn

    Directory of Open Access Journals (Sweden)

    Volkan Hürmeriç

    2012-12-01

    Full Text Available A 21-year-old male presented with corneal injury in his left eye after one of his friends had moved his arm backwards and accidentally hit his eye with the lit end of a cigarette. Slit lamp examination revealed epithelial defect and significant stromal edema at the superior temporal quadrant of the cornea. Cigarette ashes were noted in his lashes and inferior conjunctival fornix at the initial examination in the emergency service. 6 weeks after the injury, slit lamp examination revealed stromal thinning and haze in the temporal part of the cornea. His best spectacle-corrected distance visual acuity was 20/25 with a refractive error of -6.75x135 diopters in the left eye. Our case demonstrates that ocular thermal injury due to cigarette smoking can cause serious damage to the ocular tissues. (Turk J Oph thal mol 2012; 42: 484-5

  11. The effects of cigarette smoking on anesthesia.

    OpenAIRE

    Rodrigo, C.

    2000-01-01

    Cigarette smoke contains over 4000 substances, some of which are harmful to the smoker. Some constituents cause cardiovascular problems, increasing the blood pressure, heart rate, and the systemic vascular resistance. Some cause respiratory problems, interfering with oxygen uptake, transport, and delivery. Further, some interfere with respiratory function both during and after anesthesia. Some also interfere with drug metabolism. Various effects on muscle relaxants have been reported. Risk of...

  12. The effects of cigarette smoking on anaesthesia

    OpenAIRE

    Rodrigo, C.

    2000-01-01

    Cigarette smoke contains over 4000 substances, some of which are harmful to the smoker. Some constituents cause cardiovascular problems, increasing the blood pressure, heart rate, and the systemic vascular resistance. Some cause respiratory problems, interfering with oxygen uptake, transport, and delivery. Further, some interfere with respiratory function both during and after anesthesia. Some also interfere with drug metabolism. Various effects on muscle relaxants have been reported. Risk of...

  13. Exposure of a 23F Serotype Strain of Streptococcus pneumoniae to Cigarette Smoke Condensate Is Associated with Selective Upregulation of Genes Encoding the Two-Component Regulatory System 11 (TCS11

    Directory of Open Access Journals (Sweden)

    Riana Cockeran

    2014-01-01

    Full Text Available Alterations in whole genome expression profiles following exposure of the pneumococcus (strain 172, serotype 23F to cigarette smoke condensate (160 μg/mL for 15 and 60 min have been determined using the TIGR4 DNA microarray chip. Exposure to CSC resulted in the significant (P<0.014–0.0006 upregulation of the genes encoding the two-component regulatory system 11 (TCS11, consisting of the sensor kinase, hk11, and its cognate response regulator, rr11, in the setting of increased biofilm formation. These effects of cigarette smoke on the pneumococcus may contribute to colonization of the airways by this microbial pathogen.

  14. Exposure of a 23F Serotype Strain of Streptococcus pneumoniae to Cigarette Smoke Condensate Is Associated with Selective Upregulation of Genes Encoding the Two-Component Regulatory System 11 (TCS11)

    Science.gov (United States)

    Herbert, Jenny A.; Mitchell, Timothy J.; Dix-Peek, Thérèse; Dickens, Caroline; Anderson, Ronald; Feldman, Charles

    2014-01-01

    Alterations in whole genome expression profiles following exposure of the pneumococcus (strain 172, serotype 23F) to cigarette smoke condensate (160 μg/mL) for 15 and 60 min have been determined using the TIGR4 DNA microarray chip. Exposure to CSC resulted in the significant (P < 0.014–0.0006) upregulation of the genes encoding the two-component regulatory system 11 (TCS11), consisting of the sensor kinase, hk11, and its cognate response regulator, rr11, in the setting of increased biofilm formation. These effects of cigarette smoke on the pneumococcus may contribute to colonization of the airways by this microbial pathogen. PMID:25013815

  15. Histological and biochemical effects of cigarette smoke on lungs.

    Science.gov (United States)

    Ozan, E; Kükner, A; Canpolat, L; Oner, H; Gezen, M R; Yilmaz, S; Ozan, S

    2001-01-01

    In this study, rats were made to inhale cigarette smoke in a specifically prepared container for different periods. The lung tissue samples of the subjects were examined by light microscopy, transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Malonaldehyde, one of the free oxygen radicals was determined in lungs and plasma. The catalase activity level of erythrocyte and arginase levels were determined. Three groups were formed. The rats in the Ist and IInd groups were made to inhale cigarette smoke for 30 and 60 minutes a day for a total period of 3 months. Control group, the rats in the IIIrd group (controls) were made to inhale clean air during the same periods. An increase in the number of macrophages was observed in the pulmonary tissue of the exposed groups. Especially in the group that inhaled the smoke for long periods, the number of macrophages and the inclusion bodies contained in them increased. These differences could easily be observed in TEM studies. In the light microscopy and SEM observations, it arouse attention that the alveolar macrophages occurred as sets and their activation increased. Depending on the length of the exposure to cigarette smoke, an increase in the number of macrophages was observed. Statistically significant increases were determined in the malonaldehyde levels of pulmonary tissue and plasma when compared to the control group. Besides significant increases were found in the catalase activity levels of erythrocytes in the experimental groups.

  16. p53- and PAI-1-mediated induction of C-X-C chemokines and CXCR2: importance in pulmonary inflammation due to cigarette smoke exposure.

    Science.gov (United States)

    Tiwari, Nivedita; Marudamuthu, Amarnath S; Tsukasaki, Yoshikazu; Ikebe, Mitsuo; Fu, Jian; Shetty, Sreerama

    2016-03-15

    We previously demonstrated that tumor suppressor protein p53 augments plasminogen activator inhibitor-1 (PAI-1) expression in alveolar epithelial cells (AECs) during chronic cigarette smoke (CS) exposure-induced lung injury. Chronic lung inflammation with elevated p53 and PAI-1 expression in AECs and increased susceptibility to and exacerbation of respiratory infections are all associated with chronic obstructive pulmonary disease (COPD). We recently demonstrated that preventing p53 from binding to the endogenous PAI-1 mRNA in AECs by either suppressing p53 expression or blockading p53 interactions with the PAI-1 mRNA mitigates apoptosis and lung injury. Within this context, we now show increased expression of the C-X-C chemokines (CXCL1 and CXCL2) and their receptor CXCR2, and the intercellular cellular adhesion molecule-1 (ICAM-1), in the lung tissues of patients with COPD. We also found a similar increase in lung tissues and AECs from wild-type (WT) mice exposed to passive CS for 20 wk and in primary AECs treated with CS extract in vitro. Interestingly, passive CS exposure of mice lacking either p53 or PAI-1 expression resisted an increase in CXCL1, CXCL2, CXCR2, and ICAM-1. Furthermore, inhibition of p53-mediated induction of PAI-1 expression by treatment of WT mice exposed to passive CS with caveolin-1 scaffolding domain peptide reduced CXCL1, CXCL2, and CXCR2 levels and lung inflammation. Our study reveals that p53-mediated induction of PAI-1 expression due to chronic CS exposure exacerbates lung inflammation through elaboration of CXCL1, CXCL2, and CXCR2. We further provide evidence that targeting this pathway mitigates lung injury associated with chronic CS exposure.

  17. A Systems Biology Approach Reveals the Dose- and Time-Dependent Effect of Primary Human Airway Epithelium Tissue Culture After Exposure to Cigarette Smoke In Vitro

    OpenAIRE

    2015-01-01

    To establish a relevant in vitro model for systems toxicology-based mechanistic assessment of environmental stressors such as cigarette smoke (CS), we exposed human organotypic bronchial epithelial tissue cultures at the air liquid interface (ALI) to various CS doses. Previously, we compared in vitro gene expression changes with published human airway epithelia in vivo data to assess their similarities. Here, we present a follow-up evaluation of these in vitro transcriptomics data, using comp...

  18. Cigarette access and pupil smoking rates: a circular relationship?

    Science.gov (United States)

    Turner, Katrina M; Gordon, Jacki; Young, Robert

    2004-12-01

    Adolescents obtain cigarettes from both commercial and social sources. While the relationship between commercial access and adolescent smoking has been researched, no one has considered in detail whether rates of peer smoking affect cigarette availability. In two relatively deprived Scottish schools that differed in their pupil smoking rates, we assess pupil access to cigarettes. 896 13 and 15 year olds were surveyed, and 25 single-sex discussion groups held with a sub-sample of the 13 year olds. Smokers in both schools obtained cigarettes from shops, food vans and other pupils. However, pupils in the 'high' smoking school perceived greater access to both commercial and social sources, and had access to an active 'peer market'. These findings suggest that variations in cigarette access may contribute to school differences in pupil smoking rates, and that the relationship between access and adolescent smoking is circular, with greater availability increasing rates, and higher rates enhancing access.

  19. Waterpipes and e-cigarettes: Impact of alternative smoking techniques on indoor air quality and health

    Science.gov (United States)

    Fromme, Hermann; Schober, Wolfgang

    2015-04-01

    Waterpipe (WP) smoking is growing as an alternative to cigarette smoking, especially in younger age groups. E-cigarette use has also increased in recent years. A majority of smokers mistakenly believe that WP smoking is a social entertainment practice that leads to more social behavior and relaxation and that this type of smoking is safe or less harmful and less addictive than cigarette smoking. In reality, WP smokers are exposed to hundreds of toxic substances that include known carcinogens. High exposures to carbon monoxide and nicotine are major health threats. Persons exposed to secondhand WP smoke are also at risk. There is growing evidence that WP smoke causes adverse effects on the pulmonary and cardiovascular systems and is responsible for cancer. E-cigarettes are marketed as a smokeless and safe way to inhale nicotine without being exposed to the many toxic components of tobacco cigarettes, and as an aid to smoking cessation. In fact, consumers (vapers) and secondhand vapers can be exposed to substantial amounts of VOC, PAH or other potentially harmful substances. Of major health concern is the inhalation of fine and ultrafine particles formed from supersaturated 1,2-propanediol vapor. Such particles can be deposited in the deeper parts of the lung and may harm the respiratory system or increase the risk of acquiring asthma. More research on the safety of e-cigarettes needs to be conducted to ensure a high level of public health protection in the long-term.

  20. Cigarette Smoking-Induced Cardiac Hypertrophy, Vascular Inflammation and Injury are Attenuated by Antioxidant Supplementation in An Animal Model

    Directory of Open Access Journals (Sweden)

    Moustafa Al Hariri

    2016-11-01

    Full Text Available BackgroundCardiovascular diseases are the leading causes of morbidity and mortality worldwide. Cigarette smoking remains a global health epidemic with associated detrimental effects on the cardiovascular system. In this work, we investigated the effects of cigarette smoke exposure on cardiovascular system in an animal model. The study then evaluated the effects of antioxidants (AO, represented by pomegranate juice, on cigarette smoke induced cardiovascular injury. This study aims at evaluating the effect of pomegranate juice supplementation on the cardiovascular system of an experimental rat model of smoke exposure.Methods Adult rats were divided into four different groups: Control, Cigarette smoking (CS, AO, and CS + AO. Cigarette smoke exposure was for 4 weeks (5 days of exposure/week and AO group received pomegranate juice while other groups received placebo. Assessment of cardiovascular injury was documented by assessing different parameters of cardiovascular injury mediators including: 1 cardiac hypertrophy, 2 oxidative stress (OS, 3 expression of inflammatory markers, 3 expression of Bradykinin receptor 1 (Bdkrb1, Bradykinin receptor 2 (Bdkrb2, and 4 altered expression expression of fibrotic/atherogenic markers [(Fibronectin (Fn1 and leptin receptor (ObR].ResultsData from this work demonstrated that cigarette smoke exposure induced cardiac hypertrophy, which was reduced upon administration of pomegranate in CS + AO group. Cigarette smoke exposure was associated with elevation in oxidative stress, significant increase in the expression of IL-1β, TNFα, Fn1 and ObR in rat’s aorta. In addition, an increase in aortic calcification was observed after one month of Cigarette smoke exposure. Furthermore, Cigarette smoke induced a significant up regulation in Bdkrb1 and Bdkrb2 expression levels. Finally, pomegranate supplementation exhibited cardiovascular protection assessed by the above findings and partly contributed to ameliorating cardiac

  1. Association between Family and Friend Smoking Status and Adolescent Smoking Behavior and E-Cigarette Use in Korea

    Directory of Open Access Journals (Sweden)

    Myoung Jin Joung

    2016-11-01

    Full Text Available Smoking is harmful to the health of adolescents because their bodies are still growing. The aim of this study was to analyze the association between the smoking status of Korean adolescents’ parents and friends and their own smoking behavior. The study assessed a nationwide sample of 72,060 middle and high students from the 10th Korea Youth Risk Behavior Web-based Survey (2014. Descriptive analysis, chi-square tests, and multiple logistic regression analysis were used to probe the association between family and friend smoking status and adolescent smoking behavior. The current cigarette smoking rates were 13.3% of boys and 4.1% of girls. The corresponding rates for electronic cigarette smoking were 4.1% and 1.5%, respectively. Higher exposure to secondhand smoke, smoking by any family member, more friends smoking, and witnessed smoking at school were associated with current smoking and electronic smoking. The smoking status of family and friends was significantly related to adolescent smoking behavior. These results should be considered in designing programs to control adolescent smoking.

  2. Effect of Cigarette Smoke on Surface Roughness of Different Denture Base Materials

    Science.gov (United States)

    Mahross, Hamada Zaki; Mohamed, Mahmoud Darwish; Hassan, Ahmed Mohammed

    2015-01-01

    Background Surface roughness is an important property of denture bases since denture bases are in contact with oral tissues and a rough surface may affect tissues health due to microorganism accumulation. Therefore, the effect of cigarette smoke on the surface roughness of two commercially available denture base materials was evaluated to emphasize which type has superior properties for clinical use. Materials and Methods A total numbers of 40 specimens were constructed from two commercially available denture base materials; heat-cured PMMA and visible light cured UDMA resins (20 for each). The specimens for each type were randomly divided into: Group I: Heat cured resin control group; Group II: Heat cured acrylic resin specimens exposed to cigarette smoking; Group III: Light cured resin control group; Group IV: Light cured resin specimens exposed to cigarette smoking. The control groups used for immersion in distilled water and the smoke test groups used for exposure to cigarette smoking. The smoke test groups specimens were exposed to smoking in a custom made smoking chamber by using 20 cigarettes for each specimen. The surface roughness was measured by using Pocket SurfPS1 profilometer and the measurements considered as the difference between the initial and final roughness measured before and after smoking. Results The t-test for paired observation of test specimens after exposure to smoking was indicated significant change in surface roughness for Group II (pdentures constructed from heat cured acrylic resin had been increased after exposure to cigarette smoke but had no impact on the dentures constructed from visible light cured resin. PMID:26501010

  3. [Electronic Cigarettes: Lifestyle Gadget or Smoking Cessation Aid?].

    Science.gov (United States)

    Schuurmans, Macé M

    2015-07-01

    Electronic cigarettes (e-cigarettes) are vaporisers of liquids often containing nicotine. In the inhaled aerosol carcinogens, ultrafine and metal particles are detected usually in concentrations below those measured in tobacco smoke. Therefore, these products are expected to be less harmful. This has not yet been proven. The long-term safety of e-cigarettes is unknown. Short duration use leads to airway irritation and increased diastolic blood pressure. So far only two randomised controlled trials have investigated efficacy and safety of e-cigarettes for smoking cessation: No clear advantage was shown in comparison to smoking cessation medication. Due to insufficient evidence, e-cigarettes cannot be recommended for smoking cessation. Problematic are the lack of regulation and standardisation of e-cigarette products, which makes general conclusions impossible.

  4. Cigarette Smoke and Estrogen Signaling in Human Airway Smooth Muscle

    Directory of Open Access Journals (Sweden)

    Venkatachalem Sathish

    2015-06-01

    Full Text Available Aims: Cigarette smoke (CS in active smokers and second-hand smoke exposure exacerbate respiratory disorders such as asthma and chronic bronchitis. While women are known to experience a more asthmatic response to CS than emphysema in men, there is limited information on the mechanisms of CS-induced airway dysfunction. We hypothesize that CS interferes with a normal (protective bronchodilatory role of estrogens, thus worsening airway contractility. Methods: We tested effects of cigarette smoke extract (CSE on 17β-estradiol (E2 signaling in enzymatically-dissociated bronchial airway smooth muscle (ASM obtained from lung samples of non-smoking female patients undergoing thoracic surgery. Results: In fura-2 loaded ASM cells, CSE increased intracellular calcium ([Ca2+]i responses to 10µM histamine. Acute exposure to physiological concentrations of E2 decreased [Ca2+]i responses. However, in 24h exposed CSE cells, although expression of estrogen receptors was increased, the effect of E2 on [Ca2+]i was blunted. Acute E2 exposure also decreased store-operated Ca2+ entry and inhibited stromal interaction molecule 1 (STIM1 phosphorylation: effects blunted by CSE. Acute exposure to E2 increased cAMP, but less so in 24h CSE-exposed cells. 24h CSE exposure increased S-nitrosylation of ERα. Furthermore, 24h CSE-exposed bronchial rings showed increased bronchoconstrictor agonist responses that were not reduced as effectively by E2 compared to non-CSE controls. Conclusion: These data suggest that CS induces dysregulation of estrogen signaling in ASM, which could contribute to increased airway contractility in women exposed to CS.

  5. Identification of possible cigarette smoke constituents responsible for muscle catabolism.

    Science.gov (United States)

    Rom, Oren; Kaisari, Sharon; Aizenbud, Dror; Reznick, Abraham Z

    2012-08-01

    The age-related loss of muscle mass and strength also known as sarcopenia is significantly influenced by life style factors such as physical inactivity and impaired nutrition. Cigarette smoking is another life style habit that has been shown to be associated with sarcopenia and to affect skeletal muscle. Even today, smoking is still prevalent worldwide and is probably the most significant source of toxic chemicals exposure to humans. Cigarette smoke (CS) is a complex aerosol consisting of thousands of various constituents including reactive oxygen and nitrogen free radicals, toxic aldehydes and more. Previous epidemiological studies have identified tobacco smoking as a risk factor for sarcopenia. Clinical, in vivo and in vitro studies have revealed CS-induced skeletal muscle damage due to impaired muscle metabolism, increased inflammation and oxidative stress, over-expression of atrophy related genes and activation of various intracellular signaling pathways. This review aims to discuss and identify the components of CS that may promote catabolism of skeletal muscle.

  6. Is the smokers exposure to environmental tobacco smoke negligible?

    Directory of Open Access Journals (Sweden)

    Valerio Federico

    2010-01-01

    Full Text Available Abstract Background Very few studies have evaluated the adverse effect of passive smoking exposure among active smokers, probably due to the unproven assumption that the dose of toxic compounds that a smoker inhales by passive smoke is negligible compared to the dose inhaled by active smoke. Methods In a controlled situation of indoor active smoking, we compared daily benzo(apyrene (BaP dose, estimated to be inhaled by smokers due to the mainstream (MS of cigarettes they have smoked, to the measured environmental tobacco smoke (ETS they inhaled in an indoor environment. For this aim, we re-examined our previous study on daily personal exposure to BaP of thirty newsagents, according to their smoking habits. Results Daily BaP dose due to indoor environmental contamination measured inside newsstands (traffic emission and ETS produced by smoker newsagents was linearly correlated (p = 0.001 R2 = 0.62 with estimated BaP dose from MS of daily smoked cigarettes. In smoker subjects, the percentage of BaP daily dose due to ETS, in comparison to mainstream dose due to smoked cigarettes, was estimated with 95% confidence interval, between 14.6% and 23% for full flavour cigarettes and between 21% and 34% for full flavour light cigarettes. Conclusions During indoor smoking, ETS contribution to total BaP dose of the same smoker, may be not negligible. Therefore both active and passive smoking exposures should be considered in studies about health of active smokers.

  7. Synergistic effect of polonium-210 and cigarette smoke in rats. Final report

    Energy Technology Data Exchange (ETDEWEB)

    Black, S.C.; Bretthauer, E.W.

    1975-06-01

    An experimental procedure was devised to test the possible synergistic effect of polonium-210 and cigarette smoke in rats. Appropriate techniques were developed to expose the rats to cigarette smoke through mouth-breathing and to add known amounts of polonium-210 to the cigarette smoke. The findings from this experiment included: (1) lung deposition of polonium-210 was 31 plus or minus 2%, (2) early retention of polonium was two-phased with half-times of 4 and 84 hours, and (3) bronchitis, emphysema and lung tumors were observed in the experimental animals. Though the spontaneous occurrence of two lung tumors in the number of animals at risk was highly improbable, any conclusion that this resulted from the exposure to cigarette smoke must be highly qualified. (GRA)

  8. Effects of cigarette smoking and nicotine metabolite ratio on leukocyte telomere length.

    Science.gov (United States)

    Verde, Zoraida; Reinoso-Barbero, Luis; Chicharro, Luis; Garatachea, Nuria; Resano, Pilar; Sánchez-Hernández, Ignacio; Rodríguez González-Moro, Jose Miguel; Bandrés, Fernando; Santiago, Catalina; Gómez-Gallego, Félix

    2015-07-01

    Studies of the effects of smoking on leukocyte telomere length (LTL) using cigarettes smoked per day or pack years smoked (PYS) present limitations. Reported high levels of smoking may not increase toxin exposure levels proportionally. Nicotine metabolism ratio (NMR) predicts total cigarette puff volume and overall exposure based on total N-nitrosamines, is highly reproducible and independent of time since the last cigarette. We hypothesized that smokers with higher NMRs will exhibit increased total puff volume, reflecting efforts to extract more nicotine from their cigarettes and increasing toxin exposure. In addition, higher levels of smoking could cause a gross damage in LTL. The urinary cotinine, 3-OH cotinine and nicotine levels of 147 smokers were analyzed using a LC/MS system Triple-Q6410. LTL and CYP2A6 genotype was determined by PCR in blood samples. We found a significant association between NMR and CYP2A6 genotype. Reduction in LTL was seen in relation to accumulated tobacco consumption and years smoking when we adjusted for age and gender. However, there were no significant differences between NMR values and LTL. In our study the higher exposure was associated with lower number of PYS. Smokers with reduced cigarette consumption may exhibit compensatory smoking behavior that results in no reduced tobacco toxin exposure. Our results suggest that lifetime accumulated smoking exposure could cause a gross damage in LTL rather than NMR or PYS. Nevertheless, a combination of smoking topography (NMR) and consumption (PYS) measures may provide useful information about smoking effects on health outcomes.

  9. Are E-cigarettes a safe and good alternative to cigarette smoking?

    Science.gov (United States)

    Rom, Oren; Pecorelli, Alessandra; Valacchi, Giuseppe; Reznick, Abraham Z

    2015-03-01

    Electronic cigarettes (E-cigarettes) are devices that can vaporize a nicotine solution combined with liquid flavors instead of burning tobacco leaves. Since their emergence in 2004, E-cigarettes have become widely available, and their use has increased exponentially worldwide. E-cigarettes are aggressively advertised as a smoking cessation aid; as healthier, cheaper, and more socially acceptable than conventional cigarettes. In recent years, these claims have been evaluated in numerous studies. This review explores the development of the current E-cigarette and its market, prevalence of awareness, and use. The review also explores the beneficial and adverse effects of E-cigarettes in various aspects in accordance with recent research. The discussed aspects include smoking cessation or reduction and the health risks, social impact, and environmental consequences of E-cigarettes.

  10. Infrared spectroscopy study of the influence of inhaled vapors/smoke produced by cigarettes of active smokers

    Science.gov (United States)

    Popa, Cristina

    2015-05-01

    While much is known about the effect of smoke and vapors on the composition of blood, little is known about their impact on the composition of breath. When tobacco from traditional cigarettes (T) is burned, it produces harmful smoke compared with the vapor produced when using electronic cigarettes (E). Using a noninvasive, safe, and rapid CO2 laser-photoacoustic method, this study aimed to examine the ethylene changes at different time intervals in the exhaled breath composition of E-cigarette smokers and T-cigarette smokers, before and after the consecutive exposures to cigarettes. Oxidative stress from exposure to tobacco smoke has a role in the pathogenic process, leading to chronic obstructive pulmonary disease. The evidence on the mechanisms by which T-smoking causes damage indicates that there is no risk-free level of exposure to tobacco smoke. The study revealed that the ethylene level (in the E-cigarette smoker's case) was found to be in smaller concentrations (compared with T-cigarette smoker's case) and that E-cigarettes may provide an alternative to T-cigarette smoking.

  11. Electronic Cigarettes Use and Intention to Cigarette Smoking among Never-Smoking Adolescents and Young Adults: A Meta-Analysis.

    Science.gov (United States)

    Zhong, Jieming; Cao, Shuangshuang; Gong, Weiwei; Fei, Fangrong; Wang, Meng

    2016-05-03

    Electronic cigarettes (e-cigarettes) use is becoming increasingly common, especially among adolescents and young adults, and there is little evidence on the impact of e-cigarettes use on never-smokers. With a meta-analysis method, we explore the association between e-cigarettes use and smoking intention that predicts future cigarette smoking. Studies were identified by searching three databases up to January 2016. The meta-analysis results were presented as pooled odds ratio (OR) with 95% confidence interval (CI) calculated by a fixed-effects model. A total of six studies (91,051 participants, including 1452 with ever e-cigarettes use) were included in this meta-analysis study. We found that never-smoking adolescents and young adults who used e-cigarettes have more than 2 times increased odds of intention to cigarette smoking (OR = 2.21, 95% CI: 1.86-2.61) compared to those who never used, with low evidence of between-study heterogeneity (p = 0.28, I² = 20.1%). Among never-smoking adolescents and young adults, e-cigarettes use was associated with increased smoking intention.

  12. Information Management Strategies within Conversations about Cigarette Smoking: Parenting Correlates and Longitudinal Associations with Teen Smoking

    Science.gov (United States)

    Metzger, Aaron; Wakschlag, Lauren S.; Anderson, Ryan; Darfler, Anne; Price, Juliette; Flores, Zujeil; Mermelstein, Robin

    2013-01-01

    The present study examined smoking-specific and general parenting predictors of in vivo observed patterns of parent-adolescent discussion concerning adolescents' cigarette smoking experiences and associations between these observed patterns and 24-month longitudinal trajectories of teen cigarette smoking behavior (nonsmokers, current…

  13. Reinforcing effects of cigarette advertising on under-age smoking.

    Science.gov (United States)

    Aitken, P P; Eadie, D R

    1990-03-01

    Interviews were conducted with 848 Glasgow children aged between 11 and 14 years. There were consistent differences between smokers and non-smokers. Smokers tended to be more adept at recalling, recognizing and identifying cigarette advertisements. This suggests they tend to pay more attention to cigarette advertising. Smokers also tended to be generally more appreciative of cigarette advertising. Moreover, this greater awareness and appreciation of cigarette advertising was independent of other important predictors of under-age smoking, such as smoking by peers, siblings and parents. These findings, taken in conjunction with previous research, indicate that cigarette advertising is reinforcing under-age smoking. The smokers showed an enhanced or heightened preference for Kensitas Club, the brand favoured by adults. This is consistent with previous research indicating that promotional devices which help determine and reinforce adult cigarette brand preferences have an even greater effect on under-age smokers.

  14. Assessment of global DNA methylation in the first trimester fetal tissues exposed to maternal cigarette smoking

    DEFF Research Database (Denmark)

    Fa, Svetlana; Larsen, Trine Vilsbøll; Bilde, Katrine;

    2016-01-01

    AIMS: Maternal cigarette smoking during pregnancy increases the risk of negative health consequences for the exposed child. Epigenetic mechanisms constitute a likely link between the prenatal exposure to maternal cigarette smoking and the increased risk in later life for diverse pathologies....... Maternal smoking induces gene-specific DNA methylation alterations as well as global DNA hypermethylation in the term placentas and hypomethylation in the cord blood. Early pregnancy represents a developmental time where the fetal epigenome is remodeled and accordingly can be expected to be highly prone...... to exposures with an epigenetic impact. We have assessed the influence of maternal cigarette smoking during the first trimester for fetal global DNA methylation. METHODS AND RESULTS: We analyzed the human fetal intestines and livers as well as the placentas from the first trimester pregnancies. Global DNA...

  15. Cigarette Smoking and the Risk of Bladder Cancer in Men and Women

    Directory of Open Access Journals (Sweden)

    Quirk Jeffrey T

    2004-09-01

    Full Text Available Abstract Although cigarette smoking is a principal risk factor for bladder cancer in both men and women, few studies have statistically evaluated whether gender modifies the effect of smoking on bladder cancer risk. We initiated the present case-control study at Roswell Park Cancer Institute in Buffalo, New York, U.S., to provide further data on this important issue. We observed similar risk estimates for men and women with comparable smoking exposures, but did not observe a statistically significant interaction between gender and lifetime smoking exposure. We conclude that cigarette smoking is a major risk factor for bladder cancer in both sexes, but that gender does not modify the effect of smoking on bladder cancer risk.

  16. Exposure to teachers smoking and adolescent smoking behaviour: analysis of cross sectional data from Denmark

    DEFF Research Database (Denmark)

    Poulsen, Lis Hentze; Osler, M; Roberts, C

    2002-01-01

    OBJECTIVE: To determine whether adolescent smoking behaviour is associated with their perceived exposure to teachers or other pupils smoking at school, after adjustment for exposure to smoking at home, in school, and best friends smoking. DESIGN: Logistic regression analysis of cross sectional data...... at school, as well as the smoking behaviour of mother, father, and best friend (odds ratio (OR) 1.8, 95% confidence interval 1.2 to 2.8). Adolescents' perceived exposure to teachers smoking inside the school building was not associated with daily smoking (OR 0.9, 95% CI 0.5 to 1.6) and perceived exposure...... from students in Denmark. SUBJECTS: 1515 grade 9 students (mean age 15.8) from 90 classes in 48 Danish schools. Outcome measure: Self reported smoking behaviour; daily smoking and heavy smoking, defined as those smoking more than 20 cigarettes per week. RESULTS: Of the students in this study, 62...

  17. Branched-chain amino acid-rich diet improves skeletal muscle wasting caused by cigarette smoke in rats.

    Science.gov (United States)

    Tomoda, Koichi; Kubo, Kaoru; Hino, Kazuo; Kondoh, Yasunori; Nishii, Yasue; Koyama, Noriko; Yamamoto, Yoshifumi; Yoshikawa, Masanori; Kimura, Hiroshi

    2014-04-01

    Cigarette smoke induces skeletal muscle wasting by a mechanism not yet fully elucidated. Branched-chain amino acids (BCAA) in the skeletal muscles are useful energy sources during exercise or systemic stresses. We investigated the relationship between skeletal muscle wasting caused by cigarette smoke and changes in BCAA levels in the plasma and skeletal muscles of rats. Furthermore, the effects of BCAA-rich diet on muscle wasting caused by cigarette smoke were also investigated. Wistar Kyoto (WKY) rats that were fed with a control or a BCAA-rich diet were exposed to cigarette smoke for four weeks. After the exposure, the skeletal muscle weight and BCAA levels in plasma and the skeletal muscles were measured. Cigarette smoke significantly decreased the skeletal muscle weight and BCAA levels in both plasma and skeletal muscles, while a BCAA-rich diet increased the skeletal muscle weight and BCAA levels in both plasma and skeletal muscles that had decreased by cigarette smoke exposure. In conclusion, skeletal muscle wasting caused by cigarette smoke was related to the decrease of BCAA levels in the skeletal muscles, while a BCAA-rich diet may improve cases of cigarette smoke-induced skeletal muscle wasting.

  18. E-cigarette use results in suppression of immune and inflammatory-response genes in nasal epithelial cells similar to cigarette smoke.

    Science.gov (United States)

    Martin, Elizabeth M; Clapp, Phillip W; Rebuli, Meghan E; Pawlak, Erica A; Glista-Baker, Ellen; Benowitz, Neal L; Fry, Rebecca C; Jaspers, Ilona

    2016-07-01

    Exposure to cigarette smoke is known to result in impaired host defense responses and immune suppressive effects. However, the effects of new and emerging tobacco products, such as e-cigarettes, on the immune status of the respiratory epithelium are largely unknown. We conducted a clinical study collecting superficial nasal scrape biopsies, nasal lavage, urine, and serum from nonsmokers, cigarette smokers, and e-cigarette users and assessed them for changes in immune gene expression profiles. Smoking status was determined based on a smoking history and a 3- to 4-wk smoking diary and confirmed using serum cotinine and urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) levels. Total RNA from nasal scrape biopsies was analyzed using the nCounter Human Immunology v2 Expression panel. Smoking cigarettes or vaping e-cigarettes resulted in decreased expression of immune-related genes. All genes with decreased expression in cigarette smokers (n = 53) were also decreased in e-cigarette smokers. Additionally, vaping e-cigarettes was associated with suppression of a large number of unique genes (n = 305). Furthermore, the e-cigarette users showed a greater suppression of genes common with those changed in cigarette smokers. This was particularly apparent for suppressed expression of transcription factors, such as EGR1, which was functionally associated with decreased expression of 5 target genes in cigarette smokers and 18 target genes in e-cigarette users. Taken together, these data indicate that vaping e-cigarettes is associated with decreased expression of a large number of immune-related genes, which are consistent with immune suppression at the level of the nasal mucosa.

  19. Factors Associated with American Indian Cigarette Smoking in Rural Settings

    OpenAIRE

    Karabi Nandy; Felicia Hodge

    2011-01-01

    Introduction: This paper reports on the prevalence, factors and patterns of cigarette smoking among rural California American Indian (AI) adults. Methods: Thirteen Indian health clinic registries formed the random household survey sampling frame (N = 457). Measures included socio-demographics, age at smoking initiation, intention to quit, smoking usage, smoking during pregnancy, health effects of smoking, suicide attempts or ideation, history of physical abuse, neglect and the role of the env...

  20. A Wearable Sensor System for Monitoring Cigarette Smoking

    Science.gov (United States)

    Sazonov, Edward; Lopez-Meyer, Paulo; Tiffany, Stephen

    2013-01-01

    Objective: Available methods of smoking assessment (e.g., self-report, portable puff-topography instruments) do not permit the collection of accurate measures of smoking behavior while minimizing reactivity to the assessment procedure. This article suggests a new method for monitoring cigarette smoking based on a wearable sensor system (Personal Automatic Cigarette Tracker [PACT]) that is completely transparent to the end user and does not require any conscious effort to achieve reliable monitoring of smoking in free-living individuals. Method: The proposed sensor system consists of a respiratory inductance plethysmograph for monitoring of breathing and a hand gesture sensor for detecting a cigarette at the mouth. The wearable sensor system was tested in a laboratory study of 20 individuals who performed 12 different activities including cigarette smoking. Signal processing was applied to evaluate the uniqueness of breathing patterns and their correlation with hand gestures. Results: The results indicate that smoking manifests unique breathing patterns that are highly correlated with hand-to-mouth cigarette gestures and suggest that these signals can potentially be used to identify and characterize individual smoke inhalations. Conclusions: With the future development of signal processing and pattern-recognition methods, PACT can be used to automatically assess the frequency of smoking and inhalation patterns (such as depth of inhalation and smoke holding) throughout the day and provide an objective method of assessing the effectiveness of behavioral and pharmacological smoking interventions. PMID:24172124

  1. Influence of cigarette smoking on thyroid gland--an update.

    Science.gov (United States)

    Sawicka-Gutaj, Nadia; Gutaj, Paweł; Sowiński, Jerzy; Wender-Ożegowska, Ewa; Czarnywojtek, Agata; Brązert, Jacek; Ruchała, Marek

    2014-01-01

    Many studies have shown that cigarette smoking exerts multiple effects on the thyroid gland. Smoking seems to induce changes in thyroid function tests, like decrease in TSH and increase in thyroid hormones. However, these alterations are usually mild. In addition, tobacco smoking may also play a role in thyroid autoimmunity. Many studies have confirmed a significant influence of smoking on Graves' hyperthyroidism and particularly on Graves' orbitopathy. Here, smoking may increase the risk of disease development, may reduce the effectiveness of treatment, and eventually induce relapse. The role of smoking in Hashimoto's thyroiditis is not as well established as in Graves' disease. Nonetheless, lower prevalence of thyroglobulin antibodies, thyroperoxidase antibodies and hypothyroidism were found in smokers. These findings contrast with a study that reported increased risk of hypothyroidism in smokers with Hashimoto's thyroiditis. Moreover, cigarette smoking increases the incidence of multinodular goitre, especially in iodine-deficient areas. Some studies have examined cigarette smoking in relation to the risk of thyroid cancer. Interestingly, many of them have shown that smoking may reduce the risk of differentiated thyroid cancer. Furthermore, both active and passive smoking during pregnancy might modify maternal and foetal thyroid function. This review evaluates the current data concerning the influence of cigarette smoking on thyroid gland, including hormonal changes, autoimmunity and selected diseases. These findings, however, in our opinion, should be carefully evaluated and some of them are not totally evidence-based. Further studies are required to explain the effects of smoking upon thyroid pathophysiology.

  2. Cigarette smoking and genetic alterations in sporadic colon carcinomas

    NARCIS (Netherlands)

    Diergaarde, B.; Vrieling, A.; Kraats, van A.A.; Muijen, van G.N.P.; Kok, F.J.; Kampman, E.

    2003-01-01

    Cigarette smoking has been inconsistently associated with colon cancer risk. To evaluate the hypothesis that smoking is primarily linked to a specific colon tumor subgroup(s), we assessed associations between smoking and the occurrence of mutations in the APC, K-ras and p53 genes, p53 overexpression

  3. Cigarette Smoking by Adolescent Females: Implications for Health and Behavior.

    Science.gov (United States)

    Gritz, Ellen R.

    Cigarette smoking is a behavior with profound biomedical and psychosocial consequences across the life span. Although it is advertised in terms of youth, beauty, sexual appeal, success and independence, smoking is intimately linked with addiction, disease and death. Smoking has been shown to be a leading contributer to several kinds of cancer,…

  4. The epigenetics of maternal cigarette smoking during pregnancy and effects on child development.

    Science.gov (United States)

    Knopik, Valerie S; Maccani, Matthew A; Francazio, Sarah; McGeary, John E

    2012-11-01

    The period of in utero development is one of the most critical windows during which adverse intrauterine conditions and exposures can influence the growth and development of the fetus as well as the child's future postnatal health and behavior. Maternal cigarette smoking during pregnancy remains a relatively common but nonetheless hazardous in utero exposure. Previous studies have associated prenatal smoke exposure with reduced birth weight, poor developmental and psychological outcomes, and increased risk for diseases and behavioral disorders later in life. Researchers are now learning that many of the mechanisms whereby maternal smoke exposure may affect key pathways crucial for proper fetal growth and development are epigenetic in nature. Maternal cigarette smoking during pregnancy has been associated with altered DNA methylation and dysregulated expression of microRNA, but a deeper understanding of the epigenetics of maternal cigarette smoking during pregnancy as well as how these epigenetic changes may affect later health and behavior remain to be elucidated. This article seeks to explore many of the previously described epigenetic alterations associated with maternal cigarette smoking during pregnancy and assess how such changes may have consequences for both fetal growth and development, as well as later child health, behavior, and well-being. We also outline future directions for this new and exciting field of research.

  5. Differential Effects between Cigarette Total Particulate Matter and Cigarette Smoke Extract on Blood and Blood Vessel

    Science.gov (United States)

    Park, Jung-Min; Chang, Kyung-Hwa; Park, Kwang-Hoon; Choi, Seong-Jin; Lee, Kyuhong; Lee, Jin-Yong; Satoh, Masahiko; Song, Seong-Yu; Lee, Moo-Yeol

    2016-01-01

    The generation and collection of cigarette smoke (CS) is a prerequisite for any toxicology study on smoking, especially an in vitro CS exposure study. In this study, the effects on blood and vascular function were tested with two widely used CS preparations to compare the biological effects of CS with respect to the CS preparation used. CS was prepared in the form of total particulate matter (TPM), which is CS trapped in a Cambridge filter pad, and cigarette smoke extract (CSE), which is CS trapped in phosphate-buffered saline. TPM potentiated platelet reactivity to thrombin and thus increased aggregation at a concentration of 25~100 μg/mL, whereas 2.5~10% CSE decreased platelet aggregation by thrombin. Both TPM and CSE inhibited vascular contraction by phenylephrine at 50~100 μg/mL and 10%, respectively. TPM inhibited acetylcholine-induced vasorelaxation at 10~100 μg/mL, but CSE exhibited a minimal effect on relaxation at the concentration that affects vasoconstriction. Neither TPM nor CSE induced hemolysis of erythrocytes or influenced plasma coagulation, as assessed by prothrombin time (PT) and activated partial thromboplastin time (aPTT). Taken together, CS affects platelet activity and deteriorates vasomotor functions in vitro. However, the effect on blood and blood vessels may vary depending on the CS preparation. Therefore, the results of experiments conducted with CS preparations should be interpreted with caution.

  6. Differences in Electronic Cigarette Awareness, Use History, and Advertisement Exposure Between Black and White Hospitalized Cigarette Smokers.

    Science.gov (United States)

    Baumann, Angela Warren; Kohler, Connie; Kim, Young-il; Cheong, JeeWon; Hendricks, Peter; Bailey, William C; Harrington, Kathleen F

    2015-12-01

    E-cigarette use has increased rapidly over the past decade. There is growing concern about e-cigarette use and advertising given limited regulation of these products. This cross-sectional study reports on data collected at baseline from hospitalized cigarette smokers (N=944) recruited in monthly cohorts between December 2012 and September 2013. Participants were queried regarding e-cigarette awareness and use, and number and sources of e-cigarette advertisement exposures in the previous 6 months. Most Whites (99%) reported ever hearing of an e-cigarette compared to 96% of Blacks (padvertisement exposure reported for the previous 6 months, with a 14% increase each month (padvertisement exposure than Blacks (mean=25 vs. 8 in month 1 to 79 vs. 45 in month 9, respectively; padvertisement exposure was significantly associated with e-cigarette use (padvertisement exposure from stores and the Internet, and Blacks reported more advertisement exposure from radio or television. Results suggest that e-cigarette marketing is beginning to breach the Black population who are, as a consequence, "catching up" with Whites with regard to e-cigarette use. Given the significant disparities for smoking-related morbidity and mortality between Blacks and Whites, these findings identify new areas for future research and policy.

  7. The comparative in vitro assessment of e-cigarette and cigarette smoke aerosols using the γH2AX assay and applied dose measurements.

    Science.gov (United States)

    Thorne, David; Larard, Sophie; Baxter, Andrew; Meredith, Clive; Gaҫa, Marianna

    2017-01-04

    DNA damage can be caused by a variety of external and internal factors and together with cellular responses, can establish genomic instability through multiple pathways. DNA damage therefore, is considered to play an important role in the aetiology and early stages of carcinogenesis. The DNA-damage inducing potential of tobacco smoke aerosols in vitro has been extensively investigated; however, the ability of e-cigarette aerosols to induce DNA damage has not been extensively investigated. E-cigarette use has grown globally in recent years and the health implications of long term e-cigarette use are still unclear. Therefore, this study has assessed the induction of double-strand DNA damage in vitro using human lung epithelial cells to e-cigarette aerosols from two different product variants (a "cigalike" and a closed "modular" system) and cigarette smoke. A Vitrocell(®) VC 10 aerosol exposure system was used to generate and dilute cigarette smoke and e-cigarette aerosols, which were delivered to human bronchial epithelial cells (BEAS-2Bs) housed at the air-liquid-interface (ALI) for up to 120min exposure (diluting airflow, 0.25-1L/min). Following exposure, cells were immediately fixed, incubated with primary (0.1% γH2AX antibody in PBS) and secondary antibodies (DyLight™ 549 conjugated goat anti-mouse IgG) containing Hoechst dye DNA staining solution (0.2% secondary antibody and 0.01% Hoechst in PBS), and finally screened using the Cellomics Arrayscan VTI platform. The results from this study demonstrate a clear DNA damage-induced dose response with increasing smoke concentrations up to cytotoxic levels. In contrast, e-cigarette aerosols from two product variants did not induce DNA damage at equivalent to or greater than doses of cigarette smoke aerosol. In this study dosimetry approaches were used to contextualize exposure, define exposure conditions and facilitate comparisons between cigarette smoke and e-cigarette aerosols. Quartz crystal microbalance (QCM

  8. Protective effect of bacoside A on cigarette smoking-induced brain mitochondrial dysfunction in rats.

    Science.gov (United States)

    Anbarasi, Kothandapani; Vani, Ganapathy; Devi, Chennam Srinivasulu Shyamala

    2005-01-01

    Chronic exposure to cigarette smoke affects the structure and function of mitochondria, which may account for the pathogenesis of smoking-related diseases. Bacopa monniera Linn., used in traditional Indian medicine for various neurological disorders, was shown to possess mitrochondrial membrane-stabilizing properties in the rat brain during exposure to morphine. We investigated the protective effect of bacoside A, the active principle of Bacopa monniera, against mitochondrial dysfunction in rat brain induced by cigarette smoke. Male Wistar albino rats were exposed to cigarette smoke and administered bacoside A for a period of 12 weeks. The mitochondrial damage in the brain was assessed by examining the levels of lipid peroxides, cholesterol, phospholipid, cholesterol/phospholipid (C/P) ratio, and the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase, and cytochrome C oxidase. The oxidative phosphorylation (rate of succinate oxidation, respiratory control ratio and ADP/O ratio, and the levels of ATP) was evaluated for the assessment of mitochondrial functional capacity. We found significantly elevated levels of lipid peroxides, cholesterol, and C/P ratio, and decreased levels of phospholipids and mitochondrial enzymes in the rats exposed to cigarette smoke. Measurement of oxidative phosphorylation revealed a marked depletion in all the variables studied. Administration of bacoside A prevented the structural and functional impairment of mitochondria upon exposure to cigarette smoke. From the results, we suggest that chronic cigarette smoke exposure induces damage to the mitochondria and that bacoside A protects the brain from this damage by maintaining the structural and functional integrity of the mitochondrial membrane.

  9. Cigarette smoking induces heat shock protein 70 kDa expression and apoptosis in rat brain: Modulation by bacoside A.

    Science.gov (United States)

    Anbarasi, K; Kathirvel, G; Vani, G; Jayaraman, G; Shyamala Devi, C S

    2006-01-01

    Cigarette smoking is associated with the development of several diseases and antioxidants play a major role in the prevention of smoking-related diseases. Apoptosis is suggested as a possible contributing factor in the pathogenesis of smoking-induced toxicity. Therefore the present study was designed to investigate the influence of chronic cigarette smoke exposure on apoptosis and the modulatory effect of bacoside A (triterpenoid saponin isolated from the plant Bacopa monniera) on smoking-induced apoptosis in rat brain. Adult male albino rats of Wistar strain were exposed to cigarette smoke and simultaneously administered with bacoside A (10 mg/kg b.w./day, orally) for a period of 12 weeks. Expression of brain hsp70 was analyzed by Western blotting. Apoptosis was identified by DNA fragmentation, terminal deoxynucleotidyl transferase-mediated deoxy uridine triphosphate nick end labeling (TUNEL) staining and transmission electron microscopy. The results showed that exposure to cigarette smoke induced hsp70 expression and apoptosis as characterized by DNA laddering, increased TUNEL-positive cells and ultrastructural apoptotic features in the brain. Administration of bacoside A prevented expression of hsp70 and neuronal apoptosis during cigarette smoking. We speculate that apoptosis may be responsible for the smoking-induced brain damage and bacoside A can protect the brain from the toxic effects of cigarette smoking.

  10. Smoking behaviors and intentions among current e-cigarette users, cigarette smokers, and dual users: A national survey of U.S. high school seniors.

    Science.gov (United States)

    McCabe, Sean Esteban; Veliz, Phil; McCabe, Vita V; Boyd, Carol J

    2017-03-01

    E-cigarette use among adolescents has increased significantly in recent years, but it remains unclear whether cigarette smoking behaviors and intentions for future cigarette smoking differ among current (i.e., 30-day) non-users, only e-cigarette users, only cigarette smokers, and dual users. A nationally representative sample of 4385 U.S. high school seniors were surveyed during the spring of their senior year via self-administered questionnaires in 2014. An estimated 9.6% of U.S. high school seniors reported current e-cigarette use only, 6.3% reported current cigarette smoking only, and 7.2% reported current dual use of e-cigarettes and cigarette smoking. There were no significant differences between current only cigarette smokers and dual users in the odds of early onset of cigarette smoking, daily cigarette smoking, intentions for future cigarette smoking, friends' cigarette smoking behaviors, attempts to quit cigarette smoking, or the inability to quit cigarette smoking. Adolescents who only used e-cigarettes had higher odds of intentions for future cigarette smoking in the next 5years (AOR=2.57, 95% CI: 1.21-5.24) than current non-users. Dual users and only cigarette smokers had higher odds of cigarette smoking behaviors and intentions for future cigarette smoking than non-users or only e-cigarette users. Adolescents who engage in current dual use have cigarette smoking behaviors and intentions for future cigarette smoking that more closely resemble cigarette smokers than e-cigarette users. Adolescents who only use e-cigarettes have higher intentions to engage in future cigarette smoking relative to their peers who do not engage in e-cigarette use or cigarette smoking.

  11. Cigarette Smoke Extract Inhibits the Proliferation of Alveolar Epithelial Cells and Augments the Expression of P21WAF1

    Institute of Scientific and Technical Information of China (English)

    Zongxian JIAO; Qilin AO; Xiaona GE; Mi XIONG

    2008-01-01

    Cigarette smoking is intimately related with the development of chronic obstructive pulmonary diseases, and alveolar epithelium is a major target for the exposure of cigarette smoke ex- tract. In order to investigate the effect of cigarette smoke extract on the proliferation of alveolar epithelial cell type Ⅱand its relationship with P21WAF1, the alveolar epithelial type Ⅱ cell line (A549) cells were chosen as surrogate cells to represent alveolar epithelial type Ⅱ cells. MTT assay was used to detect cell viability after interfered with different concentrations of cigarette smoke ex-tract. It was observed cigarette smoke extract inhibited the growth of A549 cells in a dose- and time-dependent manner. The morphological changes, involving the condensation and margination of nuclear chromatin, even karyorrhexis, were observed by both Hoechst staining and electronic mi-croscopy. Flow cytometry analysis demonstrated the increased cell percentages in G1 and subG1phases after the cells were incubated with cigarette smoke extract. The expression of p21WAF1 protein and mRNA was also significantly increased as detected by the methods of Western blot or reverse transcription-polymerase chain reaction respectively. In conclusion, cigarette smoke extract inhibits the proliferation of alveolar epithelial cell type Ⅱ and blocks them in G1/S phase. The intracellular accumulation of P21WAF1 may be one of the mechanisms which contribute to cigarette smoke ex-tract-induced inhibition of cell proliferation.

  12. Electronic cigarettes and thirdhand tobacco smoke: two emerging health care challenges for the primary care provider

    Directory of Open Access Journals (Sweden)

    Nidhi Mehrotra

    2011-02-01

    Full Text Available Ware G Kuschner, Sunayana Reddy, Nidhi Mehrotra, Harman S PaintalDivision of Pulmonary and Critical Care Medicine, Stanford University School of Medicine, Palo Alto, CA, USAAbstract: Primary care providers should be aware of two new developments in nicotine addiction and smoking cessation: 1 the emergence of a novel nicotine delivery system known as the electronic (e- cigarette; and 2 new reports of residual environmental nicotine and other biopersistent toxicants found in cigarette smoke, recently described as “thirdhand smoke”. The purpose of this article is to provide a clinician-friendly introduction to these two emerging issues so that clinicians are well prepared to counsel smokers about newly recognized health concerns relevant to tobacco use. E-cigarettes are battery powered devices that convert nicotine into a vapor that can be inhaled. The World Health Organization has termed these devices electronic nicotine delivery systems (ENDS. The vapors from ENDS are complex mixtures of chemicals, not pure nicotine. It is unknown whether inhalation of the complex mixture of chemicals found in ENDS vapors is safe. There is no evidence that e-cigarettes are effective treatment for nicotine addiction. ENDS are not approved as smoking cessation devices. Primary care givers should anticipate being questioned by patients about the advisability of using e-cigarettes as a smoking cessation device. The term thirdhand smoke first appeared in the medical literature in 2009 when investigators introduced the term to describe residual tobacco smoke contamination that remains after the cigarette is extinguished. Thirdhand smoke is a hazardous exposure resulting from cigarette smoke residue that accumulates in cars, homes, and other indoor spaces. Tobacco-derived toxicants can react to form potent cancer causing compounds. Exposure to thirdhand smoke can occur through the skin, by breathing, and by ingestion long after smoke has cleared from a room

  13. Cigarette smoking and short-term addiction treatment outcome.

    Science.gov (United States)

    Harrell, P T; Montoya, I D; Preston, K L; Juliano, L M; Gorelick, D A

    2011-06-01

    Cigarette smoking is common among patients in cocaine and opioid dependence treatment, and may influence treatment outcome. We addressed this issue in a secondary analysis of data from an outpatient clinical trial of buprenorphine treatment for concurrent cocaine and opioid dependence (13 weeks, N=200). The association between cigarette smoking (lifetime cigarette smoking status, number of cigarettes smoked per day prior to study entry) and short-term treatment outcome (% of urine samples positive for cocaine or opioids, treatment retention) was evaluated with analysis of covariance, bivariate correlations, and multivariate linear regression. Nicotine-dependent smokers (66% of participants) had a significantly higher percentage of cocaine-positive urine samples than non-smokers (12% of participants) (76% vs. 62%), but did not differ in percentage of opioid-positive urine samples or treatment retention. Number of cigarettes smoked per day at baseline was positively associated with percentage of cocaine-positive urine samples, even after controlling for baseline sociodemographic and drug use characteristics, but was not significantly associated with percentage of opioid-positive urine samples or treatment retention. These results suggest that cigarette smoking is associated with poorer short-term outcome of outpatient treatment for cocaine dependence, but perhaps not of concurrent opioid dependence, and support the importance of offering smoking cessation treatment to cocaine-dependent patients.

  14. Cigarette smoking during pregnancy in two regions:cross-sectional study

    Institute of Scientific and Technical Information of China (English)

    Marcel Leppe; Josip Culig; Mirela Eric

    2012-01-01

    Objective:To assess the prevalence of cigarette smoking in pregnancy, and the rate of congenital malformations in children at in utero exposure.Methods:The trial was designed as a cross-sectional study to measure exposure of pregnant women to adverse influence of smoking and their health status.The study consists of two arms: one was conducted at fourZagreb maternity hospitals(Croatia) and the other at the same hospitals inNoviSad(Serbia).Results:Data analysis revealed the habit of cigarette smoking during pregnancy in829(11.9%) of6992(6099+893) women.Malformations were found in105(1.5%) fetuses and newborns.Major congenital malformations were present in4(0.6%), minor malformations in73(10.5%) and low birth weight in12(1.7%) newborns.In all these pregnant women smoked until becoming aware of pregnancy or during pregnancy.Tobacco smoking and congenital abnormalities that define the contingency table were not significantly related inZagreb(P=0.385), as well as inNoviSad(P=0.345). Conclusions:The proportion of pregnant women reporting cigarette smoking was quite similar in Zagreb andNoviSad.There is no statistically significant association between cigarette smoking and congenitalmalformations.

  15. Trans-resveratrol reduces cardiac oxidative stress in rats exposed to cigarette smoke

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    Melina Hauck

    2015-07-01

    Full Text Available Differences between reactive oxygen species and antioxidant defense system unbalance the redox status. The exposure to cigarette smoke can increase this imbalance. Trans-resveratrol is a polyphenol with great antioxidant action that reduces the oxidative stress. This study investigated the effect of the trans-resveratrol supplementation on the cardiac oxidative stress in rats exposed to cigarette smoke. Male Wistar rats were randomized into four groups: Control Group (CG, Exposure to Smoke Group (ESG, Antioxidant Group (AG and Exposure to Smoke plus Antioxidant Group (ESAG. Animals were exposed to cigarette smoke and supplemented with trans-resveratrol (6.0 mg kg-1 for two months. The lipid peroxidation (TBARS and the enzymatic activity of catalase (CAT were measured in the cardiac muscle. The ESG presented the highest lipid peroxidation level compared with CG (p < 0.001, AG (p < 0.001 and ESAG (p < 0.006. The CAT activity was higher in the AG (p < 0.001 and ESAG (p < 0.001 compared with CG. The ESG presented lower CAT activity compared with the ESAG (p < 0.001. The supplementation of Trans-resveratrol attenuated the cardiac oxidative stress and increased the activity of catalase. Our findings evidenced the cardioprotective effect of trans-resveratrol in rats exposed to cigarette smoke.

  16. The Contribution of cocoa additive to cigarette smoking addiction

    NARCIS (Netherlands)

    Rambali B; Andel I van; Schenk E; Wolterink G; Werken G van de; Stevenson H; Vleeming W; TOX; SIR; LVM; PZO

    2003-01-01

    In this report the effect of these compounds on the addiction to cigarette smoking was assessed, using currently available information in the literature on psychoactive compounds of cocoa. The investigated psychoactive cocoa compounds were theobromine, caffeine, serotonin, histamine, tryptophan, try

  17. Cigarette smoke toxins deposited on surfaces: implications for human health.

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    Manuela Martins-Green

    Full Text Available Cigarette smoking remains a significant health threat for smokers and nonsmokers alike. Secondhand smoke (SHS is intrinsically more toxic than directly inhaled smoke. Recently, a new threat has been discovered - Thirdhand smoke (THS - the accumulation of SHS on surfaces that ages with time, becoming progressively more toxic. THS is a potential health threat to children, spouses of smokers and workers in environments where smoking is or has been allowed. The goal of this study is to investigate the effects of THS on liver, lung, skin healing, and behavior, using an animal model exposed to THS under conditions that mimic exposure of humans. THS-exposed mice show alterations in multiple organ systems and excrete levels of NNAL (a tobacco-specific carcinogen biomarker similar to those found in children exposed to SHS (and consequently to THS. In liver, THS leads to increased lipid levels and non-alcoholic fatty liver disease, a precursor to cirrhosis and cancer and a potential contributor to cardiovascular disease. In lung, THS stimulates excess collagen production and high levels of inflammatory cytokines, suggesting propensity for fibrosis with implications for inflammation-induced diseases such as chronic obstructive pulmonary disease and asthma. In wounded skin, healing in THS-exposed mice has many characteristics of the poor healing of surgical incisions observed in human smokers. Lastly, behavioral tests show that THS-exposed mice become hyperactive. The latter data, combined with emerging associated behavioral problems in children exposed to SHS/THS, suggest that, with prolonged exposure, they may be at significant risk for developing more severe neurological disorders. These results provide a basis for studies on the toxic effects of THS in humans and inform potential regulatory policies to prevent involuntary exposure to THS.

  18. Coffee drinking enhances the analgesic effect of cigarette smoking

    DEFF Research Database (Denmark)

    Nastase, Anca; Ioan, Silvia; Braga, Radu I

    2007-01-01

    Nicotine (from cigarette smoke) and caffeine (from coffee) have analgesic effects in humans and experimental animals. We investigated the combined effects of coffee drinking and cigarette smoking on pain experience in a group of moderate nicotine-dependent, coffee drinking, young smokers. Pain...... threshold and pain tolerance were measured during cold pressor test following the habitual nocturnal deprivation of smoking and coffee drinking. Smoking increased pain threshold and pain tolerance in both men and women. Coffee drinking, at a dose that had no independent effect, doubled the increase in pain...

  19. Microbiological components in mainstream and sidestream cigarette smoke

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    Larsson Lennart

    2012-08-01

    Full Text Available Abstract Background Research has shown that tobacco smoke contains substances of microbiological origin such as ergosterol (a fungal membrane lipid and lipopolysaccharide (LPS (in the outer membrane of Gram-negative bacteria. The aim of the present study was to compare the amounts of ergosterol and LPS in the tobacco and mainstream (MS and sidestream (SS smoke of some popular US cigarettes. Methods We measured LPS 3-hydroxy fatty acids and fungal biomass biomarker ergosterol in the tobacco and smoke from cigarettes of 11 popular brands purchased in the US. University of Kentucky reference cigarettes were also included for comparison. Results The cigarette tobacco of the different brands contained 6.88-16.17 (mean 10.64 pmol LPS and 8.27-21.00 (mean 14.05 ng ergosterol/mg. There was a direct correlation between the amounts of ergosterol and LPS in cigarette tobacco and in MS smoke collected using continuous suction; the MS smoke contained 3.65-8.23% (ergosterol and 10.02-20.13% (LPS of the amounts in the tobacco. Corresponding percentages were 0.30-0.82% (ergosterol and 0.42-1.10% (LPS for SS smoke collected without any ongoing suction, and 2.18% and 2.56% for MS smoke collected from eight two-second puffs. Conclusions Tobacco smoke is a bioaerosol likely to contain a wide range of potentially harmful bacterial and fungal components.

  20. Impact of cigarette smoking in type 2 diabetes development

    Institute of Scientific and Technical Information of China (English)

    Xi-tao XIE; Qiang LIU; Jie WU; Makoto WAKUI

    2009-01-01

    Many patients with type 2 diabetes mellitus (DM2) are at risk for micro and macro vascular complications, which could be observed in heavy smokers. Cigarette smoking increases the risk for type 2 diabetes incidence. Nicotine, acknowledged as the major pharmacologically active chemical in tobacco, is responsible for the association between cigarette smoking and development of diabetes. This minireview summarized recent studies on nicotine effects on insulin action and insulin secretion, indicating the impact of nicotine on type 2 diabetes development.

  1. Impact of cigarette smoking in type 2 diabetes development

    OpenAIRE

    Xie, Xi-tao; Liu, Qiang; WU, JIE; Wakui, Makoto

    2009-01-01

    Many patients with type 2 diabetes mellitus (DM2) are at risk for micro and macro vascular complications, which could be observed in heavy smokers. Cigarette smoking increases the risk for type 2 diabetes incidence. Nicotine, acknowledged as the major pharmacologically active chemical in tobacco, is responsible for the association between cigarette smoking and development of diabetes. This minireview summarized recent studies on nicotine effects on insulin action and insulin secretion, indica...

  2. Prophylactic Anti-inflammation Inhibits Cigarette Smoke-induced Emphysema in Guinea Pigs

    Institute of Scientific and Technical Information of China (English)

    张劲农; 陶晓南; 谢建敏; 向敏; 付薇

    2003-01-01

    In this study, the effect of prophylactic anti-inflammation on the development of smokeinduced emphysema was investigated. Young male guinea-pigs aged 1.5 - 2 months (weighing 198.3±26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only),group B (cigarette smoke exposure plus pentoxifylline-rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3mg, im, every three weeks) and control group (group D: animals with sham smoke exposure,raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air-space size, mean linear intercept (Lm): 120.6±16.0 μm in Group A; 89.8±9.2 μm in Group B and 102.4±17.7 μm in Group C. The average Lm in either group B or group C was shorter than that in Group A (ANOVA and Newman-Keuls test, F=8.80, P=0.0002) but comparable to that (94.8±13.2 μm) in group D (P>0.05). It is concluded that longterm prophylactic anti-inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.

  3. In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome.

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    Kenneth R Eyring

    Full Text Available Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. In a house dust mite (HDM model of allergic airway disease, we measured airway hyperresponsiveness (AHR and airway inflammation between mice exposed prenatally to cigarette smoke (CS or filtered air (FA. DNA methylation and gene expression were then measured in lung tissue. We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3 are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease; however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease.

  4. Cigarette smoking: knowledge and attitudes among Mexican physicians

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    TAPIA-CONYER ROBERTO

    1997-01-01

    Full Text Available Objective. To determine the prevalence of the smoking habit among Mexican physicians as well as some of their attitudes and information on specific issues concerning smoking. Material and methods. In 1993, a survey was carried out among 3 568 physicians of the three major official health care institutions in Mexico City. A questionnaire designed for The Mexican National Survey of Addictions (ENA 1993 was used. Prevalence of cigarette smoking, age of onset, number of cigarettes per day; also information and attitudes concerning smoking were assessed. Results. The mean age was 37, 66% were males. Of the 3,488 (98% surveyed, 26.9% were smokers (62% daily, 20.6% were ex-smokers and 52.5% non-smokers. There were differences related to age and sex (p< 0.05. Of daily smokers, 36% smoked between 1 and 5 cigarettes. There was a significant trend among ex-smokers that linked the time they had ceased smoking with the fear to start smoking again. Physicians were well informed of the relationship between cigarette smoking and lung cancer. Over 80% considered tobacco an addictive drug but only 65% were in favor of banning smoking from their workplaces and over 10% were not aware that it is forbidden to smoke inside health care facilities. Conclusions. These results differ from other studies that find the prevalence of smoking among physicians lower than in the general population. Our study revealed a greater prevalence of the smoking habit among female physicians and the number of cigarettes smoked per day was greater than in the general population regardless of sex.

  5. Current Cigarette Smoking Among Adults - United States, 2005-2015.

    Science.gov (United States)

    Jamal, Ahmed; King, Brian A; Neff, Linda J; Whitmill, Jennifer; Babb, Stephen D; Graffunder, Corinne M

    2016-11-11

    Tobacco use is the leading cause of preventable disease and death in the United States, and cigarettes are the most commonly used tobacco product among U.S. adults (1,2). To assess progress toward achieving the Healthy People 2020 target of reducing the proportion of U.S. adults who smoke cigarettes to ≤12.0% (objective TU1.1),* CDC assessed the most recent national estimates of cigarette smoking prevalence among adults aged ≥18 years using data from the 2015 National Health Interview Survey (NHIS). The proportion of U.S. adults who smoke cigarettes declined from 20.9% in 2005 to 15.1% in 2015, and the proportion of daily smokers declined from 16.9% to 11.4%. However, disparities in cigarette smoking persist. In 2015, prevalence of cigarette smoking was higher among adults who were male; were aged 25-44 years; were American Indian/Alaska Native; had a General Education Development certificate (GED); lived below the federal poverty level; lived in the Midwest; were insured through Medicaid or were uninsured; had a disability/limitation; were lesbian, gay, or bisexual; or who had serious psychological distress. Proven population-based interventions, including tobacco price increases, comprehensive smoke-free laws, anti-tobacco mass media campaigns, and barrier-free access to tobacco cessation counseling and medications, are critical to reducing cigarette smoking and smoking-related disease and death among U.S. adults, particularly among subpopulations with the highest smoking prevalences (3).

  6. Cigarette Smoking and Anti-Smoking Counseling Practices among Physicians in Wuhan, China

    Science.gov (United States)

    Gong, Jie; Zhang, Zhifeng; Zhu, Zhaoyang; Wan, Jun; Yang, Niannian; Li, Fang; Sun, Huiling; Li, Weiping; Xia, Jiang; Zhou, Dunjin; Chen, Xinguang

    2012-01-01

    Purpose: The paper seeks to report data on cigarette smoking, anti-smoking practices, physicians' receipt of anti-smoking training, and the association between receipt of the training and anti-smoking practice among physicians in Wuhan, China. Design/methodology/approach: Participants were selected through the stratified random sampling method.…

  7. Health, Secondhand Smoke Exposure, and Smoking Behavior Impacts of No-Smoking Policies in Public Housing, Colorado, 2014–2015

    Science.gov (United States)

    Karp, Shelley; Bialick, Peter; Liverance, Cindy; Seder, Ashley; Berg, Erica; Karp, Liberty

    2016-01-01

    Introduction Exposure to secondhand smoke is problematic for residents living in multiunit housing, as the smoke migrates through shared ventilation systems, unsealed cracks, and door spaces. The objective of our research was to assess resident exposure to secondhand smoke, support for no-smoking policies, and the health impacts of no-smoking policies in multiunit housing. Methods Surveys of 312 heads of households who resided in 1 of 3 multiunit buildings managed by a Colorado public housing authority were administered before and after implementation of a no-smoking policy that prohibited smoking in all resident apartments and all indoor common areas. A matched-pairs analysis of initial surveys and 15-month post-policy implementation surveys for 115 respondents was conducted. Results Decreases were found in the number and percentage of smokers who smoked every day and the number of cigarettes smoked per day, and 30% had quit smoking 15 months after policy implementation. The percentage of residents who smelled secondhand smoke indoors declined significantly. A significant decrease in breathing problems was found after policy implementation. Although decreases were found in the incidence of asthma attacks, emphysema/chronic obstructive pulmonary disease, eye irritation, colds, nasal congestion, and ear/sinus infections, these decreases were not significant. Conclusion Consistent findings across nearly all variables tested suggest that no-smoking policies reduce resident exposure to secondhand smoke, lower the incidence of secondhand smoke–associated breathing problems, decrease daily smoking and cigarette consumption, encourage smoking cessation, and increase quit attempts. If implemented in all multiunit housing, these policies could reduce exposure to secondhand smoke and health problems associated with secondhand smoke, promote smoking cessation, and reduce cigarette consumption. PMID:27763830

  8. Cigarette smoking causes hearing impairment among Bangladeshi population.

    Directory of Open Access Journals (Sweden)

    Ahmed Faisal Sumit

    Full Text Available Lifestyle including smoking, noise exposure with MP3 player and drinking alcohol are considered as risk factors for affecting hearing synergistically. However, little is known about the association of cigarette smoking with hearing impairment among subjects who carry a lifestyle without using MP3 player and drinking alcohol. We showed here the influence of smoking on hearing among Bangladeshi subjects who maintain a lifestyle devoid of using MP3 player and drinking alcohol. A total of 184 subjects (smokers: 90; non-smokers: 94 were included considering their duration and frequency of smoking for conducting this study. The mean hearing thresholds of non-smoker subjects at 1, 4, 8 and 12 kHz frequencies were 5.63 ± 2.10, 8.56±5.75, 21.06 ± 11.06, 40.79 ± 20.36 decibel (dB, respectively and that of the smokers were 7 ± 3.8, 13.27 ± 8.4, 30.66 ± 12.50 and 56.88 ± 21.58 dB, respectively. The hearing thresholds of the smokers at 4, 8 and 12 kHz frequencies were significantly (p5 years showed higher level of auditory threshold (62.16 ± 19.87 dB at 12 kHz frequency compared with that (41.52 ± 19.21 dB of the subjects smoked for 1-5 years and the difference in auditory thresholds was statistically significant (p<0.0002. In this study, the Brinkman Index (BI of smokers was from 6 to 440 and the adjusted odds ratio showed a positive correlation between hearing loss and smoking when adjusted for age and body mass index (BMI. In addition, age, but not BMI, also played positive role on hearing impairment at all frequencies. Thus, these findings suggested that cigarette smoking affects hearing level at all the frequencies tested but most significantly at extra higher frequencies.

  9. The effects of cigarette smoking on male fertility.

    Science.gov (United States)

    Kovac, Jason R; Khanna, Abhinav; Lipshultz, Larry I

    2015-04-01

    Cigarette smoking, one of the main causes of preventable morbidity and mortality, has a multitude of well-known side effects. The relationship between cigarette smoking and infertility has been studied for decades; however, large-scale, population-wide prospective studies are lacking. The majority of the current literature is in the form of retrospective studies focused on the effects of smoking on semen analyses. This article discusses the results of these studies and reviews the postulated mechanisms. The effects of smoking on assisted reproduction and in vitro fertilization outcomes are noted. The consequences of smoking while pregnant on future fertility as well as the outcomes of second-hand smoke are analyzed. The current evidence suggests that men should be advised to abstain from smoking in order to improve reproductive outcomes.

  10. Macrophage elastase suppresses white adipose tissue expansion with cigarette smoking.

    Science.gov (United States)

    Tsuji, Takao; Kelly, Neil J; Takahashi, Saeko; Leme, Adriana S; Houghton, A McGarry; Shapiro, Steven D

    2014-12-01

    Macrophage elastase (MMP12) is a key mediator of cigarette smoke (CS)-induced emphysema, yet its role in other smoking related pathologies remains unclear. The weight suppressing effects of smoking are a major hindrance to cessation efforts, and MMP12 is known to suppress the vascularization on which adipose tissue growth depends by catalyzing the formation of antiangiogenic peptides endostatin and angiostatin. The goal of this study was to determine the role of MMP12 in adipose tissue growth and smoking-related suppression of weight gain. Whole body weights and white adipose depots from wild-type and Mmp12-deficient mice were collected during early postnatal development and after chronic CS exposure. Adipose tissue specimens were analyzed for angiogenic and adipocytic markers and for content of the antiangiogenic peptides endostatin and angiostatin. Cultured 3T3-L1 adipocytes were treated with adipose tissue homogenate to examine its effects on vascular endothelial growth factor (VEGF) expression and secretion. MMP12 content and activity were increased in the adipose tissue of wild-type mice at 2 weeks of age, leading to elevated endostatin production, inhibition of VEGF secretion, and decreased adipose tissue vascularity. By 8 weeks of age, adipose MMP12 levels subsided, and the protein was no longer detectable. However, chronic CS exposure led to macrophage accumulation and restored adipose MMP12 activity, thereby suppressing adipose tissue mass and vascularity. Our results reveal a novel systemic role for MMP12 in postnatal adipose tissue expansion and smoking-associated weight loss by suppressing vascularity within the white adipose tissue depots.

  11. Effect of Sugar Content on Acetaldehyde Yield in Cigarette Smoke

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    Cahours X

    2014-12-01

    Full Text Available The relationship between cigarette blend sugar and acetaldehyde formed in its smoke is a matter of current regulatory interest. This paper provides a re-analysis of data from 83 European commercial cigarettes studied in the 1970s and more modern data on sugar levels and acetaldehyde yields from a series of 97 European commercial cigarettes containing both inherent sugar and in other cases inherent and added sugar. It also provides data from 65 experimental cigarette products made from single curing grades of tobacco, having a wide range of inherent sugar levels but no added sugar.

  12. Toxic Chemicals in Cigarette Mainstream Smoke - Hazard and Hoopla

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    Rodgman A

    2014-12-01

    Full Text Available These are curious times. The Canadian government has passed legislation that requires cigarette manufacturers to routinely test and publish the amounts of 44 toxic substances in cigarette mainstream smoke (MSS. Following in the footsteps of their northern neighbor, various US legislators and regulators are considering modifications to their cigarette testing and reporting programs that will also list toxicants in MSS. Across the Atlantic Ocean, the European Commission has passed a directive that may also follow the North American lead for public disclosure of MSS toxic chemicals for each brand of cigarette sold in the marketplace. United Kingdom authorities have also expressed their intention to follow this mandate.

  13. Comparison of Select Analytes in Exhaled Aerosol from E-Cigarettes with Exhaled Smoke from a Conventional Cigarette and Exhaled Breaths

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    Gerald A. Long

    2014-10-01

    Full Text Available Exhaled aerosols were collected following the use of two leading U.S. commercial electronic cigarettes (e-cigarettes and a conventional cigarette by human subjects and analyzed for phenolics, carbonyls, water, glycerin and nicotine using a vacuum-assisted filter pad capture system. Exhaled breath blanks were determined for each subject prior to each product use and aerosol collection session. Distribution and mass balance of exhaled e-cigarette aerosol composition was greater than 99.9% water and glycerin, and a small amount (<0.06% of nicotine. Total phenolic content in exhaled e-cigarette aerosol was not distinguishable from exhaled breath blanks, while total phenolics in exhaled cigarette smoke were significantly greater than in exhaled e-cigarette aerosol and exhaled breaths, averaging 66 µg/session (range 36 to 117 µg/session. The total carbonyls in exhaled e-cigarette aerosols were also not distinguishable from exhaled breaths or room air blanks. Total carbonyls in exhaled cigarette smoke was significantly greater than in exhaled e-cigarette aerosols, exhaled breath and room air blanks, averaging 242 µg/session (range 136 to 352 µg/session. These results indicate that exhaled e-cigarette aerosol does not increase bystander exposure for phenolics and carbonyls above the levels observed in exhaled breaths of air.

  14. Egr-1 regulates autophagy in cigarette smoke-induced chronic obstructive pulmonary disease.

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    Zhi-Hua Chen

    Full Text Available BACKGROUND: Chronic obstructive pulmonary disease (COPD is a progressive lung disease characterized by abnormal cellular responses to cigarette smoke, resulting in tissue destruction and airflow limitation. Autophagy is a degradative process involving lysosomal turnover of cellular components, though its role in human diseases remains unclear. METHODOLOGY AND PRINCIPAL FINDINGS: Increased autophagy was observed in lung tissue from COPD patients, as indicated by electron microscopic analysis, as well as by increased activation of autophagic proteins (microtubule-associated protein-1 light chain-3B, LC3B, Atg4, Atg5/12, Atg7. Cigarette smoke extract (CSE is an established model for studying the effects of cigarette smoke exposure in vitro. In human pulmonary epithelial cells, exposure to CSE or histone deacetylase (HDAC inhibitor rapidly induced autophagy. CSE decreased HDAC activity, resulting in increased binding of early growth response-1 (Egr-1 and E2F factors to the autophagy gene LC3B promoter, and increased LC3B expression. Knockdown of E2F-4 or Egr-1 inhibited CSE-induced LC3B expression. Knockdown of Egr-1 also inhibited the expression of Atg4B, a critical factor for LC3B conversion. Inhibition of autophagy by LC3B-knockdown protected epithelial cells from CSE-induced apoptosis. Egr-1(-/- mice, which displayed basal airspace enlargement, resisted cigarette-smoke induced autophagy, apoptosis, and emphysema. CONCLUSIONS: We demonstrate a critical role for Egr-1 in promoting autophagy and apoptosis in response to cigarette smoke exposure in vitro and in vivo. The induction of autophagy at early stages of COPD progression suggests novel therapeutic targets for the treatment of cigarette smoke induced lung injury.

  15. Emotional, behavioural problems and cigarette smoking in adolescence: findings of a Greek cross-sectional study

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    Rotsika Vasiliki

    2010-02-01

    Full Text Available Abstract Background Although several studies have reported findings concerning the association between smoking and emotional/behavioural problems, little research has investigated this association after controlling for confounding factors which have been found to be significantly correlated with both cigarette smoking and emotional/behavioural problems and may have a strong effect on the relationship between adolescents' mental health and smoking. The present study attempted to assess the association between adolescents' smoking status and their emotional/behavioural problems after controlling for a number of possible confounders (i.e. age, gender, parental smoking status, exposure to family smoking, family socioeconomic status, adolescents' leisure time in a Greek nation-wide school-based sample. Methods Participants completed a questionnaire which retrieved information about age, gender, family socioeconomic status, smoking status, parental smoking, adolescents' leisure time and emotional/behavioural problems. Data were modelled using multiple logistic regression analysis with adolescents' smoking status as the dependent variable. Results A total of 1194 (i.e. 63% response rate of self-reported questionnaires (40.1% boys, 59.9% girls; 12-18 years old were returned. Data from 1030 participants with full data were analyzed. Cigarette smoking was strongly associated with higher levels of emotional/behavioural problems (p Conclusions This study supports the association between smoking and emotional/behavioural problems among adolescents. Addressing adolescents' needs regarding their emotional/behavioural health could be helpful in the development of effective anti-smoking strategies in school environment and elsewhere.

  16. Counseling Chinese Patients about Cigarette Smoking: The Role of Nurses

    Science.gov (United States)

    Li, Han Zao; Zhang, Yu; MacDonell, Karen; Li, Xiao Ping; Chen, Xinguang

    2012-01-01

    Purpose: The main purpose of this study is to determine the cigarette smoking rate and smoking cessation counseling frequency in a sample of Chinese nurses. Design/methodology/approach: At the time of data collection, the hospital had 260 nurses, 255 females and five males. The 200 nurses working on the two daytime shifts were given the…

  17. Good relationship between saliva cotinine kinetics and plasma cotinine kinetics after smoking one cigarette.

    Science.gov (United States)

    Yuki, Dai; Kikuchi, Akira; Miura, Naoki; Kakehi, Aoi; Onozawa, Masahiro

    2013-11-01

    This study investigated the relationship between plasma and saliva cotinine kinetics after smoking one cigarette and the relationship between cotinine kinetics and estimated nicotine intake, which was calculated as mouth level exposure (MLE) of nicotine, from smoking two test cigarettes with different nicotine yields. This study was conducted in 16 healthy adult Japanese smokers, who did not have null nor reduced-activity alleles of CYP2A6, with a quasi-randomized crossover design of smoking a low-tar cigarette or a high-tar cigarette. Saliva cotinine showed similar concentration profiles to plasma cotinine, and all of the calculated pharmacokinetic parameters of cotinine showed the same values in plasma and saliva. The Cmax and AUC of cotinine showed almost the same dose-responsiveness to the estimated MLE of nicotine between plasma and saliva, but the tmax and t1/2 of cotinine were not affected by the estimated MLE of nicotine in either plasma or saliva. The results show that saliva cotinine kinetics reflects plasma cotinine kinetics, and measurement of saliva cotinine concentration gives the same information as plasma cotinine on the nicotine intake. Thus, saliva cotinine would be a good and less-invasive exposure marker of cigarette smoke, reflecting the plasma cotinine concentration and kinetics.

  18. Determination of Carbonyl Compounds in Exhaled Cigarette Smoke

    Directory of Open Access Journals (Sweden)

    Moldoveanu S

    2014-12-01

    Full Text Available This paper presents the findings on a quantitative evaluation of carbonyl levels in exhaled cigarette smoke from human subjects. The cigarettes evaluated include products with 5.0 mg ‘tar’, 10.6 mg ‘tar’ and 16.2 mg ‘tar’, where ‘tar’ is defined as the weight of total wet particulate matter (TPM minus the weight of nicotine and water, and the cigarettes are smoked following U.S. Federal Trade Commission (FTC recommendations. The measured levels of carbonyls in the exhaled smoke were compared with calculated yields of carbonyls in the inhaled smoke and a retention efficiency was obtained. The number of human subjects included a total of ten smokers for the 10.6 mg ‘tar’, five for the 16.2 mg ‘tar’, and five for the 5.0 mg ‘tar’ product, each subject smoking three cigarettes. The analyzed carbonyl compounds included several aldehydes (formaldehyde, acetaldehyde, acrolein, propionaldehyde, crotonaldehyde and n-butyraldehyde, and two ketones (acetone and 2-butanone. The smoke collection from the human subjects was vacuum assisted. Exhaled smoke was collected on Cambridge pads pretreated with a solution of dinitrophenylhydrazine (DNPH followed by high performance liquid chromatography (HPLC analysis of the dinitrophenylhydrazones of the carbonyl compounds. The cigarette butts from the smokers were collected and analyzed for nicotine. The nicotine levels for the cigarette butts from the smokers were used to calculate the level of carbonyls in the inhaled smoke, based on calibration curves. These were generated separately by analyzing the carbonyls in smoke and the nicotine in the cigarette butts obtained by machine smoking under different puffing regimes. The comparison of the level of carbonyl compounds in exhaled smoke with that from the inhaled smoke showed high retention of all the carbonyls. The retention of aldehydes was above 95% for all three different ‘tar’ levels cigarettes. The ketones were retained with a

  19. Adverse health effects of cigarette smoke: aldehydes Crotonaldehyde, butyraldehyde, hexanal and malonaldehyde

    NARCIS (Netherlands)

    Andel I van; Sleijffers A; Schenk E; Rambali B; Wolterink G; Werken G van de; Aerts LAGJM van; Vleeming W; Amsterdam JGC van; TOX

    2006-01-01

    Crotonaldehyde in cigarette smoke can be concluded to induce airway damage in humans. This is one conclusion derived from the existing data found in the literature and reported here in the discussion on adverse health effects and possible addictive effects due to the exposure of crotonaldehyde, buty

  20. Pim1 kinase protects airway epithelial cells from cigarette smoke-induced damage and airway inflammation

    NARCIS (Netherlands)

    de Vries, M.; Heijink, Hilde; Gras, R.; den Boef, L. E.; Reinders-Luinge, M.; Pouwels, S. D.; Hylkema, Machteld; van der Toorn, Marco; Brouwer, U.; van Oosterhout, A. J. M.; Nawijn, M. C.

    2014-01-01

    Exposure to cigarette smoke (CS) is the main risk factor for developing chronic obstructive pulmonary disease and can induce airway epithelial cell damage, innate immune responses, and airway inflammation. We hypothesized that cell survival factors might decrease the sensitivity of airway epithelial

  1. Modeling the influence of vitamin D deficiency on cigarette smoke-induced emphysema.

    Directory of Open Access Journals (Sweden)

    Mardi A. Crane-Godreau

    2013-06-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is a major cause of morbidity and mortality worldwide. While the primary risk factor for COPD is cigarette smoke exposure, vitamin D deficiency has been epidemiologically implicated as a factor in the progressive development of COPD-associated emphysema. Because of difficulties inherent to studies involving multiple risk factors in the progression of COPD in humans, we developed a murine model in which to study the separate and combined effects of vitamin D deficiency and cigarette smoke exposure. During a 16 week period, mice were exposed to one of four conditions, control diet breathing room air (CD-NS, control diet with cigarette smoke exposure (CD-CSE, vitamin D deficient diet breathing room air (VDD-NS or vitamin D deficient diet with cigarette smoke exposure (VDD-CSE. At the end of the exposure period, the lungs were examined by a pathologist and separately by morphometric analysis. In parallel experiments, mice were anesthetized for pulmonary function testing followed by sacrifice and analysis. Emphysema (determined by an increase in alveolar mean linear intercept length was more severe in the VDD-CSE mice compared to control animals and animals exposed to VDD or CSE alone. The VDD-CSE and the CD-CSE mice had increased total lung capacity and increased static lung compliance. There was also a significant increase in the matrix metalloproteinase-9: tissue inhibitor of metalloproteinases-1 ratio in VDD-CSE mice compared with all controls. Alpha-1 antitrypsin expression was reduced in VDD-CSE mice as well. In summary, vitamin D deficiency, when combined with cigarette smoke exposure, seemed to accelerate the appearance of emphysemas, perhaps by virtue of an increased protease-antiprotease ratio in the combined VDD-CSE animals. These results support the value of our mouse model in the study of COPD.

  2. [Assessment of cadmium and lead released from cigarette smoke].

    Science.gov (United States)

    Suna, S; Asakawa, F; Jitsunari, F; Manabe, Y; Gotou, A; Fukunaga, I; Nakajima, T

    1991-12-01

    Cigarette smoke, which contains many harmful compounds, affects not only the smoker's health but also indoor air quality. To evaluate indoor air contamination by cadmium (Cd) and lead (Pb), we measured Cd and Pb contained in the mainstream and sidestream smoke exhaled by experimental smoking of Japanese cigarettes and also determined urinary and blood Cd and Pb levels in smokers and non-smokers and air Cd and Pb levels in smoky environments. 1. One cigarette of each of 7 Japanese brands contained about 1 microgram each of Cd and Pb, of which about 50 ng each was released to the mainstream and 250 ng of Cd and 50 ng of Pb to the sidestream by smoking. 2. The blood Cd level in the smokers was significantly higher than that in the non-smokers. The urinary Cd level in the smokers was slightly higher than that in the non-smokers. The blood Cd level was related to the number of cigarettes smoked daily. Blood and urinary Pb levels did not differ between the smokers and non-smokers, but the blood Pb level was also related to the number of cigarettes smoked daily. 3. The air Cd levels in smoky places such as the smoking car of the special express train, an office, and a pachinko parlor were markedly higher than that in outdoor air. The air Cd concentration was well correlated with the environmental tobacco smoke concentration. On the other hand, the air Pb level was slightly higher in the above smoky places than outdoors. The mean air Pb concentration was not correlated with the environmental tobacco smoke concentration but was higher at higher environmental tobacco smoke concentration in each place.

  3. The human laryngeal microbiome: effects of cigarette smoke and reflux

    Science.gov (United States)

    Jetté, Marie E.; Dill-McFarland, Kimberly A.; Hanshew, Alissa S.; Suen, Garret; Thibeault, Susan L.

    2016-01-01

    Prolonged diffuse laryngeal inflammation from smoking and/or reflux is commonly diagnosed as chronic laryngitis and treated empirically with expensive drugs that have not proven effective. Shifts in microbiota have been associated with many inflammatory diseases, though little is known about how resident microbes may contribute to chronic laryngitis. We sought to characterize the core microbiota of disease-free human laryngeal tissue and to investigate shifts in microbial community membership associated with exposure to cigarette smoke and reflux. Using 454 pyrosequencing of the 16S rRNA gene, we compared bacterial communities of laryngeal tissue biopsies collected from 97 non-treatment-seeking volunteers based on reflux and smoking status. The core community was characterized by a highly abundant OTU within the family Comamonadaceae found in all laryngeal tissues. Smokers demonstrated less microbial diversity than nonsmokers, with differences in relative abundances of OTUs classified as Streptococcus, unclassified Comamonadaceae, Cloacibacterium, and Helicobacter. Reflux status did not affect microbial diversity nor community structure nor composition. Comparison of healthy laryngeal microbial communities to benign vocal fold disease samples revealed greater abundance of Streptococcus in benign vocal fold disease suggesting that mucosal dominance by Streptococcus may be a factor in disease etiology. PMID:27775059

  4. Differences in cardiovascular toxicities associated with cigarette smoking and snuff use revealed using novel zebrafish models

    Directory of Open Access Journals (Sweden)

    Maggie Folkesson

    2016-07-01

    Full Text Available Tobacco use is strongly associated with cardiovascular disease and the only avoidable risk factor associated with development of aortic aneurysm. While smoking is the most common form of tobacco use, snuff and other oral tobacco products are gaining popularity, but research on potentially toxic effects of oral tobacco use has not kept pace with the increase in its use. Here, we demonstrate that cigarette smoke and snuff extracts are highly toxic to developing zebrafish embryos. Exposure to such extracts led to a palette of toxic effects including early embryonic mortality, developmental delay, cerebral hemorrhages, defects in lymphatics development and ventricular function, and aneurysm development. Both cigarette smoke and snuff were more toxic than pure nicotine, indicating that other compounds in these products are also associated with toxicity. While some toxicities were found following exposure to both types of tobacco product, other toxicities, including developmental delay and aneurysm development, were specifically observed in the snuff extract group, whereas cerebral hemorrhages were only found in the group exposed to cigarette smoke extract. These findings deepen our understanding of the pathogenic effects of cigarette smoking and snuff use on the cardiovascular system and illustrate the benefits of using zebrafish to study mechanisms involved in aneurysm development.

  5. E-Cigarette Use Among Never-Smoking California Students.

    Science.gov (United States)

    Bostean, Georgiana; Trinidad, Dennis R; McCarthy, William J

    2015-12-01

    We determined the extent to which adolescents who have never used tobacco try e-cigarettes. Data on the prevalence and correlates of e-cigarette use among 482,179 California middle and high school students are from the 2013-2014 California Healthy Kids Survey. Overall, 24.4% had ever used e-cigarettes (13.4% have never used tobacco and 11.0% have used tobacco), and 12.9% were current e-cigarette users (5.9% have never used tobacco). Among those who have never used tobacco, males and older students were more likely to use e-cigarettes than females and younger students. Hispanics (odds ratio [OR] = 1.60; confidence interval [CI] = 1.53, 1.67) and those of other races (OR = 1.24; CI = 1.19, 1.29) were more likely than Whites to have ever used e-cigarettes, but only among those who had never used smokeless tobacco and never smoked a whole cigarette. E-cigarette use is very prevalent among California students who have never smoked tobacco, especially among Hispanic and other race students, males, and older students.

  6. Exposure to teachers smoking and adolescent smoking behaviour

    DEFF Research Database (Denmark)

    Poulsen, L H; Osler, M; Roberts, C

    2002-01-01

    To determine whether adolescent smoking behaviour is associated with their perceived exposure to teachers or other pupils smoking at school, after adjustment for exposure to smoking at home, in school, and best friends smoking.......To determine whether adolescent smoking behaviour is associated with their perceived exposure to teachers or other pupils smoking at school, after adjustment for exposure to smoking at home, in school, and best friends smoking....

  7. Factors Associated with American Indian Cigarette Smoking in Rural Settings

    Directory of Open Access Journals (Sweden)

    Karabi Nandy

    2011-03-01

    Full Text Available Introduction: This paper reports on the prevalence, factors and patterns of cigarette smoking among rural California American Indian (AI adults. Methods: Thirteen Indian health clinic registries formed the random household survey sampling frame (N = 457. Measures included socio-demographics, age at smoking initiation, intention to quit, smoking usage, smoking during pregnancy, health effects of smoking, suicide attempts or ideation, history of physical abuse, neglect and the role of the environment (smoking at home and at work. Statistical tests included Chi Square and Fisher’s Exact test, as well as multiple logistic regression analysis among never, former, and current smokers. Results: Findings confirm high smoking prevalence among male and female participants (44% and 37% respectively. American Indians begin smoking in early adolescence (age 14.7. Also, 65% of current smokers are less than 50% Indian blood and 76% of current smokers have no intention to quit smoking. Current and former smokers are statistically more likely to report having suicidal ideation than those who never smoked. Current smokers also report being neglected and physically abused in childhood and adolescence, are statistically more likely to smoke ½ pack or less (39% vs. 10% who smoke 1+ pack, smoke during pregnancy, and have others who smoke in the house compared with former and never smokers. Conclusion: Understanding the factors associated with smoking will help to bring about policy changes and more effective programs to address the problem of high smoking rates among American Indians.

  8. The Relation between Frequency of E-Cigarette Use and Frequency and Intensity of Cigarette Smoking among South Korean Adolescents

    Directory of Open Access Journals (Sweden)

    Jung Ah Lee

    2017-03-01

    Full Text Available Introduction: The prevalence of adolescent electronic cigarette (e-cigarette use has increased in most countries. This study aims to determine the relation between the frequency of e-cigarette use and the frequency and intensity of cigarette smoking. Additionally, the study evaluates the association between the reasons for e-cigarette use and the frequency of its use. Materials and Methods: Using the 2015 Korean Youth Risk Behavior Web-Based Survey, we included 6655 adolescents with an experience of e-cigarette use who were middle and high school students aged 13–18 years. We compared smoking experience, the frequency and intensity of cigarette smoking, and the relation between the reasons for e-cigarette uses and the frequency of e-cigarette use. Results: The prevalence of e-cigarette ever and current (past 30 days users were 10.1% and 3.9%, respectively. Of the ever users, approximately 60% used e-cigarettes not within 1 month. On the other hand, 8.1% used e-cigarettes daily. The frequent and intensive cigarette smoking was associated with frequent e-cigarette uses. The percentage of frequent e-cigarette users (≥10 days/month was 3.5% in adolescents who did not smoke within a month, but 28.7% among daily smokers. Additionally, it was 9.1% in smokers who smoked less than 1 cigarette/month, but 55.1% in smokers who smoked ≥20 cigarettes/day. The most common reason for e-cigarette use was curiosity (22.9%, followed by the belief that they are less harmful than conventional cigarettes (18.9%, the desire to quit smoking (13.1%, and the capacity for indoor use (10.7%. Curiosity was the most common reason among less frequent e-cigarette users; however, the desire to quit smoking and the capacity for indoor use were the most common reasons among more frequent users. Conclusions: Results showed a positive relation between frequency or intensity of conventional cigarette smoking and the frequency of e-cigarette use among Korean adolescents, and

  9. The Relation between Frequency of E-Cigarette Use and Frequency and Intensity of Cigarette Smoking among South Korean Adolescents

    Science.gov (United States)

    Lee, Jung Ah; Lee, Sungkyu; Cho, Hong-Jun

    2017-01-01

    Introduction: The prevalence of adolescent electronic cigarette (e-cigarette) use has increased in most countries. This study aims to determine the relation between the frequency of e-cigarette use and the frequency and intensity of cigarette smoking. Additionally, the study evaluates the association between the reasons for e-cigarette use and the frequency of its use. Materials and Methods: Using the 2015 Korean Youth Risk Behavior Web-Based Survey, we included 6655 adolescents with an experience of e-cigarette use who were middle and high school students aged 13–18 years. We compared smoking experience, the frequency and intensity of cigarette smoking, and the relation between the reasons for e-cigarette uses and the frequency of e-cigarette use. Results: The prevalence of e-cigarette ever and current (past 30 days) users were 10.1% and 3.9%, respectively. Of the ever users, approximately 60% used e-cigarettes not within 1 month. On the other hand, 8.1% used e-cigarettes daily. The frequent and intensive cigarette smoking was associated with frequent e-cigarette uses. The percentage of frequent e-cigarette users (≥10 days/month) was 3.5% in adolescents who did not smoke within a month, but 28.7% among daily smokers. Additionally, it was 9.1% in smokers who smoked less than 1 cigarette/month, but 55.1% in smokers who smoked ≥20 cigarettes/day. The most common reason for e-cigarette use was curiosity (22.9%), followed by the belief that they are less harmful than conventional cigarettes (18.9%), the desire to quit smoking (13.1%), and the capacity for indoor use (10.7%). Curiosity was the most common reason among less frequent e-cigarette users; however, the desire to quit smoking and the capacity for indoor use were the most common reasons among more frequent users. Conclusions: Results showed a positive relation between frequency or intensity of conventional cigarette smoking and the frequency of e-cigarette use among Korean adolescents, and frequency of e-cigarette

  10. Factors affecting exposure to nicotine and carbon monoxide in adult cigarette smokers.

    Science.gov (United States)

    Muhammad-Kah, Raheema; Liang, Qiwei; Frost-Pineda, Kimberly; Mendes, Paul E; Roethig, Hans J; Sarkar, Mohamadi

    2011-10-01

    Exposure to cigarette smoke among smokers is highly variable. This variability has been attributed to differences in smoking behavior as measured by smoking topography, as well as other behavioral and subjective aspects of smoking. The objective of this study was to determine the factors affecting smoke exposure as estimated by biomarkers of exposure to nicotine and carbon monoxide (CO). In a multi-center cross-sectional study of 3585 adult smokers and 1077 adult nonsmokers, exposure to nicotine and CO was estimated by 24h urinary excretion of nicotine and five of its metabolites and by blood carboxyhemoglobin, respectively. Number of cigarettes smoked per day (CPD) was determined from cigarette butts returned. Puffing parameters were determined through a CreSS® micro device and a 182-item adult smoker questionnaire (ASQ) was administered. The relationship between exposure and demographic factors, smoking machine measured tar yield and CPD was examined in a statistical model (Model A). Topography parameters were added to this model (Model B) which was further expanded (Model C) by adding selected questions from the ASQ identified by a data reduction process. In all the models, CPD was the most important and highest ranking factor determining daily exposure. Other statistically significant factors were number of years smoked, questions related to morning smoking, topography and tar yield categories. In conclusion, the models investigated in this analysis, explain about 30-40% of variability in exposure to nicotine and CO.

  11. Acute effects of cigarette smoking on pattern electroretinogram.

    Science.gov (United States)

    Gundogan, Fatih C; Durukan, A Hakan; Mumcuoglu, Tarkan; Sobaci, Gungor; Bayraktar, M Zeki

    2006-09-01

    In this study, acute effects of cigarette smoking on the pattern electroretinogram (PERG) were investigated. First, variability of the PERG was studied in a group of young male smokers (26 right eyes of 26 subjects). Then PERGs were investigated in a group of habitual smokers (17 right eyes of 17 subjects) in separate real smoking and sham smoking sessions. On each session PERGs were recorded pre-smoking (PS), immediately after smoking (IAS) and 5 min after smoking (5th) conditions. Real smoking significantly increased P50 amplitudes and decreased N95 latencies. Regarding P50 amplitudes in the real smoking sessions, the differences were significant between PS and IAS (PS: 3.3 +/- 0.5 muV, IAS: 3.7 +/- 0.7microV, P = 0.015) and between PS-5th (PS: 3.3 +/- 0.5microV, 5th: 4.1 +/- 0.9microV, P = 0.039). There was significant difference (P = 0.024) between N95 latencies of PS (98.5 +/- 6.9 ms) and IAS (94.7 +/- 5.1 ms) in the real smoking sessions. No statistically significant difference was observed in sham smoking sessions. Our results indicated, for the first time, that cigarette smoking may influence PERG amplitude and latency significantly in habitual smokers.

  12. Medicalisation, smoking and e-cigarettes: evidence and implications.

    Science.gov (United States)

    Morphett, Kylie; Carter, Adrian; Hall, Wayne; Gartner, Coral

    2016-11-30

    There is debate in the tobacco control literature about the value of a medical model in reducing smoking-related harm. The variety of medical treatments for smoking cessation has increased, health professionals are encouraged to use them to assist smoking cessation and tobacco dependence is being described as a 'chronic disease'. Some critics suggest that the medicalisation of smoking undermines the tobacco industry's responsibility for the harms of smoking. Others worry that it will lead smokers to deny personal responsibility for cessation, create beliefs in 'magic bullets' for smoking cessation, or erode smokers' confidence in their ability to quit. We argue that the medicalisation of smoking will have limited impact due to the emphasis on population-based interventions in tobacco control, the ambiguous place of nicotine among other drugs and the modest efficacy of current pharmacotherapies. These factors, as well as lay understandings of smoking that emphasise willpower, personal choice and responsibility, have contributed to the limited success of medical approaches to smoking cessation. While the rapid uptake of e-cigarettes in some countries has provided an option for those who reject medical treatments for smoking cessation, current regulatory developments could limit the potential of e-cigarettes to provide non-therapeutic nicotine for those who currently smoke tobacco.

  13. Switching from usual brand cigarettes to a tobacco-heating cigarette or snus: Part 2. Biomarkers of exposure.

    Science.gov (United States)

    Ogden, Michael W; Marano, Kristin M; Jones, Bobbette A; Morgan, Walter T; Stiles, Mitchell F

    2015-01-01

    A randomized, multi-center study of adult cigarette smokers switched to tobacco-heating cigarettes, snus or ultra-low machine yield tobacco-burning cigarettes (50/group) was conducted, and subjects' experience with the products was followed for 24 weeks. Differences in biomarkers of tobacco exposure between smokers and never smokers at baseline and among groups relative to each other and over time were assessed. Results indicated reduced exposure to many potentially harmful constituents found in cigarette smoke following product switching. Findings support differences in exposure from the use of various tobacco products and are relevant to the understanding of a risk continuum among tobacco products (ClinicalTrials.gov Identifier: NCT02061917).

  14. Lethal impacts of cigarette smoke in cultured tobacco cells

    Directory of Open Access Journals (Sweden)

    Kawano Tomonori

    2011-07-01

    Full Text Available Abstract Background In order to understand and generalize the toxic mechanism of cigarette smoke in living cells, comparison of the data between animal systems and other biological system such as microbial and plant systems is highly beneficial. Objective By employing the tobacco cells as model materials for cigarette smoke toxicity assay, the impacts of the combustion by-products such as nitrogen oxides could be highlighted as the toxic impacts of the plant-derived endogenous chemicals could be excluded in the plant cells. Methods Cigarette smoke-induced cell death was assessed in tobacco cell suspension cultures in the presence and absence of pharmacological inhibitors. Results Cigarette smoke was effective in induction of cell death. The smoke-induced cell death could be partially prevented by addition of nitric oxide (NO scavenger, suggesting the role for NO as the cell death mediator. Addition of NO donor to tobacco cells also resulted in development of partial cell death further confirming the role of NO as cell death mediator. Members of reactive oxygen species and calcium ion were shown to be protecting the cells from the toxic action of smoke-derived NO.

  15. In Adult Smokers Unwilling or Unable to Quit, Does Changing From Tobacco Cigarettes to Electronic Cigarettes Decrease the Incidence of Negative Health Effects Associated With Smoking Tobacco? A Clin-IQ

    Directory of Open Access Journals (Sweden)

    Jennifer Brown

    2014-05-01

    Full Text Available Data from a randomized controlled trial and systematic review support the claim that switching from tobacco cigarettes to electronic cigarettes (e-cigarettes can reduce the short-term negative health effects of smoking. In adult smokers unwilling or unable to quit, exhaled carbon monoxide levels, total number of cigarettes smoked, and exposure to nitrosamine chemicals were reduced within a 12-month period. While the e-cigarette industry remains largely unregulated thus far, these studies provide encouraging hope in the uphill battle toward helping patients make informed and healthy choices.

  16. Opinions of Turkish University Students on Cigarette Smoking at Schools

    Science.gov (United States)

    Keloglu-Isler, Esra; Erdogan, Irfan

    Cigarette smoking among college students is a critical public health problem with serious personal and social consequences. This study examined college student opinions about smoking in the student cafeteria, hallways and offices, considering smoking as freedom of choice, complying with the cigarette law and policy of universities on smoking. A sample of 1527 students (53.9% female, 46.1% male) attending to the six prestigious universities in Ankara, Turkey, completed a ten-item questionnaire. Results of the study showed that nonsmoking students reported the most favorable opinions toward the issues questioned, whereas occasional smokers and regular smokers reported the least favorable opinions. The highest level of disagreement by smokers and nonsmokers was provided for banning cigarette smoking in the cafeteria. Students generally agreed on that teachers should not smoke in the classrooms and in their offices with doors open. Recommended actions include campus-wide no-smoking policies embracing indoors and outdoors and identification and use of new ways of providing smoking prevention and cessation programs and services.

  17. Neural correlates of response inhibition and cigarette smoking in late adolescence.

    Science.gov (United States)

    Galván, Adriana; Poldrack, Russell A; Baker, Christine M; McGlennen, Kristine M; London, Edythe D

    2011-04-01

    Smoking is usually initiated in adolescence, and is the leading preventable cause of death in the United States. Little is known, however, about the links between smoking and neurobiological function in adolescent smokers. This study aimed to probe prefrontal cortical function in late adolescent smokers, using a response inhibition task, and to assess possible relationships between inhibition-related brain activity, clinical features of smoking behavior, and exposure to cigarette smoking. Participants in this study were otherwise healthy late adolescent smokers (15-21 years of age; n=25), who reported daily smoking for at least the 6 months before testing, and age- and education-matched nonsmokers (16-21 years of age; n=25), who each reported smoking fewer than five cigarettes in their lifetimes. The subjects performed the Stop-signal Task, while undergoing functional magnetic resonance imaging. There were no significant group differences in prefrontal cortical activity during response inhibition, but the Heaviness of Smoking Index, a measure of smoking behavior and dependence, was negatively related to neural function in cortical regions of the smokers. These findings suggest that smoking can modulate prefrontal cortical function. Given the late development of the prefrontal cortex, which continues through adolescence, it is possible that smoking may influence the trajectory of brain development during this critical developmental period.

  18. Biomarkers of exposure to environmental tobacco smoke in infants

    DEFF Research Database (Denmark)

    Sørensen, M; Bisgaard, H; Stage, M;

    2007-01-01

    Non-invasive biomonitoring of exposure to environmental tobacco smoke (ETS) by means of hair is attractive in children, although systematic evaluation is required in infants. The objective was to compare nicotine and cotinine concentrations in hair and plasma and parentally reported exposure to ETS...... microl plasma. Information was obtained on the number of days with ETS exposure during the first year of life, the smoking habits of the parents, and the number of cigarettes smoked per day in the home. All three parentally reported indices of ETS exposure were significantly associated...

  19. Racial differences in cigarette brand recognition and impact on youth smoking

    Directory of Open Access Journals (Sweden)

    Dauphinee Amanda L

    2013-02-01

    Full Text Available Abstract Background African Americans are disproportionately exposed to cigarette advertisements, particularly for menthol brands. Tobacco industry documents outline strategic efforts to promote menthol cigarettes to African Americans at the point of sale, and studies have observed more outdoor and retail menthol advertisements in neighborhoods with more African-American residents. Little research has been conducted to examine the effect of this target marketing on adolescents’ recognition of cigarette brand advertising and on smoking uptake. To our knowledge, this is the first study to examine racial differences in brand recognition and to assess the prospective relationship between brand recognition and smoking uptake. Methods School-based surveys assessing tobacco use and environmental and social influences to smoke were administered to 6th through 9th graders (ages 11 to 15 in an urban and racially diverse California school district. The primary outcome for the cross-sectional analysis (n = 2,589 was brand recognition, measured by students’ identification of masked tobacco advertisements from the point of sale. The primary outcome for the longitudinal analysis (n = 1,179 was progression from never to ever smoking within 12 months. Results At baseline, 52% of students recognized the Camel brand, 36% Marlboro, and 32% Newport. African-American students were three times more likely than others to recognize Newport (OR = 3.03, CI = 2.45, 3.74, p  Conclusions The study findings illustrate that African-American youth are better able to recognize Newport cigarette advertisements, even after adjustment for exposure to smoking by parents and peers. In addition, recognition of Newport cigarette advertising predicted smoking initiation, regardless of race. This longitudinal study contributes to a growing body of evidence that supports a ban on menthol flavored cigarettes in the US as well as stronger regulation of tobacco

  20. Evaluation of the effect of cigarette smoking on the olfactory neuroepithelium of New Zealand white rabbit, using scanning electron microscope.

    Science.gov (United States)

    Iskander, Nagi M; El-Hennawi, Diaa M; Yousef, Tarek F; El-Tabbakh, Mohammed T; Elnahriry, Tarek A

    2017-03-01

    To detect ultra-structural changes of Rabbit's olfactory neuro-epithelium using scanning electron microscope after exposure to cigarette smoking. Sixty six rabbits (Pathogen free New Zealand white rabbits weighing 1-1.5 kg included in the study were randomly assigned into one of three groups: control group did not expose to cigarette smoking, study group 1 was exposed to cigarette smoking for 3 months and study group 2 was exposed to cigarette smoking 3 months and then stopped for 2 months. Olfactory neuro-epithelium from all rabbits were dissected and examined under Philips XL-30 scanning electron microscope. Changes that were found in the rabbits of study group 1 in comparison to control group were loss of microvilli of sustentacular cells (p = 0.016) and decreases in distribution of specialized cilia of olfactory receptor cells (p = 0.046). Also respiratory metaplasia was detected. These changes were reversible in study group 2. Cigarette smoking causes ultra-structural changes in olfactory neuro-epithelium which may explain why smell was affected in cigarette smokers. Most of these changes were reversible after 45 days of cessation of cigarette smoking to the rabbits.

  1. Humic acid enhances cigarette smoke-induced lung emphysema in mice and IL-8 release of human monocytes

    NARCIS (Netherlands)

    Eijl, S. van; Mortaz, E.; Ferreira, A.F.; Kuper, F.; Nijkamp, F.P.; Folkerts, G.; Bloksma, N.

    2011-01-01

    Tobacco smoke is the main factor in the etiology of lung emphysema. Generally prolonged, substantial exposure is required to develop the disease. Humic acid is a major component of cigarette smoke that accumulates in smokers' lungs over time and induces tissue damage. Objectives: To investigate whet

  2. Heme oxygenase-1 alleviates cigarette smoke-induced restenosis after vascular angioplasty by attenuating inflammation in rat model.

    Science.gov (United States)

    Ni, Leng; Wang, Zhanqi; Yang, Genhuan; Li, Tianjia; Liu, Xinnong; Liu, Changwei

    2016-03-14

    Cigarette smoke is not only a profound independent risk factor of atherosclerosis, but also aggravates restenosis after vascular angioplasty. Heme oxygenase-1 (HO-1) is an endogenous antioxidant and cytoprotective enzyme. In this study, we investigated whether HO-1 upregulating by hemin, a potent HO-1 inducer, can protect against cigarette smoke-induced restenosis in rat's carotid arteries after balloon injury. Results showed that cigarette smoke exposure aggravated stenosis of the lumen, promoted infiltration of inflammatory cells, and induced expression of inflammatory cytokines and adhesion molecules after balloon-induced carotid artery injury. HO-1 upregulating by hemin treatment reduced these effects of cigarette smoke, whereas the beneficial effects were abolished in the presence of Zincprotoporphyrin IX, an HO-1 inhibitor. To conclude, hemin has potential therapeutic applications in the restenosis prevention after the smokers' vascular angioplasty.

  3. Repeated whole cigarette smoke exposure alters cell differentiation and augments secretion of inflammatory mediators in air-liquid interface three-dimensional co-culture model of human bronchial tissue.

    Science.gov (United States)

    Ishikawa, Shinkichi; Ito, Shigeaki

    2017-02-01

    In vitro models of human bronchial epithelium are useful for toxicological testing because of their resemblance to in vivo tissue. We constructed a model of human bronchial tissue which has a fibroblast layer embedded in a collagen matrix directly below a fully-differentiated epithelial cell layer. The model was applied to whole cigarette smoke (CS) exposure repeatedly from an air-liquid interface culture while bronchial epithelial cells were differentiating. The effects of CS exposure on differentiation were determined by histological and gene expression analyses on culture day 21. We found a decrease in ciliated cells and perturbation of goblet cell differentiation. We also analyzed the effects of CS exposure on the inflammatory response, and observed a significant increase in secretion of IL-8, GRO-α, IL-1β, and GM-CSF. Interestingly, secretion of these mediators was augmented with repetition of whole CS exposure. Our data demonstrate the usefulness of our bronchial tissue model for in vitro testing and the importance of exposure repetition in perturbing the differentiation and inflammation processes.

  4. Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats.

    Science.gov (United States)

    Morimoto, Y; Kido, M; Tanaka, I; Fujino, A; Higashi, T; Yokosaki, Y

    1993-10-01

    The objective of this study was to evaluate the combined effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor (TNF) by alveolar macrophages. Rats were exposed to cigarette smoke in vivo, and production of TNF by alveolar macrophages was measured in the presence of mineral fibres in vitro. For smoke exposure, rats were divided into two groups. Five were exposed to a daily concentration of 10 mg/m3 of cigarette smoke for an eight hour period, and five rats (controls) were not exposed to smoke. Bronchoalveolar lavage was performed after exposure to smoke and the recovered alveolar macrophages were incubated with either chrysotile or ceramic fibres on a microplate for 24 hours. Activity of TNF in the supernatant was determined by the L-929 fibroblast cell bioassay. When alveolar macrophages were not stimulated by mineral fibres, production of TNF by rats exposed to smoke and unexposed rats was essentially the same. When alveolar macrophages were stimulated in vitro by chrysotile or ceramic fibres, production of TNF by alveolar macrophages from rats exposed to smoke was higher than that by alveolar macrophages from unexposed rats. The findings suggest that cigarette smoke and mineral fibres have a synergistic effect on TNF production by alveolar macrophages.

  5. The Effect of Cigarette Smoking on Gingival Crevicular Fluid Flow.

    Science.gov (United States)

    1986-01-01

    Gregory, G.: An epidemiological study of chronic periodontal disease . Arch Oral Biol 10:553-566, 1965. 52. Shuler, R.L.: Effect of cigarette smoking on the... studies . Researchers have attempted to correlate plaque accumulation, calculus deposition, gingivitis, periodontal disease , and oral hygiene practices...in the etiology of periodontal disease . 15 In 1970 Alexander studied the relationship between tobacco smoking and periodontal health in 200 dental

  6. Behavior of cardiac variables in animals exposed to cigarette smoke

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    Sergio Alberto Rupp de Paiva

    2003-09-01

    Full Text Available OBJECTIVE: To assess the behavior of cardiac variables in animals exposed to cigarette smoke. METHODS: Two groups of Wistar rats were studied as follows: control group (C, comprising 28 animals; and smoking group (S, comprising 23 animals exposed to cigarette smoke for 30 days. Left ventricular cardiac function was assessed in vivo with transthoracic echocardiography, and myocardial performance was analyzed in vitro in preparations of isolated left ventricular papillary muscle. The cardiac muscle was assessed in isometric contractions with an extracellular calcium concentration of 2.5 mmol/L. RESULTS: No statistical difference was observed in the values of the body variables of the rats and in the mechanical data obtained from the papillary muscle between the control and smoking groups. The values of left ventricular systolic diameter were significantly greater in the smoking animals than in the control animals (C= 3.39 ± 0.4 mm and S= 3.71 ± 0.51 mm, P=0.02. A significant reduction was observed in systolic shortening fraction (C= 56.7 ± 4.2% and S= 53.5 ± 5.3%, P=0.02 and in ejection fraction (C= 0.92 ± 0.02 and S= 0.89 ± 0.04, P=0.01. CONCLUSION: The rats exposed to cigarette smoke had a reduction in left ventricular systolic function, although their myocardial function was preserved.

  7. Effects of Cigarette Smoking on Transplant Survival: Extending or Shortening It?

    Science.gov (United States)

    Qiu, Feifei; Fan, Ping; Nie, Golay D.; Liu, Huazhen; Liang, Chun-Ling; Yu, Wanlin; Dai, Zhenhua

    2017-01-01

    Cigarette smoking (CS) regulates both innate and adaptive immunity and causes numerous diseases, including cardiovascular, respiratory, and autoimmune diseases, allergies, cancers, and transplant rejection. Therefore, smoking poses a serious challenge to the healthcare system worldwide. Epidemiological studies have always shown that CS is one of the major risk factors for transplant rejection, even though smoking plays redundant roles in regulating immune responses. The complex roles for smoking in immunoregulation are likely due to molecular and functional diversities of cigarette smoke components, including carbon monoxide (CO) and nicotine. Especially, CO has been shown to induce immune tolerance. Although CS has been shown to impact transplantation by causing complications and subsequent rejection, it is overlooked whether CS interferes with transplant tolerance. We have previously demonstrated that cigarette smoke exposure reverses long-term allograft survival induced by costimulatory blockade. Given that CS impacts both adaptive and innate immunity and that it hinders long-term transplant survival, our perspective is that CS impacts transplant tolerance. Here, we review impacts of CS on major immune cells that are critical for transplant outcomes and propose the cellular and molecular mechanisms underlying its effects on alloimmunity and transplant survival. Further investigations are warranted to fully understand why CS exerts deleterious rather than beneficial effects on transplant survival even if some of its components are immunosuppressive.

  8. Perlite filtration of phenolic compounds from cigarette smoke.

    Science.gov (United States)

    Rostami-Charati, Faramarz; Robati, Gholamreza Moradi; Naghizadeh, Farhad; Hosseini, Shahnaz; Chaichi, Mohammad Javad

    2013-01-01

    Adsorption of phenolic compounds and chemical analysis of them from a local production cigarette (named by Farvardin cigarette) smoke have been investigated by using perlite filtration. In this research, the mainstream smoke was tested by three filtration methods: Perlite filter, Cambridge filter and general cigarette filter. Then the used filter was extracted by pure methanol as solvent. After that, the extracted solution was analysed by GC-MS. By this consideration, the phenolic derivatives such as phenol, hydroquinone, resorcinol, pyrocatechol, m-cresol, p-cresol and o-cresol were detected. The structure of the perlite filtration after absorption was studied by SEM. In addition, its chemical structure was investigated by XRD and XRF.

  9. Lung emphysema induced by cigarette smoke: Studies in mice

    NARCIS (Netherlands)

    Eijl, Teunis Jan Ahasuerus van

    2006-01-01

    The experiments described in this thesis were designed to shed some more light on the mechanisms underlying cigarette smoke-induced lung emphysema. We used elastase instillation to induce lung emphysema, and subsequently perfused the lungs ex-vivo with buffer at a range of flows to measure changes i

  10. Cigarette smoke-induced mitochondrial dysfunction and oxidative stress in

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    Toorn, Marco van der

    2009-01-01

    In this thesis we studied the effects of cigarette smoke (CS) on mitochondrial function and oxidative stress in epithelial cells and discussed the potential of these phenomena in the pathogenesis of chronic obstructive pulmonary diseases (COPD). In the first three chapters we demonstrated that CS di

  11. Determination of Polycyclic Aromatic Hydrocarbons In Exhaled Cigarette Smoke

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    Moldoveanu SC

    2014-12-01

    Full Text Available The retention by humans of 20 polycyclic aromatic hydrocarbons (PAHs from mainstream cigarette smoke was evaluated. The analysis was done by a new technique using solid phase extraction (SPE for the cleanup and the concenration of PAHs. The new technique has excellent sensitivity and accuracy, which were necessary for the analysis of the very low levels of PAHs present in the exhaled cigarette smoke. The study was done on a common commercial cigarette with 10.6 mg ‘tar’ by U.S. Federal Trade Commission (FTC recommendation. The results were obtained from ten human subjects, each smoking three cigarettes. The exhaled smoke was collected using a vacuum assisted procedure that avoids strain in exhaling. The study showed that the PAHs with a molecular weight lower than about 170 Daltons are retained with high efficiency. The heavier molecules are less retained, but even compounds such as indeno[1,2,3-cd]pyrene, dibenz[a, h]anthracene, and benzoperylene are retained with efficiencies around 50%. The dependence of retention efficiency for PAHs (in % on their octanol-water partition coefficient (LogPow was found to be nonlinear and showed considerable variability for several compounds that have very close LogPow values. Better correlation was obtained between the retention efficiency and PAHs vapor pressure (Log VP.

  12. Cigarette smoking during pregnancy in two regions:cross-sectional study

    Institute of Scientific and Technical Information of China (English)

    Marcel Leppe; Josip Culig; Mirela Eric

    2012-01-01

    Objective:Smoking in pregnancy is associated with the risk of congenital malformations and functional disorders.The aim of the study was to assess the prevalence of cigarette smoking in pregnancy, and the rate of congenital malformations in children at in utero exposure.Methods:The trial was designed as a cross-sectional study to measure exposure of pregnant women to adverse influence of smoking and their health status.The study consists of two arms: one was conducted at fourZagreb maternity hospitals(Croatia) and the other at the same hospitals inNovi Sad(Serbia).Results:Data analysis revealed the habit of cigarette smoking during pregnancy in829(11.9%) of6992(6099+893) women.Malformations were found in105(1.5%) fetuses and newborns.Major congenital malformations were present in four(0.6%), minor malformations in73 (10.5%) andLBW in12(1.7%) newborns.In all these cases pregnant women smoked until becoming aware of pregnancy or during pregnancy.Tobacco smoking and congenital abnormalities that define the contingency table are not significantly related inZagreb(P=0.385), as well as in NoviSad(P=0.345).Conclusions:The rate of congenital malformations is higher in fetuses and newborns at in utero exposure to maternal cigarette smoking as well as to alcohol consumption and drug abuse than in the general population.The results of the present study did not identify the exact cause of these malformations because of fetal concurrent exposure to multiple teratogenic factors.

  13. Toxicological effects of cigarette smoke on Ana-1 macrophages in vitro.

    Science.gov (United States)

    Yuan, Fengjiao; Dong, Ping; Wang, Xiang; Fu, Xiao; Dai, Mingjun; Zhang, Weiyun

    2013-11-01

    Cigarette smoke exposure is associated with increased risk of different disorders. Immunological dysfunction especially in macrophages is one of important reasons in the initiation, progression and exacerbation of smoke-related pulmonary illnesses. However, it is still obscure how cigarette smoke impacts the vitality and functions of macrophages. In the present study, we examined the effects of cigarette smoke extract (CSE) on mouse Ana-1 macrophages and tried to elucidate the involved mechanism. The results showed CSE induced cell apoptosis accompanied by increased releasing of lactate dehydrogenase (LDH), mitochondrial injury and oxidative stress. It also inhibited anti-apoptosis protein Bcl-2 expression and promoted pro-apoptosis protein Bax and Bad expressions. Moreover, low-dose CSE increased nuclear NF-κB levels of macrophages; on the contrary, high-dose CSE or long-time treatment decreased it. These observations were in correspondence with changes of intracellular ROS level and antioxidant enzymes' activity. Furthermore, pretreatment with 10μM of NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) for 1h significantly enhanced macrophage apoptosis. Taken together, these data implied that mitochondrial dysfunction and oxidative stress played important roles in the injury of Ana-1 cells caused by CSE, which was related to NF-κB pathway; an anti-apoptotic program played a dominant role at low doses/short-term exposure to CSE, whereas a pro-apoptotic program was initiated at high doses/long-term exposure.

  14. Socioeconomic Distinction, Cultural Tastes, and Cigarette Smoking.

    Science.gov (United States)

    Pampel, Fred C

    2006-03-01

    OBJECTIVES: The inverse relationship between socioeconomic status (SES) and smoking is typically seen in terms of the greater economic and social resources of advantaged groups, but it may also relate to cultural resources. This study aims to test theories of symbolic distinction by examining relationships between smoking and ostensibly unrelated cultural preferences. METHODS: Using the 1993 General Social Survey, ordinal logistic regression models, and a three-category dependent variable (never, former, and current smoker), the analysis estimates relationships of musical likes and dislikes with smoking while controlling for SES and social strain. RESULTS: Preferences for classical music are associated with lower smoking, while preferences for bluegrass, jazz, and heavy metal music are associated with higher smoking. CONCLUSIONS: The results suggest that SES groups may use smoking, like other cultural tastes, to distinguish their lifestyles from those of others.

  15. Mechanisms of Cigarette Smoke Effects on Human Airway Smooth Muscle.

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    Mark E Wylam

    Full Text Available 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 Ca(2+ ([Ca(2+]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 Ca(2+ regulatory proteins leading to increased store operated Ca(2+ entry (SOCE and cell proliferation. Using isolated human ASM (hASM cells, incubated in the presence and absence cigarette smoke extract (CSE we determined ([Ca(2+]i responses and expression of relevant proteins as well as ASM proliferation, reactive oxidant species (ROS and cytokine generation. CSE enhanced [Ca(2+]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 Ca(2+ regulatory proteins and enhanced SOCE to alter airway structure and function in smoking-related airway disease.

  16. The Effects of Maternal Cigarette Smoking on Infant Anthropometric Measurements

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    F Sahin Mutlu

    2008-12-01

    Full Text Available "nBackground: The association between maternal smoking and poor pregnancy outcome, which is well established in medi­cal literature, has also been corroborated by the results of this study conducted in a Turkish hospital. Our objective was to investi­gate the effects of cigarette smoking during pregnancy on infant head circumference, height, weight, and body mass in­dex (BMI."nMethods: In this retrospective study, the data was collected from the Medical Live Birth Registry in a maternity hospital with the largest capacity of births in a city of northwest Turkey during 2002."nResults: We found that 16.4% (1040/6332 of mothers investigated had smoked during their pregnancy, with a mean of 5 ciga­rettes per day. Head circumference, height, weight and BMI values of male infants whose mothers smoked were found to be less than those of infants whose mothers did not smoke (P> 0.05, for each one. Head circumference, height, weight and BMI values of female infants whose mothers smoked were less than those whose mothers did not smoke (P> 0.05, P< 0.01, P< 0.05 and P> 0.05, respectively. According to analysis of variance, infant head circumferences, heights and weights in all infants decreased as the rate of the mother's smoking increased (P> 0.05, P< 0.001 and P> 0.05, respec­tively."nConclusions: The results support that maternal smoking during pregnancy was associated with a linear reduction of height meas­urement, and the infants appeared to be more susceptible to the growth retarding effects of cigarette smoking on height. Thus, if cessation-of-smoking programs are initiated before conception, many of the harmful effects of smoking on fe­tal growth might be prevented.

  17. Non-smoking male adolescents' reactions to cigarette warnings.

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    Jessica K Pepper

    Full Text Available BACKGROUND: The U.S. Food and Drug Administration (FDA is working to introduce new graphic warning labels for cigarette packages, the first change in cigarette warnings in more than 25 years. We sought to examine whether warnings discouraged participants from wanting to smoke and altered perceived likelihood of harms among adolescent males and whether these warning effects varied by age. METHODS: A national sample of 386 non-smoking American males ages 11-17 participated in an online experiment during fall 2010. We randomly assigned participants to view warnings using a 2 × 2 between-subjects design. The warnings described a harm of smoking (addiction or lung cancer using text only or text plus an image used on European cigarette package warnings. Analyses tested whether age moderated the warnings' impact on risk perceptions and smoking motivations. RESULTS: The warnings discouraged most adolescents from wanting to smoke, but lung cancer warnings discouraged them more than addiction warnings did (60% vs. 34% were "very much" discouraged, p<.001. Including an image had no effect on discouragement. The warnings affected several beliefs about the harms from smoking, and age moderated these effects. Adolescents said addiction was easier to imagine and more likely to happen to them than lung cancer. They also believed that their true likelihood of experiencing any harm was lower than what an expert would say. CONCLUSIONS: Our findings suggest that warnings focusing on lung cancer, rather than addiction, are more likely to discourage wanting to smoke among adolescent males and enhance their ability to imagine the harmful consequences of smoking. Including images on warnings had little effect on non-smoking male adolescents' discouragement or beliefs, though additional research on the effects of pictorial warnings for this at-risk population is needed as the FDA moves forward with developing new graphic labels.

  18. Glaucoma and cigarette smoking: a review of narrative reviews

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    Francesca Di Murro

    2016-12-01

    Full Text Available Background: Glaucoma is an optic neuropathy associated with visual field changes for which high intra-ocular pressure is a major risk factor. Emerging research indicates that modifiable factors, among which the cigarette smoke, besides IOP may be associated with the presence of glaucoma. Objective: The objective of the study was to perform a review of narrative reviews to examine on the relationship between cigarette smoking and glaucoma. Methods: The results of all narrative reviews in the scientific literature about glaucoma and tobacco smoking were analyzed. A quality assessment was performed according to an easy and convenient tool for the quality assessment of narrative reviews for systematic reviews (International Narrative Systematic assessment the INSA tool. Literature searches were performed using PubMed. Results: 20 studies about relation between glaucoma and smoke were collected, no restriction language was applied. 15 of these studies have been excluded. We selected among them 5 reviews. With the INSA tool we measured the quality of the 5 selected narrative reviews. Studies that had a highest score with the INSA tool were two: A. Coleman et al. “Risk Factors for Glaucoma Needing More Attention” and R. Salowe et al. “Primary Open-Angle Glaucoma in Individuals of African Descent: A Review of Risk Factors”. Conclusion: The narrative reviews analyzed underline that there is no definitive association between cigarette smoking.

  19. Cigarette smoking among Chinese PLWHA: An exploration of changes in smoking after being tested HIV positive.

    Science.gov (United States)

    Wang, Yuanhui; Chen, Xinguang; Li, Xiaoming; Wang, Yan; Shan, Qiao; Zhou, Yuejiao; Shen, Zhiyong

    2016-01-01

    Prevention and cessation of Tobacco use among persons living with HIV/AIDS (PLWHA) represents a significant challenge for HIV/AIDS patient care in China and across the globe. Awareness of HIV-positive status may alter the likelihood for PLWHA smokers to change their smoking habit. In this study, we tested the risk enhancement and risk reduction hypotheses by assessing changes in cigarette smoking behavior among PLWHA after they received the positive results of their HIV tests. Cross-sectional survey data collected from a random sample of 2973 PLWHA in care in Guangxi, China were analyzed. Changes in cigarette smoking after receiving the HIV-positive test results, as well as the current levels of cigarette smoking were measured. Among the total participants, 1529 (51.7%) were self-identified as cigarette smokers, of whom 436 (28.9%) reduced smoking and 286 (19.0%) quit after receiving their HIV-positive test results. Among the quitters, 210 (73.9%) remained abstinent for a median duration of two years. There were also 124 (8.2%) who increased cigarette smoking. Older age, female gender, more education, and receiving antiretroviral therapy were associated with quitting. In conclusion, our study findings support the risk reduction and risk enhancement hypotheses. A large proportion of smoking PLWHA reduced or quit smoking, while a small proportion increased smoking. Findings of this study suggest that the timing when a person receives his or her HIV-positive test result may be an ideal opportunity for care providers to deliver tobacco cessation interventions. Longitudinal studies are indicated to verify the findings of this study and to support smoking cessation intervention among PLWHA in the future.

  20. An international literature survey of "IARC Group I carcinogens" reported in mainstream cigarette smoke.

    Science.gov (United States)

    Smith, C J; Livingston, S D; Doolittle, D J

    1997-01-01

    The International Agency for Research on Cancer (IARC) currently lists 44 individual chemical agents, 12 groups or mixtures of chemicals and 13 exposure circumstances as "Group 1 human carcinogens". A comprehensive search of the published literature revealed that nine of the 44 chemical agents classified as "Group I carcinogens" by IARC have been reported to occur in mainstream cigarette smoke. The other 35 have never been reported to occur in cigarette smoke. The nine agents reported are benzene, cadmium, arsenic, nickel, chromium, 2-naphthyl-amine, vinyl chloride, 4-aminobiphenyl and beryllium. The reported yields of each of these nine agents in mainstream smoke varies widely. The range of yields reported for a given compound is influenced by the type of cigarette tested and when the analysis was conducted. In micrograms/cigarette, the ranges that have been reported for each of the nine compounds are: benzene (0.05-104), cadmium (0-6.67), arsenic (0-1.4), nickel (0-0.51), chromium (0.0002-0.5), 2-naphthylamine (0.0002-0.022), vinyl chloride (0.0013-0.0158), 4-aminobiphenyl (0.00019-0.005) and beryllium (0-0.0005). Although some of the variation in reported yields may be due to differences in analytical methodology, several correlations between the yield of a particular chemical in mainstream smoke and certain cigarette characteristics were observed. For example, charcoal filtration was associated with reduced vinyl chloride, and the concentration of sodium nitrate in the tobacco was positively correlated with the mainstream yield of both 2-naphthylamine and 4-aminobiphenyl. Benzene yield in mainstream cigarette smoke was correlated with the amount of tobacco burned and with the 'tar' level. Agronomic factors such as production practices and soil characteristics, and environmental conditions such as rainfall, reportedly influence the accumulation of metals, for example, cadmium, beryllium, chromium, nickel and arsenic, in the leaf. The use of fertilizers low in

  1. Effect of bacoside A on brain antioxidant status in cigarette smoke exposed rats.

    Science.gov (United States)

    Anbarasi, K; Vani, G; Balakrishna, K; Devi, C S Shyamala

    2006-02-16

    Free radicals mediated oxidative stress has been implicated in the pathogenesis of smoking-related diseases and antioxidant nutrients are reported to prevent the oxidative damage induced by smoking. Therefore, the present study was conducted to evaluate the antioxidant role of bacoside A (triterpenoid saponin isolated from Bacopa monniera) against chronic cigarette smoking induced oxidative damage in rat brain. Adult male albino rats were exposed to cigarette smoke for a period of 12 weeks and simultaneously administered with bacoside A (10 mg/kg b.w./day, p.o.). Antioxidant status of the brain was assessed from the levels of reduced glutathione, vitamin C, vitamin E, and vitamin A and the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. The levels of copper, iron, zinc and selenium in brain and serum ceruloplasmin activity were also measured. Oxidative stress was evident from the diminished levels of both enzymatic and non-enzymatic antioxidants. Alterations in the levels of trace elements with accumulation of copper and iron, and depletion of zinc and selenium were also observed. Bacoside A administration improved the antioxidant status and maintained the levels of trace elements. These results suggest that chronic cigarette smoke exposure enhances oxidative stress, thereby disturbing the tissue defense system and bacoside A protects the brain from the oxidative damage through its antioxidant potential.

  2. Effect of epimedium pubescen flavonoid on bone mineral status and bone turnover in male rats chronically exposed to cigarette smoke

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    Gao Shu-guang

    2012-06-01

    Full Text Available Abstract Background Epimedii herba is one of the most frequently used herbs in formulas that are prescribed for the treatment of osteoporosis in China and its main constituent is Epimedium pubescen flavonoid (EPF. However, it is unclear whether EPF during chronic exposure to cigarette smoke may have a protective influence on the skeleton. The present study investigated the effect of EPF on bone mineral status and bone turnover in a rat model of human relatively high exposure to cigarette smoke. Methods Fifty male Wistar rats were randomized into five groups: controls, passive smoking groups and passive smoking rats administered EPF at three dosage levels (75, 150 or 300 mg/kg/day in drinking water for 4 months. A rat model of passive smoking was prepared by breeding male rats in a cigarette-smoking box. Bone mineral content (BMC, bone mineral density (BMD, bone turnover markers, bone histomorphometric parameters and biomechanical properties were examined. Results Smoke exposure decreased BMC and BMD, increased bone turnover (inhibited bone formation and stimulated its resorption, affected bone histomorphometry (increased trabecular separation and osteoclast surface per bone surface; decreased trabecular bone volume, trabecular thickness, trabecular number, cortical thickness, bone formation rate and osteoblast surface per bone surface, and reduced mechanical properties. EPF supplementation during cigarette smoke exposure prevented smoke-induced changes in bone mineral status and bone turnover. Conclusion The results suggest that EPF can prevent the adverse effects of smoke exposure on bone by stimulating bone formation and inhibiting bone turnover and bone resorption.

  3. Chinese green tea ameliorates lung injury in cigarette smoke-exposed rats

    OpenAIRE

    Koo, MWL; Ip, MSM; Man, RYK; Mak, JCW; Chan, KH; Ho, SP; Yeung, SC; So, WHL; Cho, CH; Lam, WK

    2009-01-01

    Background: Epigallocatechin-3-gallate (EGCG), which has been shown to have potent antioxidant effect, comprises 80% of catechins in Chinese green tea. This study was to investigate whether cigarette smoke (CS) exposure would induce lung morphological changes and oxidative stress in the CS-exposed rat model, and whether Chinese green tea (Lung Chen tea with EGCG as its main active ingredient) consumption would alter oxidative stress in sera and lung leading to protection of CS-induced lung da...

  4. Analysis of the effects of cigarette smoke on staphylococcal virulence phenotypes.

    Science.gov (United States)

    McEachern, Elisa K; Hwang, John H; Sladewski, Katherine M; Nicatia, Shari; Dewitz, Carola; Mathew, Denzil P; Nizet, Victor; Crotty Alexander, Laura E

    2015-06-01

    Cigarette smoking is the leading preventable cause of death, disease, and disability worldwide. It is well established that cigarette smoke provokes inflammatory activation and impairs antimicrobial functions of human immune cells. Here we explore whether cigarette smoke likewise affects the virulence properties of an important human pathogen, Staphylococcus aureus, and in particular methicillin-resistant S. aureus (MRSA), one of the leading causes of invasive bacterial infections. MRSA colonizes the nasopharynx and is thus exposed to inhalants, including cigarette smoke. MRSA exposed to cigarette smoke extract (CSE-MRSA) was more resistant to macrophage killing (4-fold higher survival; P cigarette smoke-induced immune resistance phenotypes in MRSA may be an additional factor contributing to susceptibility to infectious disease in cigarette smokers.

  5. Analysis of the smoke of cigarettes containing Salvia divinorum.

    Science.gov (United States)

    Krstenansky, John L; Muzzio, Miguel

    2014-09-01

    Salvia divinorum is a hallucinogen sold over the internet in several forms. Perhaps the most common method of use is smoking the dried leaf material. The sole presumed active constituent, salvinorin A, is a selective kappa-opioid receptor agonist. Upon smoking of the dried leaf material, some of the salvinorin A is destroyed or converted to other materials, leaving in question the actual amount of salvinorin A delivered that leads to the psychotomimetic effect. On average, 133 μg of salvinorin A was delivered in the smoke from an 830 mg per cigarette, which contained ∼2.7 mg of salvinorin A. Hence, only ∼5% of the salvinorin A available in the dried plant material was delivered in the smoke. Upon smoking, hydrolysis of salvinorin A to salvinorin B, an inactive and minor component of the leaf material, also occurs as evidenced by a higher delivered amount of salvinorin B vs salvinorin A (217 vs 133 μg per cigarette). Since smoking is an effective means of achieving the hallucinogenic effect and salvinorin A is the presumed sole active ingredient in the plant, the estimated effective dose of salvinorin A by inhalation is <133 μg per person. Considering the reported rapid metabolism of salvinorin A in vivo, the dose reaching the brain would be substantially less.

  6. IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke.

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    Kong Chen

    Full Text Available Chronic Obstructive Pulmonary Disease (COPD is characterized by airspace enlargement and peribronchial lymphoid follicles; however, the immunological mechanisms leading to these pathologic changes remain undefined. Here we show that cigarette smoke is a selective adjuvant that augments in vitro and in vivo Th17, but not Th1, cell differentiation via the aryl hydrocarbon receptor. Smoke exposed IL-17RA(-/- mice failed to induce CCL2 and MMP12 compared to WT mice. Remarkably, in contrast to WT mice, IL-17RA(-/- mice failed to develop emphysema after 6 months of cigarette smoke exposure. Taken together, these data demonstrate that cigarette smoke is a potent Th17 adjuvant and that IL-17RA signaling is required for chemokine expression necessary for MMP12 induction and tissue emphysema.

  7. Cigarette smoking substantially alters plasma microRNA profiles in healthy subjects

    Energy Technology Data Exchange (ETDEWEB)

    Takahashi, Kei; Yokota, Shin-ichi; Tatsumi, Naoyuki; Fukami, Tatsuki; Yokoi, Tsuyoshi; Nakajima, Miki, E-mail: nmiki@p.kanazawa-u.ac.jp

    2013-10-01

    Circulating microRNAs (miRNAs) are receiving attention as potential biomarkers of various diseases, including cancers, chronic obstructive pulmonary disease, and cardiovascular disease. However, it is unknown whether the levels of circulating miRNAs in a healthy subject might vary with external factors in daily life. In this study, we investigated whether cigarette smoking, a habit that has spread throughout the world and is a risk factor for various diseases, affects plasma miRNA profiles. We determined the profiles of 11 smokers and 7 non-smokers by TaqMan MicroRNA array analysis. A larger number of miRNAs were detected in smokers than in non-smokers, and the plasma levels of two-thirds of the detected miRNAs (43 miRNAs) were significantly higher in smokers than in non-smokers. A principal component analysis of the plasma miRNA profiles clearly separated smokers and non-smokers. Twenty-four of the miRNAs were previously reported to be potential biomarkers of disease, suggesting the possibility that smoking status might interfere with the diagnosis of disease. Interestingly, we found that quitting smoking altered the plasma miRNA profiles to resemble those of non-smokers. These results suggested that the differences in the plasma miRNA profiles between smokers and non-smokers could be attributed to cigarette smoking. In addition, we found that an acute exposure of ex-smokers to cigarette smoke (smoking one cigarette) did not cause a dramatic change in the plasma miRNA profile. In conclusion, we found that repeated cigarette smoking substantially alters the plasma miRNA profile, interfering with the diagnosis of disease or signaling potential smoking-related diseases. - Highlights: • Plasma miRNA profiles were unambiguously different between smokers and non-smokers. • Smoking status might interfere with the diagnosis of disease using plasma miRNAs. • Changes of plasma miRNA profiles may be a signal of smoking-related diseases.

  8. Effects of Cigarette Smoke Extract on E-cadherin Expression in Cultured Airway Epithelial Cells

    Institute of Scientific and Technical Information of China (English)

    WANG Xi; WU Renling; CHEN Fang; HAO Tianling

    2000-01-01

    To investigate whether the change of E-cadherin (ECD) expression plays a role in the injury and repair of airway epithelial cells (AEC) caused by smoking, porcine AECs were cultured by using an enzyme-dispersed method. After exposure of the AECs to cigarette smoke extract(CSE), the ECD expression in the cells was detected by using immunocytochemistry and in situ hybridization. The results showed that ECD was distributed on the plasma membrane at the cell junctions of AECs. After exposure to 20% CSE, the membranous ECD expression was decreased, the cytoplasmic ECD expression was increased (P<0.01) as the exposure time went on.But the content of ECD mRNA in the AECs did not chang. It suggests that the change of ECD expression is regulated at the posttranslational level and plays a role in the injury and repair of AEC caused by smoking.

  9. Prisoners' attitudes towards cigarette smoking and smoking cessation: a questionnaire study in Poland

    Directory of Open Access Journals (Sweden)

    Konopa Krzysztof

    2006-07-01

    Full Text Available Abstract Background In the last decade Poland has successfully carried out effective anti-tobacco campaigns and introduced tobacco control legislation. This comprehensive strategy has focused on the general population and has led to a considerable decrease in tobacco consumption. Prisoners constitute a relatively small part of the entire Polish population and smoking habits in this group have been given little attention. The aim of the study was to assess the prevalence of cigarette smoking in Polish male prisoners, factors determining smoking in this group, prisoners' attitudes towards smoking cessation, and to evaluate prisoners' perception of different anti-tobacco measures. Methods An anonymous questionnaire including personal, demographic and smoking data was distributed among 944 male inmates. Of these, 907 men aged between 17 and 62 years (mean 32.3 years met the inclusion criteria of the study. For the comparison of proportions, a chi-square test was used with continuity correction whenever appropriate. Results In the entire group, 81% of the subjects were smokers, 12% – ex-smokers, and 7% – never smokers. Current smokers had significantly lower education level than non-smokers (p Conclusion The prevalence of cigarette smoking among Polish prisoners is high. However, a majority of smokers attempt to quit, and they should be encouraged and supported. Efforts to reduce cigarette smoking in prisons need to take into consideration the specific factors influencing smoking habits in prisons.

  10. Microscopical examination of particles on smoked cigarette filters.

    Science.gov (United States)

    Linch, Charles A; Prahlow, Joseph A

    2008-01-01

    Cigarette butts collected from crime scenes can play an important role in forensic investigations by providing a DNA link to a victim or suspect. Microscopic particles can frequently be seen on smoked cigarette filters with stereomicroscopy. The authors are not aware of previous published attempts to identify this material. These particles were examined with transmission and scanning electron microscopy and were found to consist of two types of superficial epithelial tissue, consistent with two areas of the lip surface. The particles were often composed of several layers of non-nucleated and nucleated epithelium with the former being the most common. It was further determined that both of these cell types are easily transferred from the lip. The results of this study indicate that the most visible source of DNA obtained from cigarette butts and other objects in contact with the lip may be lip epithelial tissue.

  11. Cigarette smoke-induced damage-associated molecular pattern release from necrotic neutrophils triggers proinflammatory mediator release.

    Science.gov (United States)

    Heijink, Irene H; Pouwels, Simon D; Leijendekker, Carin; de Bruin, Harold G; Zijlstra, G Jan; van der Vaart, Hester; ten Hacken, Nick H T; van Oosterhout, Antoon J M; Nawijn, Martijn C; van der Toorn, Marco

    2015-05-01

    Cigarette smoking, the major causative factor for the development of chronic obstructive pulmonary disease, is associated with neutrophilic airway inflammation. Cigarette smoke (CS) exposure can induce a switch from apoptotic to necrotic cell death in airway epithelium. Therefore, we hypothesized that CS promotes neutrophil necrosis with subsequent release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), alarming the innate immune system. We studied the effect of smoking two cigarettes on sputum neutrophils in healthy individuals and of 5-day CS or air exposure on neutrophil counts, myeloperoxidase, and HMGB1 levels in bronchoalveolar lavage fluid of BALB/c mice. In human peripheral blood neutrophils, mitochondrial membrane potential, apoptosis/necrosis markers, caspase activity, and DAMP release were studied after CS exposure. Finally, we assessed the effect of neutrophil-derived supernatants on the release of chemoattractant CXCL8 in normal human bronchial epithelial cells. Cigarette smoking caused a significant decrease in sputum neutrophil numbers after 3 hours. In mice, neutrophil counts were significantly increased 16 hours after repeated CS exposure but reduced 2 hours after an additional exposure. In vitro, CS induced necrotic neutrophil cell death, as indicated by mitochondrial dysfunction, inhibition of apoptosis, and DAMP release. Supernatants from CS-treated neutrophils significantly increased the release of CXCL8 in normal human bronchial epithelial cells. Together, these observations show, for the first time, that CS exposure induces neutrophil necrosis, leading to DAMP release, which may amplify CS-induced airway inflammation by promoting airway epithelial proinflammatory responses.

  12. Active and passive smoking - New insights on the molecular composition of different cigarette smoke aerosols by LDI-FTICRMS

    Science.gov (United States)

    Schramm, Sébastien; Carré, Vincent; Scheffler, Jean-Luc; Aubriet, Frédéric

    2014-08-01

    The aerosol generated when a cigarette is smoked is a significant indoor contaminant. Both smokers and non-smokers can be exposed to this class of pollutants. Nevertheless, they are not exposed to the same kind of smoke. The active smoker breathes in the mainstream smoke (MSS) during a puff, whereas the passive smoker inhales not only the smoke generated by the lit cigarette between two puffs (SSS) but also the smoke exhaled by active smokers (EXS). The aerosol fraction of EXS has until now been poorly documented; its composition is expected to be different from MSS. This study aims to investigate the complex composition of aerosol from EXS to better understand the difference in exposure between active and passive smokers. To address this, the in-situ laser desorption ionisation Fourier transform ion cyclotron mass spectrometry (LDI-FTICRMS) was used to characterise the aerosol composition of EXS from two different smokers. Results clearly indicated many similarities between EXS samples but also significant differences with MSS and SSS aerosol. The comparison of MSS and EXS aerosol allowed the chemicals retained by the active smoker's lungs to be identified, whereas the convolution of the EXS and SSS aerosol compositions were considered relevant to the exposition of a passive smoker. As a consequence, active smokers are thought to be mainly exposed to polar and poorly unsaturated oxygenated and nitrogenated organics, compared with poorly oxygenated but highly unsaturated compounds in passive smokers.

  13. Does Cigarette Smoking Affect Seminal Fluid Parameters? A Comparative Study

    Directory of Open Access Journals (Sweden)

    Zakarya Bani Meri

    2013-01-01

    Full Text Available Objective: To study the effect of cigarette smoking on seminal fluid parameters, namely; volume, sperm concentration, and motility, as well as morphology, leukocyte infiltration, among males complaining of infertility.Methods: Between August 2010 and July 2011, seminal fluid analysis was done for 1438 males who are partners of couples who visited the infertility clinic at Prince Rashid Ben Al Hassan Hospital (PRH for infertility. The men who fit the inclusion criteria (n=960 were classified into two groups: group a (non-smokers; n=564 and group B (smokers; n=396, which represents 41.25% of the study group. Seminal fluid was collected using masturbation after 3-5 days of abstinence then analyzed for volume, sperm count, sperm concentration, motility and morphology. In order to analyze whether the number of cigarettes smoked per day has an effect on the spermatogram; the smoking men were divided into two subgroups: the heavy smokers (n=266 and non-heavy smokers (n=130.Results: A total of 960 adult males were enrolled. Their age ranged between 21 and 76 years, 564 were non-smokers with mean age of 36. 45±6.27 (Mean±SD. Three-hundred-and-ninety-six were smokers with a mean age of 34.35±4.25 (Mean±SD. There was a significant effect of smoking on the motility of sperms and the ratios of abnormality (p<0.005. Concentration appeared not to be affected by smoking. Furthermore, the group of heavy smokers were found to have lower sperm concentrations and a higher percentage of abnormal sperms compared to the non-heavy smokers.Conclusion: Cigarette smoking has a deleterious effect on some of the seminal fluid parameters (motility, morphology and leukocyte count which in turn may result in male subfertility.

  14. Smoking and symbolism: children, communication and cigarettes.

    Science.gov (United States)

    Rugkåsa, J; Kennedy, O; Barton, M; Abaunza, P S; Treacy, M P; Knox, B

    2001-04-01

    Health promotion, with its concern with empowerment and autonomy, must recognize the agency of its target population. Based on 85 in-depth interviews with 10- to 11-year-old children throughout Northern Ireland, this paper argues that it is necessary to focus on the social relations of children if we are to understand and prevent childhood smoking. Addressing the complex issue of childhood agency, it is argued that regardless of various restrictions to their choices, children can act intentionally in constructing their identities. Instead of viewing the smoking children as communicating with the adult world, we focus on smoking as negotiation of status within the children's culture. Such negotiations utilize symbolism derived from and shared with the 'adult world'. It is important that those analyzing children's lives understand children's ideas and behaviour on their own terms. We must make sure that the very concepts in which the children's experiences are put are appropriate ones. It is suggested that the metaphor 'rite of passage' and terminology such as peer 'pressure' versus adult 'influence', commonly used to analyse the children's smoking behaviour, may actually conceal important aspects of childhood agency.

  15. Up-regulation of endothelin receptors induced by cigarette smoke--involvement of MAPK in vascular and airway hyper-reactivity

    DEFF Research Database (Denmark)

    Zhang, Yaping; Edvinsson, Lars; Xu, Cang-Bao

    2010-01-01

    and airway diseases. In the vasculature and airways, the main functional consequences of up-regulated endothelin receptors by cigarette smoke exposure are enhanced contraction and proliferation of the smooth muscle cells, which subsequently result in abnormal contraction (spasm) and adverse proliferation......Cigarette smoke exposure is well known to cause cardiovascular and airway diseases, both of which are leading causes of death and disability in the world. However, the molecular mechanisms that link cigarette smoke to cardiovascular and airway diseases are not fully understood. Vascular and airway...... (remodeling) of the vasculature and airways. The structural alteration by adverse remodeling involves changes in cell growth, cell death, cell migration, and production or degradation of the extracellular matrix. This review focuses on cigarette smoke exposure that induces activation of intracellular mitogen...

  16. Cigarette smoking and tooth loss experience among young adults: a national record linkage study

    Directory of Open Access Journals (Sweden)

    Tanaka Keiko

    2007-11-01

    Full Text Available Abstract Background Various factors affect tooth loss in older age including cigarette smoking; however, evidence regarding the association between smoking and tooth loss during young adulthood is limited. The present study examined the association between cigarette smoking and tooth loss experience among adults aged 20–39 years using linked data from two national databases in Japan. Methods Two databases of the National Nutrition Survey (NNS and the Survey of Dental Diseases (SDD, which were conducted in 1999, were obtained from the Ministry of Health, Labor and Welfare with permission for analytical use. In the NNS, participants received physical examinations and were interviewed regarding dietary intake and health practices including cigarette smoking, whereas in the SDD, participants were asked about their frequency of daily brushing, and received oral examinations by certified dentists. Among 6,805 records electronically linked via household identification code, 1314 records of individuals aged 20 to 39 years were analyzed. The prevalence of 1+ tooth loss was compared among non-, former, and current smokers. Multiple logistic regression models were constructed including confounders: frequency of tooth brushing, body mass index, alcohol consumption, and intake of vitamins C and E. Results Smoking rates differed greatly in men (53.3% and women (15.5%. The overall prevalence of tooth loss was 31.4% (31.8% men and 31.1% women. Tooth loss occurred more frequently among current smokers (40.6% than former (23.1% and non-smokers (27.9%. Current smoking showed a significant association with 1+ tooth loss in men (adjusted OR = 2.21 [1.40–3.50], P = 0.0007 and women (1.70 [1.13–2.55], P = 0.0111. A significant positive exposure-related relationship between cigarette smoking status and tooth loss was observed (P for trend Conclusion An association between cigarette smoking and tooth loss was evident among young adults throughout Japan. Due to

  17. The social dynamics of cigarette smoking: a family systems perspective.

    Science.gov (United States)

    Doherty, W J; Whitehead, D A

    1986-09-01

    This paper uses family systems concepts and the Family FIRO model to show how cigarette smoking occurs in the context of the important relationships in a smoker's life. Specifically, smoking is viewed as a way a person is included in relationships, is in control in relationships, and perhaps is intimate in relationships. When smoking is well-established in the relationship, predictable interaction patterns surround it. When a person tries to quit or succeeds in quitting, these patterns change and may need to be replaced by nonsmoking alternatives. Partners may respond with support and willingness to create alternative patterns, or with undermining behavior stemming from a perceived threat to the established patterns. The model is offered for its heuristic value in guiding research and clinical experimentation. The paper also describes implications for family therapists as consultants to smoking-cessation programs.

  18. Validation of Methods for Determining Consumer Smoked Cigarette Yields from Cigarette Filter Analysis

    Directory of Open Access Journals (Sweden)

    Shepperd CJ

    2014-12-01

    Full Text Available Methods based on the analyses of cigarette filters have been used to estimate ‘tar’ and nicotine yields to smokers. These methods rely on the measurement of filtration efficiencies (FEs. However FEs may be influenced by both cigarette design features e.g., type of filter and levels of filter ventilation, and human smoking behaviour factors such as puff flow-rates and cigarette butt lengths. Two filter analysis methods are considered in our study. One is based on the analysis of whole filters using average values of FEs obtained from a range of machine smoking regimes. The other, a ‘part filter’ method, analyses a 10 mm section from the mouth end of the filter where the FE remains relatively constant irrespective of puff flow rates and butt lengths. Human puffing behaviour records were obtained from 10 smokers, each smoking six commercial cigarettes ranging from 1 mg to 12 mg ‘tar’ yields [International Standard (ISO values]. These records were used to drive a human smoke duplicator and the resulting ‘tar’ and nicotine yields obtained from duplication were compared with the estimates obtained from ‘whole’ and ‘part filter’ analysis. The results indicated that whilst both filter methods gave good correlations with nicotine and ‘tar’ yields obtained from smoke duplication, the ‘part filter’ method was less susceptible to the effect of nicotine condensation and changes in FEs and hence gave a more accurate assessment of yields than the ‘whole filter’ method.

  19. Study on the effect of cigarette smoke exposure on hippocampal LTP and effect of cigarette smoke extractant on the growth of hippocam-pal neurons in vivo%香烟烟雾暴露对小鼠海马LTP效应及神经元存活的影响

    Institute of Scientific and Technical Information of China (English)

    姜丽娜; 杨杰; 马强; 李君文

    2015-01-01

    Objective To explore the influence of passive smoking in different periods on LTP and the neural mechanism of mice,and to demonstrate the effect of cigarette smoke extractant( CSE)in different concentrations on the growth of primitive culture of hippocampal neurons of mice. Methods Models of passive smoking were established in different exposure periods(1 day,1 week,2 weeks,4 weeks and 8 weeks),and the effect of hippocampal synaptic long-term potentiation had been studied. Primitive hippocampal neurons of mice were cultured and evaluated. Morphological features,MTT assay and neuron apoptosis were tested by flow cytometry,DNA damage in neuron was tested by comet assay when neurons were exposed to CSE with different ending concentrations(35 μg/ml,14 μg/ml,4 μg/ml,0. 4 μg/ml and 0. 04 μg/ml). Results PS range of passive smoking in 1d group had no obvious change compared with control group,PS range of passive smoking in 1w and 2w groups were lower than those of control group,PS ranges of passive smoking in 4w and 8w groups were obviously higher( P ﹤0. 05). Apoptosis of neurons treated with CSE was lower than that of control group. Neurons treated with decreasing concentration of CSE,showed a trend of decline in rate of apoptosis. DNA damage had not been found in neurons. Conclusion Short-term smoking inhibited the formation of LTP in hippocampal dentate gyrus and CA1 areas,but with increasing in smoking period,suggested that long-term passive smoking can lead to increase the excitability of nerve cells and plasticity of nerve synapse. CSE had no injurious effect on neurons.%目的:探讨香烟烟雾暴露对小鼠长时程增强( LTP)效应的影响;及烟草提取液( CSE)对原代培养的小鼠海马神经轴突生长和神经元存活的影响。方法将小鼠按1d、1w、2w、4w和8w不同时间进行香烟烟雾暴露染毒,采用神经电生理技术检测小鼠海马突触传递LTP效应的变化;原代培养小鼠海马神经元,用35

  20. EL CIGARRILLO: IMPLICACIONES PARA LA SALUD CIGARETTE SMOKE HEALTH IMPLICATIONS

    Directory of Open Access Journals (Sweden)

    Manuel Antonio Ballén

    2006-07-01

    Full Text Available Antecedentes. El consumo de cigarrillo, según cálculos de la Organización Mundial de la Salud (OMS, es la causa de por lo menos cuatro millones de muertes al año. Las consecuencias de fumar cigarrillo van desde cambios fisiopatológicos en los sistemas respiratorio, cardiovascular y digestivo, hasta trastornos mentales asociados a la dependencia a la nicotina. Objetivo. Realizar una revisión narrativa de la literatura médica mostrando los efectos del consumo de cigarrillo sobre la salud física y mental en los fumadores activos y pasivos. Material y métodos. El artículo se basa en la revisión de artículos a través de la base de datos del MEDLINE y de la biblioteca Virtual de la OMS. Se emplearon en la búsqueda las palabras clave “Cigarette Smoke”, “Cancer AND smoke”, “COPD AND smoke”, “Nicotine Dependence”. Se escogieron artículos y libros publicados en idioma inglés entre los años 1994 y 2006, realizando una lectura crítica (análisis de posibles conflictos de interés y errores de diseño. Conclusión. El humo del cigarrillo contiene partículas potencialmente peligrosas para la salud de quien está expuesto a ellas. De este modo, fumar cigarrillo se convierte en un factor etiológico común a muchos tipos de cáncer. Además los componentes del cigarrillo están relacionados con el desarrollo de otros estados patológicos (enfermedad cardiovascular y enfermedad pulmonar obstructiva crónica. La nicotina, uno de sus componentes, es un potente agente adictivo. Todo esto en su conjunto hace del cigarrillo un importante problema de salud pública.Background. According to World Health Organization (WHO, cigarette smoke causes four million deaths each year. The consequences of cigarette smoke are phatophysiological changes in pulmonary cardiovascular and digestive systems, and mental dysfunctions associated to nicotine dependence. Objective. To show the effects of cigarette smoke in active and passive smokers

  1. Nanoparticles in cigarette smoke; real-time undiluted measurements by a scanning mobility particle sizer

    NARCIS (Netherlands)

    Dijk, W.D. van; Gopal, S.R.; Scheepers, P.T.J.

    2011-01-01

    Cigarette smoke is a complex mixture of smoke constituents, often characterised by size-resolved particle distributions. Since descriptions of ultrafine particles <50 nm are absent, our aim was to explore the existence of these nanoparticles in fresh and undiluted cigarette smoke. We measured und

  2. Smoking, epidemiology and e-cigarettes

    Directory of Open Access Journals (Sweden)

    Raschke RA

    2013-07-01

    Full Text Available No abstract available. Article truncated at 150 words. “The true face of smoking is disease, death and horror - not the glamour and sophistication the pushers in the tobacco industry try to portray.” - David Byrne In our fellows’ conference we recently reviewed the evolution of the science of clinical epidemiology as it relates to the association of smoking and lung cancer and the concurrent history of tobacco marketing in the United States. This story begins in 1950, when Richard Doll and Austin Bradford Hill published their landmark case control study demonstrating the association between smoking and lung cancer (1. This study was performed with methodological standards that have rarely been matched in the 63 years since. Exhaustive analysis of possible confounders, a multi-stage evaluation of study blinding, determination of dose-effect, and the use of multiple analyses to establish consistency are among many examples of superb attention to detail exercised by Doll and Hill in this study. The …

  3. Impact of cigarette smoke on the human and mouse lungs: a gene-expression comparison study.

    Directory of Open Access Journals (Sweden)

    Mathieu C Morissette

    Full Text Available Cigarette smoke is well known for its adverse effects on human health, especially on the lungs. Basic research is essential to identify the mechanisms involved in the development of cigarette smoke-related diseases, but translation of new findings from pre-clinical models to the clinic remains difficult. In the present study, we aimed at comparing the gene expression signature between the lungs of human smokers and mice exposed to cigarette smoke to identify the similarities and differences. Using human and mouse whole-genome gene expression arrays, changes in gene expression, signaling pathways and biological functions were assessed. We found that genes significantly modulated by cigarette smoke in humans were enriched for genes modulated by cigarette smoke in mice, suggesting a similar response of both species. Sixteen smoking-induced genes were in common between humans and mice including six newly reported to be modulated by cigarette smoke. In addition, we identified a new conserved pulmonary response to cigarette smoke in the induction of phospholipid metabolism/degradation pathways. Finally, the majority of biological functions modulated by cigarette smoke in humans were also affected in mice. Altogether, the present study provides information on similarities and differences in lung gene expression response to cigarette smoke that exist between human and mouse. Our results foster the idea that animal models should be used to study the involvement of pathways rather than single genes in human diseases.

  4. Effect of Cigarette and Cigar Smoking on Peak Expiratory Flow Rate

    OpenAIRE

    Medabala, Tambi; B.N., Rao; Mohesh M.I., Glad; Kumar M., Praveen

    2013-01-01

    Background: Tobacco smoking in India has been increasing alarmingly. Smoking is a known risk factor for chronic obstructive pulmonary disease (COPD), cardiovascular diseases and certain cancers, especially, the lung cancer. The percentage prevalence of cigarette smoking (18.5%) and cigar smoking (4%) in males is high in Andhra Pradesh compared to other southern states. There is not enough scientific literature to correlate about intensity of cigarette and cigar smoking and their impact on lun...

  5. Reduced inflammatory response in cigarette smoke exposed Mrp1/Mdr1a/1b deficient mice

    Directory of Open Access Journals (Sweden)

    Postma Dirkje S

    2007-07-01

    Full Text Available Abstract Background Tobacco smoke is the principal risk factor for chronic obstructive pulmonary disease (COPD, though the mechanisms of its toxicity are still unclear. The ABC transporters multidrug resistance-associated protein 1 (MRP1 and P-glycoprotein (P-gp/MDR1 extrude a wide variety of toxic substances across cellular membranes and are highly expressed in bronchial epithelium. Their impaired function may contribute to COPD development by diminished detoxification of noxious compounds in cigarette smoke. Methods We examined whether triple knock-out (TKO mice lacking the genes for Mrp1 and Mdr1a/1b are more susceptible to develop COPD features than their wild-type (WT littermates. TKO and WT mice (six per group were exposed to 2 cigarettes twice daily by nose-only exposure or room air for 6 months. Inflammatory infiltrates were analyzed in lung sections, cytokines and chemokines in whole lung homogenates, emphysema by mean linear intercept. Multiple linear regression analysis with an interaction term was used to establish the statistical significances of differences. Results TKO mice had lower levels of interleukin (IL-7, KC (mouse IL-8, IL-12p70, IL-17, TNF-alpha, G-CSF, GM-CSF and MIP-1-alpha than WT mice independent of smoke exposure (P P P Conclusion Mrp1/Mdr1a/1b knock-out mice have a reduced inflammatory response to cigarette smoke. In addition, the expression levels of several cytokines and chemokines were also lower in lungs of Mrp1/Mdr1a/1b knock-out mice independent of smoke exposure. Further studies are required to determine whether dysfunction of MRP1 and/or P-gp contribute to the pathogenesis of COPD.

  6. Cigarette smoke causes caspase-independent apoptosis of bronchial epithelial cells from asthmatic donors.

    Directory of Open Access Journals (Sweden)

    Fabio Bucchieri

    Full Text Available Epidemiologic studies have demonstrated important links between air pollution and asthma. Amongst these pollutants, environmental cigarette smoke is a risk factor both for asthma pathogenesis and exacerbation. As the barrier to the inhaled environment, the bronchial epithelium is a key structure that is exposed to cigarette smoke.Since primary bronchial epithelial cells (PBECs from asthmatic donors are more susceptible to oxidant-induced apoptosis, we hypothesized that they would be susceptible to cigarette smoke-induced cell death.PBECs from normal and asthmatic donors were exposed to cigarette smoke extract (CSE; cell survival and apoptosis were assessed by fluorescence-activated cell sorting, and protective effects of antioxidants evaluated. The mechanism of cell death was evaluated using caspase inhibitors and immunofluorescent staining for apoptosis-inducing factor (AIF.Exposure of PBEC cultures to CSE resulted in a dose-dependent increase in cell death. At 20% CSE, PBECs from asthmatic donors exhibited significantly more apoptosis than cells from non-asthmatic controls. Reduced glutathione (GSH, but not ascorbic acid (AA, protected against CSE-induced apoptosis. To investigate mechanisms of CSE-induced apoptosis, caspase-3 or -9 inhibitors were tested, but these failed to prevent apoptosis; in contrast, CSE promoted nuclear translocation of AIF from the mitochondria. GSH reduced the number of nuclear-AIF positive cells whereas AA was ineffective.Our results show that PBECs from asthmatic donors are more susceptible to CSE-induced apoptosis. This response involves AIF, which has been implicated in DNA damage and ROS-mediated cell-death. Epithelial susceptibility to CSE may contribute to the impact of environmental tobacco smoke in asthma.

  7. Smoke and mirrors: magnified beliefs that cigarette smoking suppresses weight.

    Science.gov (United States)

    White, Marney A; McKee, Sherry A; O'malley, Stephanie S

    2007-10-01

    Research suggests that for some smokers, weight concerns interfere with smoking cessation. Studies with individuals with eating disorders and weight concerns have indicated that weight-concerned individuals place undue faith in the effectiveness of certain weight control strategies; i.e., adopt a brand of magical thinking pertaining to food rules and dieting behaviors. The current study investigated whether weight-concerned smokers endorsed exaggerated beliefs in the ability of smoking to suppress body weight. Participants were 385 individuals undergoing treatment for smoking cessation. Prior to treatment, participants completed the Smoking Consequences Questionnaire-Adult (SCQ-A), the Dieting and Bingeing Severity Scale, and the Perceived Risks and Benefits Questionnaire (PBRQ). Results indicated that heightened beliefs in the effectiveness of smoking to control weight were related to eating and weight concerns; specifically, strong associations were observed between SCQ-A Weight Control scores and fear of weight gain, loss of control over eating, and body dissatisfaction. Although SCQ-A Weight Control scores were related to (self-reported) weight gain during a previous quit attempt, scores did not predict actual weight gain over the course of the cessation trial. Reported weight gain at previous attempts was also unrelated to actual weight gain over the current trial. These findings indicate that eating and weight-concerned smokers may benefit from psychoeducation concerning the relatively modest and temporary ability of nicotine to suppress weight.

  8. Association of cigarette smoking with drug use and risk taking behaviour in Irish teenagers.

    LENUS (Irish Health Repository)

    O'Cathail, S M

    2011-05-01

    Cigarette smoking has been shown to act as a \\'gateway\\' to cannabis use and further risk taking behaviours. This study aims to (1) establish the prevalence of cigarette smoking and cannabis use in Irish teenagers, (2) to quantify the strength and significance of the association of cigarette smoking and cannabis use and other high risk behaviours and (3) examine whether the above associations are independent of the extent of social networking.

  9. Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes

    OpenAIRE

    McEachern, Elisa K.; Hwang, John H.; Sladewski, Katherine M.; Nicatia, Shari; Dewitz, Carola; Mathew, Denzil P.; Nizet, Victor; Crotty Alexander, Laura E.

    2015-01-01

    Cigarette smoking is the leading preventable cause of death, disease, and disability worldwide. It is well established that cigarette smoke provokes inflammatory activation and impairs antimicrobial functions of human immune cells. Here we explore whether cigarette smoke likewise affects the virulence properties of an important human pathogen, Staphylococcus aureus, and in particular methicillin-resistant S. aureus (MRSA), one of the leading causes of invasive bacterial infections. MRSA colon...

  10. Selected constituents in the smokes of foreign commercial cigaretts: tar, nicotine, carbon monoxide, and carbon dioxide

    Energy Technology Data Exchange (ETDEWEB)

    Jenkins, R.A.; Quincy, R.B.; Guerin, M.R.

    1979-05-01

    The tar, nicotine, carbon monoxide, and carbon dioxide contents of the smokes of 220 brands of foreign commercial cigarettes are reported. In some instances, filter cigarettes of certain brands were found to deliver as much or more smoke constituents than their nonfilter counterparts. Also, data indicated that there can be a great variation in the tar, nicotine, or carbon monoxide content of the smoke of samples of a given brand of cigarettes, depending on the nation in which they are purchased. 24 tables.

  11. The electronic-cigarette: effects on desire to smoke, withdrawal symptoms and cognition

    OpenAIRE

    Dawkins, Lynne; Turner, John J.D.; Hasna, Surrayyah; Soar, Kirstie

    2012-01-01

    Electronic cigarettes (e-cigarettes) are battery operated devices that deliver nicotine via inhaled vapour. Few studies have evaluated acute effects on craving and mood, and none have explored effects on cognition. This study aimed to explore the effects of the White Super e-cigarette on desire to smoke, nicotine withdrawal symptoms, attention and working memory. Eighty-six smokers were randomly allocated to either: 18mg nicotine e-cigarette (nicotine), 0mg e-cigarette (placebo), or just hold...

  12. Cigarettes vs. e-cigarettes: Passive exposure at home measured by means of airborne marker and biomarkers

    Energy Technology Data Exchange (ETDEWEB)

    Ballbè, Montse [Tobacco Control Unit, Cancer Prevention and Control Program, Institut Català d' Oncologia, L’Hospitalet de Llobregat, Barcelona (Spain); Catalan Network of Smoke-free Hospitals, L' Hospitalet de Llobregat, Barcelona (Spain); Cancer Prevention and Control Group, Institut d' Investigació Biomèdica de Bellvitge – IDIBELL, L’Hospitalet de Llobregat, Barcelona (Spain); Addictions Unit, Institute of Neurosciences, Hospital Clínic de Barcelona – IDIBAPS, Barcelona (Spain); Department of Clinical Sciences, Universitat de Barcelona, Barcelona (Spain); Martínez-Sánchez, Jose M., E-mail: jmmartinez@iconcologia.net [Tobacco Control Unit, Cancer Prevention and Control Program, Institut Català d' Oncologia, L’Hospitalet de Llobregat, Barcelona (Spain); Cancer Prevention and Control Group, Institut d' Investigació Biomèdica de Bellvitge – IDIBELL, L’Hospitalet de Llobregat, Barcelona (Spain); Biostatistics Unit, Department of Basic Sciences, Universitat Internacional de Catalunya, Sant Cugat del Vallès, Barcelona (Spain); Sureda, Xisca; Fu, Marcela [Tobacco Control Unit, Cancer Prevention and Control Program, Institut Català d' Oncologia, L’Hospitalet de Llobregat, Barcelona (Spain); Cancer Prevention and Control Group, Institut d' Investigació Biomèdica de Bellvitge – IDIBELL, L’Hospitalet de Llobregat, Barcelona (Spain); Department of Clinical Sciences, Universitat de Barcelona, Barcelona (Spain); and others

    2014-11-15

    Background: There is scarce evidence about passive exposure to the vapour released or exhaled from electronic cigarettes (e-cigarettes) under real conditions. The aim of this study is to characterise passive exposure to nicotine from e-cigarettes' vapour and conventional cigarettes' smoke at home among non-smokers under real-use conditions. Methods: We conducted an observational study with 54 non-smoker volunteers from different homes: 25 living at home with conventional smokers, 5 living with nicotine e-cigarette users, and 24 from control homes (not using conventional cigarettes neither e-cigarettes). We measured airborne nicotine at home and biomarkers (cotinine in saliva and urine). We calculated geometric mean (GM) and geometric standard deviations (GSD). We also performed ANOVA and Student's t tests for the log-transformed data. We used Bonferroni-corrected t-tests to control the family error rate for multiple comparisons at 5%. Results: The GMs of airborne nicotine were 0.74 μg/m{sup 3} (GSD=4.05) in the smokers’ homes, 0.13 μg/m{sup 3} (GSD=2.4) in the e-cigarettes users’ homes, and 0.02 μg/m{sup 3} (GSD=3.51) in the control homes. The GMs of salivary cotinine were 0.38 ng/ml (GSD=2.34) in the smokers’ homes, 0.19 ng/ml (GSD=2.17) in the e-cigarettes users’ homes, and 0.07 ng/ml (GSD=1.79) in the control homes. Salivary cotinine concentrations of the non-smokers exposed to e-cigarette's vapour at home (all exposed ≥2 h/day) were statistically significant different that those found in non-smokers exposed to second-hand smoke ≥2 h/day and in non-smokers from control homes. Conclusions: The airborne markers were statistically higher in conventional cigarette homes than in e-cigarettes homes (5.7 times higher). However, concentrations of both biomarkers among non-smokers exposed to conventional cigarettes and e-cigarettes’ vapour were statistically similar (only 2 and 1.4 times higher, respectively). The levels of airborne

  13. Chitosan Removes Toxic Heavy Metal Ions from Cigarette Mainstream Smoke

    Institute of Scientific and Technical Information of China (English)

    ZHOU Wen; XU Ying; WANG Dongfeng; ZHOU Shilu

    2013-01-01

    This study investigated the removal of heavy metal ions from cigarette mainstream smoke using chitosan.Chitosan of various deacetylation degrees and molecular weights were manually added to cigarette filters in different dosages.The mainstream smoke particulate matter was collected by a Cambridge filter pad,digested by a microwave digestor,and then analyzed for contents of heavy metal ions,including As(Ⅲ/Ⅴ),Pb(Ⅱ),Cd(Ⅱ),Cr(Ⅲ/Ⅵ) and Ni(Ⅱ),by graphite furnace atomic absorption spectrometry (GFAAS).The results showed that chitosan had a removal effect on Pb(Ⅱ),Cd(Ⅱ),Cr(Ⅲ/Ⅵ) and Ni(Ⅱ).Of these,the percent removal of Ni(Ⅱ) was elevated with an increasing dosage of chitosan.Chitosan of a high deace tylation degree exhibited good binding performance toward Cd(Ⅱ),Cr(Ⅲ/Ⅵ) and Ni(Ⅱ),though with poor efficiency for Pb(Ⅱ).Except As(Ⅲ/Ⅴ),all the tested metal ions showed similar tendencies in the growing contents with an increasing chitosan molecular weight.Nonetheless,the percent removal of Cr(Ⅲ/Ⅵ) peaked with a chitosan molecular weight of 200 kDa,followed by a dramatic decrease with an increasing chitosan molecular weight.Generally,chitosan had different removal effects on four out of five tested metal ions,and the percent removal of Cd(Ⅱ),Pb(Ⅱ),Cr(Ⅲ/Ⅵ) and Ni(Ⅱ) was approximately 55%,45%,50%,and 16%,respectively.In a word,chitosan used in cigarette filter can remove toxic heavy metal ions in the mainstream smoke,improve cigarette safety,and reduce the harm to smokers.

  14. Correlates of Cigarette Smoking among Male Chinese College Students in China--A Preliminary Study

    Science.gov (United States)

    Li, Kaigang; Kay, Noy S.

    2009-01-01

    The main purpose of this preliminary study was to examine the association between four constructs of the Health Belief Model (HBM) (i.e. perceived severity of smoking-related health problems, perceived susceptibility to smoking-health related problems, perceived barriers to non-smoking and perceived benefits of non-smoking) and cigarette smoking

  15. Cigarette Smoking Practice and Attitudes, and Proposed Effective Smoking Cessation Measures among College Student Smokers in China

    Science.gov (United States)

    Cui, Yanping; Ying, Mao; Fan, Hongqi

    2012-01-01

    Purpose: This paper aims to investigate the average daily consumption of cigarettes and its correlates, attitudes toward smoking, and suggestions for anti-smoking measures in a sample of Chinese college student smokers. Design/methodology/approach: A sample of 150 college student cigarette smokers in Baoding, a city near Beijing, filled out a…

  16. Pentoxifylline attenuates cigarette smoke-induced overexpression of CXCR3 and IP-10 in mice

    Institute of Scientific and Technical Information of China (English)

    WANG Zheng; CHEN Yan-wei; ZHANG Jin-nong; HU Xiao-fei; PENG Mei-jun

    2012-01-01

    Background Cigarette smoke-induced emphysema is associated with overexpression of the chemokine receptor CXCR3 and its ligands.Previously,we have demonstrated that pentoxifylline (PTX) alleviated cigarette smoke-induced emphysema.The aim of this study was to determine if the overexpression of CXCR3 and its ligand interferon-inducible protein-10 (IP-10) that was elicited by smoke exposure were attenuated by PTX.Methods (1) The study in vitro:a given number of RAW264.7 macrophages with decreasing concentrations of PTX in the culture medium were challenged with cigarette smoke extract (CSE); (2) The study in vivo:male BALB/c mice were randomized into four groups,i.e.,sham-smoke,smoke only,smoke with 2 mg/kg PTX,and smoke with 10 mg/kg PTX.The smoke exposure time was 90 minutes once a day,6 days a week for 16 weeks.PTX was given intraperitoneally before each episode of smoke exposure.Interferon (IFN)-y and IP-10 in broncho-alveolar lavage fluid (BALF) and in culture medium were measured by enzyme-linked immunosorbent assay (ELISA).IP-10 mRNA in lung tissue was assessed by RT-PCR.CXCR3 positive cells in lung sections were visualized by immunochemistry staining.Results Up-regulation of IFN-y and IP-10 in the culture medium of macrophages elicited by CSE was inhibited by PTX in a dose-dependent manner.Chronic cigarette smoke exposure led to overexpression of IFN-y and IP-10 in BALF,upregulation of IP-10 mRNA and increased infiltration of CXCR3+ cells into lung parenchyma.Administration of PTX decreased the level of IFN-y from (6.26±1.38) ng/ml to (4.43±0.66) ng/ml by low dose PTX or to (1.74±0.28) ng/ml by high dose PTX.IP-10 was reduced from (10.35±1.49) ng/ml to (8.19±0.79) ng/ml by low dose PTX or to (7.51±0.60)ng/ml by high dose PTX.The expression of IP-10 mRNA was also down-regulated (P <0.05).But only with a high dose of PTX was the ratio of CXCR3+ cells decreased; 15.2±7.3 vs.10.4±1.8 (P <0.05).Conclusion PTX attenuates cigarette smoke

  17. E-Cigarettes: The Science Behind the Smoke and Mirrors.

    Science.gov (United States)

    Cobb, Nathan K; Sonti, Rajiv

    2016-08-01

    E-cigarettes are a diverse set of devices that are designed for pulmonary delivery of nicotine through an aerosol, usually consisting of propylene glycol, nicotine, and flavorings. The devices heat the nicotine solution using a battery-powered circuit and deliver the resulting vapor into the proximal airways and lung. Although the current devices on the market appear to be safer than smoking combusted tobacco, they have their own inherent risks, which remain poorly characterized due to widespread product variability. Despite rising use throughout the United States, predominantly by smokers, limited evidence exists for their efficacy in smoking cessation. Pending regulation by the FDA will enforce limited disclosures on the industry but will not directly impact safety or efficacy. Meanwhile, respiratory health practitioners will need to tailor their discussions with patients, taking into account the broad range of existing effective smoking cessation techniques, including pharmaceutical nicotine replacement therapy.

  18. Telephone surveys underestimate cigarette smoking among African-Americans

    Directory of Open Access Journals (Sweden)

    Hope eLandrine

    2013-09-01

    Full Text Available Background. This study tested the hypothesis that data from random digit-dial telephone surveys underestimate the prevalence of cigarette smoking among African-American adults. Method. A novel, community-sampling method was used to obtain a statewide, random sample of N= 2118 California (CA African-American/Black adults, surveyed door-to-door. This Black community sample was compared to the Blacks in the CA Health Interview Survey (N = 2315, a statewide, random digit-dial telephone-survey conducted simultaneously. Results. Smoking prevalence was significantly higher among community (33% than among telephone-survey (19% Blacks, even after controlling for sample-differences in demographics.Conclusions. Telephone surveys underestimate smoking among African-Americans and probably underestimate other health risk behaviors as well. Alternative methods are needed to obtain accurate data on African-American health behaviors and on the magnitude of racial disparities in them.

  19. Ependymal alterations in sudden intrauterine unexplained death and sudden infant death syndrome: possible primary consequence of prenatal exposure to cigarette smoking

    Directory of Open Access Journals (Sweden)

    Matturri Luigi

    2010-07-01

    Full Text Available Abstract Background The ependyma, the lining providing a protective barrier and filtration system separating brain parenchyma from cerebrospinal fluid, is still inadequately understood in humans. In this study we aimed to define, by morphological and immunohistochemical methods, the sequence of developmental steps of the human ependyma in the brainstem (ventricular ependyma and thoracic spinal cord (central canal ependyma of a large sample of fetal and infant death victims, aged from 17 gestational weeks to 8 postnatal months. Additionally, we investigated a possible link between alterations of this structure, sudden unexplained fetal and infant death and maternal smoking. Results Our results demonstrate that in early fetal life the human ependyma shows a pseudostratified cytoarchitecture including many tanycytes and ciliated cells together with numerous apoptotic and reactive astrocytes in the subependymal layer. The ependyma is fully differentiated, with a monolayer of uniform cells, after 32 to 34 gestational weeks. We observed a wide spectrum of ependymal pathological changes in sudden death victims, such as desquamation, clusters of ependymal cells in the subventricular zone, radial glial cells, and the unusual presence of neurons within and over the ependymal lining. These alterations were significantly related to maternal smoking in pregnancy. Conclusions We conclude that in smoking mothers, nicotine and its derivatives easily reach the cerebrospinal fluid in the fetus, immediately causing ependymal damage. Consequently, we suggest that the ependyma should be examined in-depth first in victims of sudden fetal or infant death with mothers who smoke.

  20. Impaired Transcriptional Response of the Murine Heart to Cigarette Smoke in the Setting of High Fat Diet and Obesity

    Energy Technology Data Exchange (ETDEWEB)

    Tilton, Susan C.; Karin, Norman J.; Webb-Robertson, Bobbie-Jo M.; Waters, Katrina M.; Mikheev, Vladimir B.; Lee, K. M.; Corley, Richard A.; Pounds, Joel G.; Bigelow, Diana J.

    2013-07-01

    Smoking and obesity are each well-established risk factors for cardiovascular heart disease, which together impose earlier onset and greater severity of disease. To identify early signaling events in the response of the heart to cigarette smoke exposure within the setting of obesity, we exposed normal weight and high fat diet-induced obese (DIO) C57BL/6 mice to repeated inhaled doses of mainstream (MS) or sidestream (SS) cigarette smoke administered over a two week period, monitoring effects on both cardiac and pulmonary transcriptomes. MS smoke (250 μg wet total particulate matter (WTPM)/L, 5 h/day) exposures elicited robust cellular and molecular inflammatory responses in the lung with 1466 differentially expressed pulmonary genes (p < 0.01) in normal weight animals and a much-attenuated response (463 genes) in the hearts of the same animals. In contrast, exposures to SS smoke (85 μg WTPM/L) with a CO concentration equivalent to that of MS smoke (250 CO ppm) induced a weak pulmonary response (328 genes) but an extensive cardiac response (1590 genes). SS smoke and to a lesser extent MS smoke preferentially elicited hypoxia- and stress-responsive genes as well as genes predicting early changes of vascular smooth muscle and endothelium, precursors of cardiovascular disease. The most sensitive smoke-induced cardiac transcriptional changes of normal weight mice were largely absent in DIO mice after smoke exposure, while genes involved in fatty acid utilization were unaffected. At the same time, smoke exposure suppressed multiple proteome maintenance genes induced in the hearts of DIO mice. Together, these results underscore the sensitivity of the heart to SS smoke and reveal adaptive responses in healthy individuals that are absent in the setting of high fat diet and obesity.

  1. Indoor exposure to environmental cigarette smoke, but not other inhaled particulates associates with respiratory symptoms and diminished lung function in adults

    DEFF Research Database (Denmark)

    Hersoug, Lars-Georg; Husemoen, Lise L N; Sigsgaard, Torben;

    2010-01-01

    Exposure to particulate matter (PM) can induce airway inflammation and exacerbation of asthma. However, there is limited knowledge about the effects of exposure to indoor sources of PM. We investigated the associations between self-reported exposure to indoor sources of PM and lower airway sympto...

  2. Smoking and reproduction: The oviduct as a target of cigarette smoke

    Directory of Open Access Journals (Sweden)

    Riveles Karen

    2005-09-01

    Full Text Available Abstract The oviduct is an exquisitely designed organ that functions in picking-up ovulated oocytes, transporting gametes in opposite directions to the site of fertilization, providing a suitable environment for fertilization and early development, and transporting preimplantation embryos to the uterus. A variety of biological processes can be studied in oviducts making them an excellent model for toxicological studies. This review considers the role of the oviduct in oocyte pick-up and embryo transport and the evidence that chemicals in both mainstream and sidestream cigarette smoke impair these oviductal functions. Epidemiological data have repeatedly shown that women who smoke are at increased risk for a variety of reproductive problems, including ectopic pregnancy, delay to conception, and infertility. In vivo and in vitro studies indicate the oviduct is targeted by smoke components in a manner that could explain some of the epidemiological data. Comparisons between the toxicity of smoke from different types of cigarettes, including harm reduction cigarettes, are discussed, and the chemicals in smoke that impair oviductal functioning are reviewed.

  3. Associations between phenylthiocarbamide gene polymorphisms and cigarette smoking.

    Science.gov (United States)

    Cannon, Dale S; Baker, Timothy B; Piper, Megan E; Scholand, Mary Beth; Lawrence, Daniel L; Drayna, Dennis T; McMahon, William M; Villegas, G Martin; Caton, Trace C; Coon, Hilary; Leppert, Mark F

    2005-12-01

    Phenotypic evidence indicates that the ability to taste the bitter compounds phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) may protect against cigarette smoking. In this study, PTC gene haplotypes were found to be associated with both the odds of being a smoker and the importance of cigarette taste as a smoking motive. Smokers (n = 384) and nonsmokers (n = 183) were genotyped for polymorphisms that affect taste sensitivity to PTC and PROP. The "taster" PAV haplotype, relative to the "nontaster" AVI haplotype, was predicted to be associated with reduced odds of being a smoker and lower taste motivation as measured by the Wisconsin Inventory of Smoking Dependence Motives-68 taste/sensory processes scale. The results did not support the predicted association between the PAV and AVI haplotypes and smoker odds, but the AAV haplotype, which confers intermediate PTC/PROP taste sensitivity, was associated with reduced smoker prevalence (49% vs. 70%), chi(2)(1, N = 567) = 10.392, p = .001. The predicted relationship between PAV and AVI and taste motivation was found, F(2, 348) = 3.303, p = .038. The results encourage further exploration of the role of taste/sensory processes in tobacco dependence.

  4. [Cigarette as "companion": a critical gender approach to women's smoking].

    Science.gov (United States)

    Borges, Márcia Terezinha Trotta; Simões-Barbosa, Regina Helena

    2008-12-01

    This article presents the main results of a study that examined the symbolic and material meanings of women's smoking, adopting a critical and qualitative gender approach. Semi-structured interviews were held with 14 women smokers in different stages of the smoking cessation process. The research locus was a tobacco treatment program located in a public hospital in Rio de Janeiro, Brazil. The findings showed how deeply smoking is interwoven in these women's social and gender trajectories, playing a decisive support role when they have to deal with various difficulties in life. The cigarette as a "companion" emerged as the main empirical category, as something always available to quell anxiety and loneliness, as well as a source of pleasure and relaxation. The critical gender approach evidenced how women's reproductive and productive work overload reinforces their tobacco dependency. In health care, in order to attain women smokers' adherence to the arduous cessation process, it is crucial to consider the complex relations between social and gender dimensions when cigarettes are viewed as a "companion".

  5. A protocol for detecting and scavenging gas-phase free radicals in mainstream cigarette smoke.

    Science.gov (United States)

    Yu, Long-Xi; Dzikovski, Boris G; Freed, Jack H

    2012-01-02

    Cigarette smoking is associated with human cancers. It has been reported that most of the lung cancer deaths are caused by cigarette smoking (5,6,7,12). Although tobacco tars and related products in the particle phase of cigarette smoke are major causes of carcinogenic and mutagenic related diseases, cigarette smoke contains significant amounts of free radicals that are also considered as an important group of carcinogens(9,10). Free radicals attack cell constituents by damaging protein structure, lipids and DNA sequences and increase the risks of developing various types of cancers. Inhaled radicals produce adducts that contribute to many of the negative health effects of tobacco smoke in the lung(3). Studies have been conducted to reduce free radicals in cigarette smoke to decrease risks of the smoking-induced damage. It has been reported that haemoglobin and heme-containing compounds could partially scavenge nitric oxide, reactive oxidants and carcinogenic volatile nitrosocompounds of cigarette smoke(4). A 'bio-filter' consisted of haemoglobin and activated carbon was used to scavenge the free radicals and to remove up to 90% of the free radicals from cigarette smoke(14). However, due to the cost-ineffectiveness, it has not been successfully commercialized. Another study showed good scavenging efficiency of shikonin, a component of Chinese herbal medicine(8). In the present study, we report a protocol for introducing common natural antioxidant extracts into the cigarette filter for scavenging gas phase free radicals in cigarette smoke and measurement of the scavenge effect on gas phase free radicals in mainstream cigarette smoke (MCS) using spin-trapping Electron Spin Resonance (ESR) Spectroscopy(1,2,14). We showed high scavenging capacity of lycopene and grape seed extract which could point to their future application in cigarette filters. An important advantage of these prospective scavengers is that they can be obtained in large quantities from byproducts of

  6. Orofacial clefts, parental cigarette smoking, and transforming growth factor-alpha gene variants

    Energy Technology Data Exchange (ETDEWEB)

    Shaw, G.M.; Wasserman, C.R.; O`Malley, C.D. [California Birth Defects Monitoring Program, Emeryville, CA (United States)] [and others

    1996-03-01

    Results of studies determine whether women who smoke during early pregnancy are at increased risk of delivering infants with orofacial clefts have been mixed, and recently a gene-environment interaction between maternal smoking, transforming growth factor-alpha (TGFa), and clefting has been reported. Using a large population-based case-control study, we investigated whether parental periconceptional cigarette smoking was associated with an increased risk for having offspring with orofacial clefts. We also investigated the influence of genetic variation of the TGFa locus on the relation between smoking and clefting. Parental smoking information was obtained from telephone interviews with mothers of 731 (84.7% of eligible) orofacial cleft case infants and with mothers of 734 (78.2%) nonmalformed control infants. DNA was obtained from newborn screening blood spots and genotyped for the allelic variants of TGFa. We found that risks associated with maternal smoking were most elevated for isolated cleft lip with or without cleft palate, (odds ratio 2.1 [95% confidence interval 1.3-3.6]) and for isolated cleft palate (odds ratio 2.2 [1.1-4.5]) when mothers smoked {ge} 20 cigarrettes/d. These risks for white infants ranged from 3-fold to 11-fold across phenotypic groups. Paternal smoking was not associated with clefting among the offspring of nonsmoking mothers, and passive smoke exposures were associated with at most slightly increased risks. This study offers evidence that the risk for orofacial clefting in infants may be influenced by maternal smoke exposures alone as well as in combination (gene-environment interaction) with the presence of the uncommon TGFa allele. 56 refs., 5 tabs.

  7. Exposure to celebrity-endorsed small cigar promotions and susceptibility to use among young adult cigarette smokers.

    Science.gov (United States)

    Sterling, Kymberle L; Moore, Roland S; Pitts, Nicole; Duong, Melissa; Ford, Kentya H; Eriksen, Michael P

    2013-01-01

    Small cigar smoking among young adult cigarette smokers may be attributed to their exposure to its advertisements and promotions. We examined the association between exposure to a celebrity music artist's endorsement of a specific brand of small cigars and young adult cigarette smokers' susceptibility to smoking that brand. Venue-based sampling procedures were used to select and survey a random sample of 121 young adult cigarette smokers, aged 18-35. Fourteen percent reported exposure to the artist's endorsement of the small cigar and 45.4% reported an intention to smoke the product in the future. The odds of small cigar smoking susceptibility increased threefold for those who reported exposure to the endorsement compared to those not exposed (OR = 3.64, 95% CI 1.06 to 12.54). Past 30-day small cigar use (OR = 3.30, 95% CI 1.24 to 8.74) and past 30-day cigar use (OR = 5.08, 95% CI 1.23, 21.08) were also associated with susceptibility to smoke a small cigar. An association between young adult cigarette smokers' exposure to the music artist's small cigar endorsement and their susceptibility to smoke small cigars was found. This association underscores the importance of monitoring small cigar promotions geared toward young people and their impact on small cigar product smoking.

  8. Exposure to Celebrity-Endorsed Small Cigar Promotions and Susceptibility to Use among Young Adult Cigarette Smokers

    Directory of Open Access Journals (Sweden)

    Kymberle L. Sterling

    2013-01-01

    Full Text Available Small cigar smoking among young adult cigarette smokers may be attributed to their exposure to its advertisements and promotions. We examined the association between exposure to a celebrity music artist’s endorsement of a specific brand of small cigars and young adult cigarette smokers’ susceptibility to smoking that brand. Venue-based sampling procedures were used to select and survey a random sample of 121 young adult cigarette smokers, aged 18–35. Fourteen percent reported exposure to the artist’s endorsement of the small cigar and 45.4% reported an intention to smoke the product in the future. The odds of small cigar smoking susceptibility increased threefold for those who reported exposure to the endorsement compared to those not exposed (OR = 3.64, 95% CI 1.06 to 12.54. Past 30-day small cigar use (OR = 3.30, 95% CI 1.24 to 8.74 and past 30-day cigar use (OR = 5.08, 95% CI 1.23, 21.08 were also associated with susceptibility to smoke a small cigar. An association between young adult cigarette smokers’ exposure to the music artist’s small cigar endorsement and their susceptibility to smoke small cigars was found. This association underscores the importance of monitoring small cigar promotions geared toward young people and their impact on small cigar product smoking.

  9. Heterogeneity in Past Year Cigarette Smoking Quit Attempts among Latinos

    Directory of Open Access Journals (Sweden)

    Daniel A. Gundersen

    2012-01-01

    Full Text Available Objective. Examine the association between English language proficiency (ELP and immigrant generation and having made a cigarette smoking quit attempt in the past 12 months among Latinos. Examine if gender moderates the association between acculturation and quit attempts. Methods. Latino past year smokers from the 2003 and 2006/07 Tobacco Use Supplement to the Current Population Survey were analyzed. Logistic regression was used to examine the association between quit attempt and ELP and immigrant generation, controlling for demographics and smoking characteristics. Results. Latinos with poor ELP were more likely to have made a quit attempt compared to those with good ELP (adjusted odds ratio [AOR]=1.22, confidence interval [CI]: 1.02–1.46 after controlling for demographic and smoking characteristics. First (AOR=1.21, CI: 1.02–1.43 and second generation immigrants (AOR=1.36, CI: 1.12–1.64 were more likely than third generation immigrants to have made a quit attempt in the past 12 months. Conclusion. Quit behaviors are shaped by differences in language ability and generational status among Latinos. This underscores the need to disaggregate Latinos beyond racial/ethnic categories to identify subgroup differences relevant for smoking and smoking cessation behaviors in this population.

  10. Physical exercise is effective in preventing cigarette smoke-induced pulmonary oxidative response in mice

    Directory of Open Access Journals (Sweden)

    Nesi RT

    2016-03-01

    Full Text Available Renata Tiscoski Nesi,1 Priscila Soares de Souza,1 Giulia Pedroso dos Santos,1 Anand Thirupathi,1 Bruno T Menegali,1 Paulo Cesar Lock Silveira,1 Luciano Acordi da Silva,1 Samuel Santos Valença,2 Ricardo Aurino Pinho11Laboratory of Exercise Biochemistry and Physiology, Graduate Program in Health Sciences, Health Sciences Unit, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil; 2Biomedical Science Institute, Federal University of Rio de Janeiro, Rio de Janeiro, BrazilAbstract: Reactive oxygen species (ROS are important in the pathogenesis of pulmonary injury induced by cigarette smoke (CS exposure, and physical exercise (Ex is useful in combating impaired oxidative process. We verified the preventive effects of Ex on lung oxidative markers induced by smoking. In this study, 36 mice (C57BL-6, 30–35 g were split into four groups: control, CS, Ex, and CS plus Ex. Ex groups were given prior physical training in water (2×30 min/d, 5 days/wk, 8 weeks. After training, the CS groups were subjected to passive exposure to four cigarettes, 3 × per day, for 60 consecutive days. After 24 hours from the last exposure, CS animals were sacrificed, and lung samples were collected for further analysis. Left lung sample was prepared for histological analysis, and right lung was used for biochemical analysis (superoxide, hydroxyproline, lipid peroxidation [thiobarbituric acid reactive species], protein carbonylation [carbonyl groups formation], superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GPx] activities. Group comparisons were evaluated by analysis of variance (ANOVA. Results were expressed as mean ± standard deviation, with P<0.05 considered significantly different. Preventive Ex impeded histological changes and increased the enzymatic defense system (SOD and GPx by reducing oxidative damage in lipids and proteins. This preventive effect of prior physical Ex alleviates damage caused by CS exposure.Keywords: exercise

  11. CT findings of respiratory bronchiolitis caused by cigarette smoking

    Energy Technology Data Exchange (ETDEWEB)

    Katagiri, Siro; Osima, K.; Kim, S. [Chiba Tokusyukai Hospital, Funabashi (Japan)

    1998-07-01

    CT scans were performed in 11 cases of respiratory bronchiolitis caused by cigarette smoking. Characteristics of CT findings were as follows: Remarkable visualization of the branching in peripheral bronchi within secondary lobules, multiple ground-glass opacities of centrilobular or lobular size adjacent to the above mentioned bronchial branching, thickening of the bronchial wall without dilatation, and no or minimal centrilobular emphysema. These characteristic CT findings were observed in all of 11 cases, who are current smokers, and never observed in non-smokers, ex-smokers and patients with apparent centrilobular emphysema. (author)

  12. Cigarette smoking during pregnancy and hyperactive-distractible preschooler's: a follow-up study

    DEFF Research Database (Denmark)

    Linnet, K. M.; Obel, C; Bonde, E

    2006-01-01

    singletons born to Danish-speaking mothers. Information on smoking habits during pregnancy and other lifestyle factors was obtained from self-administered questionnaires filled in during second and third trimester. Approximately 3.5 years later, the parents provided information on their child's behaviour...... born to women who smoked 10 or more cigarettes per day had a 60% increased risk of hyperactivity and distractibility perceived by the parents (OR 1.6; 95% CI 1.0-2.3; P lifestyle factors and socioeconomic characteristics. Additional adjustment...... for perinatal factors and parental psychiatric hospitalization did not change the results substantially (OR 1.7; 95% CI 1.1-2.6). We found no statistically significant association between maternal smoking in pregnancy and hostile-aggressive and anxious-fearful behaviour in the offspring. CONCLUSION: Exposure...

  13. A exposição crônica à fumaça do cigarro resulta em remodelação cardíaca e prejuízo da função ventricular em ratos Chronic cigarette smoke exposure results in cardiac remodeling and impaired ventricular function in rats

    Directory of Open Access Journals (Sweden)

    Édson Castardeli

    2005-04-01

    Full Text Available OBJETIVO: Determinar as alterações cardíacas estruturais e funcionais causadas pela exposição à fumaça do cigarro em ratos. MÉTODOS: Os animais foram aleatoriamente distribuídos em dois grupos: fumante (F, composto por 10 animais, expostos à fumaça do cigarro, na taxa de 40 cigarros/dia e controle (C, constituído por 10 animais não submetidos à exposição. Após 4 meses, os animais foram submetidos a estudo morfológico e funcional por meio do ecocardiograma. As variáveis estudadas foram analisadas pelo teste t ou pelo teste de Mann-Whitney. RESULTADOS: Os ratos fumantes apresentaram maior átrio esquerdo (F=4,2± 0,7mm; C=3,5±0,6mm; pOBJECTIVE: To determine the cardiac structural and functional alterations caused by cigarette smoke exposure in rats. METHODS: The animals were randomly distributed into the following 2 groups: 1 smokers (S, comprising 10 animals exposed to cigarette smoke at a rate of 40 cigarettes/day; and 2 control (C, comprising 10 animals not exposed to cigarette smoke. After 4 months, the animals underwent morphological and functional study with echocardiography. The variables studied were analyzed by use of the t test or the Mann-Whitney test. RESULTS: The smoking rats had a greater left atrium (S=4.2±0.7mm; C=3.5±0.6mm; P<0.05, and greater left ventricular diastolic (S=7.9±0.7mm; C=7.2±0.5mm; P<0.05 and systolic (S=4.1±0.5; C=3.4±0.5; P<0.05 diameters. The left ventricular mass index was greater in the smoking animals (S=1.5mg/kg±0.2; C=1.3mg/kg±0.2; P<0.05, and the ejection fraction (S=0.85±0.03; C=0.89±0.03; P<0.05 and the shortening fraction (S=47.8%±3.7; C=52.7%±4.6; P<0.05 were greater in the control group. No differences were observed in the diastolic transmitral flow variables (E wave, A wave, and E/A ratio. CONCLUSION: Chronic cigarette smoke exposure results in cardiac remodeling with a decrease in ventricular functional capacity.

  14. Plasmacytoid dendritic cells prevent cigarette smoke and Chlamydophila pneumoniae-induced Th2 inflammatory responses.

    Science.gov (United States)

    Sorrentino, Rosalinda; Gray, Pearl; Chen, Shuang; Shimada, Kenichi; Crother, Timothy R; Arditi, Moshe

    2010-10-01

    Smoking promotes the development of allergic asthma and pneumonia. Chlamydophila pneumoniae lung infection is associated with an increased risk for asthma, inducing an immune response regulated by dendritic cells (DCs). This study sought to determine whether exposure to cigarette smoke modulates the functional activity of CD11c-positive DCs in the lung, with and without concomitant C. pneumoniae infection. Bone marrow-derived DCs (BMDCs) were exposed in vitro to cigarette smoke extract (CSE) and/or live C. pneumoniae (Cpn), and then adoptively transferred intratracheally into wild-type mice. Although CSE plus Cpn appeared to exert an additive effect on the production of Th2 cytokines in vitro, we did not see this effect in vivo. However, the adoptive transfer of DCs pulsed with both CSE and C. pneumoniae into the lungs of naive mice led to an influx of plasmacytoid DCs (pDCs) that suppressed the Th2 skewing ability of the transferred BMDCs. The depletion of pDCs by antibody restored the Th2 skewing ability of the BMDCs. The expression of indoleamine-2,3-dioxygenase in the lung was reduced after the depletion of pDCs, and blocking IFN-α in vitro prevented the ability of pDCs to inhibit the Th2 responses induced by myeloid DCs (mDCs), suggesting their potential involvement in the mechanism of altered polarization. In conclusion, exposure to cigarette smoke skews C. pneumoniae-induced mDCs responses toward a Th2 bias in the lung, which is prevented by pDCs. We propose that pDCs may play a major role in the immunosuppressive lung environment in smokers with C. pneumoniae infection.

  15. Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells.

    Science.gov (United States)

    Checa, Marco; Hagood, James S; Velazquez-Cruz, Rafael; Ruiz, Victor; García-De-Alba, Carolina; Rangel-Escareño, Claudia; Urrea, Francisco; Becerril, Carina; Montaño, Martha; García-Trejo, Semiramis; Cisneros Lira, José; Aquino-Gálvez, Arnoldo; Pardo, Annie; Selman, Moisés

    2016-01-01

    Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease of unknown etiology. A growing body of evidence indicates that it may result from an aberrant activation of alveolar epithelium, which induces the expansion of the fibroblast population, their differentiation to myofibroblasts and the excessive accumulation of extracellular matrix. The mechanisms that activate the alveolar epithelium are unknown, but several studies indicate that smoking is the main environmental risk factor for the development of IPF. In this study we explored the effect of cigarette smoke on the gene expression profile and signaling pathways in alveolar epithelial cells. Lung epithelial cell line from human (A549), was exposed to cigarette smoke extract (CSE) for 1, 3, and 5 weeks at 1, 5 and 10% and gene expression was evaluated by complete transcriptome microarrays. Signaling networks were analyzed with the Ingenuity Pathway Analysis software. At 5 weeks of exposure, alveolar epithelial cells acquired a fibroblast-like phenotype. At this time, gene expression profile revealed a significant increase of more than 1000 genes and deregulation of canonical signaling pathways such as TGF-β and Wnt. Several profibrotic genes involved in EMT were over-expressed, and incomplete EMT was observed in these cells, and corroborated in mouse (MLE-12) and rat (RLE-6TN) epithelial cells. The secretion of activated TGF-β1 increased in cells exposed to cigarette smoke, which decreased when the integrin alpha v gene was silenced. These findings suggest that the exposure of alveolar epithelial cells to CSE induces the expression and release of a variety of profibrotic genes, and the activation of TGF-β1, which may explain at least partially, the increased risk of developing IPF in smokers.

  16. Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells.

    Directory of Open Access Journals (Sweden)

    Marco Checa

    Full Text Available Idiopathic pulmonary fibrosis (IPF is a progressive and lethal disease of unknown etiology. A growing body of evidence indicates that it may result from an aberrant activation of alveolar epithelium, which induces the expansion of the fibroblast population, their differentiation to myofibroblasts and the excessive accumulation of extracellular matrix. The mechanisms that activate the alveolar epithelium are unknown, but several studies indicate that smoking is the main environmental risk factor for the development of IPF. In this study we explored the effect of cigarette smoke on the gene expression profile and signaling pathways in alveolar epithelial cells. Lung epithelial cell line from human (A549, was exposed to cigarette smoke extract (CSE for 1, 3, and 5 weeks at 1, 5 and 10% and gene expression was evaluated by complete transcriptome microarrays. Signaling networks were analyzed with the Ingenuity Pathway Analysis software. At 5 weeks of exposure, alveolar epithelial cells acquired a fibroblast-like phenotype. At this time, gene expression profile revealed a significant increase of more than 1000 genes and deregulation of canonical signaling pathways such as TGF-β and Wnt. Several profibrotic genes involved in EMT were over-expressed, and incomplete EMT was observed in these cells, and corroborated in mouse (MLE-12 and rat (RLE-6TN epithelial cells. The secretion of activated TGF-β1 increased in cells exposed to cigarette smoke, which decreased when the integrin alpha v gene was silenced. These findings suggest that the exposure of alveolar epithelial cells to CSE induces the expression and release of a variety of profibrotic genes, and the activation of TGF-β1, which may explain at least partially, the increased risk of developing IPF in smokers.

  17. Influence of heavy cigarette smoking on heart rate variability and heart rate turbulence parameters

    DEFF Research Database (Denmark)

    Cagirci, Goksel; Cay, Serkan; Karakurt, Ozlem;

    2009-01-01

    BACKGROUND: Cigarette smoking increases the risk of cardiovascular events related with several mechanisms. The most suggested mechanism is increased activity of sympathetic nervous system. Heart rate variability (HRV) and heart rate turbulence (HRT) has been shown to be independent and powerful...... predictors of mortality in a specific group of cardiac patients. The goal of this study was to assess the effect of heavy cigarette smoking on cardiac autonomic function using HRV and HRT analyses. METHODS: Heavy cigarette smoking was defined as more than 20 cigarettes smoked per day. Heavy cigarette smokers......, 69 subjects and nonsmokers 74 subjects (control group) were enrolled in this study. HRV and HRT analyses [turbulence onset (TO) and turbulence slope (TS)] were assessed from 24-hour Holter recordings. RESULTS: The values of TO were significantly higher in heavy cigarette smokers than control group...

  18. How people think about the chemicals in cigarette smoke: a systematic review.

    Science.gov (United States)

    Morgan, Jennifer C; Byron, M Justin; Baig, Sabeeh A; Stepanov, Irina; Brewer, Noel T

    2017-02-21

    Laws and treaties compel countries to inform the public about harmful chemicals (constituents) in cigarette smoke. To encourage relevant research by behavioral scientists, we provide a primer on cigarette smoke toxicology and summarize research on how the public thinks about cigarette smoke chemicals. We systematically searched PubMed in July 2016 and reviewed citations from included articles. Four central findings emerged across 46 articles that met inclusion criteria. First, people were familiar with very few chemicals in cigarette smoke. Second, people knew little about cigarette additives, assumed harmful chemicals are added during manufacturing, and perceived cigarettes without additives to be less harmful. Third, people wanted more information about constituents. Finally, well-presented chemical information increased knowledge and awareness and may change behavior. This research area is in urgent need of behavioral science. Future research should investigate whether educating the public about these chemicals increases risk perceptions and quitting.

  19. An Integrated Framework for the Analysis of Adolescent Cigarette Smoking in Middle School Latino Youth

    Science.gov (United States)

    Guilamo-Ramos, Vincent; Dittus, Patricia; Holloway, Ian; Bouris, Alida; Crossett, Linda

    2011-01-01

    A framework based on five major theories of health behavior was used to identify the correlates of adolescent cigarette smoking. The framework emphasizes intentions to smoke cigarettes, factors that influence these intentions, and factors that moderate the intention-behavior relationship. Five hundred sixteen randomly selected Latino middle school…

  20. Impact of Cigarette Smoke on the Human and Mouse Lungs : A Gene-Expression Comparison Study

    NARCIS (Netherlands)

    Morissette, Mathieu C.; Lamontagne, Maxime; Berube, Jean-Christophe; Gaschler, Gordon; Williams, Andrew; Yauk, Carole; Couture, Christian; Laviolette, Michel; Hogg, James C.; Timens, Wim; Halappanavar, Sabina; Stampfli, Martin R.; Bosse, Yohan

    2014-01-01

    Cigarette smoke is well known for its adverse effects on human health, especially on the lungs. Basic research is essential to identify the mechanisms involved in the development of cigarette smoke-related diseases, but translation of new findings from pre-clinical models to the clinic remains diffi

  1. Cigarette smoke impairs airway epithelial barrier function and cell-cell contact recovery

    NARCIS (Netherlands)

    Heijink, I H; Brandenburg, S M; Postma, D S; van Oosterhout, A J M

    2012-01-01

    Cigarette smoking, the major cause of chronic obstructive pulmonary disease (COPD), induces aberrant airway epithelial structure and function. The underlying mechanisms are unresolved so far. We studied effects of cigarette smoke extract (CSE) on epithelial barrier function and wound regeneration in

  2. Examining Demographic Factors Related to Cigarette Smoking among Undergraduate Students at a Turkish University

    Science.gov (United States)

    Oktay, Erkan; Çelik, Ali Kemal; Akbaba, Ahmet Ilker

    2013-01-01

    Cigarette smoking is the leading global preventable health risk, and it is associated with well-known health risks such as morbidity, mortality, cancer, cardiovascular disease, and nicotine addiction. When analyzed by age group, cigarette smoking in Turkey is the most prevalent among younger adult populations. The college years appear to be a time…

  3. Evaluation of Nationwide Health Costs of Air Pollution and Cigarette Smoking

    Science.gov (United States)

    Williams, J. R.; Justus, C. G.

    1974-01-01

    The findings of this study indicate cigarette smoking causes more respiratory diseases than does air pollution. The 1970 nationwide health cost of respiratory diseases is estimated at $6.22 billion. The effect of air pollution accounts for between 1 and 5 percent of this total cost while cigarette smoking represents 68 percent. (MLB)

  4. Community and Individual Factors Associated with Cigarette Smoking among Young Men Who Have Sex with Men

    Science.gov (United States)

    Holloway, Ian W.; Traube, Dorian E.; Rice, Eric; Schrager, Sheree M.; Palinkas, Lawrence A.; Richardson, Jean; Kipke, Michele D.

    2012-01-01

    Young men who have sex with men (YMSM) have higher rates of cigarette smoking than their heterosexual counterparts, yet few studies have examined factors associated with cigarette smoking among YMSM. The present study sought to understand how different types of gay community connection (i.e., gay community identification and involvement, gay bar…

  5. NOS3 polymorphisms, cigarette smoking, and cardiovascular disease risk: The Atherosclerosis Risk in Communities study

    Science.gov (United States)

    Endothelial nitric oxide synthase (NOS3) activity and cigarette smoking significantly influence endothelial function. We sought to determine whether cigarette smoking modified the association between NOS3 polymorphisms and risk of coronary heart disease or stroke. All 1085 incident coronary heart di...

  6. Pulmonary cytokine composition differs in the setting of alcohol use disorders and cigarette smoking.

    Science.gov (United States)

    Burnham, Ellen L; Kovacs, Elizabeth J; Davis, Christopher S

    2013-06-15

    Alcohol use disorders (AUDs), including alcohol abuse and dependence, and cigarette smoking are widely acknowledged and common risk factors for pneumococcal pneumonia. Reasons for these associations are likely complex but may involve an imbalance in pro- and anti-inflammatory cytokines within the lung. Delineating the specific effects of alcohol, smoking, and their combination on pulmonary cytokines may help unravel mechanisms that predispose these individuals to pneumococcal pneumonia. We hypothesized that the combination of AUD and cigarette smoking would be associated with increased bronchoalveolar lavage (BAL) proinflammatory cytokines and diminished anti-inflammatory cytokines, compared with either AUDs or cigarette smoking alone. Acellular BAL fluid was obtained from 20 subjects with AUDs, who were identified using a validated questionnaire, and 19 control subjects, matched on the basis of age, sex, and smoking history. Half were current cigarette smokers; baseline pulmonary function tests and chest radiographs were normal. A positive relationship between regulated and normal T cell expressed and secreted (RANTES) with increasing severity of alcohol dependence was observed, independent of cigarette smoking (P = 0.0001). Cigarette smoking duration was associated with higher IL-1β (P = 0.0009) but lower VEGF (P = 0.0007); cigarette smoking intensity was characterized by higher IL-1β and lower VEGF and diminished IL-12 (P = 0.0004). No synergistic effects of AUDs and cigarette smoking were observed. Collectively, our work suggests that AUDs and cigarette smoking each contribute to a proinflammatory pulmonary milieu in human subjects through independent effects on BAL RANTES and IL-1β. Furthermore, cigarette smoking additionally influences BAL IL-12 and VEGF that may be relevant to the pulmonary immune response.

  7. The effects of repeated exposure to graphic fear appeals on cigarette packages: A field experiment.

    Science.gov (United States)

    Dijkstra, Arie; Bos, Colin

    2015-03-01

    Experimental studies on the effects of graphic fear appeals on cigarette packages typically expose smokers in a single session to a fear appeal, although in practice the exposure is always repeated. The present study applied an improved study design with repeated exposure to fear appeals on cigarette packages. In this field-experiment, 118 smokers were assigned to 1 of 2 conditions with either graphic fear appeals or textual warnings on their cigarette packages. During 3 weeks, fear and disgust were assessed 6 times. The intention to quit smoking after 3 weeks and quitting activity during the 3 weeks were the dependent measures. The effects of 3 pretest individual difference moderators were tested: disengagement beliefs, number of cigarettes smoked a day, and readiness to quit. Three weeks of exposure to the graphic fear appeals led to a stronger intention to quit, but only when smokers scored low on disengagement beliefs, or were heavier smokers. In addition, smokers low in disengagement more often reported to have cut down on smoking in the graphic condition. There were no indications of habituation of fear and disgust over the 3 weeks. The effects of graphic fear appeals depended on smokers' characteristics: The moderators may explain the mixed findings in the literature. The lack of habituation may be caused by the renewal of the graphics every few days. The used field-experimental design with natural repeated exposure to graphics is promising.

  8. Estimating cotinine associations and a saliva cotinine level to identify active cigarette smoking in alaska native pregnant women.

    Science.gov (United States)

    Smith, Julia J; Robinson, Renee F; Khan, Burhan A; Sosnoff, Connie S; Dillard, Denise A

    2014-01-01

    Studies indicate nicotine metabolism varies by race and can change during pregnancy. Given high rates of tobacco use and limited studies among Alaska Native (AN) women, we estimated associations of saliva cotinine levels with cigarette use and second-hand smoke (SHS) exposure and estimated a saliva cotinine cutoff to distinguish smoking from non-smoking pregnant AN women. Using questionnaire data and saliva cotinine, we utilized multi-variable linear regression (n = 370) to estimate cotinine associations with tobacco use, SHS exposure, demographic, and pregnancy-related factors. Additionally, we estimated an optimal saliva cotinine cutoff for indication of active cigarette use in AN pregnant women using receiver operating characteristic (ROC) curve analysis (n = 377). Saliva cotinine significantly decreased with maternal age and significantly increased with cigarettes smoked per day, SHS exposure, and number of previous full term pregnancies. Using self-reported cigarette use in the past 7 days as indication of active smoking, the area under the ROC curve was 0.975 (95 % CI: 0.960-0.990). The point closest to 100 % specificity and sensitivity occurred with a cotinine concentration of 1.07 ng/mL, which corresponded to sensitivity of 94 % and specificity of 94 %. We recommend using a saliva cotinine cutoff of 1 ng/mL to distinguish active smoking in pregnant AN women. This cutoff is lower than used in other studies with pregnant women, most likely due to high prevalence of light or intermittent smoking in the AN population. Continued study of cotinine levels in diverse populations is needed.

  9. Vertical Equity Consequences of Very High Cigarette Tax Increases: If the Poor Are the Ones Smoking, How Could Cigarette Tax Increases Be Progressive?

    Science.gov (United States)

    Colman, Gregory J.; Remler, Dahlia K.

    2008-01-01

    Cigarette smoking is concentrated among low-income groups. Consequently, cigarette taxes are considered regressive. However, if poorer individuals are much more price sensitive than richer individuals, then tax increases would reduce smoking much more among the poor and their cigarette tax expenditures as a share of income would rise by much less…

  10. Does cigarette smoking relieve stress? Evidence from the event-related potential (ERP).

    Science.gov (United States)

    Choi, Damee; Ota, Shotaro; Watanuki, Shigeki

    2015-12-01

    Previous studies have reported a paradox that cigarette smoking reduces stress psychologically; however, it increases the arousal level physiologically. To examine this issue, our study aimed to investigate whether cigarette smoking relieves stress by measuring the late positive potential (LPP), a component of the event-related potential (ERP). In Experiment 1, participants first watched emotionally neutral images; second, they received a break; and finally, they watched emotionally neutral images again. In the break, they smoked a cigarette (smoking condition) or simply rested without smoking (non-smoking condition). The procedure of Experiment 2 was the same as that of Experiment 1, except that the participants watched unpleasant images as stress stimuli before the break. In Experiment 1, the LPP decreased from before to after the break in the smoking condition, but not in the non-smoking condition, suggesting that smoking cigarettes in the neutral state reduces the arousal level. In Experiment 2, the LPP for 400-600 ms decreased from before to after the break, both in the smoking and non-smoking conditions; however, the LPP for 200-400 ms decreased from before to after the break only in the smoking condition. This suggests the possibility that cigarette smoking in the unpleasant state may facilitate a decrease in the arousal level faster than with non-smoking. In both Experiments 1 and 2, the subjective rating results also suggested that cigarette smoking decreased anxiety. Taken together, both the physiological (LPP) and the psychological responses from our study suggest that cigarette smoking perhaps relieves stress.

  11. Big five personality factors and cigarette smoking: a 10-year study among US adults.

    Science.gov (United States)

    Zvolensky, Michael J; Taha, Farah; Bono, Amanda; Goodwin, Renee D

    2015-04-01

    The present study examined the relation between the big five personality traits and any lifetime cigarette use, progression to daily smoking, and smoking persistence among adults in the United States (US) over a ten-year period. Data were drawn from the Midlife Development in the US (MIDUS) I and II (N = 2101). Logistic regression was used to examine the relationship between continuously measured personality factors and any lifetime cigarette use, smoking progression, and smoking persistence at baseline (1995-1996) and at follow-up (2004-2006). The results revealed that higher levels of openness to experience and neuroticism were each significantly associated with increased risk of any lifetime cigarette use. Neuroticism also was associated with increased risk of progression from ever smoking to daily smoking and persistent daily smoking over a ten-year period. In contrast, conscientiousness was associated with decreased risk of lifetime cigarette use, progression to daily smoking, and smoking persistence. Most, but not all, associations between smoking and personality persisted after adjusting for demographic characteristics, depression, anxiety disorders, and substance use problems. The findings suggest that openness to experience and neuroticism may be involved in any lifetime cigarette use and smoking progression, and that conscientiousness appears to protect against smoking progression and persistence. These data add to a growing literature suggesting that certain personality factors--most consistently neuroticism--are important to assess and perhaps target during intervention programs for smoking behavior.

  12. Cigarette smoking and mammographic density in the Danish Diet, Cancer and Health cohort

    DEFF Research Database (Denmark)

    Jacobsen, Katja Kemp; Lynge, Elsebeth; Vejborg, Ilse;

    2016-01-01

    between smoking and MD was strongest in women who initiated smoking before age of 16 years (0.79, 0.64-0.96), smoked ≥15 cigarettes/day (0.83, 0.71-0.98), smoked ≥5 pack-years (0.62, 0.43-0.89), smoked >30 years (0.86, 0.75-0.99), and smoked ≥11 years before first childbirth (0.70, 0.51-0.96). Association...

  13. Up-Regulation of Endothelin Receptors Induced by Cigarette Smoke — Involvement of MAPK in Vascular and Airway Hyper-Reactivity

    Directory of Open Access Journals (Sweden)

    Yaping Zhang

    2010-01-01

    Full Text Available Cigarette smoke exposure is well known to cause cardiovascular and airway diseases, both of which are leading causes of death and disability in the world. However, the molecular mechanisms that link cigarette smoke to cardiovascular and airway diseases are not fully understood. Vascular and airway hyper-reactivity plays an important role in the pathogenesis of cardiovascular and airway diseases. Recent studies have demonstrated that endothelin receptor up-regulation mediates vascular and airway hyper-reactivity in response to endothelin-1 (ET-1, endothelin receptor agonist in cardiovascular and airway diseases. In the vasculature and airways, the main functional consequences of up-regulated endothelin receptors by cigarette smoke exposure are enhanced contraction and proliferation of the smooth muscle cells, which subsequently result in abnormal contraction (spasm and adverse proliferation (remodeling of the vasculature and airways. The structural alteration by adverse remodeling involves changes in cell growth, cell death, cell migration, and production or degradation of the extracellular matrix. This review focuses on cigarette smoke exposure that induces activation of intracellular mitogen-activated protein kinase (MAPK and subsequently results in the up-regulation of endothelin receptors in the vasculature and airways, which mediates vascular and airway hyper-reactivity, one of the important pathogenic characteristics of cardiovascular and airway diseases. Understanding the molecular mechanisms of how cigarette smoke causes up-regulation of endothelin receptors in the vasculature and airways may provide new strategies for the treatment of cigarette smoke—associated cardiovascular and lung diseases.

  14. Cigarette smoke promotes dendritic cell accumulation in COPD; a Lung Tissue Research Consortium study

    Directory of Open Access Journals (Sweden)

    Yi Eunhee S

    2010-04-01

    Full Text Available Abstract Background Abnormal immune responses are believed to be highly relevant in the pathogenesis of chronic obstructive pulmonary disease (COPD. Dendritic cells provide a critical checkpoint for immunity by their capacity to both induce and suppress immunity. Although evident that cigarette smoke, the primary cause of COPD, significantly influences dendritic cell functions, little is known about the roles of dendritic cells in the pathogenesis of COPD. Methods The extent of dendritic cell infiltration in COPD tissue specimens was determined using immunohistochemical localization of CD83+ cells (marker of matured myeloid dendritic cells, and CD1a+ cells (Langerhans cells. The extent of tissue infiltration with Langerhans cells was also determined by the relative expression of the CD207 gene in COPD versus control tissues. To determine mechanisms by which dendritic cells accumulate in COPD, complimentary studies were conducted using monocyte-derived human dendritic cells exposed to cigarette smoke extract (CSE, and dendritic cells extracted from mice chronically exposed to cigarette smoke. Results In human COPD lung tissue, we detected a significant increase in the total number of CD83+ cells, and significantly higher amounts of CD207 mRNA when compared with control tissue. Human monocyte-derived dendritic cells exposed to CSE (0.1-2% exhibited enhanced survival in vitro when compared with control dendritic cells. Murine dendritic cells extracted from mice exposed to cigarette smoke for 4 weeks, also demonstrated enhanced survival compared to dendritic cells extracted from control mice. Acute exposure of human dendritic cells to CSE induced the cellular pro-survival proteins heme-oxygenase-1 (HO-1, and B cell lymphoma leukemia-x(L (Bcl-xL, predominantly through oxidative stress. Although activated human dendritic cells conditioned with CSE expressed diminished migratory CCR7 expression, their migration towards the CCR7 ligand CCL21 was not

  15. Bayesian Network Inference Enables Unbiased Phenotypic Anchoring of Transcriptomic Responses to Cigarette Smoke in Humans.

    Science.gov (United States)

    Jennen, Danyel G J; van Leeuwen, Danitsja M; Hendrickx, Diana M; Gottschalk, Ralph W H; van Delft, Joost H M; Kleinjans, Jos C S

    2015-10-19

    Microarray-based transcriptomic analysis has been demonstrated to hold the opportunity to study the effects of human exposure to, e.g., chemical carcinogens at the whole genome level, thus yielding broad-ranging molecular information on possible carcinogenic effects. Since genes do not operate individually but rather through concerted interactions, analyzing and visualizing networks of genes should provide important mechanistic information, especially upon connecting them to functional parameters, such as those derived from measurements of biomarkers for exposure and carcinogenic risk. Conventional methods such as hierarchical clustering and correlation analyses are frequently used to address these complex interactions but are limited as they do not provide directional causal dependence relationships. Therefore, our aim was to apply Bayesian network inference with the purpose of phenotypic anchoring of modified gene expressions. We investigated a use case on transcriptomic responses to cigarette smoking in humans, in association with plasma cotinine levels as biomarkers of exposure and aromatic DNA-adducts in blood cells as biomarkers of carcinogenic risk. Many of the genes that appear in the Bayesian networks surrounding plasma cotinine, and to a lesser extent around aromatic DNA-adducts, hold biologically relevant functions in inducing severe adverse effects of smoking. In conclusion, this study shows that Bayesian network inference enables unbiased phenotypic anchoring of transcriptomics responses. Furthermore, in all inferred Bayesian networks several dependencies are found which point to known but also to new relationships between the expression of specific genes, cigarette smoke exposure, DNA damaging-effects, and smoking-related diseases, in particular associated with apoptosis, DNA repair, and tumor suppression, as well as with autoimmunity.

  16. Neurobehavioral Consequences of Prenatal Exposure to Smoking at 6 to 8 Months of Age

    Science.gov (United States)

    Willoughby, Michael; Greenberg, Mark; Blair, Clancy; Stifter, Cynthia

    2007-01-01

    Between 400,000 and 800,000 infants are born in the United States each year to women who smoked cigarettes during their pregnancy. Whereas the physical health consequences to infants of prenatal exposure to smoking are well established, the early neurobehavioral consequences are less well understood. This study investigated the neurobehavioral…

  17. Influence of filter ventilation on the chemical composition of cigarette mainstream smoke

    Energy Technology Data Exchange (ETDEWEB)

    Adam, Thomas, E-mail: dr-thomas-adam@gmx.net [Analytical Chemistry, Institute of Physics, University of Augsburg, 86159 Augsburg (Germany); Institute of Ecological Chemistry, Helmholtz Zentrum Muenchen, 85764 Neuherberg (Germany); McAughey, John [British American Tobacco, Group R and D, Southampton SO15 8TL (United Kingdom); Mocker, Christoph [Institute of Ecological Chemistry, Helmholtz Zentrum Muenchen, 85764 Neuherberg (Germany); Analytical Chemistry, Institute of Chemistry, University of Rostock, 18051 Rostock (Germany); McGrath, Conor [British American Tobacco, Group R and D, Southampton SO15 8TL (United Kingdom); Zimmermann, Ralf [Institute of Ecological Chemistry, Helmholtz Zentrum Muenchen, 85764 Neuherberg (Germany); BIfA-Umweltinstitut - Bavarian Institute of Applied Environmental Research and Technology GmbH, Environmental Chemistry, 86167 Augsburg (Germany); Analytical Chemistry, Institute of Chemistry, University of Rostock, 18051 Rostock (Germany)

    2010-01-04

    Total yields of cigarette smoke constituents are greatly influenced by smoking behaviour, the tobacco blend as well as a variety of cigarette design parameters. Thereby, filter ventilation, i.e. diluting the smoke by providing a zone of microscopic holes around the circumference of the filter is one method to reduce the yield of 'tar' and other smoke compounds. However, little is known how these design variations influence the combustion conditions, and therefore, the overall chemical pattern of the smoke. In this paper single photon ionization-time-of-flight mass spectrometry (SPI-TOFMS) is used to characterize and compare cigarettes on a puff-by-puff basis, which differ only in filter ventilation magnitude. The research cigarettes investigated were made from Virginia tobacco and featured filter ventilations of 0% (no ventilation), 35%, and 70%. The cigarettes were smoked under two different puffing regimes, one using the puffing parameters of the conventional International Organization for Standardization (ISO) smoking regime and a more intense smoking condition. Results show that every variation entails a change of the chemical pattern, whereby, in general, cigarettes with 0% filter ventilation as well as the intense smoking regime lead to a more complete combustion compared to the ISO smoking conditions and the high ventilated cigarettes. Changes in the overall patterns can also be observed during the smoking for individual puffs. Some substances dominate the first puff, some species are more pronounced in the middle puffs, whereas others are preferably formed in the last puffs. This demonstrates the high complexity of the occurring processes. Results might help to understand the formation and decomposition reactions taking place when a cigarette is smoked and offer scope for targeted reduction strategies for specific toxicants or groups of toxicants in the smoke.

  18. Magnitudes of biomarker reductions in response to controlled reductions in cigarettes smoked per day: a one-week clinical confinement study.

    Science.gov (United States)

    Theophilus, Eugenia H; Coggins, Christopher R E; Chen, Peter; Schmidt, Eckhardt; Borgerding, Michael F

    2015-03-01

    Tobacco toxicant-related exposure reduction is an important tool in harm reduction. Cigarette per day reduction (CPDR) occurs as smokers migrate from smoking cigarettes to using alternative tobacco/nicotine products, or quit smoking. Few reports characterize the dose-response relationships between CPDR and effects on exposure biomarkers, especially at the low end of CPD exposure (e.g., 5 CPD). We present data on CPDR by characterizing magnitudes of biomarker reductions. We present data from a well-controlled, one-week clinical confinement study in healthy smokers who were switched from smoking 19-25 CPD to smoking 20, 10, 5 or 0 CPD. Biomarkers were measured in blood, plasma, urine, and breath, and included smoke-related toxicants, urine mutagenicity, smoked cigarette filter analyses (mouth level exposure), and vital signs. Many of the biomarkers (e.g., plasma nicotine) showed strong CPDR dose-response reductions, while others (e.g., plasma thiocyanate) showed weaker dose-response reductions. Factors that lead to lower biomarker reductions include non-CPD related contributors to the measured response (e.g., other exposure sources from environment, life style, occupation; inter-individual variability). This study confirms CPDR dose-responsive biomarkers and suggests that a one-week design is appropriate for characterizing exposure reductions when smokers switch from cigarettes to new tobacco products.

  19. Intrauterine Tobacco Smoke Exposure and Congenital Heart Defects.

    Science.gov (United States)

    Forest, Sharron; Priest, Sandra

    2016-01-01

    Tobacco use and second-hand smoke exposure during pregnancy are linked to a host of deleterious effects on the pregnancy, fetus, and infant. Health outcomes improve when women quit smoking at any time during the pregnancy. However, the developing heart is vulnerable to noxious stimuli in the early weeks of fetal development, a time when many women are not aware of being pregnant. Congenital heart defects are the most common birth defects. Research shows an association between maternal tobacco exposure, both active and passive, and congenital heart defects. This article presents recent evidence supporting the association between intrauterine cigarette smoke exposure in the periconceptional period and congenital heart defects and discusses clinical implications for practice for perinatal and neonatal nurses.

  20. Cigarette Smoke-Exposed Candida albicans Increased Chitin Production and Modulated Human Fibroblast Cell Responses

    Directory of Open Access Journals (Sweden)

    Humidah Alanazi

    2014-01-01

    Full Text Available The predisposition of cigarette smokers for development of respiratory and oral bacterial infections is well documented. Cigarette smoke can also contribute to yeast infection. The aim of this study was to investigate the effect of cigarette smoke condensate (CSC on C. albicans transition, chitin content, and response to environmental stress and to examine the interaction between CSC-pretreated C. albicans and normal human gingival fibroblasts. Following exposure to CSC, C. albicans transition from blastospore to hyphal form increased. CSC-pretreated yeast cells became significantly (P<0.01 sensitive to oxidation but significantly (P<0.01 resistant to both osmotic and heat stress. CSC-pretreated C. albicans expressed high levels of chitin, with 2- to 8-fold recorded under hyphal conditions. CSC-pretreated C. albicans adhered better to the gingival fibroblasts, proliferated almost three times more and adapted into hyphae, while the gingival fibroblasts recorded a significantly (P<0.01 slow growth rate but a significantly higher level of IL-1β when in contact with CSC-pretreated C. albicans. CSC was thus able to modulate both C. albicans transition through the cell wall chitin content and the interaction between C. albicans and normal human gingival fibroblasts. These findings may be relevant to fungal infections in the oral cavity in smokers.

  1. Impacts of cigarette smoking on immune responsiveness: Up and down or upside down?

    Science.gov (United States)

    Qiu, Feifei; Liang, Chun-Ling; Liu, Huazhen; Zeng, Yu-Qun; Hou, Shaozhen; Huang, Song; Lai, Xiaoping; Dai, Zhenhua

    2017-01-01

    Cigarette smoking is associated with numerous diseases and poses a serious challenge to the current healthcare system worldwide. Smoking impacts both innate and adaptive immunity and plays dual roles in regulating immunity by either exacerbation of pathogenic immune responses or attenuation of defensive immunity. Adaptive immune cells affected by smoking mainly include T helper cells (Th1/Th2/Th17), CD4+CD25+ regulatory T cells, CD8+ T cells, B cells and memory T/B lymphocytes while innate immune cells impacted by smoking are mostly DCs, macrophages and NK cells. Complex roles of cigarette smoke have resulted in numerous diseases, including cardiovascular, respiratory and autoimmune diseases, allergies, cancers and transplant rejection etc. Although previous reviews have described the effects of smoking on various diseases and regional immunity associated with specific diseases, a comprehensive and updated review is rarely seen to demonstrate impacts of smoking on general immunity and, especially on major components of immune cells. Here, we aim to systematically and objectively review the influence of smoking on major components of both innate and adaptive immune cells, and summarize cellular and molecular mechanisms underlying effects of cigarette smoking on the immune system. The molecular pathways impacted by cigarette smoking involve NFκB, MAP kinases and histone modification. Further investigations are warranted to understand the exact mechanisms responsible for smoking-mediated immunopathology and to answer lingering questions over why cigarette smoking is always harmful rather than beneficial even though it exerts dual effects on immune responses. PMID:27902485

  2. Paternal smoking and germ cell death: A mechanistic link to the effects of cigarette smoke on spermatogenesis and possible long-term sequelae in offspring.

    Science.gov (United States)

    Esakky, Prabagaran; Moley, Kelle H

    2016-11-05

    Paternal exposure to constituents of cigarette smoke (CS) is reportedly associated with infertility, birth defects and childhood cancers even though the mechanism behind this relationship is still unclear. Chronic cigarette smoking by men leads to poor sperm quality and quantity mainly through oxidative stress and also direct assault by CS metabolites. Among several carcinogenic and teratogenic components of cigarette smoke condensate (CSC), polycyclic aromatic hydrocarbons (PAHs) display a preeminent role in accelerating germ cell death via the cytoplasmic transcription factor, aryl hydrocarbon receptor (AHR) that is present across all stages of spermatogenesis. Activation of AHR by growth factors though benefits normal cellular functions, its mediation by CSC in a spermatocyte cell line [Gc2(spd)ts] adversely affects the expression of a battery of genes associated with antioxidant mechanisms, cell proliferation and apoptosis, and cell cycle progress. Besides, the CSC-mediated cross talk either between AHR and NRF2 or AHR-NRF2 and MAPKs pathways inhibits normal proliferation of the spermatogenic GC-2spd(ts) cells in vitro and cell death of spermatocytes in vivo. Pharmacological inactivation of CSC-induced AHR but not its genetic manipulation seems preventing DNA and cell membrane damage in Gc2(spd)ts. Data from recent reports suggest that the cigarette smoke affects both the genomic and epigenomic components of the sperm and attributes any associated changes to developmental defects in the offspring. Thus, the studies discussed here in this review shed light on possible mechanistic factors that could probably be responsible for the paternally mediated birth defects in the offspring following exposure to the toxic constituents of cigarette smoke.

  3. 卷烟烟气暴露对大鼠学习记忆功能及海马组织病理和BDNF表达的影响%Influence of cigarette smoke exposure on learning and memory function,histologic changes and brain-derived neurotrophic factor in rats

    Institute of Scientific and Technical Information of China (English)

    李跃; 潘秀颉; 杨陟华; 齐绍武; 朱茂祥

    2012-01-01

    设对照组(未染毒)、低剂量组(约2.5支烟,每天染毒10 min)、中剂量组(约5支烟,每天染毒20 min)及高剂量组(约10支烟,每天染毒40 min)4个处理,将雄性SD大鼠置于气体染毒箱内行被动吸烟,研究卷烟烟气暴露对大鼠学习记忆功能及海马病理和脑源性神经营养因子(brain-derived neurotrophicfactor,BDNF)的影响.结果表明:染毒30d,染毒组大鼠潜伏时间均显著短于对照组,BDNF表达显著高于对照组;染毒60 d,中剂量组大鼠潜伏时间显著短于对照组,BDNF表达显著高于对照组;染毒180 d,染毒组大鼠潜伏时间显著长于对照组,BDNF表达显著高于对照组;不同剂量处理大鼠的海马HE染色均无明显变化,大鼠的海马组织均无器质性损伤;短期烟气暴露可提高大鼠学习记忆功能,随染毒时间的延长,大鼠学习记忆功能下降,该作用与海马BDNF的表达密切相关.%Male SD rats were randomly divided into normal control group and cigarette smoke group (CS group). Rats in CS group were exposed to cigarette smoke in ventilated smoking chambers and divided into low-dose group (about 2.5 cigarettes, exposed for 10 minutes a day), medium-dose group (about 5 cigarettes, exposed for 20 minutes a day) and high-dose group (about 10 cigarettes, exposed for 40 minutes a day). The influence of cigarette smoke exposure on learning and memory function of rats, on pathological changes of hippocampus and on the expression of brain-derived neurotrophicfactor (BDNF) was explored by Morris water maze, H-E staining and immunohistochemistry staining, respectively. The results showed that the escape latency of CS group was significantly decreased and the expression of BDNF was significantly increased compared to normal control group 30 d after exposure; the escape latency of medium-dose group was shorter than that of the normal control group and the expression of BDNF of CS group was significantly increased 60 d after exposure

  4. Effect of Cigarette and Cigar Smoking on Peak Expiratory Flow Rate

    Science.gov (United States)

    Medabala, Tambi; B.N., Rao; Mohesh M.I., Glad; Kumar M., Praveen

    2013-01-01

    Background: Tobacco smoking in India has been increasing alarmingly. Smoking is a known risk factor for chronic obstructive pulmonary disease (COPD), cardiovascular diseases and certain cancers, especially, the lung cancer. The percentage prevalence of cigarette smoking (18.5%) and cigar smoking (4%) in males is high in Andhra Pradesh compared to other southern states. There is not enough scientific literature to correlate about intensity of cigarette and cigar smoking and their impact on lung function though high prevalence is reported in Andhra Pradesh, India. Objectives: The purpose of this study was to examine whether PEFR differs between cigarette and cigar smokers compared to non-smokers and also to estimate the intensity of cigarette and cigar smoking on PEFR. Methods: PEFR was recorded in cigarette smokers (n=49) and cigar smokers (n=10) as well as in non-smokers (n=64) using Wright’s mini Peak Flow Meter. Results: PEFR is decreased in both cigarette as well in cigar smokers compared to non-smokers and the magnitude of decline was higher in cigar smoking elderly individuals. Conclusion: The intensity of cigarette and cigar smoking (pack-years) emerged as the main variable to influence airway obstruction in smokers that caused greater reduction in PEFR. PMID:24179889

  5. The frequency of cigarette smoking in patients with psoriasis vulgaris: a comparative study

    Directory of Open Access Journals (Sweden)

    Ashkevari Sh

    2011-07-01

    Full Text Available "n 800x600 Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-parent:""; mso-padding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin:0in; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:10.0pt; font-family:"Times New Roman","serif";} Background: Psoriasis is a chronic, inflammatory disease of the skin. Recently, nicotinic cholinergic receptors have been demonstrated on keratinocytes, stimulating calcium influx and accelerating cell differentiation. Therefore, smoking and nicotine seem to influence inflammatory processes in psoriatic skin. The aim of this study was to determine the frequency of cigarette smoking as an independent risk factor in patients with psoriasis who attended the department of dermatology at Razi Hospital in Rasht during the years 2008 and 2009. "n"nMethods : In this descriptive-inferential study, we recruited 96 patients with psoriasis vulgaris and 96 individuals as the controls. The participants were adjusted for sex, age and body mass index. The collected data related to smoking status, duration of smoking habit, smoking intensity, pack-year smoking history, and passively exposure to smoking were documented in a researcher-devised questionnaire. Subsequently, the data were analyzed by descriptive and inferential statistics such as χ2, t-test and Mann-Whitney U test by SPSS software."n"nResults : The smoking rate was 33.3% in the patients and 19.4% in the controls. Pack-year history, regarded as the intensity and duration (years of smoking, significantly increased the risk of psoriasis vulgaris (P<0.05, OR=2.07, 95% CI=1.17-3.68. Being a passive smoker did not make significant differences between the cases and the controls. "n"nConclusion: Our study demonstrated that psoriasis vulgaris had a

  6. Cognitive regulation of smoking behavior within a cigarette: Automatic and nonautomatic processes.

    Science.gov (United States)

    Motschman, Courtney A; Tiffany, Stephen T

    2016-06-01

    There has been limited research on cognitive processes governing smoking behavior in individuals who are tobacco dependent. In a replication (Baxter & Hinson, 2001) and extension, this study examined the theory (Tiffany, 1990) that drug use may be controlled by automatic processes that develop over repeated use. Heavy and occasional cigarette smokers completed a button-press reaction time (RT) task while concurrently smoking a cigarette, pretending to smoke a lit cigarette, or not smoking. Slowed RT during the button-press task indexed the cognitive disruption associated with nonautomatic control of behavior. Occasional smokers' RTs were slowed when smoking or pretending to smoke compared with when not smoking. Heavy smokers' RTs were slowed when pretending to smoke versus not smoking; however, their RTs were similarly fast when smoking compared with not smoking. The results indicated that smoking behavior was more highly regulated by controlled, nonautomatic processes among occasional smokers and by automatic processes among heavy smokers. Patterns of RT across the interpuff interval indicated that occasional smokers were significantly slowed in anticipation of and immediately after puffing onset, whereas heavy smokers were only slowed significantly after puffing onset. These findings suggest that the entirety of the smoking sequence becomes automatized, with the behaviors leading up to puffing becoming more strongly regulated by automatic processes with experience. These results have relevance to theories on the cognitive regulation of cigarette smoking and support the importance of interventions that focus on routinized behaviors that individuals engage in during and leading up to drug use. (PsycINFO Database Record

  7. Subjective Reactivity to the First Cigarette of the Day as a Predictor of Smoking Relapse: A Preliminary Study

    OpenAIRE

    Toll, Benjamin A.; Schepis, Ty S.; O’Malley, Stephanie S.; McKee, Sherry A.; Krishnan-Sarin, Suchitra

    2007-01-01

    We examined subjective responses to smoking the first cigarette of the day and investigated how these responses related to smoking cessation treatment outcome. Data from participants (N = 207) in a clinical trial of message framing for smoking cessation with bupropion, obtained prior to the targeted quit day, were used to examine indices of craving, withdrawal, and affect before and after smoking the first cigarette of the day. After smoking the initial cigarette, craving, withdrawal symptoms...

  8. Earlier age of smoking initiation may not predict heavier cigarette consumption in later adolescence.

    Science.gov (United States)

    Morrell, Holly E R; Song, Anna V; Halpern-Felsher, Bonnie L

    2011-09-01

    Previous studies suggest that earlier cigarette smoking initiation in adolescence predicts greater cigarette consumption later in adolescence or adulthood. Results from these studies have been used to inform interventions for adolescent smoking. However, previous studies suffer from several important methodological limitations. The objective of the present study was to address these limitations by longitudinally and prospectively examining whether and how age of initiation of smoking among adolescents predicts cigarette consumption by age 16 or 17. Participants completed an in-class survey every 6 months for 2-3 school years. Participants included 395 adolescents (Mean age=14 years at baseline; 53.2% female) from two public high schools in Northern California (Schools A and B) who completed self-report measures of smoking initiation, number of friends who smoke, and number of whole cigarettes smoked by the final survey time point. Adolescents who were older when they first smoked one whole cigarette were 5.3 to 14.6 times more likely in School A and 2.9 to 4.3 times more likely in School B to have smoked a greater number of cigarettes by age 16 or 17. Results suggested that earlier smoking initiation may not lead to heavier cigarette consumption later in time, as has been previously shown. There may be a period of heightened vulnerability in mid- or late adolescence where smoking experimentation is more likely to lead to greater cigarette consumption. Targeting prevention efforts to adolescents aged 14 to 17 years may further reduce smoking initiation among youth, thus limiting subsequent smoking-related morbidity and mortality in adulthood.

  9. Glucosamine attenuates cigarette smoke-induced lung inflammation by inhibiting ROS-sensitive inflammatory signaling.

    Science.gov (United States)

    Wu, Yuh-Lin; Lin, An-Hsuan; Chen, Chao-Hung; Huang, Wen-Chien; Wang, Hsin-Yi; Liu, Meng-Han; Lee, Tzong-Shyuan; Ru Kou, Yu

    2014-04-01

    Cigarette smoking causes persistent lung inflammation that is mainly regulated by redox-sensitive pathways. We have reported that cigarette smoke (CS) activates a NADPH oxidase-dependent reactive oxygen species (ROS)-sensitive AMP-activated protein kinase (AMPK) signaling pathway leading to induction of lung inflammation. Glucosamine, a dietary supplement used to treat osteoarthritis, has antioxidant and anti-inflammatory properties. However, whether glucosamine has similar beneficial effects against CS-induced lung inflammation remains unclear. Using a murine model we show that chronic CS exposure for 4 weeks increased lung levels of 4-hydroxynonenal (an oxidative stress biomarker), phospho-AMPK, and macrophage inflammatory protein 2 and induced lung inflammation; all of these CS-induced events were suppressed by chronic treatment with glucosamine. Using human bronchial epithelial cells, we demonstrate that cigarette smoke extract (CSE) sequentially activated NADPH oxidase; increased intracellular levels of ROS; activated AMPK, mitogen-activated protein kinases (MAPKs), nuclear factor-κB (NF-κB), and signal transducer and activator of transcription proteins 3 (STAT3); and induced interleukin-8 (IL-8). Additionally, using a ROS scavenger, a siRNA that targets AMPK, and various pharmacological inhibitors, we identified the signaling cascade that leads to induction of IL-8 by CSE. All these CSE-induced events were inhibited by glucosamine pretreatment. Our findings suggest a novel role for glucosamine in alleviating the oxidative stress and lung inflammation induced by chronic CS exposure in vivo and in suppressing the CSE-induced IL-8 in vitro by inhibiting both the ROS-sensitive NADPH oxidase/AMPK/MAPK signaling pathway and the downstream transcriptional factors NF-κB and STAT3.

  10. Biomarkers of polycyclic aromatic hydrocarbon-DNA damage and cigarette smoke exposures in paired maternal and newborn blood samples as a measure of differential susceptibility

    Energy Technology Data Exchange (ETDEWEB)

    Whyatt, R.M.; Jedrychowski, W.; Hemminki, K.; Santella, R.M.; Tsai WeiYann; Yang Ke; Perera, F.P. [Columbia University, New York, NY (US). Division of Environmental Health Sciences, Mailman School of Public Health

    2001-07-01

    In this study, we report on three biomarkers measured in paired blood samples collected at birth from 160 mother/newborn pairs from Poland: 70 pairs from Krakow (a city with high air pollution including PAHs) and 90 pairs from Limanowa (an area with lower ambient pollution but greater indoor coal use). Field studies were conducted during January-March 1992. Biomarkers were: WBC aromatic-DNA adducts by {sup 32}P-postlabeling and PAH-DNA adducts by ELISA and plasma cotinine. Correlations were assessed by Spearman's rank test, and differences in biomarker levels were assessed by the Wilcoxon signed-ranks test. A significant correlation between paired newborn/maternal samples was seen for aromatic-DNA adduct levels and plasma cotinine, but not PAH-DNA adduct levels. Among the total cohort, levels of the three biomarkers were higher in newborn samples compared with paired maternal samples. The difference was significant for aromatic-DNA adduct levels (16.6 plus or minus 12.5 versus 14.21 plus or minus 15.4/10{sup 8} nucleotides; P=0.002) and plasma cotinine, but not for PAH-DNA adduct levels. When analyses were restricted to the 80 mother/newborn pairs from whom the blood sample was drawn concurrently, levels of all of the three biomarkers were significantly higher in the newborn compared with paired maternal blood samples (P {lt} 0.05). These results suggest that the fetus has reduced detoxification capabilities and increased susceptibility to DNA damage, especially in light of experimental evidence that transplacental exposures to PAHs are 10-fold lower than paired maternal exposures. Also, these results have implications for risk assessment, which currently does not adequately account for sensitive subsets of the population. 64 refs.

  11. Cigarette smoking contributes to idiopathic pulmonary fibrosis associated with emphysema

    Institute of Scientific and Technical Information of China (English)

    Ye Qiao; Huang Kewu; Ding Yi; Lou Baohui; Hou Ziliang; Dai Huaping; Wang Chen

    2014-01-01

    Background Combined emphysema and pulmonary fibrosis,including idiopathic pulmonary fibrosis (IPF),is a distinct disorder described with upper-lobe emphysema and lower-lobe fibrosis on chest computed tomography.Smoking appears to be the predominant risk factor for this disorder.We aimed to compare clinical features,smoking history,physiological and radiological findings between IPF with and without emphysema.Methods A sample of 125 IPF patients over a period of 48 months were evaluated.High resolution CT scans were reviewed blinded to clinical data.The IPF patients with or without emphysema were classified accordingly.Results The prevalence of emphysema in this IPF sample was 70/125.IPF with emphysema was significantly associated with smoking status (OR 63; 95% CI 4.4 to 915; P=0.002) and smoking pack year (OR 1.1; 95% CI 1.05 to 1.13; P=-0.000).The patients with IPF and emphysema had a higher decrease in carbon monoxide diffusing capacity adjusted for alveolar volume ((58±19)% pred vs.(66:±:21)% pred; P=-0.021) and a higher prevalence of pulmonary hypertension (24/70 vs.7/55; P=0.006).The two groups of patients had similar forced and residual volumes.No significant differences were found in cell differentials of bronchoalveolar lavage or the scores of fibrosis on chest CT.Survival of the patients with emphysema was significantly less than that of patients with IPF alone.Conclusions Cigarette smoking induces IPF combined with emphysema.Emphysema further impairs physiological function and increases the prevalence of pulmonary hypertension that leads to poor prognosis.The inclusion of the patients with combined pulmonary fibrosis and emphysema in IPF clinical trials may lead to under evaluation of the effect of treatment in patients.

  12. Pharmacological Treatment for Pregnant Women who Smoke Cigarettes

    Directory of Open Access Journals (Sweden)

    Koren G

    2003-09-01

    Full Text Available Abstract Smoking has been associated with several concerns in pregnancy including miscarriage, preterm delivery and stillbirth. Unfortunately, approximately 12% of the pregnant population continue to smoke cigarettes, suggesting a need for additional therapy beyond behavioural change. This paper reviews the literature on the use of nicotine replacement therapy and bupropion (Zyban® in the pregnant human population, the pharmacokinetics of nicotine in the pregnant woman, and current guidelines for smoking cessation for pregnant patients. There are currently four studies that have investigated the use of nicotine patch, three for nicotine gum, and registry and preliminary reports for bupropion. These studies did not show any adverse pregnancy outcomes with the use of pharmacological aid for smoking cessation. All the nicotine replacement therapy studies, with the exception of one randomized-controlled nicotine patch trial had small sample sizes and looked at short-term use of drug in the third trimester. Two studies have examined the pharmacokinetics of nicotine in the pregnant woman. The results from these studies reveal greater nicotine metabolism in pregnant individuals who continue to smoke during pregnancy. Current guidelines from several organizations uniformly recommend that Nicotine Replacement Therapy should be considered if non-pharmacological therapies have been unsuccessful. Bupropion is recommended in pregnancy if the benefits outweigh the risks. There is a need for further studies on the safety and effectiveness of Nicotine Replacement therapy and bupropion in pregnancy. However, considering the current research and guidelines, pharmacological cessation aids should be considered if non-pharmacological therapies have not been effective.

  13. Do cigarette smoking and alcohol consumption associate with cannabis use and problem gambling among Spanish adolescents?

    Science.gov (United States)

    Míguez Varela, M Del Carmen; Becoña, Elisardo

    2015-03-01

    This article examined the relationship between cigarette smoking or alcohol consumption and cannabis use and problem gambling among a random and representative sample of 1447 Spanish adolescents (797 males and 650 females with an average of 12.8 years). An ad-hoc questionnaire was used to assess cigarette smoking, alcohol consumption (beer, wine and spirits) and cannabis use. Gambling was assessed with the South Oaks Gambling Screen Revised for Adolescents (SOGS-RA). Results indicated a positive and significant association between cigarette smoking and alcohol consumption and the two aforementioned variables. A larger percentage of cigarette smokers and drinkers was found among those participants who had consumed cannabis before or scored significantly in problem gambling. Additionally, multiple regression analysis confirmed that both cigarette smoking and alcohol consumption (beer and wine) were the most determinant variables for cannabis use and problem gambling.

  14. Vam3, a derivative of resveratrol, attenuates cigarette smoke-induced autophagy

    Institute of Scientific and Technical Information of China (English)

    Ji SHI; Ning YIN; Ling-ling XUAN; Chun-suo YAO; Ai-min MENG; Qi HOU

    2012-01-01

    Aim:To appraise the efficacy of Vam3 (Amurensis H),a dimeric derivative of resveratrol,at inhibiting cigarette smoke-induced autophagy.Methods:Human bronchial epithelial cells were treated with cigarette smoke condensates,and a chronic obstructive pulmonary disease (COPD) model was established by exposing male BALB/c mice to cigarette smoke.The protein levels of the autophagic marker microtubule-associated protein 1A/1B-light chain 3 (LC3),Sirtuin 1 (Sirt1),and foxhead box O 3a (FoxO3a) were examined using Western blotting and Immunohistochemistry.LC3 punctae were detected by immunofluorescence.The levels of FoxO3a acetylation were examined by immunoprecipitation.The level of intracellular oxidation was assessed by detecting ROS and GSH-Px.Results:Vam3 attenuated cigarette smoke condensate-induced autophagy in human bronchial epithelial cells,and restored the expression levels of Sift1 and FoxO3a that had been reduced by cigarette smoke condensates.Similar protective effects of Vam3,reducing autophagy and restoring the levels of Sirt1 and FoxO3a,were observed in the COPD animal model.Additionally,Vam3 also diminished the oxidative stress that was induced by the cigarette smoke condensates.Conclusion:Vam3 decreases cigarette smoke-induced autophagy via up-regulating/restoring the levels of Sirt1 and FoxO3a and inhibiting the induced oxidative stress.

  15. Acculturation and cigarette smoking in Hispanic women: A meta-analysis.

    Science.gov (United States)

    Kondo, Karli K; Rossi, Joseph S; Schwartz, Seth J; Zamboanga, Byron L; Scalf, Carissa D

    2016-01-01

    The present study was a random-effects model meta-analysis of 26 studies published between 1990 and 2010 (k = 32; n = 39,777) that (a) examined the association between acculturation and cigarette smoking in Hispanic women and (b) evaluated age, national origin, and measure and dimensionality (unidimensional vs. bidimensional) of acculturation as moderating variables. Results indicate a strong positive relationship and suggest larger effects of acculturation on cigarette smoking in women of Mexican descent as compared with women originating from other Latin American countries for current and lifetime smoking, as well as smoking overall. The effect of acculturation on cigarette smoking was larger in adults as compared with adolescents for current smoking and smoking overall. Few differences in effect size by measure or dimensionality of acculturation emerged. Results are discussed with regard to implications for future research and the measurement of acculturation.

  16. Determination of Carbon Dioxide, Carbon Monoxide, and Methane Concentrations in Cigarette Smoke by Fourier Transform Infrared Spectroscopy

    Science.gov (United States)

    Tan, T. L.; Lebron, G. B.

    2012-01-01

    The integrated absorbance areas of vibrational bands of CO[subscript 2], CO, and CH[subscript 4] gases in cigarette smoke were measured from Fourier transform infrared (FTIR) spectra to derive the partial pressures of these gases at different smoke times. The quantity of the three gas-phase components of cigarette smoke at different smoke times…

  17. Passive cigarette smoking induces inflammatory injury in human arterial walls

    Institute of Scientific and Technical Information of China (English)

    ZOU Ni; HONG Jiang; DAI Qiu-yan

    2009-01-01

    Background Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis. But very little is known about the biological processes induced by passive cigarette smoking that contribute to atheresclerosis. We observe the expression of a few of biological and inflammatory markers in human arterial walls in vitro which were treated with the second-hand smoke solution (sidestream whole, SSW), and discuss the possible mechanism of inflammatory injury induced by second-hand smoke.Methods The biological markers (platelet endothelial cell adhesion molecule-1, PECAM-1; α-smooth muscle actin, α-SMA; collagen Ⅳ, Col Ⅳ) and inflammatory markers (vascular cell adhesion molecule-1, VCAM-1; monocyte chemoattractant protein-1, MCP-1; interleukin-8, IL-8) of human aortal wall were tested by immunofluorescence staining. The levels of MCP-1 and IL-8 mRNA expression were detected by reverse transcription-polymerase chain reaction (RT-PCR).Results No distinct difference was observed between SSW and the control group on the expression of biological markers as assessed by the light microscope. But the inflammatory markers VCAM-1, MCP-1 and IL-8 on the subendothelial layer and smooth muscle cell layers, which are near the endothelium of arterial wall, were strongly stained in the SSW group compared with the control group. Their fluorescence intensities in the 1:40 SSW group (VCAM-1: 0.35±0.04, MCP-1: 0.34±0.05, IL-8: 0.37±0.05) and the 1:20 SSW group (VCAM-1: 0.40±0.04, MCP-1: 0.52±0.09, IL-8: 0.51±0.07) were significantly stronger than the control group (VCAM-1: 0.12±0.04, MCP-1: 0.06±0.02, IL-8: 0.24±0.03) by semi-quantitative analysis of immunofluorescence (P <0.001 vs control). MCP-1 mRNA expression in the 1:40 SSW (0.15±0.04) and the 1:20 SSW (0.19±0.06) group was significantly higher than in the control group (0.09±0.03) (P <0.05, P <0.01 vs control); IL-8 mRNA expression in the 1:40 SSW (0.64±0.12) and 1

  18. Cigarette smoke effects on innate immune mechanisms in the nasal mucosa. Potential effects on the microbiome.

    Science.gov (United States)

    Jaspers, Ilona

    2014-01-01

    It is well established that exposure to cigarette smoke (CS), through active smoking and through exposure to secondhand smoke, has immunosuppressive effects, yet how this might affect the microbiome is not known. In this manuscript we focus on the effects of CS on innate host defense response, with particular emphasis on the role of epithelial cells and mucosal immune responses in the nose and the potential effects on the microbiome. The studies described here briefly summarize the effects of CS on specific innate immune cells, such as neutrophils, macrophages/monocytes, natural killer cells, and dendritic cells. A detailed description of how CS affects epithelial cells and why we consider this to be a central defect in the overall immunosuppressive effects of CS in the lung is provided. We summarize data on the role of the "epimmunome" in the context of CS exposure, including the effects on soluble mediator production, such as cytokines, chemokines, and antimicrobial defense mediators. Separate emphasis is put on the expression of ligands on epithelial cells, which directly interact with receptors on immune cells, and the effects of CS on these interactions. We introduce the nose and nasal mucosa as a model to study the effects of CS exposure on host defense responses and changes in the microbiome in humans in vivo. Understanding the dynamics of a healthy microbiome and how CS affects this balance is important to uncovering the mechanisms of CS-induced disease.

  19. Smoking among construction workers: the nonlinear influence of the economy, cigarette prices, and antismoking sentiment.

    Science.gov (United States)

    Okechukwu, Cassandra; Bacic, Janine; Cheng, Kai-Wen; Catalano, Ralph

    2012-10-01

    Little research has been conducted on the influence of macroeconomic environments on smoking among blue-collar workers, a group with high smoking prevalence and that is especially vulnerable to the effects of changing economic circumstances. Using data from 52,418 construction workers in the Tobacco Use Supplement to the United States Current Population Survey, we examined the association of labor market shock, cigarette prices, and state antismoking sentiments with smoking status and average number of cigarettes smoked daily. Data analysis included the use of multiple linear and logistic regressions, which employed the sampling and replicate weights to account for sampling design. Unemployed, American-Indian, lower-educated and lower-income workers had higher smoking rates. Labor market shock had a quadratic association, which was non-significant for smoking status and significant for number of cigarettes. The association of cigarette prices with smoking status became non-significant after adjusting for state-level antismoking sentiment. State-level antismoking sentiment had significant quadratic association with smoking status among employed workers and significant quadratic association with number of cigarettes for all smokers. The study highlights how both workplace-based smoking cessation interventions and antismoking sentiments could further contribute to disparities in smoking by employment status.

  20. Factors Related to Cigarette Smoking Initiation and Use among College Students

    Directory of Open Access Journals (Sweden)

    Ebert Sheryl

    2005-01-01

    Full Text Available Abstract The purpose of this cross-sectional study was to examine the impact of personality factors (neuroticism, extraversion, openness, agreeableness, and conscientiousness, cognitive factors (sense of coherence and self-efficacy, coping resources (family and friend social support and demographic factors (gender and ethnicity on cigarette smoking behaviors (initiation, frequency, and amount of cigarette smoking among college students. A total of 161 U.S. college students, aged 18–26, who enrolled in an introductory psychology course completed self-report questionnaires. The majority of the students had tried smoking (55%; among those who had tried, 42% were current smokers. The majority (77% who had smoked a whole cigarette did so at age 16 years or younger. Students who reported lower levels of conscientiousness and self-efficacy had a greater likelihood to had tried cigarette smoking. Also, students who had lower levels of self-efficacy reported smoking more frequently and greater quantities of cigarettes than students with higher levels of self-efficacy. Self-efficacy was the most significant predictor of smoking behaviors. Health promotion programs focused on self-efficacy may be an effective tool for reducing the initiation, frequency, and amount of cigarette smoking among college students.

  1. Method for the Determination of Ammonia in Mainstream Cigarette Smoke Using Ion Chromatography

    Science.gov (United States)

    Watson, Christina Vaughan; Feng, June; Valentin-Blasini, Liza; Stanelle, Rayman; Watson, Clifford H.

    2016-01-01

    Ammonia in mainstream smoke is present in both the particulate and vapor phases. The presence of ammonia in the cigarette filler material and smoke is of significance because of the potential role ammonia could have in raising the “smoke pH.” An increased smoke pH could shift a fraction of total nicotine to free-base nicotine, which is reportedly more rapidly absorbed by the smoker. Methods measuring ammonia in smoke typically employ acid filled impingers to trap the smoke. We developed a fast, reliable method to measure ammonia in mainstream smoke without the use of costly and time consuming impingers to examine differences in ammonia delivery. The method uses both a Cambridge filter pad and a Tedlar bag to capture particulate and vapor phases of the smoke. We quantified ammonia levels in the mainstream smoke of 50 cigarette brands from 5 manufacturers. Ammonia levels ranged from approximately 1μg to 23μg per cigarette for ISO smoking conditions and 38μg to 67μg per cigarette for Canadian intense smoking conditions and statistically significance differences were observed between brands and manufacturers. Our findings suggest that ammonia levels vary by brand and are higher under Canadian intense smoking conditions. PMID:27415766

  2. Method for the Determination of Ammonia in Mainstream Cigarette Smoke Using Ion Chromatography.

    Directory of Open Access Journals (Sweden)

    Christina Vaughan Watson

    Full Text Available Ammonia in mainstream smoke is present in both the particulate and vapor phases. The presence of ammonia in the cigarette filler material and smoke is of significance because of the potential role ammonia could have in raising the "smoke pH." An increased smoke pH could shift a fraction of total nicotine to free-base nicotine, which is reportedly more rapidly absorbed by the smoker. Methods measuring ammonia in smoke typically employ acid filled impingers to trap the smoke. We developed a fast, reliable method to measure ammonia in mainstream smoke without the use of costly and time consuming impingers to examine differences in ammonia delivery. The method uses both a Cambridge filter pad and a Tedlar bag to capture particulate and vapor phases of the smoke. We quantified ammonia levels in the mainstream smoke of 50 cigarette brands from 5 manufacturers. Ammonia levels ranged from approximately 1μg to 23μg per cigarette for ISO smoking conditions and 38μg to 67μg per cigarette for Canadian intense smoking conditions and statistically significance differences were observed between brands and manufacturers. Our findings suggest that ammonia levels vary by brand and are higher under Canadian intense smoking conditions.

  3. Biological effects of cigarette smoke in cultured human retinal pigment epithelial cells.

    Directory of Open Access Journals (Sweden)

    Alice L Yu

    Full Text Available The goal of the present study was to determine whether treatment with cigarette smoke extract (CSE induces cell loss, cellular senescence, and extracellular matrix (ECM synthesis in primary human retinal pigment epithelial (RPE cells. Primary cultured human RPE cells were exposed to 2, 4, 8, and 12% of CSE concentration for 24 hours. Cell loss was detected by cell viability assay. Lipid peroxidation was assessed by loss of cis-parinaric acid (PNA fluorescence. Senescence-associated ß-galactosidase (SA-ß-Gal activity was detected by histochemical staining. Expression of apolipoprotein J (Apo J, connective tissue growth factor (CTGF, fibronectin, and laminin were examined by real-time PCR, western blot, or ELISA experiments. The results showed that exposure of cells to 12% of CSE concentration induced cell death, while treatment of cells with 2, 4, and 8% CSE increased lipid peroxidation. Exposure to 8% of CSE markedly increased the number of SA-ß-Gal positive cells to up to 82%, and the mRNA expression of Apo J, CTGF, and fibronectin by approximately 3-4 fold. Treatment with 8% of CSE also increased the protein expression of Apo J and CTGF and the secretion of fibronectin and laminin. Thus, treatment with CSE can induce cell loss, senescent changes, and ECM synthesis in primary human RPE cells. It may be speculated that cigarette smoke could be involved in cellular events in RPE cells as seen in age-related macular degeneration.

  4. Cigarette and waterpipe smoking among Lebanese adolescents, a cross-sectional study, 2003-2004.

    Science.gov (United States)

    El-Roueiheb, Zana; Tamim, Hala; Kanj, Mayada; Jabbour, Samer; Alayan, Iman; Musharrafieh, Umayya

    2008-02-01

    Waterpipe or "argileh" is a form of smoking other than cigarettes that is currently spreading among people of all ages. The objective of the present study was to assess tobacco smoking practices (waterpipe and/or cigarette) among public and private adolescent school students in Beirut, Lebanon. A sample of 2,443 students selected from 10 private and 3 public schools with intermediate/secondary classes filled out a self-administered anonymous questionnaire that inquired about sociodemographic characteristics, and behavior about tobacco smoking. Binary analysis was performed as well as three regression models for the relationship between exclusive cigarettes smoking, exclusive waterpipe smoking and both cigarettes and waterpipe as the dependent variables and gender, type of school, and class as the independent variables. The current prevalence of cigarettes smoking was 11.4%, and that of waterpipe smoking was 29.6%. Gender was significantly associated with cigarettes (OR=3.2, 95% CI 1.8-5.6) but not waterpipe smoking. Public school students were, respectively, 3.2 (95% CI 1.8-5.6) and 1.7 (95% CI 1.4-2.1) times more likely to be exclusive cigarettes smokers, and exclusive waterpipe smokers. Class was not significantly associated with exclusive cigarette smoking; however, students attending secondary classes were 1.3 (95% CI 1.1-1.6) times more likely to be exclusive waterpipe smokers. The reasons behind the high prevalence of both types of smoking are presented and discussed. The present study calls for school-based prevention programs and other types of interventions such as tax increases, and age-restrictions on tobacco sales. More aggressive interventions to disseminate education and awareness among parents and students altogether are warranted.

  5. Cigarette smoking and risk of gestational diabetes: a systematic review of observational studies

    Directory of Open Access Journals (Sweden)

    Belizán José M

    2008-12-01

    Full Text Available Abstract Background Gestational diabetes is a prevalent disease associated with adverse outcomes of pregnancy. Smoking as been associated with glucose intolerance during pregnancy in some but not all studies. Therefore, we aimed to systematically review all epidemiological evidence to examine the association between cigarette smoking during pregnancy and risk of developing gestational diabetes mellitus. Methods We conducted a systematic review of articles published up to 2007, using PubMed, Embase, LILACS e CINAHL to identify the articles. Because this review focuses on studies of smoking during pregnancy, we excluded studies evaluating smoking outside pregnancy. Two investigators independently abstracted information on participant's characteristics, assessment of exposure and outcome, and estimates for the association under study. We evaluated the studies for publication bias and performed heterogeneity analyses. We also assessed the effect of each study individually through sensitivity analysis. Results We found and critically reviewed 32 studies, of which 12 met the criteria for inclusion in the review. Most of the studies provided only unadjusted measurements. Combining the results of the individual studies, we obtained a crude odds ratio of 1.03 (99% CI 0.85–1.25. Only 4 studies presented adjusted measurements of association, and no association was found when these alone were analyzed (OR 0.95; 99% CI 0.85–1.07. Subgroup analysis could not be done due to small sample size. Conclusion The number of studies is small, with major heterogeneity in research design and findings. Taken together, current data do not support an association between cigarette smoking during pregnancy and the risk of gestational diabetes.

  6. Activated charcoal filter effectively reduces p-benzosemiquinone from the mainstream cigarette smoke and prevents emphysema

    Indian Academy of Sciences (India)

    Neekkan Dey; Archita Das; Arunava Ghosh; Indu B Chatterjee

    2010-06-01

    In this paper, we have made a comparative evaluation of the cytotoxicity and pathophysiological effects of mainstream smoke from cellulose acetate (CA)-filtered cigarettes with that of charcoal-filtered cigarettes developed in our laboratory. Previously, we had demonstrated that the mainstream smoke from an Indian CA-filtered commercial cigarette contains p-benzosemiquinone (p-BSQ), a major, highly toxic, long-lived water-soluble radical. Here, we have examined 16 brands of different CA-filtered cigarettes including Kentucky research cigarettes, and observed that mainstream smoke from all the cigarettes contains substantial amounts of p-BSQ (100–200 g/cigarette). We also show that when the CA filter is replaced by a charcoal filter, the amount of p-BSQ in the mainstream smoke is reduced by 73–80%, which is accompanied by a reduction of carbonyl formation in bovine serum albumin to the extent of 70–90%. The charcoal filter also prevented cytotoxicity in A549 cells as evidenced by MTT assay, apoptosis as evidenced by FACS analysis, TUNEL assay, overexpression of Bax, activation of p53 and caspase 3, as well as emphysematous lung damage in a guinea pig model as seen by histology and morphometric analysis. The results indicate that the charcoal filter developed in our laboratory may protect smokers from cigarette smoke-induced cytotoxity, protein modification, apoptosis and emphysema.

  7. Tobacco and Pregnancy: Overview of exposures and effects

    Science.gov (United States)

    This opening paper will review the epidemiology of the impact of cigarette smoking and other forms of tobacco exposure on human development. Sources of exposure described include cigarettes and other forms of smoked tobacco, secondhand (environmental) tobacco smoke, several forms...

  8. Cigarette smoke and nicotine protect dopaminergic neurons against the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine Parkinsonian toxin.

    Science.gov (United States)

    Parain, Karine; Hapdey, Céline; Rousselet, Estelle; Marchand, Véronique; Dumery, Bernard; Hirsch, Etienne C

    2003-09-12

    Epidemiological studies have found a negative association between cigarette smoking and Parkinson's disease (PD). In order to analyze the putative neuroprotective effect of cigarette smoke and nicotine, one of its major constituents, we examined their effects in an animal model of PD provoked by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication. Two groups of mice were chronically exposed to cigarette smoke (a low exposure subgroup and a high exposure subgroup; 5 exposures per day at 2-h intervals), two other groups received nicotine treatment (two doses tested 0.2 and 2 mg/kg, 5 injections i.p. per day at 2-h intervals) and one group placebo. On day 8 after the beginning of the treatment, 4 injections of MPTP hydrochloride (15 mg/kg, i.p., at 2-h intervals) or saline were administered to these animals. Nicotine and cotinine plasmatic concentration was quantified by the HPLC method, and degeneration of the nigrostriatal system was assessed by tyrosine hydroxylase (TH) immunohistochemistry. The loss of dopaminergic neurons induced by MPTP in the substantia nigra was significantly less severe in the chronic nicotine treatment groups (at 0.2 and 2 mg/kg) and the low exposure to cigarette smoke group than in the high exposure to cigarette smoke subgroup and the placebo treated subgroup. In contrast, no preservation of TH immunostaining of nerve terminals was observed in the striatum in any group. This suggests that nicotine and low exposure to cigarette smoke may have a neuroprotective effect on the dopaminergic nigrostriatal system by an as yet unknown mechanism.

  9. Simultaneous analysis of 22 volatile organic compounds in cigarette smoke using gas sampling bags for high-throughput solid-phase microextraction.

    Science.gov (United States)

    Sampson, Maureen M; Chambers, David M; Pazo, Daniel Y; Moliere, Fallon; Blount, Benjamin C; Watson, Clifford H

    2014-07-15

    Quantifying volatile organic compounds (VOCs) in cigarette smoke is necessary to establish smoke-related exposure estimates and evaluate emerging products and potential reduced-exposure products. In response to this need, we developed an automated, multi-VOC quantification method for machine-generated, mainstream cigarette smoke using solid-phase microextraction gas chromatography-mass spectrometry (SPME-GC-MS). This method was developed to simultaneously quantify a broad range of smoke VOCs (i.e., carbonyls and volatiles, which historically have been measured by separate assays) for large exposure assessment studies. Our approach collects and maintains vapor-phase smoke in a gas sampling bag, where it is homogenized with isotopically labeled analogue internal standards and sampled using gas-phase SPME. High throughput is achieved by SPME automation using a CTC Analytics platform and custom bag tray. This method has successfully quantified 22 structurally diverse VOCs (e.g., benzene and associated monoaromatics, aldehydes and ketones, furans, acrylonitrile, 1,3-butadiene, vinyl chloride, and nitromethane) in the microgram range in mainstream smoke from 1R5F and 3R4F research cigarettes smoked under ISO (Cambridge Filter or FTC) and Intense (Health Canada or Canadian Intense) conditions. Our results are comparable to previous studies with few exceptions. Method accuracy was evaluated with third-party reference samples (≤15% error). Short-term diffusion losses from the gas sampling bag were minimal, with a 10% decrease in absolute response after 24 h. For most analytes, research cigarette inter- and intrarun precisions were ≤20% relative standard deviation (RSD). This method provides an accurate and robust means to quantify VOCs in cigarette smoke spanning a range of yields that is sufficient to characterize smoke exposure estimates.

  10. α1-Antitrypsin reduces rhinovirus infection in primary human airway epithelial cells exposed to cigarette smoke

    Directory of Open Access Journals (Sweden)

    Berman R

    2016-06-01

    Full Text Available Reena Berman, Di Jiang, Qun Wu, Hong Wei Chu Department of Medicine, National Jewish Health, Denver, CO, USA Abstract: Human rhinovirus (HRV infections target airway epithelium and are the leading cause of acute exacerbations of COPD. Cigarette smoke (CS increases the severity of viral infections, but there is no effective therapy for HRV infection. We determined whether α1-antitrypsin (A1AT reduces HRV-16 infection in CS-exposed primary human airway epithelial cells. Brushed bronchial epithelial cells from normal subjects and patients diagnosed with COPD were cultured at air–liquid interface to induce mucociliary differentiation. These cells were treated with A1AT or bovine serum albumin for 2 hours and then exposed to air or whole cigarette smoke (WCS with or without HRV-16 (5×104 50% Tissue Culture Infective Dose [TCID50]/transwell infection for 24 hours. WCS exposure significantly increased viral load by an average of fivefold and decreased the expression of antiviral genes interferon-λ1, OAS1, and MX1. When A1AT was added to WCS-exposed cells, viral load significantly decreased by an average of 29-fold. HRV-16 infection significantly increased HRV-16 receptor intercellular adhesion molecule-1 messenger RNA expression in air-exposed cells, which was decreased by A1AT. A1AT-mediated reduction of viral load was not accompanied by increased epithelial antiviral gene expression or by inhibiting the activity of 3C protease involved in viral replication or maturation. Our findings demonstrate that A1AT treatment prevents a WCS-induced increase in viral load and for the first time suggest a therapeutic effect of A1AT on HRV infection. Keywords: α1-antitrypsin, rhinovirus, COPD, cigarette smoke, ICAM-1

  11. Differences in Electronic Cigarette Awareness, Use History, and Advertisement Exposure between Black and White Hospitalized Cigarette Smokers

    OpenAIRE

    Baumann, Angela Warren; Kohler, Connie; Kim, Young-Il; Cheong, JeeWon; Hendricks, Peter; Bailey, William C.; Harrington, Kathleen F.

    2015-01-01

    E-cigarette use has increased rapidly over the past decade. There is growing concern about e-cigarette use and advertising given limited regulation of these products. This cross-sectional study reports on data collected at baseline from hospitalized cigarette smokers (N = 944) recruited in monthly cohorts between December 2012 and September 2013. Participants were queried regarding e-cigarette awareness and use, and number and sources of e-cigarette advertisement exposures in the previous six...

  12. Maternal waterpipe smoke exposure and the risk of asthma and allergic diseases in childhood: A post hoc analysis

    Directory of Open Access Journals (Sweden)

    Mirna Waked

    2015-02-01

    Full Text Available Introduction This analysis was conducted with the objective of evaluating association between waterpipe passive smoking exposure and asthma, and allergies among Lebanese children. Material and methods Data were taken from a crosssectional study on children from public and private schools. A sample of 22 schools participated in the study, where standardized written core questionnaires were distributed. From 5 to 12-year-old students filled in the questionnaires at home, while 13–14-year-old students filled it in in the class. In total, 5522 children were evaluated for the prevalence of asthma, allergic rhinitis and atopic eczema, and their associated factors, including waterpipe exposure due to parents’ smoking. Results The descriptive results of parental smoking were, as follows: among mothers: 1609 (29% mothers smoked cigarettes, 385 (7% smoked waterpipe and 98 (1.8% smoked both; among fathers: 2449 (44.2% smoked cigarettes, 573 (10.3% smoked waterpipe and 197 (3.5% smoked both. Maternal waterpipe smoking was significantly and moderately associated with allergic diseases (p < 0.001; ORa = 1.71, including probable asthma, rhinitis and dermatitis (p < 0.001 for all. Quite on the opposite, father’s waterpipe smoking was not associated with any of the diseases. Parental cigarette smoking demonstrated some positive effects: father’s cigarette smoking did not show association with dermatitis or asthma diagnosed by a physician, while mother’s cigarette smoking showed a positive association only with probable asthma. Moreover, no interactions between cigarette and waterpipe smoking were observed. Conclusions Maternal waterpipe smoking should be regarded as a high risk behavior; however, additional studies are necessary to confirm this finding.

  13. Exposure to radionuclides in smoke from vegetation fires.

    Science.gov (United States)

    Carvalho, Fernando P; Oliveira, João M; Malta, Margarida

    2014-02-15

    Naturally occurring radionuclides of uranium, thorium, radium, lead and polonium were determined in bushes and trees and in the smoke from summer forest fires. Activity concentrations of radionuclides in smoke particles were much enriched when compared to original vegetation. Polonium-210 ((210)Po) in smoke was measured in concentrations much higher than all other radionuclides, reaching 7,255 ± 285 Bq kg(-1), mostly associated with the smaller size smoke particles (forest fires displayed volume concentrations up to 70 m Bq m(-3), while in smoke-free air (210)Po concentration was about 30 μ Bq m(-3). The estimated absorbed radiation dose to an adult member of the public or a firefighter exposed for 24h to inhalation of smoke near forest fires could exceed 5 μSv per day, i.e, more than 2000 times above the radiation dose from background radioactivity in surface air, and also higher than the radiation dose from (210)Po inhalation in a chronic cigarette smoker. It is concluded that prolonged exposure to smoke allows for enhanced inhalation of radionuclides associated with smoke particles. Due to high radiotoxicity of alpha emitting radionuclides, and in particular of (210)Po, the protection of respiratory tract of fire fighters is strongly recommended.

  14. Acculturation, Gender, Depression, and Cigarette Smoking among U.S. Hispanic Youth: The Mediating Role of Perceived Discrimination

    Science.gov (United States)

    Lorenzo-Blanco, Elma I.; Unger, Jennifer B.; Ritt-Olson, Anamara; Soto, Daniel; Baezconde-Garbanati, Lourdes

    2011-01-01

    Hispanic youth are at risk for experiencing depressive symptoms and smoking cigarettes, and risk for depressive symptoms and cigarette use increase as Hispanic youth acculturate to U.S. culture. The mechanism by which acculturation leads to symptoms of depression and cigarette smoking is not well understood. The present study examined whether…

  15. Application of the protection motivation theory in predicting cigarette smoking among adolescents in China.

    Science.gov (United States)

    Yan, Yaqiong; Jacques-Tiura, Angela J; Chen, Xinguang; Xie, Nianhua; Chen, Jing; Yang, Niannian; Gong, Jie; Macdonell, Karen Kolmodin

    2014-01-01

    Reducing tobacco use among adolescents in China represents a significant challenge for global tobacco control. Existing behavioral theories developed in the West - such as the Protection Motivation Theory (PMT) - may be useful tools to help tackle this challenge. We examined the relationships between PMT factors and self-reported cigarette smoking behavior and intention among a random sample of vocational high school students (N=553) in Wuhan, China. Tobacco-related perceptions were assessed using the PMT Scale for Adolescent Smoking. Among the total sample, 45% had initiated cigarette smoking, and 25% smoked in the past month. Among those who never smoked, 15% indicated being likely or very likely to smoke in a year. Multiple regression modeling analysis indicated the significance of the seven PMT constructs, the four PMT perceptions and the two PMT pathways in predicting intention to smoke and actual smoking behavior. Overall, perceived rewards of smoking, especially intrinsic rewards, were consistently positively related to smoking intentions and behavior, and self-efficacy to avoid smoking was negatively related to smoking. The current study suggests the utility of PMT for further research examining adolescent smoking. PMT-based smoking prevention and clinical smoking cessation intervention programs should focus more on adolescents' perceived rewards from smoking and perceived efficacy of not smoking to reduce their intention to and actual use of tobacco.

  16. A Simple Technique for Determining the pH of Whole Cigarette Smoke

    Directory of Open Access Journals (Sweden)

    Dong J

    2014-12-01

    Full Text Available A new technique has been developed to determine the pH of whole cigarette smoke. In this technique, whole smoke from ten cigarettes was trapped in 300 mL water containing 1% (w/v sodium chloride and the pH was determined on the resulting aqueous suspension of cigarette smoke. Two impingers with an extra coarse porosity fritted disc were used to dispense the smoke in the aqueous trapping medium. Cigarettes were smoked on a 20-port Borgwaldt RM 20/CS smoking machine using modified FTC (Federal Trade Commission conditions. The puff volume was adjusted to take a 35 mL puff as measured through the cigarette and the collection traps. This new technique accounts for the contributions to smoke pH from both the vapor phase and the particulate phase of smoke. The repeatability of this new technique was determined on eighteen replicates of a commercially available non-menthol, filter cigarette. Each measurement was done on a different day to check for a possible drift in pH with time. The mean pH value for the chosen sample was found to be 4.97 with a standard deviation of 0.07 pH units. The smoke pH values for over 150 commercially available cigarette brands with a variety of “tar” levels were determined. The smoke pH values had a range from 4.6 to 5.5, with an average of 4.79 and a maximum standard deviation of 0.10 pH units. An experimental flue cured cigarette had a smoke pH of around 5.0, while an experimental Burley cigarette had a smoke pH of 5.4. No correlation between smoke pH and “tar” or total particulate matter (TPM and between pH and nicotine levels was found. The purpose of the present study was to develop a practical, relatively simple laboratory method to measure the pH of a water solution of whole smoke, and was not intended to reflect, or have direct relevance for any biochemical or biological phenomena such as inhalability of smoke, flavor perception, nicotine ab-sorption, etc.”

  17. Determination of pyrethroid residues in tobacco and cigarette smoke by capillary gas chromatography.

    Science.gov (United States)

    Cai, Jibao; Liu, Baizhan; Zhu, Xiaolan; Su, Qingde

    2002-07-26

    The extraction of fenpropathrin, cyhalothrin, cypermethrin, fenvalerate and deltamethrin from tobacco (Nicotina tobaccum) and cigarette smoke condensate with acetone, followed by partition of resulting acetone mixture with petroleum ether, was investigated and found suitable for capillary gas chromatography (GC) residue analysis. Florisil column clean-up was found to provide clean-up procedure for tobacco and cigarette smoke condensate permitting analysis to < or = 0.01 microgram.g-1 for most of the pyrethroids by GC with a 63Ni electron capture detector (GC-ECD). Quantitative determination was obtained by the method of external standards. Cigarettes made from flue-cured tobacco spiked with different amounts of pyrethroids were used and the pyrethroid levels in mainstream smoke were determined. For all the pyrethroid residues, 1.51-15.50% were transferred from tobacco into cigarette smoke.

  18. The Effect of Cigarette Design on the Content of Phenols in Mainstream Tobacco Smoke

    Directory of Open Access Journals (Sweden)

    Dagnon S

    2014-12-01

    Full Text Available The influence of cigarette design on the content of phenols in mainstream tobacco smoke was studied. The most abundant phenols - catechol, hydroquinone, phenol, o-, m-, and p-cresol, and resorcinol - were determined by HPLC with fluorescence detection. Hydroquinone and catechol made the most significant contribution to the total content of phenols with maximum values of 135.0 µg/cig and 95.7 µg/cig, respectively. The highest total content of phenols (330.9 µg/cig was measured in the smoke of a Virginia tobacco cigarette. The total content of phenols (µg/cig in cigarette mainstream smoke decreased linearly with increased filter ventilation, R2 = 0.9536. The results obtained indicate that filtration and ventilation can strongly influence the mainstream tobacco smoke content of phenol and its less polar derivatives, o-, m-, and p-cresol, which were reduced by up to 85%. Hydroquinone and catechol are less affected and only cigarettes with the special “recessed charcoal filter system” and cigarettes with filter ventilation over 50% showed significant reductions. On a per mg ‘tar’ basis the largest contributor to phenols in cigarette mainstream smoke was the selection of the tobacco type. The use of any standard commercial filter on an unfiltered cigarette can substantially reduce the yield of phenols in cigarette mainstream smoke. The use of special filters (e.g., the “recessed charcoal filter system” or high levels of cigarette ventilation does not reduce the amount of phenols in tobacco smoke considerably when normalized on a per mg ‘tar’ basis.

  19. Assessing the Feasibility of Using Contingency Management to Modify Cigarette Smoking by Adolescents

    Science.gov (United States)

    Roll, John M.

    2005-01-01

    Cigarette smoking is a leading cause of preventable death in the United States. Many smokers initiate this dangerous behavior during adolescence. This report describes a contingency management intervention designed to initate and maintain a period of abstinence from cigarettes by adolescent smokers. Results suggest that the intervention was…

  20. Suicide and Other-Cause Mortality after Early Exposure to Smoking and Second Hand Smoking: A 12-Year Population-Based Follow-Up Study.

    Directory of Open Access Journals (Sweden)

    Vincent Chin-Hung Chen

    Full Text Available The association between smoking and suicide is still controversial, particular for early life cigarette smoking exposure. Few studies have investigated this association in adolescents using population-based cohorts, and the relationship with second hand smoking (SHS exposure has not been addressed.In this study, we followed a large population-based sample of younger people to investigate the association between smoking, SHS exposure and suicide mortality. Between October 1995 and June 1996, 162,682 junior high school students ages 11 to 16 years old living in a geographic catchment area in Taiwan were enrolled and then followed till December 2007 (1,948,432 person-years through linkage to the National Death Certification System. Participants who were currently smoking at baseline had a greater than six-fold higher suicide mortality than those who did not smoke (29.5 vs. 4.8 per 100,000 person-years, p20 cigarettes/per day. The estimated depression-adjusted odds ratio did not change substantially. The population attributable fractions for suicide associated with smoking and heavy SHS exposure (>20 cigarettes/per day were 9.6% and 10.6%, respectively.This study showed evidence of excess suicide mortality among young adults exposed to active or passive early life cigarette smoking.

  1. Cigarette and waterpipe smoking among adolescents in Estonia: HBSC survey results, 1994–2006

    Directory of Open Access Journals (Sweden)

    Pärna Kersti

    2008-11-01

    Full Text Available Abstract Background Smoking is a major single cause of preventable morbidity and premature mortality. Tobacco use among adolescents is a significant public health problem as smoking behaviour is undeniably established in adolescence. While cigarette smoking among adolescents has been a significant public health problem for years, waterpipe smoking is considered to be a new global public health threat. The objectives of this study were to describe trends of cigarette smoking and the prevalence of waterpipe smoking and to study the association between cigarette and waterpipe smoking among adolescents in Estonia. Methods This study was based on a four-yearly HBSC survey of health behaviour among school-aged children conducted in 1994–2006 in Estonia. It was a school-based survey of a nationally representative sample using standardized methodology. The target group of the survey were 11-, 13-, and 15-year-old schoolchildren (N = 13826, 6656 boys and 7170 girls. Cigarette and waterpipe smoking was determined on a 4-stage scale: every day, at least once a week, less than once a week, not smoking. Logistic regression analysis was applied to examine gender- and age-specific smoking trends and to study the association between cigarette and waterpipe smoking. Results Prevalence of smoking was higher among boys than girls in all age groups during the whole study period. The prevalence of cigarette smoking increased in 1994–2002 and then slightly decreased in both genders. The increase in smoking was larger among girls. Among girls, daily smoking increased during the whole study period. Among 15-year-old schoolchildren one-third of the boys and one quarter of the girls were cigarette smokers, 21% of the boys and 12% of the girls were daily smokers in 2006. One fourth of the boys and one sixth of the girls were waterpipe smokers. A logistic regression analysis revealed a strong association between cigarette and waterpipe smoking among schoolchildren

  2. The Impact of Menthol Cigarettes on Smoking Initiation among Non-Smoking Young Females in Japan

    Directory of Open Access Journals (Sweden)

    Yoneatsu Osaki

    2010-12-01

    Full Text Available Japan presents an excellent case-study of a nation with low female smoking rates and a negligible menthol market which changed after the cigarette market was opened to foreign competition. Internal tobacco industry documents demonstrate the intent of tobacco manufacturers to increase initiation among young females through development and marketing of menthol brands. Japanese menthol market share rose rapidly from less than 1% in 1980 to 20% in 2008. Menthol brand use was dominated by younger and female smokers, in contrast with non-menthol brands which were used primarily by male smokers. Nationally representative surveys confirm industry surveys of brand use and provide further evidence of the end results of the tobacco industry’s actions—increased female smoking in Japan. These findings suggest that female populations may be encouraged to initiate into smoking, particularly in developing nations or where female smoking rates remain low, if the tobacco industry can successfully tailor brands to them. The Japanese experience provides a warning to public health officials who wish to prevent smoking initiation among young females.

  3. The impact of menthol cigarettes on smoking initiation among non-smoking young females in Japan.

    Science.gov (United States)

    Connolly, Gregory N; Behm, Ilan; Osaki, Yoneatsu; Wayne, Geoffrey F

    2011-01-01

    Japan presents an excellent case-study of a nation with low female smoking rates and a negligible menthol market which changed after the cigarette market was opened to foreign competition. Internal tobacco industry documents demonstrate the intent of tobacco manufacturers to increase initiation among young females through development and marketing of menthol brands. Japanese menthol market share rose rapidly from less than 1% in 1980 to 20% in 2008. Menthol brand use was dominated by younger and female smokers, in contrast with non-menthol brands which were used primarily by male smokers. Nationally representative surveys confirm industry surveys of brand use and provide further evidence of the end results of the tobacco industry's actions-increased female smoking in Japan. These findings suggest that female populations may be encouraged to initiate into smoking, particularly in developing nations or where female smoking rates remain low, if the tobacco industry can successfully tailor brands to them. The Japanese experience provides a warning to public health officials who wish to prevent smoking initiation among young females.

  4. Oxidative stress and anxiety-like symptoms related to withdrawal of passive cigarette smoke in mice: beneficial effects of pecan nut shells extract, a by-product of the nut industry.

    Science.gov (United States)

    Reckziegel, P; Boufleur, N; Barcelos, R C S; Benvegnú, D M; Pase, C S; Muller, L G; Teixeira, A M; Zanella, R; Prado, A C P; Fett, R; Block, J M; Burger, M E

    2011-09-01

    The present study evaluated the role of pecan nut (Carya illinoensis) shells aqueous extract (AE) against oxidative damage induced by cigarette smoke exposure (CSE) and behavioral parameters of smoking withdrawal. Mice were passively exposed to cigarette smoke for 3 weeks (6, 10, and 14 cigarettes/day) and orally treated with AE (25 g/L). CSE induced lipid peroxidation in brain and red blood cells (RBC), increased catalase (CAT) activity in RBC, and decreased plasma ascorbic acid levels. AE prevented oxidative damage and increased antioxidant defenses of mice exposed to cigarette smoke. In addition, AE reduced the locomotor activity and anxiety symptoms induced by smoking withdrawal, and these behavioral parameters showed a positive correlation with RBC lipid peroxidation. Our results showed the beneficial effects of this by-product of the pecan industry, indicating its usefulness in smoking cessation.

  5. Differences in cadmium transfer from tobacco to cigarette smoke, compared to arsenic or lead

    Directory of Open Access Journals (Sweden)

    J.-J. Piadé

    2015-01-01

    Full Text Available Arsenic, cadmium and lead levels in tobacco filler and cigarette smoke were determined in a 568-sample worldwide survey. Median tobacco levels for arsenic, cadmium and lead were 237, 769 and 397 ng/g respectively, comparable to those previously reported albeit somewhat lower for lead and cadmium. Median mainstream smoke yields for arsenic, cadmium and lead were <3.75, 18.2, and <12.8 ng/cig. under ISO, and <8.71, 75.1 and <45.7 ng/cig. under Health Canada Intense (HCI smoking regime respectively. In the case of cigarettes with activated carbon, a selective retention of cadmium but not lead or arsenic was observed. This effect was more pronounced under ISO than under HCI smoking regimes. Cadmium selective retention by activated carbon was confirmed by testing specially designed prototype cigarettes and the causes for this selective filtration were investigated. The differences between cadmium, arsenic and lead in terms of their speciation in tobaccos and in cigarette smoke could be related to their distribution in the ash, butt, mainstream (in gas-phase and particulate-phase and sidestream smoke of a smoked cigarette. The possible formation of organometallic cadmium derivatives in the smoke gas-phase is discussed, the presence of which could adequately explain the observed cadmium selective filtration.

  6. E-Cigarettes for Immediate Smoking Substitution in Women Diagnosed with Cervical Dysplasia and Associated Disorders

    Directory of Open Access Journals (Sweden)

    Shirley A. James

    2016-03-01

    Full Text Available The aim of this study was to determine if 31 women with cervical dysplasia and associated conditions exacerbated by smoking would be successful substituting cigarettes with their choice of either nicotine replacement therapy (NRT or electronic cigarettes (EC. Women received motivational interviewing and tried both NRT and ECs, choosing one method to use during a six-week intervention period. Daily cigarette consumption was measured at baseline, six, and 12 weeks, with differences analyzed by the Wilcoxon signed-rank test. Study analysis consisted only of women choosing to use ECs (29/31, as only two chose NRT. At the 12-week follow-up, the seven day point prevalence abstinence from smoking was 28.6%, and the median number of cigarettes smoked daily decreased from 18.5 to 5.5 (p < 0.0001. The median number of e-cigarette cartridges used dropped from 21 at the six-week follow-up to 12.5 at the 12-week follow-up. After initiating EC use, women at risk for cervical cancer were able to either quit smoking or reduce the number of cigarettes smoked per day. Although a controlled trial with a larger sample size is needed to confirm these initial results, this study suggests that using ECs during quit attempts may reduce cigarette consumption.

  7. E-Cigarettes for Immediate Smoking Substitution in Women Diagnosed with Cervical Dysplasia and Associated Disorders.

    Science.gov (United States)

    James, Shirley A; Meier, Ellen M; Wagener, Theodore L; Smith, Katherine M; Neas, Barbara R; Beebe, Laura A

    2016-03-04

    The aim of this study was to determine if 31 women with cervical dysplasia and associated conditions exacerbated by smoking would be successful substituting cigarettes with their choice of either nicotine replacement therapy (NRT) or electronic cigarettes (EC). Women received motivational interviewing and tried both NRT and ECs, choosing one method to use during a six-week intervention period. Daily cigarette consumption was measured at baseline, six, and 12 weeks, with differences analyzed by the Wilcoxon signed-rank test. Study analysis consisted only of women choosing to use ECs (29/31), as only two chose NRT. At the 12-week follow-up, the seven day point prevalence abstinence from smoking was 28.6%, and the median number of cigarettes smoked daily decreased from 18.5 to 5.5 (p < 0.0001). The median number of e-cigarette cartridges used dropped from 21 at the six-week follow-up to 12.5 at the 12-week follow-up. After initiating EC use, women at risk for cervical cancer were able to either quit smoking or reduce the number of cigarettes smoked per day. Although a controlled trial with a larger sample size is needed to confirm these initial results, this study suggests that using ECs during quit attempts may reduce cigarette consumption.

  8. Exposure to Mosquito Coil Smoke May be a Risk Factor for Lung Cancer in Taiwan

    OpenAIRE

    Chen, Shu-Chen; Wong, Ruey-Hong; Shiu, Li-Jie; Chiou, Ming-Chih; Lee, Huei

    2008-01-01

    Background About 50% of lung cancer deaths in Taiwan are not related to cigarette smoking. Environmental exposure may play a role in lung cancer risk. Taiwanese households frequently burn mosquito coil at home to repel mosquitoes. The aim of this hospital-based case-control study was to determine whether exposure to mosquito coil smoke is a risk for lung cancer. Methods Questionnaires were administered to 147 primary lung cancer patients and 400 potential controls to ascertain demographic dat...

  9. [Effect of cigarette smoking on coexistence of cadmium and zinc in retained wisdom teeth].

    Science.gov (United States)

    Malara, Piotr; Kwapuliński, Jerzy; Drugacz, Jan; Malara, Beata

    2005-01-01

    The change in coexistence pattern of elements (antagonism-synergism) in conditions of excessive level of toxic element is observed in many biological samples. The aim of this study was to establish the cadmium and zinc content in hard tissues of retained wisdom teeth of smokers and non-smokers and to find out if active exposure to cigarette smoke has an influence on coexistence of both metals in these tissues. Material consisted of 127 retained wisdom teeth (65 from smokers and 62 from non-smokers). Cadmium and zinc contents were determined by means of atomic absorption spectrometry. We found out that retained wisdom tooth from smokers exhibited higher cadmium and zinc contents compared to non-smokers' teeth. Moreover, coexistence pattern of cadmium and zinc in teeth depends on exposure to heavy metals and exhibits strong synergism in smokers.

  10. Differential effects of cigarette smoking on birth weight by maternal body mass index.

    Science.gov (United States)

    Heinz-Partington, Sean; Condous, George; Mongelli, Max

    2016-07-01

    Links between low birth weight and tobacco exposure in utero are well established, as are associations between maternal body mass index (BMI) and birth weight. This study further develops those relationships. In particular, this article analyses whether high maternal weight acts to dampen the previously established link between tobacco exposure and low birth weight. A retrospective cohort study was undertaken, reviewing the birth weights of 13,473 live singleton pregnancies born at a Sydney regional hospital between 1998 and 2003. Results demonstrated a statistically significant decline in reduced birth weight as BMI increased. That is, as body weight increases, tobacco use has a smaller effect on reducing birth weight. Inversely, the effect on reducing birth weight for each cigarette smoked by leaner women was greater. In effect, the adverse influence of tobacco use on birth weight appears to be modulated by increasing maternal BMI.

  11. Exposure to radionuclides in smoke from vegetation fires

    Energy Technology Data Exchange (ETDEWEB)

    Carvalho, Fernando P., E-mail: carvalho@itn.pt; Oliveira, João M.; Malta, Margarida

    2014-02-01

    Naturally occurring radionuclides of uranium, thorium, radium, lead and polonium were determined in bushes and trees and in the smoke from summer forest fires. Activity concentrations of radionuclides in smoke particles were much enriched when compared to original vegetation. Polonium-210 ({sup 210}Po) in smoke was measured in concentrations much higher than all other radionuclides, reaching 7255 ± 285 Bq kg{sup −1}, mostly associated with the smaller size smoke particles (< 1.0 μm). Depending on smoke particle concentration, {sup 210}Po in surface air near forest fires displayed volume concentrations up to 70 mBq m{sup −3}, while in smoke-free air {sup 210}Po concentration was about 30 μBq m{sup −3}. The estimated absorbed radiation dose to an adult member of the public or a firefighter exposed for 24 h to inhalation of smoke near forest fires could exceed 5 μSv per day, i.e, more than 2000 times above the radiation dose from background radioactivity in surface air, and also higher than the radiation dose from {sup 210}Po inhalation in a chronic cigarette smoker. It is concluded that prolonged exposure to smoke allows for enhanced inhalation of radionuclides associated with smoke particles. Due to high radiotoxicity of alpha emitting radionuclides, and in particular of {sup 210}Po, the protection of respiratory tract of fire fighters is strongly recommended. - Highlights: • Natural radionuclides in vegetation are in low concentrations. • Forest fires release natural radionuclides from vegetation and concentrate them in inhalable ash particles. • Prolonged inhalation of smoke from forest fires gives rise enhanced radiation exposure of lungs especially due to polonium. • Respiratory protection of fire fighters and members of public is highly recommended for radioprotection reasons.

  12. The Alteration and Significance of Surfactant Protein A in Rats Chronically Exposed to Cigarette Smoke

    Institute of Scientific and Technical Information of China (English)

    Qiongjie HU; Huilan ZHANG; Shengdao XIONG; Xuemei SHI; Yongjian XU; Zhenxiang ZHANG; Guohua ZHEN; Jianping ZHAO

    2008-01-01

    In order to confirm the alteration and significance of cigarette smoke exposure on SP-A in rats, 20 Wistar rats were assigned randomly to two groups: an N group (n=10), and an S group (n=10). The ultra-structural change was observed by electron microscopy. The number of cells positive for SPA was by immunohistochemically measured. The mRNA expression in the lung tissues was deter-mined by reverse transcription polymerase chain reaction (RT-PCR). The number of cells positive for SPA of the S group (0.52±0.05) was lower than that of the N group (0.72±0.06) (P<0.05). The lev-els of mRNA of SPA in the lung tissues of the S group (0.3522±0.0512) was significantly lower than that of the N group (0.4432±0.05628) (P<0.05). It is concluded that cigarette smoke alone decreased the level of SP-A and that might have an important effect on surfactant metabolism and the host deense functions of surfactant in the peripheral airways, which might play a crucial role in the devel-opment of chronic obstructive lung disease.

  13. Oxidative stress in testicular tissues of rats exposed to cigarette smoke and protective effects of caffeic acid phenethyl ester

    Institute of Scientific and Technical Information of China (English)

    Hüseyin Ozyurt; Hidir Pekmez; Bekir Suha Parlaktas; Ilter Kus; Birsen Ozyurt; Mustafa Sarsllmaz

    2006-01-01

    Aim: To show the oxidative stress after cigarette smoke exposure in rat testis and to evaluate the effects of caffeic acid phenethyl ester (CAPE). Methods: Twenty-one rats were divided into three groups of seven. Animals in Group Ⅰwere used as control. Rats in Group Ⅱ were exposed to cigarette smoke only (4 x 30 min/d) and rats in Group Ⅲall the rats were killed and the levels of nitric oxide (NO) and anti-oxidant enzymes such as superoxide-dismutase,catalase and glutathione peroxidase (GSH-Px) and the level of malondialdehyde were studied in the testicular tissues of rats with spectrophotometric analysis. Results: There was a significant increase in catalase and superoxide-dismutase activities in Group Ⅱ when compared to the controls, but the levels of both decreased after CAPE administration in Group Ⅲ. GSH-Px activity was decreased in Group Ⅱ but CAPE caused an elevation in GSH-Px activity in Group Ⅲ.The difference between the levels of GSH-Px in Group Ⅰ and Group Ⅱ was significant, but the difference between groups Ⅱ and Ⅲ was not significant. Elevation of malondialdehyde after smoke exposure was significant and CAPE caused a decrease to a level which was not statistically different to the control group. A significantly increased level of NO after exposure to smoke was reversed by CAPE administration and the difference between NO levels in groups Ⅰ and Ⅲ was statistically insignificant. Conclusion: Exposure to cigarette smoke causes changes in the oxidative enzyme levels in rat testis, but CAPE can reverse these harmful effects.

  14. Molecular and cellular mechanisms of cigarette smoke-induced myocardial injury: prevention by vitamin C.

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    Archita Das

    Full Text Available BACKGROUND: Cardiovascular disease (CVD remains one of the major killers in modern society. One strong risk factor of CVD is cigarette smoking that causes myocardial injury and leads to the genesis of pathological cardiovascular events. However, the exact toxic component(s of cigarette smoke (CS and its molecular and cellular mechanisms for causing myocardial injury leading to heart damage and its prevention are largely unknown. METHODOLOGY/PRINCIPAL FINDINGS: Using a guinea pig model, here we show that chronic exposure to CS produces myocardial injury that is prevented by vitamin C. Male guinea pigs were fed either vitamin C-deficient (0.5 mg/day or vitamin C-sufficient (15 mg/day diet and subjected to CS exposure from 5 Kentucky Research cigarettes (3R4F/day (6 days/week in a smoke chamber up to 8 weeks. Pair-fed sham controls were subjected to air exposure instead of CS exposure under similar conditions. Myocardial injury was produced in CS-exposed marginal vitamin C-deficient guinea pigs as evidenced by release of cardiac Troponin-T and I in the serum, oxidative stress, inflammation, apoptosis, thrombosis and collagen deposition in the myocardium. Treatment of rat cardiomyocyte cells (H9c2 in vitro and guinea pigs in vivo with p-benzoquinone (p-BQ in amounts derived from CS revealed that p-BQ was a major factor responsible for CS-induced myocardial damage. A moderately large dose of vitamin C (15 mg/day prevented CS/p-BQ-induced myocardial injury. Population based studies indicated that plasma vitamin C levels of smokers without disease were significantly lower (p = 0,0000 than that of non-smokers. Vitamin C levels of CS-related cardiovascular patients were further lower (p = 0.0000 than that of smokers without disease. CONCLUSIONS/SIGNIFICANCE: The results indicate that dietary supplementation of vitamin C may be a novel and simple therapy for the prevention of pathological cardiovascular events in habitual smokers.

  15. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    Directory of Open Access Journals (Sweden)

    Rosemary Hiscock

    2015-12-01

    Full Text Available The UK Stop Smoking Services (SSS are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883 and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801. SSS monitoring data suggested 2% of clients were using e-cigarettes to quit with SSS and that clients using e-cigarettes had similar quit rates to clients using Varenicline. Most SSS personnel are waiting for licenced e-cigarettes to become available before they will recommend them to clients. However, less than a quarter view e-cigarettes as “a good thing”. Managers and commissioners were more positive than practitioners. SSS personnel working for the NHS (hospitals and GP surgeries were less positive about e-cigarettes than those employed elsewhere. E-cigarettes were cited as the most important reason for the recent decline in service footfall. Thus dissemination of information about e-cigarettes needs to be examined and services should address their stance on e-cigarettes with some urgency.

  16. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    Science.gov (United States)

    Hiscock, Rosemary; Bauld, Linda; Arnott, Deborah; Dockrell, Martin; Ross, Louise; McEwen, Andy

    2015-12-21

    The UK Stop Smoking Services (SSS) are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883) and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801). SSS monitoring data suggested 2% of clients were using e-cigarettes to quit with SSS and that clients using e-cigarettes had similar quit rates to clients using Varenicline. Most SSS personnel are waiting for licenced e-cigarettes to become available before they will recommend them to clients. However, less than a quarter view e-cigarettes as "a good thing". Managers and commissioners were more positive than practitioners. SSS personnel working for the NHS (hospitals and GP surgeries) were less positive about e-cigarettes than those employed elsewhere. E-cigarettes were cited as the most important reason for the recent decline in service footfall. Thus dissemination of information about e-cigarettes needs to be examined and services should address their stance on e-cigarettes with some urgency.

  17. β-carotene protects rats against bronchitis induced by cigarette smoking

    Institute of Scientific and Technical Information of China (English)

    庞宝森; 王辰; 翁心植; 唐小奈; 张红玉; 牛淑洁; 毛燕玲; 辛平; 黄秀霞; 张海燕; 祝锦

    2003-01-01

    Objective To investigate the protective effects of β-carotene in rats against the development of chronic bronchitis induced by cigarette smoking. Results Long-term cigarette smoking caused an obvious increase in the amount of IL-6, IL-8 and LPO and a sharp decrease in the levels of NO and SOD in smoking animals compared to controls. β-carotene intake reversed all the changes induced by smoking and alleviated the pathological changes caused by chronic bronchitis. Conclusions Quantitative oral intake of β-carotene had protective effects against chronic bronchitis induced by long-term cigarette smoking, which was associated with the increased production of NO, the clearance of some oxidative free radicals (OFR) and the alleviation of chronic inflammation.

  18. Predisposing effects of cigarette advertising on children's intentions to smoke when older.

    Science.gov (United States)

    Aitken, P P; Eadie, D R; Hastings, G B; Haywood, A J

    1991-04-01

    Six hundred and forty Glasgow children, initially aged between 11 and 14 years, were interviewed twice, with approximately one year between interviews. Children whose intentions to smoke when older became more positive between the two interviews tended to be more aware of cigarette advertising at the time of the first interview (compared with children whose intentions to smoke were negative at both interviews). Children whose intentions to smoke became more negative between the interviews tended to be less appreciative of cigarette advertisements at the time of the first interview (compared with children whose intentions to smoke were positive at both interviews). Since both groups differed from their respective contrast groups before their declared intentions changed, these findings support the view that cigarette advertising has predisposing as well as reinforcing effects on children's attitudes and behaviour with respect to smoking.

  19. Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

    DEFF Research Database (Denmark)

    Vikman, Petter; Xu, Cang-Bao; Edvinsson, Lars

    2009-01-01

    AIMS: Cigarette smoking is one of the strongest risk factors for stroke. However, the underlying molecular mechanisms that smoke leads to the pathogenesis of stroke are incompletely understood. METHODS: Dimethyl sulfoxide (DMSO)-soluble (lipid-soluble) cigarette smoking particles (DSP) were extra...

  20. Summary of the Findings from a Study About Cigarette Smoking Among Teen-Age Girls and Young Women.

    Science.gov (United States)

    Yankelovich, Skelly and White, Inc., New York, NY.

    This paper presents the major results of a study for the American Cancer Society on cigarette smoking among teen-age girls and young women, and findings relevant to the prevention and quitting of smoking. The four major trends found in this study are: (1) a dramatic increase in cigarette smoking among females; (2) an intellectual awareness of the…

  1. Effect of Cigarette Smoking on Epithelial to Mesenchymal Transition (EMT in Lung Cancer

    Directory of Open Access Journals (Sweden)

    Trung Vu

    2016-04-01

    Full Text Available Epithelial to mesenchymal transition (EMT is a process that allows an epithelial cell to acquire a mesenchymal phenotype through multiple biochemical changes resulting in an increased migratory capacity. During cancer progression, EMT is found to be associated with an invasive or metastatic phenotype. In this review, we focus on the discussion of recent studies about the regulation of EMT by cigarette smoking. Various groups of active compounds found in cigarette smoke such as polycyclic aromatic hydrocarbons (PAH, nicotine-derived nitrosamine ketone (NNK, and reactive oxygen specicies (ROS can induce EMT through different signaling pathways. The links between EMT and biological responses to cigarette smoke, such as hypoxia, inflammation, and oxidative damages, are also discussed. The effect of cigarette smoke on EMT is not only limited to cancer types directly related to smoking, such as lung cancer, but has also been found in other types of cancer. Altogether, this review emphasizes the importance of understanding molecular mechanisms of the induction of EMT by cigarette smoking and will help in identifying novel small molecules for targeting EMT induced by smoking.

  2. Effect of simvastatin on MMPs and TIMPs in cigarette smoke-induced rat COPD model

    Science.gov (United States)

    Sun, Jiawei; Bao, Jie; Shi, Yanan; Zhang, Bin; Yuan, Lindong; Li, Junhong; Zhang, Lihai; Sun, Mo; Zhang, Ling; Sun, Wuzhuang

    2017-01-01

    Background Proteases may play an important role in the development of chronic obstructive pulmonary disease and emphysema in response to cigarette smoke exposure (CSE). The current study was designed to investigate the expression of matrix metalloproteinase (MMP)-8, MMP-9, MMP-12, tissue inhibitor of MMP (TIMP)-1, and TIMP-4 in rat lung tissues in response to CSE, and assessed the effect of simvastatin in regulating expression of MMPs and TIMPs. Methods Thirty normal Sprague Dawley (SD) rats were divided into control (n=10), CSE (n=10), and CSE plus simvastatin (n=10) groups. Animals were whole-body exposed to the cigarette smoke in the box for 1 hour each time, twice a day, 5 days a week for 16 weeks. Animals of CSE + simvastatin group were intra-gastrically administered simvastatin at a dose of 5 mg/kg/day followed by CSE. Bronchoalveolar lavage fluid was harvested for inflammatory cell count and lung tissues were stained for morphologic examination. Expression of mRNA and protein level of MMP-8, MMP-9, MMP-12, TIMP-1, and TIMP-4 was assessed by real-time reverse transcription polymerase chain reaction and immunohistochemistry, respectively. Results CSE resulted in a significant increase of mean linear intercept (MLI: 34.6±2.0 μm) and bronchial wall thickness and diameter (BWT/D, 0.250±0.062) compared to control (MLI: 24.0±1.7 μm, BWT/D: 0.160±0.034, P0.01). Simvastatin slightly but not significantly prevented alteration of MLI, BWT/D, and mean alveolar number (MLI: 33.4±1.4 μm; BWT/D: 0.220±0.052; mean alveolar number: 15.5±2.5 N/μm2, P>0.05). Total white blood cell was significantly increased in the bronchoalveolar lavage fluid of smoking group (3.3±2.5×109 cells/L vs 1.1±1.3×109 cells/L of control, P0.05). In response to CSE, MMP-8, MMP-9, and MMP-12 mRNA were upregulated more than sevenfold, while TIMP-1 and TIMP-4 increased two- to fivefold. Simvastatin significantly blocked upregulation of MMP-8 and -9 (P0.05). In addition, simvastatin

  3. Effect of Permeability of Tipping Paper on Cigarette Burning Temperature and the Property of Mainstream Smoke

    Science.gov (United States)

    Yao, Zhen-Yu; Shen, Yan; Huang, Hai-Qun; Xu, Ji-Cang

    2016-05-01

    Cigarette smoke analysis of tipping paper with different permeability was carried out. The infrared thermal imager was used to measure burning temperature of cigarette with different permeability tipping paper. The results indicated that with the increase of tipping paper permeability, Tar, CO and nicotine in cigarette mainstream were significantly linear decreased, puff count was increased. Tipping paper permeability had a great influence on cigarette burning temperature. With the increase of tipping paper permeability, the third puff burning temperature and the average peak temperature values were dropped obviously, but the changes of smoldering temperature were not obvious. In addition, smoldering average temperature was significantly lower than the third puff burning temperature and peak temperature.

  4. Potential Impact of Graphic Health Warnings on Cigarette Packages in Reducing Cigarette Demand and Smoking-Related Deaths in Vietnam.

    Science.gov (United States)

    Minh, Hoang Van; Chung, Le Hong; Giang, Kim Bao; Duc, Duong Minh; Hinh, Nguyen Duc; Mai, Vu Quynh; Cuong, Nguyen Manh; Manh, Pham Duc; Duc, Ha Anh; Yang, Jui-Chen

    2016-01-01

    Two years after implementation of the graphic health warning intervention in Vietnam, it is very important to evaluate the intervention's potential impact. The objective of this paper was to predict effects of graphic health warnings on cigarette packages, particularly in reducing cigarette demand and smoking-associated deaths in Vietnam. In this study, a discrete choice experiment (DCE) method was used to evaluate the potential impact of graphic tobacco health warnings on smoking demand. To predict the impact of GHWs on reducing premature deaths associated with smoking, we constructed different static models. We adapted the method developed by University of Toronto, Canada and found that GHWs had statistically significant impact on reducing cigarette demand (up to 10.1% through images of lung damage), resulting in an overall decrease of smoking prevalence in Vietnam. We also found that between 428,417- 646,098 premature deaths would be prevented as a result of the GHW intervention. The potential impact of the GHW labels on reducing premature smoking-associated deaths in Vietnam were shown to be stronger among lower socio-economic groups.

  5. Allergic Sensitization, Rhinitis and Tobacco Smoke Exposure in US Adults.

    Directory of Open Access Journals (Sweden)

    Josef Shargorodsky

    Full Text Available Tobacco exposure has been linked with sinonasal pathology and may be associated with allergic sensitization. This study evaluates the association between exposure to active smoking or secondhand smoke (SHS and the prevalence of rhinitis and allergic sensitization in the US adult population.Cross-sectional study in 4,339 adults aged 20-85 in the National Health and Nutrition Examination Survey, 2005-2006. Never smoking was defined as reported lifetime smoking less than 100 cigarettes and serum cotinine levels 10 ng/mL. Self-reported rhinitis was based on symptoms during the past 12 months, and allergen sensitization was defined as a positive response to any of the 19 specific IgE antigens tested.Almost half of the population (43% had detectable levels of IgE specific to at least one inhaled allergen and 32% reported a history of rhinitis. After multivariate adjustment, there was a statistically significant association between the highest serum cotinine tertile and rhinitis in active smokers (OR 1.42; 95%CI 1.00-2.00. The association between active smoking and rhinitis was stronger in individuals without allergic sensitization (OR 2.47; 95%CI 1.44-4.23. There was a statistically significant association between increasing cotinine tertiles and decreased odds of inhaled allergen sensitization (p-trend <.01.Tobacco smoke exposure was associated with increased prevalence of rhinitis symptoms, but not with allergic sensitization. The results indicate that the relationship between tobacco smoke exposure and sinonasal pathology in adults may be independent of allergic sensitization.

  6. Colonic inflammation in mice is improved by cigarette smoke through iNKT cells recruitment.

    Directory of Open Access Journals (Sweden)

    Muriel Montbarbon

    Full Text Available Cigarette smoke (CS protects against intestinal inflammation during ulcerative colitis. Immunoregulatory mechanisms sustaining this effect remain unknown. The aim of this study was to assess the effects of CS on experimental colitis and to characterize the intestinal inflammatory response at the cellular and molecular levels. Using the InExpose® System, a smoking device accurately reproducing human smoking habit, we pre-exposed C57BL/6 mice for 2 weeks to CS, and then we induced colitis by administration of dextran sodium sulfate (DSS. This system allowed us to demonstrate that CS exposure improved colonic inflammation (significant decrease in clinical score, body weight loss and weight/length colonic ratio. This improvement was associated with a significant decrease in colonic proinflammatory Th1/Th17 cytokine expression, as compared to unexposed mice (TNF (p=0.0169, IFNγ (p<0.0001, and IL-17 (p=0.0008. Smoke exposure also induced an increased expression of IL-10 mRNA (p=0.0035 and a marked recruitment of iNKT (invariant Natural Killer T; CD45+ TCRβ+ CD1d tetramer+ cells in the colon of DSS-untreated mice. Demonstration of the role of iNKT cells in CS-dependent colitis improvement was performed using two different strains of NKT cells deficient mice. Indeed, in Jα18KO and CD1dKO animals, CS exposure failed to induce significant regulation of DSS-induced colitis both at the clinical and molecular levels. Thus, our study demonstrates that iNKT cells are pivotal actors in the CS-dependent protection of the colon. These results highlight the role of intestinal iNKT lymphocytes and their responsiveness to environmental stimuli. Targeting iNKT cells would represent a new therapeutic way for inflammatory bowel diseases.

  7. Cigarette smoking during pregnancy regulates the expression of specific nicotinic acetylcholine receptor (nAChR) subunits in the human placenta

    Energy Technology Data Exchange (ETDEWEB)

    Machaalani, R., E-mail: rita.machaalani@sydney.edu.au [Department of Medicine, The University of Sydney, NSW 2006 (Australia); Bosch Institute, The University of Sydney, NSW 2006 (Australia); The Children' s Hospital at Westmead, NSW 2145 (Australia); Ghazavi, E. [Bosch Institute, The University of Sydney, NSW 2006 (Australia); School of Medical Sciences (Pharmacology), The University of Sydney, NSW 2006 (Australia); Hinton, T. [School of Medical Sciences (Pharmacology), The University of Sydney, NSW 2006 (Australia); Waters, K.A. [Department of Medicine, The University of Sydney, NSW 2006 (Australia); The Children' s Hospital at Westmead, NSW 2145 (Australia); Hennessy, A. [School of Medicine, University of Western Sydney, NSW 2751 (Australia); Heart Research Institute, 7 Eliza St Newtown, NSW 2042 (Australia)

    2014-05-01

    Smoking during pregnancy is associated with low birth weight, premature delivery, and neonatal morbidity and mortality. Nicotine, a major pathogenic compound of cigarette smoke, binds to the nicotinic acetylcholine receptors (nAChRs). A total of 16 nAChR subunits have been identified in mammals (9 α, 4 β, and 1 δ, γ and ε subunits). The effect of cigarette smoking on the expression of these subunits in the placenta has not yet been determined, thus constituting the aim of this study. Using RT-qPCR and western blotting, this study investigated all 16 mammalian nAChR subunits in the normal healthy human placenta, and compared mRNA and protein expressions in the placentas from smokers (n = 8) to controls (n = 8). Our data show that all 16 subunit mRNAs are expressed in the normal, non-diseased human placenta and that the expression of α2, α3, α4, α9, β2 and β4 subunits is greater than the other subunits. For mRNA, cigarette smoke exposure was associated with increased expression of the α9 subunit, and decreased expression of the δ subunit. At the protein level, expression of both α9 and δ was increased. Thus, cigarette smoking in pregnancy is sufficient to regulate nAChR subunits in the placenta, specifically α9 and δ subunits, and could contribute to the adverse effects of vasoconstriction and decreased re-epithelialisation (α9), and increased calcification and apoptosis (δ), seen in the placentas of smoking women. - Highlights: • All 16 mammalian nAChR subunits are expressed in the human placenta. • Cigarette smoking increases α9 mRNA and protein in the placenta. • Cigarette smoking decreases δ mRNA but increases δ protein in the placenta.

  8. Urinary excretion of the acrylonitrile metabolite 2-cyanoethylmercapturic acid is correlated with a variety of biomarkers of tobacco smoke exposure and consumption

    Science.gov (United States)

    Minet, Emmanuel; Cheung, Francis; Errington, Graham; Sterz, Katharina; Scherer, Gerhard

    2011-01-01

    Acrylonitrile is an IARC class 2B carcinogen present in cigarette smoke. Urinary 2-cyanoethylmercapturic acid (CEMA) is an acrylonitrile metabolite and a potential biomarker for acrylonitrile exposure. The objective of this work was to study the dose response of CEMA in urine of non-smokers and smokers of different ISO tar yield cigarettes. We observed that smokers excreted >100-fold higher amounts of urinary CEMA than non-smokers. The CEMA levels in smokers were significantly correlated with ISO tar yield, daily cigarette consumption, and urinary biomarkers of smoke exposure. In conclusion, urinary CEMA is a suitable biomarker for assessing smoking-related exposure to acrylonitrile. PMID:21108560

  9. Urinary excretion of the acrylonitrile metabolite 2-cyanoethylmercapturic acid is correlated with a variety of biomarkers of tobacco smoke exposure and consumption.

    Science.gov (United States)

    Minet, Emmanuel; Cheung, Francis; Errington, Graham; Sterz, Katharina; Scherer, Gerhard

    2011-02-01

    Acrylonitrile is an IARC class 2B carcinogen present in cigarette smoke. Urinary 2-cyanoethylmercapturic acid (CEMA) is an acrylonitrile metabolite and a potential biomarker for acrylonitrile exposure. The objective of this work was to study the dose response of CEMA in urine of non-smokers and smokers of different ISO tar yield cigarettes. We observed that smokers excreted >100-fold higher amounts of urinary CEMA than non-smokers. The CEMA levels in smokers were significantly correlated with ISO tar yield, daily cigarette consumption, and urinary biomarkers of smoke exposure. In conclusion, urinary CEMA is a suitable biomarker for assessing smoking-related exposure to acrylonitrile.

  10. A Pilot Study to Assess Solanesol Levels in Exhaled Cigarette Smoke

    Directory of Open Access Journals (Sweden)

    Moldoveanu SC

    2014-12-01

    Full Text Available This paper describes the results obtained during the measurement of the level of solanesol in exhaled cigarette smoke from human subjects. The study was performed with three different cigarettes with U.S. Federal Trade Commission (FTC ‘tar’ values of 5.0 mg, 10.6 mg, and 16.2 mg. The number of human subjects was ten smokers for each of the evaluated products, each subject smoking three cigarettes within one hour. The exhaled smoke was collected using a vacuum assisted procedure that avoids strain in exhaling, and the solanesol was analyzed using an original high performance liquid chromatography (HPLC technique. The cigarette butts from the smokers were collected and also analyzed for solanesol. The results obtained for the cigarette butts from the smokers were used to calculate the level of solanesol delivered to the smoker, based on calibration curves. These curves were generated separately by analyzing the solanesol in smoke and in the cigarette butts obtained by machine smoking under different puffing regimes. Knowing the levels of solanesol delivered to the smoker and the exhaled levels it was possible to calculate the retention and retention % of this compound from mainstream smoke for different cigarettes types. The amount of retained solanesol is the lowest for the 5.0 mg ‘tar’ product, and the highest for the 16.2 mg ‘tar’ product, although there is not much difference between the 10.6 mg ‘tar’ product and the 16.2 mg ‘tar’ product. For the 10.6 mg ‘tar’ cigarettes the retention % was between 60% and 72%, for the 5.0 mg product the retention % was slightly lower ranging between 53% and 70%, while for the 16.2 mg ‘tar’ product, the retention % was slightly higher ranging between 62% and 82%.

  11. Prevalence and predictors of cigarette smoking among Greek urban adolescents: A cross-sectional study

    Directory of Open Access Journals (Sweden)

    Athanasia Liozidou

    2015-10-01

    Greek adolescents report lower smoking rates than previously reported, yet it is a population experimenting with tobacco products. Electronic cigarette emerged as the third most likely product of experimentation. The social origin of smoking behavior is confirmed, as well as the imperative need to encourage tobacco-free school policies and bans on tobacco advertising, promotion and sponsorship.

  12. Acute one-cigarette smoking decreases ghrelin hormone in saliva: a pilot study.

    Science.gov (United States)

    Kaabi, Yahia A; Khalifa, Mohiealdeen A

    2014-01-01

    Cigarette smoking is commonly associated with weight loss and mechanisms for these weight changes are still elusive. Ghrelin is a peptide hormone that works in a neuroendocrine fashion to stimulate hunger and the desire for food intake. Ghrelin is also secreted in saliva, probably to enhance food taste. In the current study, we tested the direct impact of acute cigarette smoking on total ghrelin found in saliva. Methods. Blood and saliva samples were collected from 30 healthy nonsmoker male volunteers before and after one-cigarette smoke. Total ghrelin in serum and saliva was measured by ELISA based method. Results. Data showed a statistically significant reduction in salivary ghrelin after smoking (P < 0.0001). In serum, total ghrelin levels were not affected before and after smoking (P = 0.1362). Additionally, positive correlation was observed between serum and salivary ghrelin before smoking (r = 0.4143 and P = 0.0158); however, this correlation was lost after smoking (r = 0.1147 and P = 0.5461). Conclusion. Acute one-cigarette smoking can negatively affect ghrelin levels in saliva that might contribute to the dull food taste in smokers.

  13. Acute One-Cigarette Smoking Decreases Ghrelin Hormone in Saliva: A Pilot Study

    Directory of Open Access Journals (Sweden)

    Yahia A. Kaabi

    2014-01-01

    Full Text Available Cigarette smoking is commonly associated with weight loss and mechanisms for these weight changes are still elusive. Ghrelin is a peptide hormone that works in a neuroendocrine fashion to stimulate hunger and the desire for food intake. Ghrelin is also secreted in saliva, probably to enhance food taste. In the current study, we tested the direct impact of acute cigarette smoking on total ghrelin found in saliva. Methods. Blood and saliva samples were collected from 30 healthy nonsmoker male volunteers before and after one-cigarette smoke. Total ghrelin in serum and saliva was measured by ELISA based method. Results. Data showed a statistically significant reduction in salivary ghrelin after smoking (P<0.0001. In serum, total ghrelin levels were not affected before and after smoking (P=0.1362. Additionally, positive correlation was observed between serum and salivary ghrelin before smoking (r=0.4143 and P=0.0158; however, this correlation was lost after smoking (r=0.1147 and P=0.5461. Conclusion. Acute one-cigarette smoking can negatively affect ghrelin levels in saliva that might contribute to the dull food taste in smokers.

  14. New interpretation of arterial stiffening due to cigarette smoking using a structurally motivated constitutive model

    DEFF Research Database (Denmark)

    Enevoldsen, Marie Sand; Henneberg, Kaj-Åge; Jensen, Jørgen Arendt

    2011-01-01

    caused by smoking was reflected by consistent increase in an elastin-associated parameter and moreover by marked increase in the collagen-associated parameters. That is, we suggest that arterial stiffening due to cigarette smoking appears to be isotropic, which may allow simpler phenomenological models...

  15. Prevalence of cigarette smoking and its predictors among school going adolescents of North India

    Directory of Open Access Journals (Sweden)

    Durgesh Thakur

    2014-01-01

    Full Text Available Background: Cigarettes smoking is a common mode of consuming tobacco in India. This habit usually starts in adolescence and tracks across the life course. Interventions like building decision making skills and resisting negative influences are effective in reducing the initiation and level of tobacco use. Aims and Objectives: The purpose of this study was to assess the prevalence of adolescent current cigarette smoking behavior and to investigate the individual and social factors, which influence them both to and not to smoke. Methodology: A cross-sectional study was carried out among school going adolescents in Shimla town of North India. After obtaining their written informed consent, a questionnaire was administered. Results: The overall prevalence of current cigarette smoking was 11.8%. The binary logistic regression model revealed that parents′ and peers′ smoking behavior influence adolescent smoking behavior. Individual self-harm tendency also significantly predicted cigarette smoking behavior. Parental active participation in keeping a track of their children′s free time activities predicted to protect adolescents from taking this habit. Conclusion: Our research lends support to the need for intervention on restricting adolescents from taking up this habit and becoming another tobacco industries′ addicted customer. Parents who smoke should quit this habit, which will not only restore their own health, but also protect their children. All parents should be counseled to carefully observe their children′s free time activities.

  16. Self-Reported Depressive Feelings and Cigarette Smoking among Mexican-American Adolescents.

    Science.gov (United States)

    Pesa, Jacqueline A.; Cowdery, Joan E.; Wang, Min Qi; Fu, Qiang

    1997-01-01

    Examined the relationship between depressive feelings and cigarette smoking in Mexican-American adolescents who participated in the 1993 Teenage Attitudes and Practices Survey II. Results suggest a relationship between certain feelings of depression and smoking, beyond that experienced by nonsmokers, which may be more evident in females.…

  17. Determination of Selected Volatiles in Cigarette Mainstream Smoke. The CORESTA 2009 Collaborative Study and Recommended Method

    Directory of Open Access Journals (Sweden)

    Intorp M

    2014-12-01

    Full Text Available A recommended method has been developed and published by CORESTA, applicable to the quantification of selected volatiles (1,3-butadiene, isoprene, acrylonitrile, benzene, and toluene in the gas phase of cigarette mainstream smoke. The method involved smoke collection in impinger traps and detection and measurement using gas chromatography/mass spectrometry techniques.

  18. Cigarette smoking is associated with reduced microstructural integrity of cerebral white matter

    NARCIS (Netherlands)

    Gons, R.A.R.; Norden, A.G.W. van; Laat, K.F. de; Oudheusden, L.J. van; Uden, I.W.M. van; Zwiers, M.P.; Norris, D.G.; Leeuw, F.E. de

    2011-01-01

    Cigarette smoking doubles the risk of dementia and Alzheimer's disease. Various pathophysiological pathways have been proposed to cause such a cognitive decline, but the exact mechanisms remain unclear. Smoking may affect the microstructural integrity of cerebral white matter. Diffusion tensor imagi

  19. Disposition of phencyclidine in mice after smoke exposure

    Energy Technology Data Exchange (ETDEWEB)

    Freeman, A.S.; Martin, B.R.

    Mice were exposed to the smoke from placebo marihuana cigarettes treated with phencyclidine hydrochloride (PCP . HCl). A dose-related decrement in motor performance was observed after exposure to the smoke from cigarettes containing 10-15 mg of PCP . HCl. Tissue levels of /sup 3/H-PCP, /sup 3/H-PC (pyrolysis product), and /sup 3/H-metabolites were measured in several tissues up to 7 days after exposure to 50 mg of /sup 3/H-PCP . HCl. /sup 3/H-PCP levels were highest in liver followed by lung, brain, fat, and plasma for the first 10 min after exposure. The /sup 3/H-PCP concentration in all tissues, except fat, declined during the subsequent 50 min. Liver and lung contained the highest levels of /sup 3/H-metabolites during this hour, followed by plasma, fat, and brain. Brain levels of /sup 3/H-PCP correlated well with the magnitude and duration of behavioral effects observed (r . 0.98). /sup 3/H-PC was also well absorbed from smoke as evidenced by initial tissue levels comparable to those of /sup 3/H-PCP, but they declined more rapidly than /sup 3/H-PCP levels. Excellent correlations were obtained between /sup 3/H-PCP and /sup 3/H-PC concentrations in plasma and those in liver, lung, and brain. /sup 3/H-PCP was not detected in any tissue 3 days after smoke exposure. At 1 and 3 days, radioactivity corresponding to metabolites persisted in liver and lung, but had largely disappeared by 7 days.

  20. Bone marrow mononuclear cells up-regulate toll-like receptor expression and produce inflammatory mediators in response to cigarette smoke extract.

    Directory of Open Access Journals (Sweden)

    Junmin Zhou

    Full Text Available Several reports link cigarette smoking with leukemia. However, the effects of cigarette smoke extract (CSE on bone marrow hematopoiesis remain unknown. The objective of this study was to elucidate the direct effects of cigarette smoke on human bone marrow hematopoiesis and characterize the inflammatory process known to result from cigarette smoking. Bone marrow mononuclear cells (BMCs from healthy individuals when exposed to CSE had significantly diminished CFU-E, BFU-E and CFU-GM. We found increased nuclear translocation of the NF-κB p65 subunit and, independently, enhanced activation of AKT and ERK1/2. Exposure of BMCs to CSE induced IL-8 and TGF-β1 production, which was dependent on NF-κB and ERK1/2, but not on AKT. CSE treatment had no effect on the release of TNF-α, IL-10, or VEGF. Finally, CSE also had a significant induction of TLR2, TLR3 and TLR4, out of which, the up-regulation of TLR2 and TLR3 was found to be dependent on ERK1/2 and NF-κB activation, but not AKT. These results indicate that CSE profoundly inhibits the growth of erythroid and granulocyte-macrophage progenitors in the bone marrow. Further, CSE modulates NF-κB- and ERK1/2-dependent responses, suggesting that cigarette smoking may impair bone marrow hematopoiesis in vivo as well as induce inflammation, two processes that proceed malignant transformation.

  1. Directly measured secondhand smoke exposure and COPD health outcomes

    Directory of Open Access Journals (Sweden)

    Balmes John

    2006-06-01

    Full Text Available Abstract Background Although personal cigarette smoking is the most important cause and modulator of chronic obstructive pulmonary disease (COPD, secondhand smoke (SHS exposure could influence the course of the disease. Despite the importance of this question, the impact of SHS exposure on COPD health outcomes remains unknown. Methods We used data from two waves of a population-based multiwave U.S. cohort study of adults with COPD. 77 non-smoking respondents with a diagnosis of COPD completed direct SHS monitoring based on urine cotinine and a personal badge that measures nicotine. We evaluated the longitudinal impact of SHS exposure on validated measures of COPD severity, physical health status, quality of life (QOL, and dyspnea measured at one year follow-up. Results The highest level of SHS exposure, as measured by urine cotinine, was cross-sectionally associated with poorer COPD severity (mean score increment 4.7 pts; 95% CI 0.6 to 8.9 and dyspnea (1.0 pts; 95% CI 0.4 to 1.7 after controlling for covariates. In longitudinal analysis, the highest level of baseline cotinine was associated with worse COPD severity (4.7 points; 95% CI -0.1 to 9.4; p = 0.054, disease-specific QOL (2.9 pts; -0.16 to 5.9; p = 0.063, and dyspnea (0.9 pts; 95% CI 0.2 to 1.6 pts; p Conclusion Directly measured SHS exposure appears to adversely influence health outcomes in COPD, independent of personal smoking. Because SHS is a modifiable risk factor, clinicians should assess SHS exposure in their patients and counsel its avoidance. In public health terms, the effects of SHS exposure on this vulnerable subpopulation provide a further rationale for laws prohibiting public smoking.

  2. Cigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats.

    Science.gov (United States)

    Ho, Yuen-Shan; Yang, Xifei; Yeung, Sze-Chun; Chiu, Kin; Lau, Chi-Fai; Tsang, Andrea Wing-Ting; Mak, Judith Choi-Wo; Chang, Raymond Chuen-Chung

    2012-01-01

    Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD). To date, little is known for how smoking can predispose our brains to dementia or cognitive impairment. This study aimed to investigate the cigarette smoke-induced pathological changes in brains. Male Sprague-Dawley (SD) rats were exposed to either sham air or 4% cigarette smoke 1 hour per day for 8 weeks in a ventilated smoking chamber to mimic the situation of chronic passive smoking. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Smoking also affected the synapse through reducing the expression of pre-synaptic proteins including synaptophysin and synapsin-1, while there were no changes in the expression of postsynaptic protein PSD95. Decreased levels of acetylated-tubulin and increased levels of phosphorylated-tau at 231, 205 and 404 epitopes were also observed in the hippocampus of the smoking rats. These results suggested that axonal transport machinery might be impaired, and the stability of cytoskeleton might be affected by smoking. Moreover, smoking affected amyloid precursor protein (APP) processing by increasing the production of sAPPβ and accumulation of β-amyloid peptide in the CA3 and dentate gyrus region. In summary, our data suggested that chronic cigarette smoking could induce synaptic changes and other neuropathological alterations. These changes might serve as evidence of early phases of neurodegeneration and may explain why smoking can predispose brains to AD and dementia.

  3. Cigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats.

    Directory of Open Access Journals (Sweden)

    Yuen-Shan Ho

    Full Text Available Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD. To date, little is known for how smoking can predispose our brains to dementia or cognitive impairment. This study aimed to investigate the cigarette smoke-induced pathological changes in brains. Male Sprague-Dawley (SD rats were exposed to either sham air or 4% cigarette smoke 1 hour per day for 8 weeks in a ventilated smoking chamber to mimic the situation of chronic passive smoking. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Smoking also affected the synapse through reducing the expression of pre-synaptic proteins including synaptophysin and synapsin-1, while there were no changes in the expression of postsynaptic protein PSD95. Decreased levels of acetylated-tubulin and increased levels of phosphorylated-tau at 231, 205 and 404 epitopes were also observed in the hippocampus of the smoking rats. These results suggested that axonal transport machinery might be impaired, and the stability of cytoskeleton might be affected by smoking. Moreover, smoking affected amyloid precursor protein (APP processing by increasing the production of sAPPβ and accumulation of β-amyloid peptide in the CA3 and dentate gyrus region. In summary, our data suggested that chronic cigarette smoking could induce synaptic changes and other neuropathological alterations. These changes might serve as evidence of early phases of neurodegeneration and may explain why smoking can predispose brains to AD and dementia.

  4. Maternal L-Carnitine Supplementation Improves Brain Health in Offspring from Cigarette Smoke Exposed Mothers.

    Science.gov (United States)

    Chan, Yik Lung; Saad, Sonia; Al-Odat, Ibrahim; Oliver, Brian G; Pollock, Carol; Jones, Nicole M; Chen, Hui

    2017-01-01

    Maternal cigarette smoke exposure (SE) causes detrimental changes associated with the development of chronic neurological diseases in the offspring as a result of oxidative mitochondrial damage. Maternal L-Carnitine administration has been shown to reduce renal oxidative stress in SE offspring, but its effect in the brain is unknown. Here, we investigated the effects of maternal L-Carnitine supplementation on brain markers of oxidative stress, autophagy, mitophagy and mitochondrial energy producing oxidative phosphorylation (OXPHOS) complexes in SE offspring. Female Balb/c mice (8 weeks) were exposed to cigarette smoke prior to mating, during gestation and lactation with or without L-Carnitine supplementation (1.5 mM in drinking water). In 1 day old male SE offspring, brain mitochondrial damage was suggested by increased mitochondrial fusion and reduced autophagosome markers; whereas at 13 weeks, enhanced brain cell damage was suggested by reduced fission and autophagosome markers, as well as increased apoptosis and DNA fragmentation markers, which were partially reversed by maternal L-Carnitine supplementation. In female SE offspring, enhanced mitochondrial regeneration was suggested by decreased fission and increased fusion markers at day 1. At 13 weeks, there was an increase in brain energy demand, oxidative stress and mitochondrial turnover, reflected by the protein changes of OXPHOS complex, fission and autophagosome markers, as well as the endogenous antioxidant, which were also partially normalized by maternal L-Carnitine supplementation. However, markers of apoptosis and DNA fragmentation were not significantly changed. Thus L-Carnitine supplementation may benefit the brain health of the offspring from smoking mothers.

  5. Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

    DEFF Research Database (Denmark)

    Vikman, Petter; Xu, Cang-Bao; Edvinsson, Lars

    2009-01-01

    AIMS: Cigarette smoking is one of the strongest risk factors for stroke. However, the underlying molecular mechanisms that smoke leads to the pathogenesis of stroke are incompletely understood. METHODS: Dimethyl sulfoxide (DMSO)-soluble (lipid-soluble) cigarette smoking particles (DSP) were...... extracted from cigarette smoke (0.8 mg nicotine per cigarette; Marlboro). Rat cerebral arteries were isolated and organ cultured in the presence of DSP (0.2 microl/ml, equivalent to the plasma level in smokers) for 24 h. The expression of matrix metalloproteinase 9 and 13 (MMP9 and MMP13), angiotensin...

  6. The cessation and detoxification effect of tea filters on cigarette smoke

    Institute of Scientific and Technical Information of China (English)

    2010-01-01

    To treat tobacco addiction,a tea filter was developed and studied for smoking cessation.This work reports the smoking cessation effect of tea when it was used as a component of cigarette filters.In one trial it was found that after using the tea filters for 2 months,the volunteer smokers decreased their cigarette consumption by 56.5%,and 31.7% of them stopped smoking.This work identified a new method and material,tea filter and theanine,which inhibit tobacco and nicotine addiction and provide an effective strategy for treating tobacco addiction.

  7. Cigarette smoke induces an unfolded protein response in the human lung: a proteomic approach.

    Science.gov (United States)

    Kelsen, Steven G; Duan, Xunbao; Ji, Rong; Perez, Oscar; Liu, Chunli; Merali, Salim

    2008-05-01

    Cigarette smoking, which exposes the lung to high concentrations of reactive oxidant species (ROS) is the major risk factor for chronic obstructive pulmonary disease (COPD). Recent studies indicate that ROS interfere with protein folding in the endoplasmic reticulum and elicit a compensatory response termed the "unfolded protein response" (UPR). The importance of the UPR lies in its ability to alter expression of a variety of genes involved in antioxidant defense, inflammation, energy metabolism, protein synthesis, apoptosis, and cell cycle regulation. The present study used comparative proteomic technology to test the hypothesis that chronic cigarette smoking induces a UPR in the human lung. Studies were performed on lung tissue samples obtained from three groups of human subjects: nonsmokers, chronic cigarette smokers, and ex-smokers. Proteomes of lung samples from chronic cigarette smokers demonstrated 26 differentially expressed proteins (20 were up-regulated, 5 were down-regulated, and 1 was detected only in the smoking group) compared with nonsmokers. Several UPR proteins were up-regulated in smokers compared with nonsmokers and ex-smokers, including the chaperones, glucose-regulated protein 78 (GRP78) and calreticulin; a foldase, protein disulfide isomerase (PDI); and enzymes involved in antioxidant defense. In cultured human airway epithelial cells, GRP78 and the UPR-regulated basic leucine zipper, transcription factors, ATF4 and Nrf2, which enhance expression of important anti-oxidant genes, increased rapidly (< 24 h) with cigarette smoke extract. These data indicate that cigarette smoke induces a UPR response in the human lung that is rapid in onset, concentration dependent, and at least partially reversible with smoking cessation. We speculate that activation of a UPR by cigarette smoke may protect the lung from oxidant injury and the development of COPD.

  8. Childhood ADHD symptoms and risk for cigarette smoking during adolescence: School adjustment as a potential mediator.

    Science.gov (United States)

    Flory, Kate; Malone, Patrick S; Lamis, Dorian A

    2011-06-01

    Although a large body of research suggests that children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for cigarette smoking during adolescence compared with their non-ADHD peers, much less research has examined why. The current study addressed this gap in the literature by examining middle school adjustment, broadly defined, as a possible mediator of the relation between childhood ADHD symptoms and cigarette smoking during middle adolescence (10th grade). Longitudinal data were collected from a community sample of 754 youth using self-report and parent report along with school records, and a novel statistical technique was used in the process of testing for mediation. Consistent with hypotheses, school adjustment was found to mediate the relation between childhood ADHD symptoms and later cigarette smoking, even after controlling for early externalizing problems. Results have implications for etiological theories of adolescent deviant behavior and suggest that successful smoking prevention programs targeting youth with ADHD should include a school adjustment component.

  9. A cross-sectional survey of cadmium biomarkers and cigarette smoking.

    Science.gov (United States)

    Hecht, Eric M; Arheart, Kris; Lee, David J; Hennekens, Charles H; Hlaing, WayWay M

    2016-07-01

    Cadmium contamination of tobacco may contribute to the health hazards of cigarette smoking. The 2005-2012 United States National Health and Nutrition Examination Survey data provided a unique opportunity to conduct a cross-sectional survey of cadmium biomarkers and cigarette smoking. Among a sample of 6761 participants, we evaluated mean differences and correlations between cadmium biomarkers in the blood and urine and characteristics of never, former and current smokers. We found statistically significant differences in mean cadmium biomarker levels between never and former smokers as well as between never and current smokers. In current smokers, duration in years had a higher correlation coefficient with urinary than blood cadmium levels. In contrast, number of cigarettes smoked per day had a higher correlation coefficient with blood than urinary cadmium levels. These data suggest that blood and urine cadmium biomarker levels differ by duration and dose. These findings should be considered in evaluating any association between cadmium and smoking related diseases, especially cardiovascular disease.

  10. The Effects of Cigarette Smoking on Cardiopulmonary Function and Exercise Tolerance in Teenagers

    Directory of Open Access Journals (Sweden)

    Dianna Louie

    2001-01-01

    Full Text Available Teenagers who smoke are frequently warned that cigarette smoking will have detrimental effects on the function of their cardiopulmonary system and on their ability to perform exercise. However, there is little published evidence to support this statement. Therefore, in the present study, peak expiratory flow was measured as an indicator of lung function, expired carbon monoxide level was measured as an indicator of current smoking and the associated reduction in the oxygen carrying capacity of the blood, and blood pressure and heart rate were measured as indicators of cardiovascular hemodynamics before and after a one-mile run in 27 teenagers. The results show that, even at a young age, cigarette smoking is associated with significant detrimental effects on cardiopulmonary function and exercise tolerance. Objective evidence of an effect of smoking on cardiopulmonary function and exercise tolerance in this age group may assist educators and health care professionals in convincing teenagers to quit smoking.

  11. Antioxidant Protective Effect of Honey in Cigarette Smoke-Induced Testicular Damage in Rats

    Directory of Open Access Journals (Sweden)

    Kuttulebbai Nainamohamed Salam Sirajudeen

    2011-08-01

    Full Text Available Cigarette smoke (CS can cause testicular damage and we investigated the possible protective effect of honey against CS-induced testicular damage and oxidative stress in rats. CS exposure (8 min, 3 times daily and honey supplementation (1.2 g/kg daily were given for 13 weeks. Rats exposed to CS significantly had smaller seminiferous tubules diameter and epithelial height, lower Leydig cell count and increased percentage of tubules with germ cell loss. CS also produced increased lipid peroxidation (TBARS and glutathione peroxidase (GPx activity, as well as reduced total antioxidant status (TAS and activities of superoxide dismutase (SOD and catalase (CAT. However, supplementation of honey significantly reduced histological changes and TBARS level, increased TAS level, as well as significantly restored activities of GPx, SOD and CAT in rat testis. These findings may suggest that honey has a protective effect against damage and oxidative stress induced by CS in rat testis.

  12. Associations of psychological capital, demographic and occupational factors with cigarette smoking among Chinese underground coal miners

    OpenAIRE

    Liu, Li; Xu, Xin; Wu, Hui; Yang, Yilong; Wang, Lie

    2015-01-01

    Background As a specific male occupational group, underground coal miners have been commonly found to have a high prevalence of cigarette smoking. It is of urgent need to explore some factors that could be intervened to reduce smoking from personal or internal perspective. The purpose of the present study was to examine the associations of psychological capital (PsyCap), demographic and occupational factors with smoking among Chinese underground coal miners. Methods A cross-sectional survey w...

  13. CIGARETTE SMOKING IN SCHIZOPHRENIC PATIENTS THAT ARE CURRENTLY TREATED IN A MEXICAN HOSPITAL

    OpenAIRE

    Oscar Rodríguez-Mayoral; Julio César Flores-Lázaro; Nuria Lanzagorta; Fernando Corona-Hernández; Humberto Nicolini

    2015-01-01

    Objective: tobacco smoking is the most commonly substance abused in psychiatric patients; among them, patients with schizophrenia are the highest abusers. Smoking is related to a decrease in the quality life and life expectancy, as well as interacting with psychotropic drugs. In Mexico, there is not basic descriptive knowledge about the main variables related to cigarette smoking in psychiatric population. The aim of this study was to know the relation among variables (beginning and course of...

  14. Respiratory effects of cigarette smoke, dust, and histamine in newborn rabbits

    Energy Technology Data Exchange (ETDEWEB)

    Trippenbach, T.; Kelly, G.

    1988-02-01

    We studied the respiratory effects of cigarette smoke, 5% histamine aerosol, and dust in unanesthetized 1- to 7-day-old rabbits in a body plethysmograph. Cigarette smoke immediately provoked the animal's arousal and irregular breathing. Histamine and dust had no effect in some of the youngest animals. In others, 5-15 s from the onset of the exposure to either of the two stimuli, respiratory rate increased and the depth of breathing decreased. These changes were more pronounced with age. The fact that effects of dust and aerosol lessened with time of exposure showed adaptation to the stimuli. The age dependence of the reflex response was also observed after injection of 50 micrograms of histamine per kilogram into the external jugular vein in anesthetized (50 mg ketamine + 3 mg acepromazine per kg) and tracheostomized rabbits during the 1st wk of life. In 1-day-old animals, a short-lasting excitation was followed by apnea or a prolongation of expiratory phase. Peak amplitude of the diaphragmatic EMG (EMGdi) increased in all animals, but only in the youngest was the EMGdi increase paralleled by an increase in tidal volume. In vagotomized animals or animals pretreated with H1-blocker, histamine never affected timing parameters in animals greater than 1 day old. In the youngest animals, respiratory depression due to histamine was not abolished after vagotomy or promethazine. The results imply that inputs from the upper airways and the rapidly adapting pulmonary mechanoreceptors exert their effects on the pattern of breathing immediately after birth in rabbits. The importance of those inputs increases with maturation.

  15. Carbonyl compounds in gas and particle phases of mainstream cigarette smoke.

    Science.gov (United States)

    Pang, Xiaobing; Lewis, Alastair C

    2011-11-01

    Carbonyl compounds (carbonyls) are important constituents of cigarette smoke and some are toxic and may be carcinogenic or mutagenic to humans. In this study carbonyl emissions in the gas and particle phases of mainstream cigarette smoke were assessed by GC-MS with pentafluorophenyl hydrazine (PFPH) derivatization. Seven brands of cigarettes and one brand of cigar common in the UK market and having differing nicotine, tar and carbon monoxide yields were investigated. Sixteen carbonyl components were identified in gaseous emissions and twenty in the particle phase. In the gaseous emissions, acetaldehyde presented as the predominant species, followed by formaldehyde, 2-propenal, and pentanal. In the particulate emissions, 1-hydroxy-2-propanone was the most abundant followed by formaldehyde, benzaldehyde, and 2,5-dimethylbenzaldehyde. Significant differences were found in carbonyl emissions among the brands of cigarettes. The gaseous carbonyl emissions varied in the range of 216-405 μg cigarette(-1) (μg cig(-1)) and the particulate carbonyl emissions varied in the range of 23-127 μg cig(-1). Positive correlations were found between the total emission of carbonyls, tar yield and carbon monoxide yield. Similar gas/particle (G/P) partitioning ratios of carbonyls were found among all cigarettes, which implies that G/P partitions of carbonyls in smoke mainly depend on the physical properties of the carbonyls. The gaseous carbonyl emissions were enhanced by 40% to 130% when some of the water, accounting for 8-12% of cigarettes in mass, was removed from the tobacco. Non-filtered cigarettes showed significantly higher carbonyl emissions compared to their filtered equivalents. Carbonyl particulate accounted for 11-19% by mass of total particulate matter from tobacco smoke. The cigar generated 806 μg cig(-1) gaseous and 141 μg cig(-1) particulate carbonyls, which is 2-4 times greater than the cigarettes.

  16. Social Network Characteristics, Social Support, and Cigarette Smoking among Asian/Pacific Islander Young Adults.

    Science.gov (United States)

    Pokhrel, Pallav; Fagan, Pebbles; Cassel, Kevin; Trinidad, Dennis R; Kaholokula, Joseph Keawe'aimoku; Herzog, Thaddeus A

    2016-06-01

    Cigarette smoking may be one of the factors contributing to the high levels of cancer-related mortality experienced by certain Asian/Pacific Islander (A/PI) subgroups (e.g., Native Hawaiian). Given the collectivist cultural orientation attributed to A/PI groups, social strategies are recommended for substance abuse or smoking cessation treatment among A/PI. However, research examining how social network characteristics and social support relate to smoking across A/PI subgroups has been lacking. This study investigated the associations between social network characteristics (e.g., size, composition), perceived social support, and recent cigarette use across Native Hawaiian, Filipino, and East Asian (e.g., Japanese, Chinese) young adults (18-35 year old). Cross-sectional, self-report data were collected from N = 435 participants (M age = 25.6, SD = 8.3; 61% women). Ethnic differences were found in a number of pathways linking social network characteristics, perceived social support, and cigarette smoking. Larger network size was strongly associated with higher perceived social support and lower recent cigarette smoking among Native Hawaiians but not Filipinos or East Asians. Higher perceived social support was associated with lower recent smoking among East Asians and Filipinos but not Native Hawaiians. Implications are discussed with regard to smoking prevention and cessation among A/PI.

  17. Association between Cigarette Smoking and Erectile Tumescence: The Mediating Role of Heart Rate Variability

    Science.gov (United States)

    Harte, Christopher B.; Meston, Cindy M.

    2012-01-01

    Cigarette smoking deleteriously affects erectile function, and conversely, quitting smoking improves erectile hemodynamics. Underlying mechanisms by which smoking (or reduction of smoking frequency) may affect erectile physiology are not well understood. This study examined the mediating role of heart rate variability (HRV; a marker of sympathovagal balance) among a sample of male chronic smokers from the United States. Sixty-two healthy men (Mage = 38.27 years; SD = 10.62) were assessed at baseline (while smoking regularly), at mid-treatment (while using a nicotine patch), and at follow-up, four weeks after patch discontinuation. Cigarette use, frequency-domain parameters of HRV (low frequency [LF], high frequency [HF], LF/HF ratio), and physiological sexual arousal responses (via penile plethysmography) were assessed at each visit. Results were consistent with mediation, in that greater reductions in cigarette use from baseline to follow-up were associated with longitudinal increases in LF, which in turn showed positive relations with across-time changes in erectile tumescence. Neither HF or LF/HF ratio mediated the relationship between smoking and erection. In conclusion, HRV mediated the inverse relationship between reductions in smoking and enhancements in erectile tumescence. Results underscore the possibility that cigarette use may deleteriously affect erectile function peripherally, in part, by disrupting cardiac autonomic function. PMID:23303335

  18. TEXT CLASSIFICATION FOR AUTOMATIC DETECTION OF E-CIGARETTE USE AND USE FOR SMOKING CESSATION FROM TWITTER: A FEASIBILITY PILOT.

    Science.gov (United States)

    Aphinyanaphongs, Yin; Lulejian, Armine; Brown, Duncan Penfold; Bonneau, Richard; Krebs, Paul

    2016-01-01

    Rapid increases in e-cigarette use and potential exposure to harmful byproducts have shifted public health focus to e-cigarettes as a possible drug of abuse. Effective surveillance of use and prevalence would allow appropriate regulatory responses. An ideal surveillance system would collect usage data in real time, focus on populations of interest, include populations unable to take the survey, allow a breadth of questions to answer, and enable geo-location analysis. Social media streams may provide this ideal system. To realize this use case, a foundational question is whether we can detect e-cigarette use at all. This work reports two pilot tasks using text classification to identify automatically Tweets that indicate e-cigarette use and/or e-cigarette use for smoking cessation. We build and define both datasets and compare performance of 4 state of the art classifiers and a keyword search for each task. Our results demonstrate excellent classifier performance of up to 0.90 and 0.94 area under the curve in each category. These promising initial results form the foundation for further studies to realize the ideal surveillance solution.

  19. The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components.

    Directory of Open Access Journals (Sweden)

    Zhen Gao

    Full Text Available 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.

  20. Natural killer cells in obesity: impaired function and increased susceptibility to the effects of cigarette smoke.

    LENUS (Irish Health Repository)

    O'Shea, Donal

    2010-01-01

    BACKGROUND: Obese individuals who smoke have a 14 year reduction in life expectancy. Both obesity and smoking are independently associated with increased risk of malignancy. Natural killer cells (NK) are critical mediators of anti-tumour immunity and are compromised in obese patients and smokers. We examined whether NK cell function was differentially affected by cigarette smoke in obese and lean subjects. METHODOLOGY AND PRINCIPAL FINDINGS: Clinical data and blood were collected from 40 severely obese subjects (BMI>40 kg\\/m(2)) and 20 lean healthy subjects. NK cell levels and function were assessed using flow cytometry and cytotoxicity assays. The effect of cigarette smoke on NK cell ability to kill K562 tumour cells was assessed in the presence or absence of the adipokines leptin and adiponectin. NK cell levels were significantly decreased in obese subjects compared to lean controls (7.6 vs 16.6%, p = 0.0008). NK function was also significantly compromised in obese patients (30% +\\/- 13% vs 42% +\\/-12%, p = 0.04). Cigarette smoke inhibited NK cell ability to kill tumour cell lines (p<0.0001). NK cells from obese subjects were even more susceptible to the inhibitory effects of smoke compared to lean subjects (33% vs 28%, p = 0.01). Cigarette smoke prevented NK cell activation, as well as perforin and interferon-gamma secretion upon tumour challenge. Adiponectin but not leptin partially reversed the effects of smoke on NK cell function in both obese (p = 0.002) and lean controls (p = 0.01). CONCLUSIONS\\/SIGNIFICANCE: Obese subjects have impaired NK cell activity that is more susceptible to the detrimental effects of cigarette smoke compared to lean subjects. This may play a role in the increase of cancer and infection seen in this population. Adiponectin is capable of restoring NK cell activity and may have therapeutic potential for immunity in obese subjects and smokers.

  1. Natural killer cells in obesity: impaired function and increased susceptibility to the effects of cigarette smoke.

    LENUS (Irish Health Repository)

    O'Shea, Donal

    2012-02-01

    BACKGROUND: Obese individuals who smoke have a 14 year reduction in life expectancy. Both obesity and smoking are independently associated with increased risk of malignancy. Natural killer cells (NK) are critical mediators of anti-tumour immunity and are compromised in obese patients and smokers. We examined whether NK cell function was differentially affected by cigarette smoke in obese and lean subjects. METHODOLOGY AND PRINCIPAL FINDINGS: Clinical data and blood were collected from 40 severely obese subjects (BMI>40 kg\\/m(2)) and 20 lean healthy subjects. NK cell levels and function were assessed using flow cytometry and cytotoxicity assays. The effect of cigarette smoke on NK cell ability to kill K562 tumour cells was assessed in the presence or absence of the adipokines leptin and adiponectin. NK cell levels were significantly decreased in obese subjects compared to lean controls (7.6 vs 16.6%, p = 0.0008). NK function was also significantly compromised in obese patients (30% +\\/- 13% vs 42% +\\/-12%, p = 0.04). Cigarette smoke inhibited NK cell ability to kill tumour cell lines (p<0.0001). NK cells from obese subjects were even more susceptible to the inhibitory effects of smoke compared to lean subjects (33% vs 28%, p = 0.01). Cigarette smoke prevented NK cell activation, as well as perforin and interferon-gamma secretion upon tumour challenge. Adiponectin but not leptin partially reversed the effects of smoke on NK cell function in both obese (p = 0.002) and lean controls (p = 0.01). CONCLUSIONS\\/SIGNIFICANCE: Obese subjects have impaired NK cell activity that is more susceptible to the detrimental effects of cigarette smoke compared to lean subjects. This may play a role in the increase of cancer and infection seen in this population. Adiponectin is capable of restoring NK cell activity and may have therapeutic potential for immunity in obese subjects and smokers.

  2. Comparison of carcinogen, carbon monoxide, and ultrafine particle emissions from narghile waterpipe and cigarette smoking: Sidestream smoke measurements and assessment of second-hand smoke emission factors

    Science.gov (United States)

    Daher, Nancy; Saleh, Rawad; Jaroudi, Ezzat; Sheheitli, Hiba; Badr, Thérèse; Sepetdjian, Elizabeth; Al Rashidi, Mariam; Saliba, Najat; Shihadeh, Alan

    2010-01-01

    The lack of scientific evidence on the constituents, properties, and health effects of second-hand waterpipe smoke has fueled controversy over whether public smoking bans should include the waterpipe. The purpose of this study was to investigate and compare emissions of ultrafine particles (UFP, carcinogenic polyaromatic hydrocarbons (PAH), volatile aldehydes, and carbon monoxide (CO) for cigarettes and narghile (shisha, hookah) waterpipes. These smoke constituents are associated with a variety of cancers, and heart and pulmonary diseases, and span the volatility range found in tobacco smoke. Sidestream cigarette and waterpipe smoke was captured and aged in a 1 m 3 Teflon-coated chamber operating at 1.5 air changes per hour (ACH). The chamber was characterized for particle mass and number surface deposition rates. UFP and CO concentrations were measured online using a fast particle spectrometer (TSI 3090 Engine Exhaust Particle Sizer), and an indoor air quality monitor. Particulate PAH and gaseous volatile aldehydes were captured on glass fiber filters and DNPH-coated SPE cartridges, respectively, and analyzed off-line using GC-MS and HPLC-MS. PAH compounds quantified were the 5- and 6-ring compounds of the EPA priority list. Measured aldehydes consisted of formaldehyde, acetaldehyde, acrolein, methacrolein, and propionaldehyde. We found that a single waterpipe use session emits in the sidestream smoke approximately four times the carcinogenic PAH, four times the volatile aldehydes, and 30 times the CO of a single cigarette. Accounting for exhaled mainstream smoke, and given a habitual smoker smoking rate of 2 cigarettes per hour, during a typical one-hour waterpipe use session a waterpipe smoker likely generates ambient carcinogens and toxicants equivalent to 2-10 cigarette smokers, depending on the compound in question. There is therefore good reason to include waterpipe tobacco smoking in public smoking bans.

  3. 76 FR 57008 - Smoking of Electronic Cigarettes on Aircraft

    Science.gov (United States)

    2011-09-15

    ... for submitting comments. Mail: Docket Management Facility, U.S. Department of Transportation, 1200 New... Journal of Medicine article, ``E-Cigarette or Drug-Delivery Device? Regulating Novel Nicotine Products... which they evaluated five electronic cigarette brands. See Anna Trtchounian & Prue Talbot,...

  4. Association of diabetes and cigarette smoke exposure on the glycemia and liver glycogen of pregnant Wistar rats Associação entre diabetes e exposição à fumaça de cigarro sobre a glicemia e glicogênio hepático de ratas Wistar prenhes

    Directory of Open Access Journals (Sweden)

    Yuri Karen Sinzato

    2008-12-01

    Full Text Available PURPOSE: To evaluate cigarette smoke exposure and/or diabetes association effects on the glycemia and liver glycogen levels of pregnant Wistar rats. METHODS: 60 adult rats were randomly distributed into (n=10/group: non-diabetic exposed to filtered air (G1; non-diabetic exposed to cigarette smoke only before pregnancy (G2; non-diabetic exposed to cigarette smoke before and during pregnancy (G3; diabetic exposed to filtered air (G4; diabetic exposed to cigarette smoke only before pregnancy (G5, and diabetic exposed to cigarette smoke before and during pregnancy (G6. Glycemia was determined at days 0 and 21 of pregnancy. Liver samples were collected for liver glycogen determinations. RESULTS: At day 21 of pregnancy, glycemia was higher in G5 and G6 compared to G4 group. G2 (2.43±0.43, G3 (3.20±0.49, G4 (2.62±0.34, G5 (2.65±0.27 and G6 groups (1.94±0.35 presented decreased liver glycogen concentrations compared to G1 (4.20±0.18 mg/100mg liver tissue (pOBJETIVO: Avaliar a associação da exposição à fumaça de cigarro e/ou diabete sobre a glicemia e concentrações de glicogênio hepático em ratas Wistar prenhes. MÉTODOS: 60 ratas adultas foram distribuídas aleatoriamente em seis grupos (n=10/grupo: não-diabético exposto ao ar filtrado (G1; não-diabético exposto à fumaça de cigarro antes da prenhez (G2; não-diabético exposto à fumaça de cigarro antes e durante a prenhez (G3; diabético exposto ao ar filtrado (G4; diabético exposto à fumaça de cigarro antes da prenhez (G5; diabético exposto à fumaça de cigarro antes e durante a prenhez (G6. A glicemia foi determinada nos dias 0 e 21 de prenhez. Foram coletadas amostras de fígado para dosagens de glicogênio. RESULTADOS: No 21º dia de prenhez, a glicemia foi maior nos grupos G5 e G6 comparados ao grupo G4. Os grupos G2 (2,43±0,43, G3 (3,20±0,49, G4 (2,62±0,34, G5 (2,65±0,27 e G6 (1,94±0,35 apresentaram concentrações de glicogênio diminuídas comparados ao grupo G1

  5. Cigarette Smoking and Alcohol Consumption among Chinese Older Adults: Do Living Arrangements Matter?

    Directory of Open Access Journals (Sweden)

    Jiaan Zhang

    2015-02-01

    Full Text Available This study used five waves of the Chinese Longitudinal Healthy Longevity Survey to examine the relationship between living arrangements, smoking, and drinking among older adults in China from 1998–2008. We found that living arrangements had strong implications for cigarette smoking and alcohol consumption among the elderly. First, the likelihood of smoking was lower among older men living with children, and older women living either with a spouse, or with both a spouse and children; and the likelihood of drinking was lower among both older men, and women living with both a spouse and children, compared with those living alone. Second, among dual consumers (i.e., being a drinker and a smoker, the amount of alcohol consumption was lower among male dual consumers living with children, while the number of cigarettes smoked was higher among female dual consumers living with others, compared with those living alone. Third, among non-smoking drinkers, the alcohol consumption was lower among non-smoking male drinkers in all types of co-residential arrangements (i.e., living with a spouse, living with children, living with both a spouse and children, or living with others, and non-smoking female drinkers living with others, compared with those living alone. Results highlighted the importance of living arrangements to cigarette smoking and alcohol consumption among Chinese elderly. Co-residential arrangements provided constraints on Chinese older adults’ health-risk behaviors, and had differential effects for men and women.

  6. Cigarette smoking and alcohol consumption among Chinese older adults: do living arrangements matter?

    Science.gov (United States)

    Zhang, Jiaan; Wu, Liyun

    2015-02-23

    This study used five waves of the Chinese Longitudinal Healthy Longevity Survey to examine the relationship between living arrangements, smoking, and drinking among older adults in China from 1998-2008. We found that living arrangements had strong implications for cigarette smoking and alcohol consumption among the elderly. First, the likelihood of smoking was lower among older men living with children, and older women living either with a spouse, or with both a spouse and children; and the likelihood of drinking was lower among both older men, and women living with both a spouse and children, compared with those living alone. Second, among dual consumers (i.e., being a drinker and a smoker), the amount of alcohol consumption was lower among male dual consumers living with children, while the number of cigarettes smoked was higher among female dual consumers living with others, compared with those living alone. Third, among non-smoking drinkers, the alcohol consumption was lower among non-smoking male drinkers in all types of co-residential arrangements (i.e., living with a spouse, living with children, living with both a spouse and children, or living with others), and non-smoking female drinkers living with others, compared with those living alone. Results highlighted the importance of living arrangements to cigarette smoking and alcohol consumption among Chinese elderly. Co-residential arrangements provided constraints on Chinese older adults' health-risk behaviors, and had differential effects for men and women.

  7. Smoking Revolution” A Content Analysis of Electronic Cigarette Retail Websites

    Science.gov (United States)

    Grana, Rachel A.; Ling, Pamela M.

    2014-01-01

    Background Electronic cigarettes (e-cigarettes) have been increasingly available and marketed in the U.S. since 2007. As patterns of product adoption are frequently driven and reinforced by marketing, it is important to understand the marketing claims encountered by consumers. Purpose To describe the main advertising claims made on branded e-cigarette retail websites. Methods Websites were retrieved from two major search engines in 2011 using iterative searches with the following terms: electronic cigarette, e-cigarette, e-cig, and personal vaporizer. Fifty-nine websites met inclusion criteria, and 13 marketing claims were coded for main marketing messages in 2012. Results Ninety-five percent of the websites made explicit or implicit health-related claims, 64% had a smoking cessation-related claim, 22% featured doctors, and 76% claimed that the product does not produce secondhand smoke. Comparisons to cigarettes included claims that e-cigarettes were cleaner (95%) and cheaper (93%). Eighty-eight percent stated that the product could be smoked anywhere and 71% mentioned using the product to circumvent clean air policies. Candy, fruit, and coffee flavors were offered on most sites. Youthful appeals included images or claims of modernity (73%), increased social status (44%), enhanced social activity (32%), romance (31%), and use by celebrities (22%). Conclusions Health claims and smoking cessation messages that are unsupported by current scientific evidence are frequently used to sell e-cigarettes. Implied and overt health claims, the presence of doctors on websites, celebrity endorsements, and the use of characterizing flavors should be prohibited. PMID:24650842

  8. Will any future increase in cigarette price reduce smoking in Saudi Arabia?

    Directory of Open Access Journals (Sweden)

    Omar A. Al-Mohrej

    2014-01-01

    Full Text Available Context: In Saudi Arabia, no studies have been conducted on the correlation between any possible cigarette′s price increase and its effects on cigarette consumption. Aims: The aim of this study was to determine the prevalence of cigarette smoking in Saudi Arabia and to predict the effect of price increase on cigarette consumption. Settings and Design: A cross-sectional study was conducted in April and May 2013. Methods: We developed an Arabic questionnaire with information on demographic and socioeconomic factors, smoking history, and personal opinion on the effect of price increase on cigarette consumption. The questionnaire was distributed in public places such as malls and posted on famous Saudi athlete media′s twitter accounts. Results: Among the 2057 included responses, 802 (39% were current smokers. The smokers′ population constituted of 746 (92% males, of which 546 (68% had a monthly income equal or greater to 800 US dollars, and 446 (55% were aged between 21 and 30 years. Multivariate analyses of the risk factors for smoking showed that male gender and older age were associated with greater risk. Despite the current low prices of 2.67 US dollars, 454 smokers (56% thought that cigarette prices are expensive. When asked about the price of cigarettes that will lead to smoking cessation, 443 smokers (55% expected that a price of 8.27 US dollars and more per pack will make them quit. Conclusions: Increasing the price of popular cigarettes pack from 2.67 US dollars to 8.27 US dollars is expected to lead to smoking cessation in a large number of smokers in the Saudi population.

  9. Cigarette Smoking and Alcohol Use among Adolescents and Young Adults with Asthma

    Directory of Open Access Journals (Sweden)

    Elizabeth Burgess Dowdell

    2011-01-01

    Full Text Available Asthma is one of the most common, serious chronic diseases in pediatric and young adult populations. Health-risk behaviors, including cigarette smoking and alcohol use, may exacerbate chronic diseases and complicate their management. The aim of this study was to longitudinally analyze rates of cigarette smoking and alcohol use in adolescents and young adults who have asthma and those who do not have asthma. A secondary analysis of data from the National Longitudinal Study of Adolescent Health was undertaken. Individuals with asthma were found to exhibit increasing rates of cigarette smoking and alcohol use as they aged. When an adolescent with a chronic health issue begins health-risk-taking behaviors, behavior change interventions must be planned. Pediatric nurses, practitioners, and clinicians are uniquely positioned to assess for health-risk behaviors in youth with asthma and to intervene with plans of care that are tailored for the needs of this vulnerable population.

  10. Pathophysiology of tobacco smoke exposure: recent insights from comparative and redox proteomics.

    Science.gov (United States)

    Colombo, Graziano; Clerici, Marco; Giustarini, Daniela; Portinaro, Nicola M; Aldini, Giancarlo; Rossi, Ranieri; Milzani, Aldo; Dalle-Donne, Isabella

    2014-01-01

    First-hand and second-hand tobacco smoke are causally linked to a huge number of deaths and are responsible for a broad spectrum of pathologies such as cancer, cardiovascular, respiratory, and eye diseases as well as adverse effects on female reproductive function. Cigarette smoke is a complex mixture of thousands of different chemical species, which exert their negative effects on macromolecules and biochemical pathways, both directly and indirectly. Many compounds can act as oxidants, pro-inflammatory agents, carcinogens, or a combination of these. The redox behavior of cigarette smoke has many implications for smoke related diseases. Reactive oxygen and nitrogen species (both radicals and non-radicals), reactive carbonyl compounds, and other species may induce oxidative damage in almost all the biological macromolecules, compromising their structure and/or function. Different quantitative and redox proteomic approaches have been applied in vitro and in vivo to evaluate, respectively, changes in protein expression and specific oxidative protein modifications induced by exposure to cigarette smoke and are overviewed in this review. Many gel-based and gel-free proteomic techniques have already been used successfully to obtain clues about smoke effects on different proteins in cell cultures, animal models, and humans. The further implementation with other sensitive screening techniques could be useful to integrate the comprehension of cigarette smoke effects on human health. In particular, the redox proteomic approach may also help identify biomarkers of exposure to tobacco smoke useful for preventing these effects or potentially predictive of the onset and/or progression of smoking-induced diseases as well as potential targets for therapeutic strategies.

  11. A Cancer That Went Up in Smoke: Pulmonary Reaction to e-Cigarettes Imitating Metastatic Cancer

    DEFF Research Database (Denmark)

    Madsen, Lene Margrethe Ring; Vinther Krarup, Niels Henrik; Bergmann, Troels Korshøj;

    2016-01-01

    e-Cigarettes have gained worldwide popularity as a substitute for smoking, but concern has been raised regarding the long-term effects associated with their use. We report a case of a 45-year-old female consumer of e-cigarettes who presented with 4 months of abdominal pain and fever. Initial....... Upon cessation of e-cigarette use (known as vaping), the lung nodules disappeared, and the liver lesions regressed. Our case report suggests that vaping can induce an inflammatory reaction mimicking metastatic cancer....

  12. Case-control study of tobacco smoke exposure and breast cancer risk in Delaware

    Directory of Open Access Journals (Sweden)

    Hathcock H Leroy

    2008-06-01

    Full Text Available Abstract Background Tobacco smoke exposure may be associated with increased breast cancer risk, although the evidence supporting the association is inconclusive. We conducted a case-control study in Delaware, incorporating detailed exposure assessment for active and secondhand smoke at home and in the workplace. Methods Primary invasive breast cancer cases diagnosed among female Delaware residents, ages 40–79, in 2000–2002 were identified through the Delaware cancer registry (n = 287. Delaware drivers license and Health Care Finance Administration records were used to select age frequency-matched controls for women Results A statistically significant increased risk of breast cancer was observed for ever having smoked cigarettes (odds ratio = 1.43, 95% confidence interval = 1.03–1.99. However, there was no evidence of a dose-response relationship between breast cancer risk and total years smoked, cigarettes per day, or pack-years. Neither residential nor workplace secondhand smoke exposure was associated with breast cancer. Recalculations of active smoking risks using a purely unexposed reference group of women who were not exposed to active or secondhand smoking did not indicate increased risks of breast cancer. Conclusion These findings do not support an association between smoking and breast cancer.

  13. Why do women stop smoking during pregnancy? Cigarettes taste and smell bad.

    Science.gov (United States)

    Pletsch, Pamela K; Kratz, Anna Thornton

    2004-08-01

    There are high rates of cigarette smoking resumption among women who have quit smoking while pregnant, and the reasons for this are poorly understood. Our purpose in this study was to obtain an in-depth description of the context surrounding smoking behaviors during pregnancy and the first 3 months after women give birth in order to gain insight into the reasons women resume smoking. We used a longitudinal qualitative descriptive approach with in-depth interviews conducted early in pregnancy, at 36 weeks of pregnancy, and 3 months postpartum. Our purposive sample consisted of 15 pregnant women who had stopped smoking without assistance by their first prenatal visit. All women smoked mentholated cigarettes prior to pregnancy and 40% were primiparas. A thematic content analysis of 43 interviews revealed that the majority of women experienced an aversion to the taste or smell of tobacco smoke while pregnant and attributed these sensation changes to being pregnant. The taste and smell of tobacco smoke returned to prepregnancy states postpartum, and by 3 months postpartum 73% of the women had resumed smoking. This physiologic change can be conceptualized as a pregnancy-specific motivation for smoking cessation that can inform our efforts toward relapse prevention.

  14. Aggravation of Allergic Airway Inflammation by Cigarette Smoke in Mice Is CD44-Dependent.

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    Smitha Kumar

    Full Text Available Although epidemiological studies reveal that cigarette smoke (CS facilitates the development and exacerbation of allergic asthma, these studies offer limited information on the mechanisms involved. The transmembrane glycoprotein CD44 is involved in cell adhesion and acts as a receptor for hyaluronic acid and osteopontin. We aimed to investigate the role of CD44 in a murine model of CS-facilitated allergic airway inflammation.Wild type (WT and CD44 knock-out (KO mice were exposed simultaneously to house dust mite (HDM extract and CS. Inflammatory cells, hyaluronic acid (HA and osteopontin (OPN levels were measured in bronchoalveolar lavage fluid (BALF. Proinflammatory mediators, goblet cell metaplasia and peribronchial eosinophilia were assessed in lung tissue. T-helper (Th 1, Th2 and Th17 cytokine production was evaluated in mediastinal lymph node cultures.In WT mice, combined HDM/CS exposure increased the number of inflammatory cells and the levels of HA and OPN in BALF and Th2 cytokine production in mediastinal lymph nodes compared to control groups exposed to phosphate buffered saline (PBS/CS, HDM/Air or PBS/Air. Furthermore, HDM/CS exposure significantly increased goblet cell metaplasia, peribronchial eosinophilia and inflammatory mediators in the lung. CD44 KO mice exposed to HDM/CS had significantly fewer inflammatory cells in BALF, an attenuated Th2 cytokine production, as well as decreased goblet cells and peribronchial eosinophils compared to WT mice. In contrast, the levels of inflammatory mediators were similar or higher than in WT mice.We demonstrate for the first time that the aggravation of pulmonary inflammation upon combined exposure to allergen and an environmental pollutant is CD44-dependent. Data from this murine model of concomitant exposure to CS and HDM might be of importance for smoking allergic asthmatics.

  15. Toxic volatile organic compounds in environmental tobacco smoke: Emission factors for modeling exposures of California populations

    Energy Technology Data Exchange (ETDEWEB)

    Daisey, J.M.; Mahanama, K.R.R.; Hodgson, A.T. [Lawrence Berkeley Lab., CA (United States)

    1994-10-01

    The primary objective of this study was to measure emission factors for selected toxic air contaminants in environmental tobacco smoke (ETS) using a room-sized environmental chamber. The emissions of 23 volatile organic compounds (VOCs), including, 1,3-butadiene, three aldehydes and two vapor-phase N-nitrosamines were determined for six commercial brands of cigarettes and reference cigarette 1R4F. The commercial brands were selected to represent 62.5% of the cigarettes smoked in California. For each brand, three cigarettes were machine smoked in the chamber. The experiments were conducted over four hours to investigate the effects of aging. Emission factors of the target compounds were also determined for sidestream smoke (SS). For almost all target compounds, the ETS emission factors were significantly higher than the corresponding SS values probably due to less favorable combustion conditions and wall losses in the SS apparatus. Where valid comparisons could be made, the ETS emission factors were generally in good agreement with the literature. Therefore, the ETS emission factors, rather than the SS values, are recommended for use in models to estimate population exposures from this source. The variabilities in the emission factors ({mu}g/cigarette) of the selected toxic air contaminants among brands, expressed as coefficients of variation, were 16 to 29%. Therefore, emissions among brands were Generally similar. Differences among brands were related to the smoked lengths of the cigarettes and the masses of consumed tobacco. Mentholation and whether a cigarette was classified as light or regular did not significantly affect emissions. Aging was determined not to be a significant factor for the target compounds. There were, however, deposition losses of the less volatile compounds to chamber surfaces.

  16. Prevalence of and Susceptibility to Cigarette Smoking Among Female Students Aged 13 to 15 Years in Vietnam, 2007

    Directory of Open Access Journals (Sweden)

    Hoang Van Minh, MD, PhD

    2010-01-01

    Full Text Available IntroductionRecent reports show a sharp increase in smoking rates among girls. We describe prevalence of cigarette smoking and susceptibility to cigarette smoking among female students aged 13 to 15 years in Vietnam and examine the associated factors.MethodsWe used data from female secondary school students aged 13 to 15 years (grades 8-10 from the 2007 Global Youth Tobacco Survey that was conducted in 9 provinces in Vietnam. We used multivariate logistic regression analysis to determine associations between independent variables with smoking status and susceptibility to smoking.ResultsPrevalence of cigarette smoking among girls was 1.2% (95% confidence interval [CI], 0.9-1.5, and 1.5% (95% CI, 1.2-1.9 of girls were susceptible to smoking. Having friends who smoke was the strongest predictor of both smoking status and susceptibility to smoking. Attendance at school classes that described the harmful effects of smoking had significant effects in reducing cigarette smoking. Girls who were exposed to billboard cigarette advertising were more likely to be susceptible to smoking than were those who had not seen advertisements.ConclusionOur findings highlight the need for pursuing school-based intervention programs in Vietnam and for countering tobacco advertising and marketing practices that target young women.

  17. Urinary 1-hydroxypyrene concentrations in Chinese coke oven workers relative to job category, respirator usage, and cigarette smoking

    Energy Technology Data Exchange (ETDEWEB)

    Bo Chen; Yunping Hu; Lixing Zheng; Qiangyi Wang; Yuanfen Zhou; Taiyi Jin [Fudan University, Shanghai (China). School of Public Health

    2007-09-15

    1-Hydroxypyrene (1-OHP) is a biomarker of recent exposure to polycyclic aromatic hydrocarbons (PAHs). We investigated whether urinary 1-OHP concentrations in Chinese coke oven workers (COWs) are modulated by job category, respirator usage, and cigarette smoking. The present cross-sectional study measured urinary 1-OHP concentrations in 197 COWs from Coking plant I and 250 COWs from Coking plant II, as well as 220 unexposed referents from Control plant I and 56 referents from Control plant II. Urinary 1-OHP concentrations (geometric mean, {mu}mol/mol creatinine) were 5.18 and 4.21 in workers from Coking plants I and II, respectively. The highest 1-OHP levels in urine were found among topside workers including lidmen, tar chasers, and whistlers. Benchmen had higher 1-OHP levels than other workers at the sideoven. Above 75% of the COWs exceeded the recommended occupational exposure limit of 2.3 {mu}mol/mol creatinine. Respirator usage and increased body mass index (BMI) slightly reduced 1-OHP levels in COWs. Cigarette smoking significantly increased urinary 1-OHP levels in unexposed referents but had no effect in COWs. Chinese COWs, especially topside workers and benchmen, are exposed to high levels of PAHs. Urinary 1-OHP concentrations appear to be modulated by respirator usage and BMI in COWs, as well as by smoking in unexposed referents.

  18. Cigarette smoking in pregnant substance users: Association with substance use and desire to quit.

    Science.gov (United States)

    Winhusen, Theresa; Lewis, Daniel

    2017-01-01

    Cigarette smoking is prevalent in pregnant substance users but receives low priority in substance use disorder treatment. This article reports the results of a secondary analysis of a randomized, multisite trial with 200 pregnant substance users, 145 (72.5%) of whom smoked at baseline. As predicted: (1) smokers had significantly greater substance use; (2) approximately half of smokers wanted to quit; and (3) smokers with a quit goal had significantly greater self-efficacy and lower perceived difficulty of quitting. Smoking may be associated with more severe substance use in pregnant substance-using patients, half of whom may be interested in smoking-cessation interventions.

  19. Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.

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    Fengjiao Yuan

    Full Text Available Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS or cigarette smoke extract (CSE. The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS and nitric oxide (NO and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the