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  1. 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.

  2. 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.

  3. Oxidative DNA damage is involved in cigarette smoke-induced lung injury in rats.

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    Chen, Zhihai; Wang, Dapeng; Liu, Xing; Pei, Weiwei; Li, Jianxiang; Cao, Yi; Zhang, Jie; An, Yan; Nie, Jihua; Tong, Jian

    2015-09-01

    Reactive oxygen species (ROS) induced by exogenous toxicants are suggested to be involved in carcinogenesis by oxidative modification of DNA. 8-Hydroxyl-2-deoxyguanosine (8-OHdG) has been considered as a reliable biomarker for oxidative DNA damage both in vivo and in vitro studies. But the effect of smoking on oxidative damage has not yet been fully elucidated. Wistar rats were exposed to cigarette smoke at concentrations of 20 and 60 % for 30 min, twice/day for 45 weeks. Then the histopathology of lung tissues, levels of ROS, 8-OHdG, and total antioxidant (T-AOC), expression of DNA repair enzymes, e.g. 8-oxyguaine DNA glycosylase (OGG1), and MutThomolog 1 (Oxidized Purine Nucleoside Triphosphatase, MTH1) were determined in urine, peripheral blood lymphocytes, and lung tissue. The results showed that long-term cigarette smoke exposure can cause obvious damages of lung tissue in rats. In addition, a significant and cigarette smoke concentration-dependent increase in ROS and 8-OHdG were observed compared with the non-exposed control rats. In contrast, the expression of OGG1 and MTH1, and T-AOC levels were obviously decreased after long-term exposure to cigarette smoke. These findings indicate that long-term exposure to cigarette smoker increases ROS levels, decreases total antioxidant capacity, and interferes DNA repair capacity that eventually induces oxidative DNA damage, which appears to play an important role in cigarette smoke-induced lung injury in rats, and determination of 8-OHdG levels might be a useful method for monitoring oxidative damage in cigarette smokers.

  4. Mechanisms of cigarette smoke-induced COPD: insights from animal models

    National Research Council Canada - National Science Library

    Andrew Churg; Manuel Cosio; Joanne L. Wright

    2008-01-01

    Cigarette smoke-induced animal models of chronic obstructive pulmonary disease support the protease-antiprotease hypothesis of emphysema, although which cells and proteases are the crucial actors remains controversial...

  5. Salidroside alleviates cigarette smoke-induced COPD in mice.

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    Luo, Fen; Liu, Jingyan; Yan, Tianhua; Miao, Mingxing

    2017-02-01

    The present study was to evaluate the effects of salidroside (Sal) on CS (cigarette smoke)-induced COPD in mice and explore its underlying mechanisms. 50 male ICR mice were randomly assigned to five groups: control group, CS group, CS+dexamethasone (2mg/kg) group, CS+salidroside (20mg/kg) group and CS+salidroside (40mg/kg) group. The COPD mice were induced by CS exposure for 8 weeks. The results of H&E staining demonstrated that Sal alleviated CS-induced pathological injury in lungs. Besides, Sal increased the activities of superoxide dismutase (SOD), reduced the content of malondialdehyde (MDA) in serum. Sal also inhibited the generations of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum and lungs. Furthermore, the administration of Sal significantly inhibited the protein levels of MAPK/NF-κB pathway in CS-induced mice. Our findings showed that Sal might effectively ameliorate the progression of COPD via MAPK/NF-κB pathway. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  6. Cigarette Smoke-Induced Collagen Destruction; Key to Chronic Neutrophilic Airway Inflammation?

    NARCIS (Netherlands)

    Overbeek, Saskia A.; Braber, Saskia; Koelink, Pim J.; Henricks, Paul A. J.; Mortaz, Esmaeil; Loi, Adele T. LoTam; Jackson, Patricia L.; Garssen, Johan; Wagenaar, Gerry T. M.; Timens, Wim; Koenderman, Leo; Blalock, J. Edwin; Kraneveld, Aletta D.; Folkerts, Gert

    2013-01-01

    Background: Cigarette smoking induces inflammatory responses in all smokers and is the major risk factor for lung disease such as chronic obstructive pulmonary disease (COPD). In this progressive disease, chronic inflammation in the lung contributes to lung tissue destruction leading to the formatio

  7. 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.

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

    NARCIS (Netherlands)

    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

  9. 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.

  10. 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

  11. Cigarette prices, cigarette expenditure and smoking-induced deprivation: findings from the International Tobacco Control Mexico survey.

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    Siahpush, Mohammad; Thrasher, James F; Yong, Hua H; Cummings, K Michael; Fong, Geoffrey T; de Miera, Belén Saenz; Borland, Ron

    2013-07-01

    Mexico implemented annual tax increases between 2009 and 2011. We examined among current smokers the association of price paid per cigarette and daily cigarette expenditure with smoking-induced deprivation (SID) and whether the association of price or expenditure with SID varies by income. We used data (n=2410) from three waves of the International Tobacco Control Mexico survey (ie, 2008, 2010, 2011) and employed logistic regression to estimate the association of price paid per cigarette and daily cigarette expenditure with the probability of SID ('In the last 6 months, have you spent money on cigarettes that you knew would be better spent on household essentials like food?'). Price paid per cigarette increased from Mex$1.24 in 2008, to Mex$1.36 in 2010, to Mex$1.64 in 2011. Daily cigarette expenditure increased from Mex$6.9, to Mex$7.6 and to Mex$8.4 in the 3 years. There was no evidence of an association between price and SID. However, higher expenditure was associated with a higher probability of SID. There was no evidence that the association of price or expenditure with SID varied by income. Tax increases in Mexico have resulted in smokers paying more and spending more for their cigarettes. Those with higher cigarette expenditure experience more SID, with no evidence that poorer smokers are more affected.

  12. 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.

  13. 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

    significantly blocked cigarette smoke-induced MMP-8 and -9 protein synthesis, while it had no significant effect on TIMP-1 and -4 protein synthesis even in the presence of cigarette smoke. Conclusion CSE resulted in imbalance of MMPs and TIMPs, and by which mechanism, cigarette smoke may lead to insufficient lung tissue repair. Simvastatin partially blocked airway inflammation and MMP production and, thus, statins may modulate composition of the lung extracellular matrix. PMID:28260878

  14. 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

    cigarette smoke-induced MMP-8 and -9 protein synthesis, while it had no significant effect on TIMP-1 and -4 protein synthesis even in the presence of cigarette smoke. CSE resulted in imbalance of MMPs and TIMPs, and by which mechanism, cigarette smoke may lead to insufficient lung tissue repair. Simvastatin partially blocked airway inflammation and MMP production and, thus, statins may modulate composition of the lung extracellular matrix.

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

    Directory of Open Access Journals (Sweden)

    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.

  16. Aging does not enhance experimental cigarette smoke-induced COPD in the mouse.

    Directory of Open Access Journals (Sweden)

    Steven Zhou

    Full Text Available It has been proposed that the development of COPD is driven by premature aging/premature senescence of lung parenchyma cells. There are data suggesting that old mice develop a greater inflammatory and lower anti-oxidant response after cigarette smoke compared to young mice, but whether these differences actually translate into greater levels of disease is unknown. We exposed C57Bl/6 female mice to daily cigarette smoke for 6 months starting at age 3 months (Ayoung@ or age 12 months (Aold@, with air-exposed controls. There were no differences in measures of airspace size between the two control groups and cigarette smoke induced exactly the same amount of emphysema in young and old. The severity of smoke-induced small airway remodeling using various measures was identical in both groups. Smoke increased numbers of tissue macrophages and neutrophils and levels of 8-hydroxyguanosine, a marker of oxidant damage, but there were no differences between young and old. Gene expression studies using laser capture microdissected airways and parenchyma overall showed a trend to lower levels in older animals and a somewhat lesser response to cigarette smoke in both airways and parenchyma but the differences were usually not marked. Telomere length was greatest in young control mice and was decreased by both smoking and age. The senescence marker p21(Waf1 was equally upregulated by smoke in young and old, but p16(INK4a, another senescence marker, was not upregulated at all. We conclude, in this model, animal age does not affect the development of emphysema and small airway remodeling.

  17. 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.

  18. Effect of simvastatin on MMPs and TIMPs in cigarette smoke-induced rat COPD model

    Directory of Open Access Journals (Sweden)

    Sun J

    2017-02-01

    /D: 0.160±0.034, P<0.01. In contrast, mean alveolar number was significantly decreased in the CSE group than that in the control group (13.5±2.0 of CSE vs 21.5±2.0 N/µm2 of control, P>0.01. 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, P<0.01, and it was significantly reduced by simvastatin (2.3±2.1×109 cells/L, P<0.01. CSE resulted in significantly increased accumulation of neutrophils and macrophages (neutrophils: 14.5%±1.3% of CSE group vs 9.1%±1.5% of control; macrophage: 91%±3% of CSE group vs 87%±2% of control, P<0.05, and simvastatin significantly reduced neutrophils (12.9%±2.0%, P<0.05 in the bronchoalveolar lavage fluid, but had no effect on macrophage (89%±1.6%, P>0.05. 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 (P<0.01, but had no effect on MMP-12, TIMP-1 and TIMP-4 mRNA (P>0.05. In addition, simvastatin significantly blocked cigarette smoke-induced MMP-8 and -9 protein synthesis, while it had no significant effect on TIMP-1 and -4 protein synthesis even in the presence of cigarette smoke.Conclusion: CSE resulted in imbalance of MMPs and TIMPs, and by which mechanism, cigarette smoke may lead to insufficient lung tissue repair. Simvastatin partially blocked airway inflammation and MMP production and, thus, statins may modulate composition of the lung extracellular matrix. Keywords: tissue injury, tissue repair, smoking

  19. Beta-Cryptoxanthin supplementation prevents cigarette smoke-induced lung inflammation, oxidative damage and squamous metaplasia in ferrets

    Science.gov (United States)

    In epidemiologic studies, high intake of beta-cryptoxanthin has been associated with a decreased risk of lung cancer, particularly among current smokers. However, data are not available from well-controlled animal studies to examine the effects of beta-cryptoxanthin on cigarette smoke-induced lung ...

  20. 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-induced

  1. Prevention of cigarette smoke induced lung cancer by low let ionizing radiation

    Energy Technology Data Exchange (ETDEWEB)

    Sanders, Charles L. [Korea Advanced Institute of Science and Technology, Daejeon (Korea, Republic of)

    2008-12-15

    Lung cancer is the most prevalent global cancer, {approx}90% of which is caused by cigarette smoking. The LNT hypothesis has been inappropriately applied to estimate lung cancer risk due to ionizing radiation. A threshold of {approx}1 Gy for lung cancer has been observed in never smokers. Lung cancer risk among nuclear workers, radiologists and diagnostically exposed patients was typically reduced by {approx}40% following exposure to <100 mSv low LET radiation. The consistency and magnitude of reduced lung cancer in nuclear workers and occurrence of reduced lung cancer in exposed non-worker populations could not be explained by the HWE. Ecologic studies of indoor radon showed highly significant reductions in lung cancer risk. A similar reduction in lung cancer was seen in a recent well designed case-control study of indoor radon, indicating that exposure to radon at the EPA action level is associated with a decrease of {approx}60% in lung cancer. A cumulative whole-body dose of {approx}1 Gy gamma rays is associated with a marked decrease in smoking-induced lung cancer in plutonium workers. Low dose, low LET radiation appears to increase apoptosis mediated removal of {alpha}-particle and cigarette smoke transformed pulmonary cells before they can develop into lung cancer.

  2. Cigarette smoke-induced collagen destruction; key to chronic neutrophilic airway inflammation?

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    Saskia A Overbeek

    Full Text Available BACKGROUND: Cigarette smoking induces inflammatory responses in all smokers and is the major risk factor for lung disease such as chronic obstructive pulmonary disease (COPD. In this progressive disease, chronic inflammation in the lung contributes to lung tissue destruction leading to the formation of chemotactic collagen fragments such as N-acetylated Proline-Glycine-Proline (N-ac-PGP. The generation of this tripeptide is mediated by a multistep pathway involving matrix metalloproteases (MMPs 8 and 9 and prolyl endopeptidase (PE. Here we investigated whether cigarette smoke extract (CSE stimulates human PMNs to breakdown whole matrix collagen leading to the generation of the chemotactic collagen fragment N-ac-PGP. METHODOLOGY/PRINCIPAL FINDINGS: Incubating PMNs with CSE led to the release of chemo-attractant CXCL8 and proteases MMP8 and MMP9. PMNs constitutively expressed PE activity as well as PE protein. Incubating CSE-primed PMNs with collagen resulted in collagen breakdown and in N-ac-PGP generation. Incubation of PMNs with the tripeptide N-ac-PGP resulted in the release of CXCL8, MMP8 and MMP9. Moreover, we tested whether PMNs from COPD patients are different from PMNs from healthy donors. Here we show that the intracellular basal PE activity of PMNs from COPD patients increased 25-fold compared to PMNs from healthy donors. Immunohistological staining of human lung tissue for PE showed that besides neutrophils, macrophages and epithelial cells express PE. CONCLUSIONS: This study indicates that neutrophils activated by cigarette smoke extract can breakdown collagen into N-ac-PGP and that this collagen fragment itself can activate neutrophils, which may lead in vivo to a self-propagating cycle of neutrophil infiltration, chronic inflammation and lung emphysema. MMP-, PE- or PGP-inhibitors can serve as an attractive therapeutic target and may open new avenues towards effective treatment of COPD.

  3. 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. Copyright © 2016. Published by Elsevier Ireland Ltd.

  4. Cigarette smoke-induced lung emphysema in mice is associated with prolyl endopeptidase, an enzyme involved in collagen breakdown

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    Koelink, Pim J.; Henricks, Paul A. J.; Jackson, Patricia L.; Nijkamp, Frans P.; Garssen, Johan; Kraneveld, Aletta D.; Blalock, J. Edwin; Folkerts, Gert

    2011-01-01

    There is increasing evidence that the neutrophil chemoattractant proline-glycine-proline (PGP), derived from the breakdown of the extracellular matrix, plays an important role in neutrophil recruitment to the lung. PGP formation is a multistep process involving neutrophils, metalloproteinases (MMPs), and prolyl endopeptidase (PE). This cascade of events is now investigated in the development of lung emphysema. A/J mice were whole body exposed to cigarette smoke for 20 wk. After 20 wk or 8 wk after smoking cessation, animals were killed, and bronchoalveolar lavage fluid and lung tissue were collected to analyze the neutrophilic airway inflammation, the MMP-8 and MMP-9 levels, the PE activity, and the PGP levels. Lung tissue degradation was assessed by measuring the mean linear intercept. Additionally, we investigated the effect of the peptide l-arginine-threonine-arginine (RTR), which binds to PGP sequences, on the smoke-induced neutrophil influx in the lung after 5 days of smoke exposure. Neutrophilic airway inflammation was induced by cigarette smoke exposure. MMP-8 and MMP-9 levels, PE activity, and PGP levels were elevated in the lungs of cigarette smoke-exposed mice. PE was highly expressed in epithelial and inflammatory cells (macrophages and neutrophils) in lung tissue of cigarette smoke-exposed mice. After smoking cessation, the neutrophil influx, the MMP-8 and MMP-9 levels, the PE activity, and the PGP levels were decreased or reduced to normal levels. Moreover, RTR inhibited the smoke-induced neutrophil influx in the lung after 5 days' smoke exposure. In the present murine model of cigarette smoke-induced lung emphysema, it is demonstrated for the first time that all relevant components (neutrophils, MMP-8, MMP-9, PE) involved in PGP formation from collagen are upregulated in the airways. Together with MMPs, PE may play an important role in the formation of PGP and thus in the pathophysiology of lung emphysema. PMID:21112944

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

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    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

  6. Could cigarette packaging be used as a tool to make prevention of smoke-induced respiratory diseases?

    Science.gov (United States)

    Sposato, Bruno; Lenzi, Piero Angelo; Carelli, Maria Rosaria

    2015-12-01

    The most important consequences of smoking are chronic obstructive pulmonary disease (COPD) and lung cancer (LC). Although the use of shocking images and warning messages on cigarette packaging is a valid tool of smoke dishabituation, unfortunately, millions of people go on smoking. Our hypotheses is that cigarette packet covers could also be used to give further messages, especially meant to spur also a screening of smoke-induced respiratory diseases. Messages on cigarette packaging suggesting smokers to perform a spirometry and a chest X-ray may persuade them not only to quit their habit but also to have a screening for COPD and LC prevention. If our hypotheses is taken into account it will have a strong worldwide impact.

  7. Cigarette smoke induces endoplasmic reticulum stress response and proteasomal dysfunction in human alveolar epithelial cells

    NARCIS (Netherlands)

    Somborac-Bacura, Anita; van der Toorn, Marco; Franciosi, Lorenza; Slebos, Dirk-Jan; Zanic-Grubisic, Tihana; Bischoff, Rainer; van Oosterhout, Antoon J. M.

    2013-01-01

    Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease. Cigarette smoke (CS) causes oxidative stress and severe damage to proteins in the lungs. One of the main systems to protect cells from the accumulation of damaged proteins is the ubiquitin-proteasome pathway. In th

  8. Proteomic Profiling of Cigarette Smoke Induced Changes in Retinal Pigment Epithelium Cells.

    Science.gov (United States)

    Merl-Pham, Juliane; Gruhn, Fabian; Hauck, Stefanie M

    2016-01-01

    Age-related macular degeneration (AMD) is a medical condition usually affecting older adults and resulting in a loss of vision in the macula, the center of the visual field. The dry form of this disease presents with atrophy of the retinal pigment epithelium, resulting in the detachment of the retina and loss of photoreceptors. Cigarette smoke is one main risk factor for dry AMD and increases the risk of developing the disease by three times. In order to understand the influence of cigarette smoke on retinal pigment epithelial cells, cultured human ARPE-19 cells were treated with cigarette smoke extract for 24 h. Using quantitative mass spectrometry more than 3000 proteins were identified and their respective abundances were compared between cigarette smoke-treated and untreated cells. Altogether 1932 proteins were quantified with at least two unique peptides, with 686 proteins found to be significantly differentially abundant with p > 0.05. Of these proteins the abundance of 64 proteins was at least 2-fold down-regulated after cigarette smoke treatment while 120 proteins were 2-fold up-regulated. The analysis of associated biological processes revealed an alteration of proteins involved in RNA processing and transport as well as extracellular matrix remodelling in response to cigarette smoke treatment.

  9. 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.

  10. 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

  11. 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.

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

    Science.gov (United States)

    Crane-Godreau, Mardi A; Black, Candice C; Giustini, Andrew J; Dechen, Tenzin; Ryu, Jihan; Jukosky, James A; Lee, Hong-Kee; Bessette, Katherine; Ratcliffe, Nora R; Hoopes, P Jack; Fiering, Steven; Kelly, John A; Leiter, J C

    2013-01-01

    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 (TIMP-1) ratio in VDD-CSE mice compared with all controls. Alpha-1 antitrypsin (A1AT) 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.

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

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    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.

  14. Inhibition by oral N-acetylcysteine of cigarette smoke-induced "bronchitis" in the rat.

    Science.gov (United States)

    Rogers, D F; Jeffery, P K

    1986-01-01

    Specific pathogen-free rats were exposed to the cigarette smoke (CS) of 25 cigarettes daily for 14 days and concurrently given N-acetylcysteine (Nac) as 1% of their drinking water (average daily dose 973 mg/kg). The thickness of the epithelium was measured at four airway levels and the numbers of mucus-containing secretory cells, stained for neutral or acidic glycoprotein (NGP or AGP respectively), were counted in surface epithelium at eight airway levels. Cigarette smoke increased the thickness of the epithelium at three of the airway levels studied by between 37 and 72%. The number of secretory cells was increased at all airway levels distal to the upper trachea by between 102 and 421%. Secretory cells containing NGP were reduced in number but this was more than offset by a large increase in the number of secretory cells containing AGP at all airway levels. N-acetylcysteine inhibited CS-induced epithelial thickening. Nac also inhibited the CS-induced increase in the number of secretory cells with AGP, but had little effect on the CS-induced reduction in the number of cells with NGP. Thus, prophylactic oral N-acetylcysteine led to an overall inhibition of CS-induced mucous cell hyperplasia and epithelial hypertrophy. The results suggest a novel anti-inflammatory action for a drug with known mucolytic effects.

  15. 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.

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

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    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

  17. Inhibitory effect of Chinese green tea on cigarette smoke-induced up-regulation of airway neutrophil elastase and matrix metalloproteinase-12 via antioxidant activity

    OpenAIRE

    Chan, CH; Yeung, SC; Man, RYK; Ip, MSM; Mak, JCW; Chan, KH

    2012-01-01

    Our recent study has indicated that Chinese green tea (Lung Chen), in which epigallocatechin-3-gallate (EGCG) accounts for 60% of catechins, protected cigarette smoke-induced lung injury. We now hypothesized that Lung Chen tea may also have potential effect on lung oxidative stress and proteases/anti-proteases in a smoking rat model. Sprague–Dawley rats were exposed to either sham air (SA) or 4% cigarette smoke (CS) plus 2% Lung Chen tea or water by oral gavage. Serine proteases, matrix metal...

  18. 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.

  19. Antioxidant Protective Effect of Honey in Cigarette Smoke-Induced Testicular Damage in Rats

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    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.

  20. (--Epigallocatechin-3-gallate Reduces Cigarette Smoke-Induced Airway Neutrophilic Inflammation and Mucin Hypersecretion in Rats

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    Yingmin Liang

    2017-09-01

    Full Text Available Background: Cigarette smoking is the leading cause of chronic obstructive pulmonary disease. (--Epigallocatechin-3-gallate (EGCG, the major catechins in Chinese green tea, has been studied for its anti-oxidative and anti-inflammatory properties in cell and animal models. In this study, we aimed to analyze the effects of EGCG on cigarette smoke (CS-induced airway inflammation and mucus secretion in the CS-exposed rat model.Methods: Male Sprague-Dawley rats were randomly divided into either sham air (SA or CS exposure. EGCG (50 mg/kg b.wt. was given by oral gavage every other day in both SA and CS-exposed animals. Oxidative stress and inflammatory markers were determined in serum and/or bronchoalveolar lavage fluid by biochemical assays or ELISA. Lung morphological changes were examined by Periodic Acid-Schiff, Masson’s Trichrome staining and immunohistochemical analysis. Western blot analysis was performed to explore the effects of EGCG on epidermal growth factor receptor (EGFR-mediated signaling pathway.Results: (--Epigallocatechin-3-gallate treatment attenuated CS-induced oxidative stress, lung cytokine-induced neutrophil chemoattractant-1 release and neutrophil recruitment. CS exposure caused an increase in the number of goblet cells in line with MUC5AC upregulation, and increased lung collagen deposition, which were alleviated in the presence of EGCG. In addition, CS-induced phosphorylation of EGFR in rat lung was abrogated by EGCG treatment.Conclusion: (--Epigallocatechin-3-gallate treatment ameliorated CS-induced oxidative stress and neutrophilic inflammation, as well as airway mucus production and collagen deposition in rats. The present findings suggest that EGCG has a therapeutic effect on chronic airway inflammation and abnormal airway mucus production probably via inhibition of EGFR signaling pathway.

  1. Attenuation of cigarette smoke-induced airway mucus production by hydrogen-rich saline in rats.

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    Yunye Ning

    Full Text Available BACKGROUND: Over-production of mucus is an important pathophysiological feature in chronic airway disease such as chronic obstructive pulmonary disease (COPD and asthma. Cigarette smoking (CS is the leading cause of COPD. Oxidative stress plays a key role in CS-induced airway abnormal mucus production. Hydrogen protected cells and tissues against oxidative damage by scavenging hydroxyl radicals. In the present study we investigated the effect of hydrogen on CS-induced mucus production in rats. METHODS: Male Sprague-Dawley rats were divided into four groups: sham control, CS group, hydrogen-rich saline pretreatment group and hydrogen-rich saline control group. Lung morphology and tissue biochemical changes were determined by immunohistochemistry, Alcian Blue/periodic acid-Schiff staining, TUNEL, western blot and realtime RT-PCR. RESULTS: Hydrogen-rich saline pretreatment attenuated CS-induced mucus accumulation in the bronchiolar lumen, goblet cell hyperplasia, muc5ac over-expression and abnormal cell apoptosis in the airway epithelium as well as malondialdehyde increase in the BALF. The phosphorylation of EGFR at Tyr1068 and Nrf2 up-regulation expression in the rat lungs challenged by CS exposure were also abrogated by hydrogen-rich saline. CONCLUSION: Hydrogen-rich saline pretreatment ameliorated CS-induced airway mucus production and airway epithelium damage in rats. The protective role of hydrogen on CS-exposed rat lungs was achieved at least partly by its free radical scavenging ability. This is the first report to demonstrate that intraperitoneal administration of hydrogen-rich saline protected rat airways against CS damage and it could be promising in treating abnormal airway mucus production in COPD.

  2. Different regulation of cigarette smoke induced inflammation in upper versus lower airways

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    Bracke Ken R

    2010-07-01

    Full Text Available Abstract Background Cigarette smoke (CS is known to initiate a cascade of mediator release and accumulation of immune and inflammatory cells in the lower airways. We investigated and compared the effects of CS on upper and lower airways, in a mouse model of subacute and chronic CS exposure. Methods C57BL/6 mice were whole-body exposed to mainstream CS or air, for 2, 4 and 24 weeks. Bronchoalveolar lavage fluid (BAL was obtained and tissue cryosections from nasal turbinates were stained for neutrophils and T cells. Furthermore, we evaluated GCP-2, KC, MCP-1, MIP-3α, RORc, IL-17, FoxP3, and TGF-β1 in nasal turbinates and lungs by RT-PCR. Results In both upper and lower airways, subacute CS-exposure induced the expression of GCP-2, MCP-1, MIP-3α and resulted in a neutrophilic influx. However, after chronic CS-exposure, there was a significant downregulation of inflammation in the upper airways, while on the contrary, lower airway inflammation remained present. Whereas nasal FoxP3 mRNA levels already increased after 2 weeks, lung FoxP3 mRNA increased only after 4 weeks, suggesting that mechanisms to suppress inflammation occur earlier and are more efficient in nose than in lungs. Conclusions Altogether, these data demonstrate that CS induced inflammation may be differently regulated in the upper versus lower airways in mice. Furthermore, these data may help to identify new therapeutic targets in this disease model.

  3. Protection from Cigarette Smoke-Induced Lung Dysfunction and Damage by H2 Relaxin (Serelaxin).

    Science.gov (United States)

    Pini, Alessandro; Boccalini, Giulia; Lucarini, Laura; Catarinicchia, Stefano; Guasti, Daniele; Masini, Emanuela; Bani, Daniele; Nistri, Silvia

    2016-06-01

    Cigarette smoke (CS) is the major etiologic factor of chronic obstructive pulmonary disease (COPD), which is characterized by airway remodeling, lung inflammation and fibrosis, emphysema, and respiratory failure. The current therapies can improve COPD management but cannot arrest its progression and reduce mortality. Hence, there is a major interest in identifying molecules susceptible of development into new drugs to prevent or reduce CS-induced lung injury. Serelaxin (RLX), or recombinant human relaxin-2, is a promising candidate because of its anti-inflammatory and antifibrotic properties highlighted in lung disease models. Here, we used a guinea pig model of CS-induced lung inflammation, and remodeling reproducing some of the hallmarks of COPD. Animals exposed chronically to CS (8 weeks) were treated with vehicle or RLX, delivered by osmotic pumps (1 or 10 μg/day) or aerosol (10 μg/ml/day) during CS treatment. Controls were nonsmoking animals. RLX maintained airway compliance to a control-like pattern, likely because of its capability to counteract lung inflammation and bronchial remodeling. In fact, treatment of CS-exposed animals with RLX reduced the inflammatory recruitment of leukocytes, accompanied by a significant reduction of the release of proinflammatory cytokines (tumor necrosis factor α and interleukin-1β). Moreover, RLX was able to counteract the adverse bronchial remodeling and emphysema induced by CS exposure by reducing goblet cell hyperplasia, smooth muscle thickening, and fibrosis. Of note, RLX delivered by aerosol has shown a comparable efficacy to systemic administration in reducing CS-induced lung dysfunction and damage. In conclusion, RLX emerges as a new molecule to counteract CS-induced inflammatory lung diseases.

  4. The influence of 5-lipoxygenase on cigarette smoke-induced emphysema in mice.

    Science.gov (United States)

    Kennedy-Feitosa, Emanuel; Pinto, Rômulo Fonseca Santos; Pires, Karla Maria Pereira; Monteiro, Ana Paula Teixeira; Machado, Mariana Nascimento; Santos, Juliana Carvalho; Ribeiro, Marcelo Lima; Zin, Walter Araújo; Canetti, Cláudio Azevedo; Romana-Souza, Bruna; Porto, Luís Cristóvão; Valenca, Samuel Santos

    2014-01-01

    Pulmonary emphysema is characterized by the loss of lung architecture. Our hypothesis is that the inhibition of 5-lipoxygenase (5-LO) production may be an important strategy to reduce inflammation, oxidative stress, and metalloproteinases in lung tissue resulting from cigarette smoke (CS)-induced emphysema. 5-LO knockout (129S2-Alox5(tm1Fun)/J) and wild-type (WT) mice (129S2/SvPas) were exposed to CS for 60days. Mice exposed to ambient air were used as Controls. Oxidative, inflammatory, and proteolytic markers were analyzed. The alveolar diameter was decreased in CS 5-LO(-/-) mice when compared with the WT CS group. The CS exposure resulted in less pronounced pulmonary inflammation in the CS 5-LO(-/-) group. The CS 5-LO(-/-) group showed leukotriene B4 values comparable to those of the Control group. The expression of MMP-9 was decreased in the CS 5-LO(-/-) group when compared with the CS WT group. The expression of superoxide dismutase, catalase, and glutathione peroxidase were decreased in the CS 5-LO(-/-) group when compared with the Control group. The protein expression of nuclear factor (erythroid-derived 2)-like 2 was reduced in the CS 5-LO(-/-) group when compared to the CS WT group. In conclusion, we show for the first time that 5-LO deficiency protects 129S2 mice against emphysema caused by CS. We suggest that the main mechanism of pathogenesis in this model involves the imbalance between proteases and antiproteases, particularly the association between MMP-9 and TIMP-1. General significance This study demonstrates the influence of 5-LO mediated oxidative stress, inflammation, and proteolytic markers in CS exposed mice. © 2013.

  5. Genetic ablation of CXCR2 protects against cigarette smoke-induced lung inflammation and injury

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    Chad A Lerner

    2016-10-01

    Full Text Available Antagonism of CXCR2 receptors, predominately located on neutrophils and critical for their immunomodulatory activity, is an attractive pharmacological therapeutic approach aimed at reducing the potentially damaging effects of heightened neutrophil influx into the lung caused by environmental agents including tobacco smoke. The role CXCR2 in lung inflammation in response to cigarette smoke (CS inhalation using the mutant mouse approach is not known. We hypothesized that genetic ablation of CXCR2 would protect mice against CS-induced inflammation and DNA damaging response. We used CXCR2 -/- deficient/mutant (knock-out, KO mice, and assessed the changes in critical lung inflammatory NF-B-driven chemokines released from the parenchyma of CS-exposed mice, and indications of the extent of tissue damage assessed by the number of DNA damaging γH2AX positive cells. CXCR2 KO mice exhibited protection from heightened levels of neutrophils measured in BALF taken from mice exposed to CS. IL-8 (KC mouse levels in the BALF from CS-exposed CXCR2 KO were elevated compared to WT. IL-6 levels in BALF were refractory to increase by CS in CXCR2 KO mice. There were no significant changes to MIP-2, MCP-1, or IL-1β. Total levels of NF-κB were maintained at lower levels in CS-exposed CXCR2 KO mice compared to WT mice exposed to CS. Finally CXCR2 KO mice were protected from increased number of lung cells positive for DNA damage response and senescence marker γH2AX, CXCR2 KO mice are protected from heightened inflammatory response mediated by increased neutrophil response as a result of acute 3 day CS exposure. This is also associated with changes in pro-inflammatory chemokines and reduced incursion of γH2AX indicating CXCR2 deficient mice are protected from lung injury. Thus CXCR2 may be a pharmacological target in setting of inflammation and DNA damage in the pathogenesis of COPD.

  6. A murine model of elastase- and cigarette smoke-induced emphysema.

    Science.gov (United States)

    Rodrigues, Rubia; Olivo, Clarice Rosa; Lourenço, Juliana Dias; Riane, Alyne; Cervilha, Daniela Aparecida de Brito; Ito, Juliana Tiyaki; Martins, Milton de Arruda; Lopes, Fernanda Degobbi Tenório Quirino Dos Santos

    2017-01-01

    To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS) and instillation of porcine pancreatic elastase (PPE). A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution); PPE (two intranasal instillations of PPE); CS (CS exposure for 60 days); and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days). At the end of the experimental protocol, all animals were anesthetized and tracheostomized for calculation of respiratory mechanics parameters. Subsequently, all animals were euthanized and their lungs were removed for measurement of the mean linear intercept (Lm) and determination of the numbers of cells that were immunoreactive to macrophage (MAC)-2 antigen, matrix metalloproteinase (MMP)-12, and glycosylated 91-kDa glycoprotein (gp91phox) in the distal lung parenchyma and peribronchial region. Although there were no differences among the four groups regarding the respiratory mechanics parameters assessed, there was an increase in the Lm in the CS + PPE group. The numbers of MAC-2-positive cells in the peribronchial region and distal lung parenchyma were higher in the CS + PPE group than in the other groups, as were the numbers of cells that were positive for MMP-12 and gp91phox, although only in the distal lung parenchyma. Our model of emphysema induced by a combination of PPE instillation and CS exposure results in a significant degree of parenchymal destruction in a shorter time frame than that employed in other models of CS-induced emphysema, reinforcing the importance of protease-antiprotease imbalance and oxidant-antioxidant imbalance in the pathogenesis of emphysema. Descrever um modelo murino de enfisema induzido por exposição a fumaça de cigarro (FC) e instilação de elastase pancreática porcina (EPP). Trinta e oito camundongos C57BL/6 foram aleatoriamente divididos em quatro grupos: controle (uma instilação intranasal

  7. Recuperating lung decoction attenuates inflammation and oxidation in cigarette smoke-induced COPD in rats via activation of ERK and Nrf2 pathways.

    Science.gov (United States)

    Li, Chunlei; Yan, Yue; Shi, Qi; Kong, Yanhua; Gao, Longxia; Bao, Haipeng; Li, Youlin

    2017-07-01

    Oxidative/antioxidative imbalance and chronic inflammation are the main contributors to the pathogenesis of chronic obstructive pulmonary disease (COPD). This study evaluated the effect of recuperating lung decoction (RLD) on inflammation and oxidative stress in rats with COPD induced by cigarette smoke and lipopolysaccharides (LPS). We used intravenous infusion of LPS combined with cigarette smoke exposure as a COPD rat model. We observed that RLD treatment increased the protein level of GSH and the ratio of GSH/GSSG but decreased 8-OHdG and 4-HNE in the serum. Furthermore, RLD significantly inhibited the expressions of IL-1β, IL-6, TNF-α, and TGF-β induced by cigarette smoke exposure, reduced the number of inflammatory cells in the bronchoalveolar lavage fluid, and alleviated the severity of cigarette smoke-induced emphysema. Mechanistically, RLD treatment prevented disease through downregulation of phosphorylated-ERK and Nrf2 expression, which regulates the production of proinflammatory cytokines. RLD treatment exerted a dramatic therapeutic effect on COPD. This study revealed a mechanism that RLD functions on the regulation of ERK signalling to inhibit inflammation. Copyright © 2017 John Wiley & Sons, Ltd.

  8. Human Tubal-Derived Mesenchymal Stromal Cells Associated with Low Level Laser Therapy Significantly Reduces Cigarette Smoke-Induced COPD in C57BL/6 mice.

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    Jean Pierre Schatzmann Peron

    Full Text Available Cigarette smoke-induced chronic obstructive pulmonary disease is a very debilitating disease, with a very high prevalence worldwide, which results in a expressive economic and social burden. Therefore, new therapeutic approaches to treat these patients are of unquestionable relevance. The use of mesenchymal stromal cells (MSCs is an innovative and yet accessible approach for pulmonary acute and chronic diseases, mainly due to its important immunoregulatory, anti-fibrogenic, anti-apoptotic and pro-angiogenic. Besides, the use of adjuvant therapies, whose aim is to boost or synergize with their function should be tested. Low level laser (LLL therapy is a relatively new and promising approach, with very low cost, no invasiveness and no side effects. Here, we aimed to study the effectiveness of human tube derived MSCs (htMSCs cell therapy associated with a 30mW/3J-660 nm LLL irradiation in experimental cigarette smoke-induced chronic obstructive pulmonary disease. Thus, C57BL/6 mice were exposed to cigarette smoke for 75 days (twice a day and all experiments were performed on day 76. Experimental groups receive htMSCS either intraperitoneally or intranasally and/or LLL irradiation either alone or in association. We show that co-therapy greatly reduces lung inflammation, lowering the cellular infiltrate and pro-inflammatory cytokine secretion (IL-1β, IL-6, TNF-α and KC, which were followed by decreased mucus production, collagen accumulation and tissue damage. These findings seemed to be secondary to the reduction of both NF-κB and NF-AT activation in lung tissues with a concomitant increase in IL-10. In summary, our data suggests that the concomitant use of MSCs + LLLT may be a promising therapeutic approach for lung inflammatory diseases as COPD.

  9. N-acetylcysteine increases the frequency of bone marrow pro-B/pre-B cells, but does not reverse cigarette smoking-induced loss of this subset.

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    Victoria L Palmer

    Full Text Available BACKGROUND: We previously showed that mice exposed to cigarette smoke for three weeks exhibit loss of bone marrow B cells at the Pro-B-to-pre-B cell transition, but the reason for this is unclear. The antioxidant N-acetylcysteine (NAC, a glutathione precursor, has been used as a chemopreventive agent to reduce adverse effects of cigarette smoke exposure on lung function. Here we determined whether smoke exposure impairs B cell development by inducing cell cycle arrest or apoptosis, and whether NAC treatment prevents smoking-induced loss of developing B cells. METHODOLOGY/PRINCIPAL FINDINGS: Groups of normal mice were either exposed to filtered room air or cigarette smoke with or without concomitant NAC treatment for 5 days/week for three weeks. Bone marrow B cell developmental subsets were enumerated, and sorted pro-B (B220(+CD43(+ and pre-B (B220(+CD43(- cell fractions were analyzed for cell cycle status and the percentage of apoptotic cells. We find that, compared to sham controls, smoke-exposed mice have ∼60% fewer pro-B/pre-B cells, regardless of NAC treatment. Interestingly, NAC-treated mice show a 21-38% increase in total bone marrow cellularity and lymphocyte frequency and about a 2-fold increase in the pro-B/pre-B cell subset, compared to sham-treated controls. No significant smoking- or NAC-dependent differences were detected in frequency of apoptotic cells or the percentage cells in the G1, S, or G2 phases of the cycle. CONCLUSIONS/SIGNIFICANCE: The failure of NAC treatment to prevent smoking-induced loss of bone marrow pre-B cells suggests that oxidative stress is not directly responsible for this loss. The unexpected expansion of the pro-B/pre-B cell subset in response to NAC treatment suggests oxidative stress normally contributes to cell loss at this developmental stage, and also reveals a potential side effect of therapeutic administration of NAC to prevent smoking-induced loss of lung function.

  10. P21-PARP-1 Pathway Is Involved in Cigarette Smoke-Induced Lung DNA Damage and Cellular Senescence

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    Yao, Hongwei; Sundar, Isaac K.; Gorbunova, Vera; Rahman, Irfan

    2013-01-01

    Persistent DNA damage triggers cellular senescence, which may play an important role in the pathogenesis of cigarette smoke (CS)-induced lung diseases. Both p21CDKN1A (p21) and poly(ADP-ribose) polymerase-1 (PARP-1) are involved in DNA damage and repair. However, the role of p21-PARP-1 axis in regulating CS-induced lung DNA damage and cellular senescence remains unknown. We hypothesized that CS causes DNA damage and cellular senescence through a p21-PARP-1 axis. To test this hypothesis, we determined the levels of γH2AX (a marker for DNA double-strand breaks) as well as non-homologous end joining proteins (Ku70 and Ku80) in lungs of mice exposed to CS. We found that the level of γH2AX was increased, whereas the level of Ku70 was reduced in lungs of CS-exposed mice. Furthermore, p21 deletion reduced the level of γH2AX, but augmented the levels of Ku70, Ku80, and PAR in lungs by CS. Administration of PARP-1 inhibitor 3-aminobenzamide increased CS-induced DNA damage, but lowered the levels of Ku70 and Ku80, in lungs of p21 knockout mice. Moreover, 3-aminobenzamide increased senescence-associated β-galactosidase activity, but decreased the expression of proliferating cell nuclear antigen in mouse lungs in response to CS. Interestingly, 3-aminobenzamide treatment had no effect on neutrophil influx into bronchoalveolar lavage fluid by CS. These results demonstrate that the p21-PARP-1 pathway is involved in CS-induced DNA damage and cellular senescence. PMID:24244594

  11. P21-PARP-1 pathway is involved in cigarette smoke-induced lung DNA damage and cellular senescence.

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    Hongwei Yao

    Full Text Available Persistent DNA damage triggers cellular senescence, which may play an important role in the pathogenesis of cigarette smoke (CS-induced lung diseases. Both p21(CDKN1A (p21 and poly(ADP-ribose polymerase-1 (PARP-1 are involved in DNA damage and repair. However, the role of p21-PARP-1 axis in regulating CS-induced lung DNA damage and cellular senescence remains unknown. We hypothesized that CS causes DNA damage and cellular senescence through a p21-PARP-1 axis. To test this hypothesis, we determined the levels of γH2AX (a marker for DNA double-strand breaks as well as non-homologous end joining proteins (Ku70 and Ku80 in lungs of mice exposed to CS. We found that the level of γH2AX was increased, whereas the level of Ku70 was reduced in lungs of CS-exposed mice. Furthermore, p21 deletion reduced the level of γH2AX, but augmented the levels of Ku70, Ku80, and PAR in lungs by CS. Administration of PARP-1 inhibitor 3-aminobenzamide increased CS-induced DNA damage, but lowered the levels of Ku70 and Ku80, in lungs of p21 knockout mice. Moreover, 3-aminobenzamide increased senescence-associated β-galactosidase activity, but decreased the expression of proliferating cell nuclear antigen in mouse lungs in response to CS. Interestingly, 3-aminobenzamide treatment had no effect on neutrophil influx into bronchoalveolar lavage fluid by CS. These results demonstrate that the p21-PARP-1 pathway is involved in CS-induced DNA damage and cellular senescence.

  12. Cigarette smoke-induced blockade of the mitochondrial respiratory chain switches lung epithelial cell apoptosis into necrosis

    NARCIS (Netherlands)

    van der Toorn, Marco; Slebos, Dirk-Jan; de Bruin, Harold G.; Leuvenink, Henri G.; Bakker, Stephan J. L.; Gans, Rijk O. B.; Koeter, Gerard H.; van Oosterhout, Antoon J. M.; Kauffman, Henk F.

    2007-01-01

    Increased lung cell apoptosis and necrosis occur in patients with chronic obstructive pulmonary disease ( COPD). Mitochondria are crucially involved in the regulation of these cell death processes. Cigarette smoke is the main risk factor for development of COPD. We hypothesized that cigarette smoke

  13. Role of extracellular signal-regulated kinase 1/2 in cigarette smoke-induced mucus hypersecretion in a rat model

    Institute of Scientific and Technical Information of China (English)

    XIAO Jun; WANG Ke; FENG Yu-lin; CHEN Xue-rong; XU Dan; ZHANG Ming-ke

    2011-01-01

    Background Airway mucus hypersecretion is an important pathophysiological feature of chronic obstructive pulmonary disease,which is closely associated with cigarette smoking.However,the signal transduction pathway from the cell surface to the nucleus through which cigarette smoke causes upregulation of mucin gene expression is not well known.This study was designed to investigate the role of extracellular signal-regulated Kinase 1/2 (ERK 1/2) in airway mucus hypersecretion induced by cigarette smoke in rats.Methods A rat model of airway mucus hypersecretion was induced by exposure to cigarette smoke for 4 weeks.Rats exposed to inhalation of cigarette smoke or normal saline were given an intraperitoneal injection of U0126,a specific MEK1 kinase inhibitor,at doses of 0.25 mg/kg,0.5 mg/kg and 1 mg/kg for 14 days.Expression of MUC5AC mRNA and protein,ERK 1/2 and phosphorylated-ERK 1/2 (p-ERK 1/2) were detected by RT-PCR,immunohistochemistry and Western blotting.Results Cigarette smoke significantly increased airway goblet cells metaplasia,induced the overexpression of MUG5AC mRNA and protein in bronchial epithelia,and increased the ratio of p-ERK 1/2 and ERK 1/2.U0126 significantly attentuated the expression of MUC5AC mRNA and protein induced by cigarette smoke (P <0.05).Moreover,there was a significant positive correlation between the ratio of p-ERK1/2 to ERK1/2 and the expression of MUC5AC mRNA and protein (P<0.05).Conclusions Inhibition of ERK 1/2 by U0126 decreased the ratio of p-ERK 1/2 to ERK 1/2 and expression of MUC5AC mRNA and protein.ERK 1/2 may play an essential role in cigarette smoke-induced mucus hypersecretion in vivo.

  14. Sestrin-2, a repressor of PDGFRβ signalling, promotes cigarette-smoke-induced pulmonary emphysema in mice and is upregulated in individuals with COPD

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    Juliana Heidler

    2013-11-01

    Chronic obstructive pulmonary disease (COPD is a leading cause of morbidity and mortality worldwide. COPD is caused by chronic exposure to cigarette smoke and/or other environmental pollutants that are believed to induce reactive oxygen species (ROS that gradually disrupt signalling pathways responsible for maintaining lung integrity. Here we identify the antioxidant protein sestrin-2 (SESN2 as a repressor of PDGFRβ signalling, and PDGFRβ signalling as an upstream regulator of alveolar maintenance programmes. In mice, the mutational inactivation of Sesn2 prevents the development of cigarette-smoke-induced pulmonary emphysema by upregulating PDGFRβ expression via a selective accumulation of intracellular superoxide anions (O2−. We also show that SESN2 is overexpressed and PDGFRβ downregulated in the emphysematous lungs of individuals with COPD and to a lesser extent in human lungs of habitual smokers without COPD, implicating a negative SESN2-PDGFRβ interrelationship in the pathogenesis of COPD. Taken together, our results imply that SESN2 could serve as both a biomarker and as a drug target in the clinical management of COPD.

  15. Inhibitory effect of Chinese green tea on cigarette smoke-induced up-regulation of airway neutrophil elastase and matrix metalloproteinase-12 via antioxidant activity.

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    Chan, Ka Ho; Chan, Stanley Chi Hang; Yeung, Sze Chun; Man, Ricky Ying Keung; Ip, Mary Sau Man; Mak, Judith Choi Wo

    2012-09-01

    Our recent study has indicated that Chinese green tea (Lung Chen), in which epigallocatechin-3-gallate (EGCG) accounts for 60% of catechins, protected cigarette smoke-induced lung injury. We now hypothesized that Lung Chen tea may also have potential effect on lung oxidative stress and proteases/anti-proteases in a smoking rat model. Sprague-Dawley rats were exposed to either sham air (SA) or 4% cigarette smoke (CS) plus 2% Lung Chen tea or water by oral gavage. Serine proteases, matrix metalloproteinases (MMPs) and their respective endogenous inhibitors were determined in bronchoalveolar lavage (BAL) and lung tissues by gelatin/casein zymography and biochemical assays. Green tea consumption significantly decreased CS-induced elevation of lung lipid peroxidation marker, malondialdehyde (MDA), and CS-induced up-regulation of neutrophil elastase (NE) concentration and activity along with that of α(1)-antitrypsin (α(1)-AT) and secretory leukoproteinase inhibitor (SLPI) in BAL and lung. In parallel, significant elevation of MMP-12 activity was found in BAL and lung of the CS-exposed group, which returned to the levels of SA-exposed group after green tea consumption but not CS-induced reduction of tissue inhibitor of metalloproteinase (TIMP)-1 activity, which was not reversed by green tea consumption. Taken together, our data supported the presence of local oxidative stress and protease/anti-protease imbalance in the airways after CS exposure, which might be alleviated by green tea consumption through its biological antioxidant activity.

  16. A novel anti-inflammatory and pro-resolving role for resolvin D1 in acute cigarette smoke-induced lung inflammation.

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    Hsi-Min Hsiao

    Full Text Available Cigarette smoke is a profound pro-inflammatory stimulus that contributes to acute lung injuries and to chronic lung disease including COPD (emphysema and chronic bronchitis. Until recently, it was assumed that resolution of inflammation was a passive process that occurred once the inflammatory stimulus was removed. It is now recognized that resolution of inflammation is a bioactive process, mediated by specialized lipid mediators, and that normal homeostasis is maintained by a balance between pro-inflammatory and pro-resolving pathways. These novel small lipid mediators, including the resolvins, protectins and maresins, are bioactive products mainly derived from dietary omega-3 and omega-6 polyunsaturated fatty acids (PUFA. We hypothesize that resolvin D1 (RvD1 has potent anti-inflammatory and pro-resolving effects in a model of cigarette smoke-induced lung inflammation.Primary human lung fibroblasts, small airway epithelial cells and blood monocytes were treated with IL-1β or cigarette smoke extract in combination with RvD1 in vitro, production of pro-inflammatory mediators was measured. Mice were exposed to dilute mainstream cigarette smoke and treated with RvD1 either concurrently with smoke or after smoking cessation. The effects on lung inflammation and lung macrophage populations were assessed.RvD1 suppressed production of pro-inflammatory mediators by primary human cells in a dose-dependent manner. Treatment of mice with RvD1 concurrently with cigarette smoke exposure significantly reduced neutrophilic lung inflammation and production of pro-inflammatory cytokines, while upregulating the anti-inflammatory cytokine IL-10. RvD1 promoted differentiation of alternatively activated (M2 macrophages and neutrophil efferocytosis. RvD1 also accelerated the resolution of lung inflammation when given after the final smoke exposure.RvD1 has potent anti-inflammatory and pro-resolving effects in cells and mice exposed to cigarette smoke. Resolvins

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

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    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.

  18. Muscarinic M3 receptors on structural cells regulate cigarette smoke-induced neutrophilic airway inflammation in mice

    NARCIS (Netherlands)

    Kistemaker, Loes E.M.; van Os, Ronald P.; Dethmers-Ausema, Albertina; Bos, I. Sophie T.; Hylkema, Machteld N.; van den Berge, Maarten; Hiemstra, Pieter S; Wess, Jürgen; Meurs, Herman; Kerstjens, Huib A.M.; Gosens, Reinoud

    2015-01-01

    Anticholinergics, blocking the muscarinic M-3 receptor, are effective bronchodilators for patients with chronic obstructive pulmonary disease. Recent evidence from M-3 receptor-deficient mice (M3R-/-) indicates that M-3 receptors also regulate neutrophilic inflammation in response to cigarette smoke

  19. 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

  20. 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

  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

  2. Cigarette smoke-induced accumulation of lung dendritic cells is interleukin-1α-dependent in mice

    Science.gov (United States)

    2012-01-01

    Background Evidence suggests that dendritic cells accumulate in the lungs of COPD patients and correlate with disease severity. We investigated the importance of IL-1R1 and its ligands IL-1α and β to dendritic cell accumulation and maturation in response to cigarette smoke exposure. Methods Mice were exposed to cigarette smoke using a whole body smoke exposure system. IL-1R1-, TLR4-, and IL-1α-deficient mice, as well as anti-IL-1α and anti-IL-1β blocking antibodies were used to study the importance of IL-1R1 and TLR4 to dendritic cell accumulation and activation. Results Acute and chronic cigarette smoke exposure led to increased frequency of lung dendritic cells. Accumulation and activation of dendritic cells was IL-1R1/IL-1α dependent, but TLR4- and IL-1β-independent. Corroborating the cellular data, expression of CCL20, a potent dendritic cells chemoattractant, was IL-1R1/IL-1α-dependent. Studies using IL-1R1 bone marrow-chimeric mice revealed the importance of IL-1R1 signaling on lung structural cells for CCL20 expression. Consistent with the importance of dendritic cells in T cell activation, we observed decreased CD4+ and CD8+ T cell activation in cigarette smoke-exposed IL-1R1-deficient mice. Conclusion Our findings convey the importance of IL-1R1/IL-1α to the recruitment and activation of dendritic cells in response to cigarette smoke exposure. PMID:22992200

  3. Pathogenesis of cigarette smoke-induced chronic obstructive pulmonary disease and therapeutic effects of glucocorticoids and N-acetylcysteine in rats

    Institute of Scientific and Technical Information of China (English)

    徐凌; 蔡柏蔷; 朱元珏

    2004-01-01

    Background T lymphocytes and matrix metalloproteinase (MMP) play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the details of the mechanisms involved are unclear. The aims of this study were to investigate the changes in interferon-γ (IFN-γ), interleukin-4 (IL-4), MMP-9, MMP-12 and tissue inhibitor of metalloproteinase-1 (TIMP-1) levels in a smoke-induced COPD rat model and the therapeutic effects of glucocorticoids and N-acetylcysteine.Methods Male Wistar rats were exposed to cigarette smoke for 3.5 months. Budesonide or N-acetylcysteine was given in the last month. Lung function was measured at the end of the study. IL-4 and IFN-γ levels were then determined in bronchoalveolar lavage fluid and lung tissue samples by enzyme-linked immunosorbent assay. The expression of MMP-9, MMP-12 and TIMP-1 mRNA in lung tissue was determined by RT-PCR. Results In comparison with the control group, rats exposed to smoke had a significant increase in IL-4 and MMP-12 levels and a significant decrease in IFN-γ levels. In addition, the IL-4/ IFN-γ ratio and MMP-12/TIMP-1 ratio were both higher. At the same time, the ratio of forced expiratory volume in 0.3 second to forced vital capacity (FEV0.3/FVC) and dynamic compliance (Cdyn) decreased and expiratory resistance (Re) increased. By measuring pulmonary mean linear intercept and mean alveolar numbers, obvious emphysematous changes were observed in the smoke exposed group. After treatment with budesonide, IL-4 and MMP-12 decreased and IFN-γ increased. The IL-4/IFN-γ ratio returned to normal, though the MMP-12/TIMP-1 ratio remained unchanged. FEV0.3/FVC was significantly higher and Re was significantly lower than that in untreated smoke exposed rats. No significant differences were found in pulmonary mean linear intercept and mean alveolar numbers. After treatment with N-acetylcysteine, IFN-γ increased and the IL-4/IFN-γ ratio decreased. The MMP-12/TIMP-1 ratio remained

  4. Essential amino acid leucine and proteasome inhibitor MG132 attenuate cigarette smoke induced catabolism in C2 myotubes.

    Science.gov (United States)

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

    2013-01-01

    Exposure to cigarette smoke (CS) and cigarette smoking have been shown to promote catabolism of skeletal muscle. Previous studies and recent findings from our laboratory have demonstrated the involvement of the ubiquitin proteasome system and the muscle-specific E3 ubiquitin ligases MAFbx/atrogin-1 and MuRF1 in CS induced skeletal muscle catabolism. The essential amino acid leucine is a known anticatabolic agent that improves skeletal muscle metabolism in various atrophic conditions. To examine the protective effect of leucine and proteasome inhibition in CS induced muscle catabolism, C2 myotubes, from an in vitro skeletal muscle cell line, were exposed to CS in the presence or absence of leucine and a proteasome inhibitor, MG132. Diameter of myotubes, levels of the main contractile proteins - myosin heavy chain and actin, expression of MAFbx/atrogin-1 and MuRF1 were studied by microscopy, Western blotting, and qPCR. Leucine pretreatment prevented the CS-induced reduction in diameter of myotubes and degradation of myosin heavy chain by suppressing the upregulation of MAFbx/atrogin-1 and MuRF1. MG132 also attenuated the CS-induced decrease in diameter of myotubes and degradation of myosin heavy chain. Our findings demonstrate that supplementation with the essential amino acid leucine and inhibition of the proteasome may protect skeletal muscle from CS induced catabolism.

  5. NADPH oxidase (NOX) 1 mediates cigarette smoke-induced superoxide generation in rat vascular smooth muscle cells.

    Science.gov (United States)

    Chang, Kyung-Hwa; Park, Jung-Min; Lee, Chang Hoon; Kim, Bumseok; Choi, Kyung-Chul; Choi, Seong-Jin; Lee, Kyuhong; Lee, Moo-Yeol

    2017-02-01

    Smoking is a well-established risk factor for cardiovascular diseases. Oxidative stress is one of the common etiological factors, and NADPH oxidase (NOX) has been suggested as a potential mediator of oxidative stress. In this study, cigarette smoke (CS)-induced superoxide production was characterized in vascular smooth muscle cells (VSMC). CS was prepared in forms of cigarette smoke extract (CSE) and total particulate matter (TPM). Several molecular probes for reactive oxygen species were trialed, and dihydroethidium (DHE) and WST-1 were chosen for superoxide detection considering the autofluorescence, light absorbance, and peroxidase inhibitory activity of CS. Both CSE and TPM generated superoxide in a VSMC culture system by stimulating cells to produce superoxide and by directly producing superoxide in the aqueous solution. NOX, specifically NOX1 was found to be an important cellular source of superoxide through experiments with the NOX inhibitors diphenyleneiodonium (DPI) and VAS2870 as well as isoform-specific NOX knockdown. NOX inhibitors and the superoxide dismutase mimetic TEMPOL reduced the cytotoxicity of CSE, thus suggesting the contribution of NOX1-derived superoxide to cytotoxicity. Since NOX1 is known to mediate diverse pathological processes in the vascular system, NOX1 may be a critical effector of cardiovascular toxicity caused by smoking. Copyright © 2016 Elsevier B.V. All rights reserved.

  6. Cigarette Smoke-Induced Lung Disease Predisposes to More Severe Infection with Nontypeable Haemophilus influenzae: Protective Effects of Andrographolide.

    Science.gov (United States)

    Tan, W S Daniel; Peh, Hong Yong; Liao, Wupeng; Pang, Chu Hui; Chan, Tze Khee; Lau, Suk Hiang; Chow, Vincent T; Wong, W S Fred

    2016-05-27

    Cigarette smoke (CS) is associated with many maladies, one of which is chronic obstructive pulmonary disease (COPD). As the disease progresses, patients are more prone to develop COPD exacerbation episodes by bacterial infection, particularly to nontypeable Haemophilus influenza (NTHi) infection. The present study aimed to develop a CS-exposed mouse model that increases inflammation induced by NTHi challenge and investigate the protective effects of andrographolide, a bioactive molecule with anti-inflammatory and antioxidant properties isolated from the plant Andrographis paniculata. Female BALB/c mice exposed to 2 weeks of CS followed by a single intratracheal instillation of NTHi developed increased macrophage and neutrophil pulmonary infiltration, augmented cytokine levels, and heightened oxidative damage. Andrographolide effectively reduced lung cellular infiltrates and decreased lung levels of TNF-α, IL-1β, CXCL1/KC, 8-OHdG, matrix metalloproteinase-8 (MMP-8), and MMP-9. The protective actions of andrographolide on CS-predisposed NTHi inflammation might be attributable to increased nuclear factor erythroid-2-related factor 2 (Nrf2) activation and decreased Kelch-like ECH-associated protein 1 (Keap1) repressor function, resulting in enhanced gene expression of antioxidant enzymes including heme oxygenase-1 (HO-1), glutathione reductase (GR), glutathione peroxidase-2 (GPx-2), glutamate-cysteine ligase modifier (GCLM), and NAD(P)H quinone oxidoreductase 1 (NQO1). Taken together, these findings strongly support a therapeutic potential for andrographolide in preventing lung inflammation caused by NTHi in cigarette smokers.

  7. Role of recently migrated monocytes in cigarette smoke-induced lung inflammation in different strain of mice.

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    Sandra Pérez-Rial

    Full Text Available This study investigates the role of proinflammatory monocytes recruited from blood circulation and recovered in bronchoalveolar lavage (BAL fluid in mediating the lung damage in a model of acute cigarette smoke (CS-induced lung inflammation in two strains of mice with different susceptibility to develop emphysema (susceptible -C57BL/6J and non susceptible -129S2/SvHsd. Exposure to whole-body CS for 3 consecutive research cigarettes in one single day induced acute inflammation in the lung of mice. Analysis of BAL fluid showed more influx of recently migrated monocytes at 72 h after CS-exposition in susceptible compared to non susceptible mice. It correlated with an increase in MMP-12 and TNF-α protein levels in the lung tissue, and with an increment of NF-κB translocation to the nucleus measured by electrophoretic mobility shift assay in C57BL/6J mice. To determine the functional role of these proinflammatory monocytes in mediating CS-induced airway inflammation, alveolar macrophages and blood monocytes were transiently removed by pretreatment with intratracheal and intravenous liposome-encapsulated CL2MDP, given 2 and 4 days prior to CS exposure and their repopulation was studied. Monocytes/macrophages were maximally depleted 48 h after last liposome application and subsequently recently migrated monocytes reappeared in BAL fluid of susceptible mice at 72 h after CS exposure. Recently migrated monocytes influx to the lung correlated with an increase in the MMP-12 protein level in the lung tissue, indicating that the increase in proinflammatory monocytes is associated with a major tissue damaging. Therefore our data confirm that the recruitment of proinflammatory recently migrated monocytes from the blood are responsible for the increase in MMP-12 and has an important role in the pathogenesis of lung disease induced by acute lung inflammation. These results could contribute to understanding the different susceptibility to CS of these strains of

  8. Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium.

    Science.gov (United States)

    Rius, Cristina; Company, Chantal; Piqueras, Laura; Cerdá-Nicolás, Jose Miguel; González, Cruz; Servera, Emilio; Ludwig, Andreas; Morcillo, Esteban J; Sanz, Maria-Jesus

    2013-02-01

    Cigarette smoking is an important risk factor for the development of cardiovascular disease, yet the pathways through which this may operate are poorly understood. Therefore, the mechanism underlying cigarette smoke (CS)-induced arterial endothelial dysfunction and the potential link with fractalkine/CX(3)CL1 upregulation were investigated. Stimulation of human arterial umbilical endothelial cells (HUAECs) with pathophysiological concentrations of CS extract (1% CSE) increased CX(3)CL1 expression. Neutralisation of CX(3)CL1 activity under dynamic flow conditions significantly inhibited CSE-induced mononuclear cell adhesion to HUAECs (67%). The use of small interfering RNA (siRNA) revealed that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 5 (Nox5) but not Nox2 or Nox4 is the main NADPH isoform involved in CSE-induced CX(3)CL1 upregulation and mononuclear cell arrest. Knock down of HUAEC tumour necrosis factor α expression with siRNA or pharmacological inhibition of p38 mitogen-activated protein kinase and nuclear factor κB also abolished these responses. Interestingly, circulating monocytes and lymphocytes from patients with chronic obstructive pulmonary disease (COPD) (n=29) versus age-matched controls (n=23) showed CX(3)CR1overexpression. Furthermore, CX(3)CL1 neutralisation dramatically diminished their enhanced adhesiveness to CSE-stimulated HUAECs. Finally, when animals were exposed for 3 days to CS, a mild inflammatory response in the lung was observed which was accompanied by enhanced CX(3)CL1 expression in the cremasteric arterioles, an organ distant from the lung. CS exposure resulted in increased leukocyte-arteriolar endothelial cell adhesion which was significantly reduced (51%) in animals lacking CX(3)CL1 receptor (CX(3)CR1). These results suggest that CS induces functional CX(3)CL1 expression in arterial endothelium and leukocytes from patients with COPD show increased CX(3)CL1-dependent adhesiveness. Therefore, targeting the CX(3)CL1

  9. Cigarette smoke induces endoplasmic reticulum stress and the unfolded protein response in normal and malignant human lung cells

    Directory of Open Access Journals (Sweden)

    Yang Jin

    2008-08-01

    Full Text Available Abstract Background Although lung cancer is among the few malignancies for which we know the primary etiological agent (i.e., cigarette smoke, a precise understanding of the temporal sequence of events that drive tumor progression remains elusive. In addition to finding that cigarette smoke (CS impacts the functioning of key pathways with significant roles in redox homeostasis, xenobiotic detoxification, cell cycle control, and endoplasmic reticulum (ER functioning, our data highlighted a defensive role for the unfolded protein response (UPR program. The UPR promotes cell survival by reducing the accumulation of aberrantly folded proteins through translation arrest, production of chaperone proteins, and increased degradation. Importance of the UPR in maintaining tissue health is evidenced by the fact that a chronic increase in defective protein structures plays a pathogenic role in diabetes, cardiovascular disease, Alzheimer's and Parkinson's syndromes, and cancer. Methods Gene and protein expression changes in CS exposed human cell cultures were monitored by high-density microarrays and Western blot analysis. Tissue arrays containing samples from 110 lung cancers were probed with antibodies to proteins of interest using immunohistochemistry. Results We show that: 1 CS induces ER stress and activates components of the UPR; 2 reactive species in CS that promote oxidative stress are primarily responsible for UPR activation; 3 CS exposure results in increased expression of several genes with significant roles in attenuating oxidative stress; and 4 several major UPR regulators are increased either in expression (i.e., BiP and eIF2α or phosphorylation (i.e., phospho-eIF2α in a majority of human lung cancers. Conclusion These data indicate that chronic ER stress and recruitment of one or more UPR effector arms upon exposure to CS may play a pivotal role in the etiology or progression of lung cancers, and that phospho-eIF2α and BiP may have

  10. Induced Pluripotent Stem Cells-Derived Mesenchymal Stem Cells Attenuate Cigarette Smoke-Induced Cardiac Remodeling and Dysfunction

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    Yingmin Liang

    2017-07-01

    Full Text Available The strong relationship between cigarette smoking and cardiovascular disease (CVD has been well-documented, but the mechanisms by which smoking increases CVD risk appear to be multifactorial and incompletely understood. Mesenchymal stem cells (MSCs are regarded as an important candidate for cell-based therapy in CVD. We hypothesized that MSCs derived from induced pluripotent stem cell (iPSC-MSCs or bone marrow (BM-MSCs might alleviate cigarette smoke (CS-induced cardiac injury. This study aimed to investigate the effects of BM-MSCs or iPSC-MSCs on CS-induced changes in serum and cardiac lipid profiles, oxidative stress and inflammation as well as cardiac function in a rat model of passive smoking. Male Sprague-Dawley rats were randomly selected for exposure to either sham air (SA as control or 4% CS for 1 h per day for 56 days. On day 29 and 43, human adult BM-MSCs, iPSC-MSCs or PBS were administered intravenously to CS-exposed rats. Results from echocardiography, serum and cardiac lipid profiles, cardiac antioxidant capacity, cardiac pro- and anti-inflammatory cytokines and cardiac morphological changes were evaluated at the end of treatment. iPSC-MSC-treated group showed a greater effect in the improvement of CS-induced cardiac dysfunction over BM-MSCs-treated group as shown by increased percentage left ventricular ejection fraction and percentage fractional shortening, in line with the greater reversal of cardiac lipid abnormality. In addition, iPSC-MSCs administration attenuated CS-induced elevation of cardiac pro-inflammatory cytokines as well as restoration of anti-inflammatory cytokines and anti-oxidative markers, leading to ameliorate cardiac morphological abnormalities. These data suggest that iPSC-MSCs on one hand may restore CS-induced cardiac lipid abnormality and on the other hand may attenuate cardiac oxidative stress and inflammation via inhibition of CS-induced NF-κB activation, leading to improvement of cardiac remodeling and

  11. Leucine and its transporter provide protection against cigarette smoke-induced cell death: A potential therapy for emphysema

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    Bannhi Das

    2014-01-01

    Full Text Available Cigarette smoke (CS is a major risk factor for emphysematous changes in the lungs and the underlying mechanism involves CS-induced cell death. In the present study we investigated the ability of nutrients to rescue CS-induced cell death. We observed that pre-treatment with excess leucine can partially rescue CS extract-induced cell death in Saccharomyces cerevisiae and alveolar epithelial A549 cells. Excess dietary leucine was also effective in alleviating effects of CS in guinea pig lungs. Further investigation to understand the underlying mechanism showed that CS exposure causes downregulation of leucine transporter that results in inactivation of mTOR, which is a positive regulator of protein synthesis and cell proliferation. Notably, leucine supplemented diet ameliorated even existing CS-induced emphysematous changes in guinea pig lung, a condition hitherto thought to be irreversible. Thus the current study documents a new mechanism by which CS affects cellular physiology wherein leucine transporter is a key target.

  12. Cigarette smoke-induced disruption of pulmonary barrier and bacterial translocation drive tumor-associated inflammation and growth.

    Science.gov (United States)

    Jungnickel, C; Wonnenberg, B; Karabiber, O; Wolf, A; Voss, M; Wolf, L; Honecker, A; Kamyschnikow, A; Herr, C; Bals, R; Beisswenger, C

    2015-09-15

    Microorganisms have an important role in tumorgenesis by the induction of inflammation and by a direct impact on tumor cells. Chronic obstructive pulmonary disease (COPD) is associated with an increased risk for lung cancer and microbial colonization. We asked whether bacterial pathogens act as tumor promoters during CS-induced pulmonary inflammation. In a metastatic lung cancer (LC) model, Lewis lung carcinoma (LLC) cells were injected in mice to initiate the growth of tumors in the lung. Exposure to the combination of cigarette smoke (CS) and nontypeable Haemophilus influenzae (NTHi) synergistically increased metastatic growth. Lung levels of albumin and LDH, translocation of bacterial factors into tumor tissue, tumor inflammation, and tumor proliferation were significantly increased in mice exposed to CS in combination with NTHi. Bacterial pathogens increased the proliferation of cultured LLC cells and human cancer cell lines. Metastatic growth induced by the exposure to CS in combination with NTHi was reduced in mice deficient for IL-17. Our data provide evidence that CS-induced loss of pulmonary barrier integrity allows bacterial factors to translocate into tumor tissue and to regulate tumor-associated inflammation and tumor proliferation. Translocation of bacterial factors in tumor tissue links CS-induced inflammation with tumor proliferation.

  13. Proliferative Activity of Liver Growth Factor is Associated with an Improvement of Cigarette Smoke-Induced Emphysema in Mice

    Science.gov (United States)

    Terrón-Expósito, Raúl; Díaz-Gil, Juan José; González-Mangado, Nicolás; Peces-Barba, Germán

    2014-01-01

    Cigarette smoke (CS)-induced emphysema is a major component of chronic obstructive pulmonary disease (COPD). COPD treatment is based on the administration of bronchodilators and corticosteroids to control symptoms and exacerbations, however, to date, there are no effective therapies to reverse disease progression. Liver growth factor (LGF) is an albumin-bilirubin complex with mitogenic properties, whose therapeutic effects have previously been reported in a model of emphysema and several rodent models of human disease. To approach the therapeutic effect of LGF in a model of previously established emphysema, morphometric and lung function parameters, matrix metalloproteinase (MMP) activity and the expression of several markers, such as VEGF, PCNA, 3NT and Nrf2, were assessed in air-exposed and CS-exposed C57BL/6J male mice with and without intraperitoneal (i.p.) injection of LGF. CS-exposed mice presented a significant enlargement of alveolar spaces, higher alveolar internal area and loss of lung function that correlated with higher MMP activity, higher expression of 3NT and lower expression of VEGF. CS-exposed mice injected with LGF, showed an amelioration of emphysema and improved lung function, which correlated with lower MMP activity and 3NT expression and higher levels of VEGF, PCNA and Nrf2. Taken together, this study suggests that LGF administration ameliorates CS-induced emphysema, highlights the ability of LGF to promote alveolar cell proliferation and may be a promising strategy to revert COPD progression. PMID:25401951

  14. Protecting the BBB Endothelium against Cigarette Smoke-Induced Oxidative Stress Using Popular Antioxidants: Are they really beneficial?

    Science.gov (United States)

    Kaisar, Mohammad Abul; Prasad, Shikha; Cucullo, Luca

    2015-01-01

    Blood Brain Barrier (BBB) exposed to realistic concentrations (comparable to a chronic heavy smoker) of Cigarette Smoke Extract (CSE) triggers a strong endothelial inflammatory which can lead to the onset of neurological disorders. The involvement of Reactive Oxygen Species (ROS) in this inflammatory cascade is evident from the up-regulation of nuclear factor erythroid 2 related factor 2 (Nrf-2), a transcription factor involved in anti-oxidant response signaling in CSE exposed endothelial cells. We have shown that pre-treatment with α-tocopherol and/or ascorbic acid is highly protective for the BBB, thus suggesting that, prophylactic administration of antioxidants can reduce CSE and/or inflammatory-dependent BBB damage. We have assessed and ranked the protective effects of 5 popular OTC antioxidants (Coenzyme Q10, Melatonin, Glutathione, Lipoic acid and Resveratrol) against CSE-induced BBB endothelial damage using hCMEC/D3 cells. The analysis of pro-inflammatory cytokines release by ELISA revealed that, resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 & IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Endothelial Cell Adhesion Molecule -1 (PECAM-1), Vascular Endothelial Cell Adhesion Molecule-1 (VCAM-1) & E-selectin and inhibited monocytes-endothelial cell adhesion. The anti-inflammatory effects correlated with the anti-oxidative protection endowed by these compounds as evidenced by upregulation of NADPH: Quinone Oxidoreductase 1 (NQO1) and reduced cellular oxidative stress. CSE-induced release of Vascular Endothelial Growth Factor (VEGF) was inhibited by all tested compounds although the effect was not strictly dose-dependent. Further in vivo studies are required to validate our results and expand our current study to include combinatorial treatments. PMID:26410779

  15. Paraoxsonase2 (PON2) and oxidative stress involvement in pomegranate juice protection against cigarette smoke-induced macrophage cholesterol accumulation.

    Science.gov (United States)

    Rom, Oren; Aviram, Michael

    2016-11-25

    Exposure to cigarette smoke (CS) promotes various stages of atherosclerosis development. Macrophages are the predominant cells in early atherogenesis, and the polyphenolic-rich pomegranate juice (PJ) is known for its protective role against macrophage atherogenicity. The aim of the current study was to examine the atherogenic effects of CS on macrophages, and to evaluate the protective effects of PJ against CS-induced macrophage atherogenicity. Murine J774A.1 macrophages were treated with CS-exposed medium in the absence or presence of PJ. Parameters of lipid peroxidation in CS-exposed medium were measured by the lipid peroxides and thiobarbituric acid reactive substances (TBARS) assays. Atherogenicity of macrophages incubated with increasing concentrations of CS-exposed medium was assessed by cytotoxicity, oxidative stress determined by generation of reactive oxygen species (ROS) using DCFH-DA, activity of the cellular anti-oxidant paraoxonase2 (PON2), macrophage accumulation of cholesterol and triglycerides, as well as through high density lipoprotein (HDL)-mediated cholesterol efflux from the cells. CS exposure resulted in significant and dose-dependent increases in lipid peroxides and TBARS medium levels (up to 3 and 8-fold, respectively). Incubation of macrophages with CS-exposed medium resulted in dose-dependent increases in macrophage damage/injury (up to 6-fold), intracellular ROS levels (up to 31%), PON2 activity (up to 2-fold), and macrophage cholesterol content (up to 24%). The latter might be explained by reduced HDL-mediated cholesterol efflux from CS-exposed macrophages (by 21%). PJ protected macrophages from CS-induced increases in intracellular ROS levels and cholesterol accumulation, as well as the attenuated efflux of cholesterol. These data indicate that CS stimulates macrophage oxidation and activates PON2 as a possible compensatory response to the oxidative burden. CS impairs HDL-mediated cholesterol efflux from macrophages leading to cellular

  16. Cigarette smoke-induced reduction in binding of the salivary translocator protein is not mediated by free radicals.

    Science.gov (United States)

    Nagler, R; Savulescu, D; Gavish, M

    2016-02-01

    Oral cancer is the most common malignancy of the head and neck and its main inducer is exposure to cigarette smoke (CS) in the presence of saliva. It is commonly accepted that CS contributes to the pathogenesis of oral cancer via reactive free radicals and volatile aldehydes. The 18 kDa translocator protein (TSPO) is an intracellular receptor involved in proliferation and apoptosis, and has been linked to various types of cancer. The presence of TSPO in human saliva has been linked to oral cancer, and its binding affinity to its ligand is reduced following exposure to CS. In the present study we wished to further investigate the mechanism behind the CS-induced reduction of TSPO binding by exploring the possible mediatory role of reactive oxygen species (ROS) and volatile aldehydes in this process. We first analyzed TSPO binding in control saliva and in saliva exposed to CS in the presence and absence of various antioxidants. These experiments found that TSPO binding ability was not reversed by any of the antioxidants added, suggesting that CS exerts its effect on TSPO via mechanisms that do not involve volatile aldehydes and free radicals tested. Next, we analyzed TSPO binding in saliva following addition of exogenous ROS in the form of H2O2. These experiments found that TSPO binding was enhanced due to the treatment, once again showing that the CS-induced TSPO binding reduction is not mediated by this common form of ROS. However, the previously reported CS-induced reduction in salivary TSPO binding together with the role of TSPO in cells and its link to cancer strongly suggest that TSPO has a critical role in the pathogenesis of CS-induced oral cancer. The importance of further elucidating the mechanisms behind it should be emphasized.

  17. Pharmacological characterisation of anti-inflammatory compounds in acute and chronic mouse models of cigarette smoke-induced inflammation

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    Mok Joanie

    2010-09-01

    Full Text Available Abstract Background Candidate compounds being developed to treat chronic obstructive pulmonary disease are typically assessed using either acute or chronic mouse smoking models; however, in both systems compounds have almost always been administered prophylactically. Our aim was to determine whether the prophylactic effects of reference anti-inflammatory compounds in acute mouse smoking models reflected their therapeutic effects in (more clinically relevant chronic systems. Methods To do this, we started by examining the type of inflammatory cell infiltrate which occurred after acute (3 days or chronic (12 weeks cigarette smoke exposure (CSE using female, C57BL/6 mice (n = 7-10. To compare the effects of anti-inflammatory compounds in these models, mice were exposed to either 3 days of CSE concomitant with compound dosing or 14 weeks of CSE with dosing beginning after week 12. Budesonide (1 mg kg-1; i.n., q.d., roflumilast (3 mg kg-1; p.o., q.d. and fluvastatin (2 mg kg-1; p.o., b.i.d. were dosed 1 h before (and 5 h after for fluvastatin CSE. These dose levels were selected because they have previously been shown to be efficacious in mouse models of lung inflammation. Bronchoalveolar lavage fluid (BALF leukocyte number was the primary endpoint in both models as this is also a primary endpoint in early clinical studies. Results To start, we confirmed that the inflammatory phenotypes were different after acute (3 days versus chronic (12 weeks CSE. The inflammation in the acute systems was predominantly neutrophilic, while in the more chronic CSE systems BALF neutrophils (PMNs, macrophage and lymphocyte numbers were all increased (p Conclusions These results demonstrate that the acute, prophylactic systems can be used to identify compounds with therapeutic potential, but may not predict a compound's efficacy in chronic smoke exposure models.

  18. Smoking-induced chromosomal segregation anomalies identified by FISH analysis of sperm

    National Research Council Canada - National Science Library

    Pereira, Ciro Silveira; Juchniuk de Vozzi, Maria Silvina; Dos Santos, Silvio Avelino; Vasconcelos, Maria Aparecida C; de Paz, Cláudia Cp; Squire, Jeremy A; Martelli, Lucia

    2014-01-01

    .... Previous studies have shown that toxic substances from cigarette smoke induce structural and numerical chromosomal aberrations in vitro and could potentially increase levels of aneusomy in sperm...

  19. Cigarette smoke induces proteasomal-mediated degradation of DNA methyltransferases and methyl CpG-/CpG domain-binding proteins in embryonic orofacial cells.

    Science.gov (United States)

    Mukhopadhyay, Partha; Greene, Robert M; Pisano, M Michele

    2015-12-01

    Orofacial clefts, the most prevalent of developmental anomalies, occur with a frequency of 1 in 700 live births. Maternal cigarette smoking during pregnancy represents a risk factor for having a child with a cleft lip and/or cleft palate. Using primary cultures of first branchial arch-derived cells (1-BA cells), which contribute to the formation of the lip and palate, the present study addressed the hypothesis that components of cigarette smoke alter global DNA methylation, and/or expression of DNA methyltransferases (Dnmts) and various methyl CpG-binding proteins. Primary cultures of 1-BA cells, exposed to 80μg/mL cigarette smoke extract (CSE) for 24h, exhibited a >13% decline in global DNA methylation and triggered proteasomal-mediated degradation of Dnmts (DNMT-1 and -3a), methyl CpG binding protein 2 (MeCP2) and methyl-CpG binding domain protein 3 (MBD-3). Pretreatment of 1-BA cells with the proteasomal inhibitor MG-132 completely reversed such degradation. Collectively, these data allow the suggestion of a potential epigenetic mechanism underlying maternal cigarette smoke exposure-induced orofacial clefting. Copyright © 2015 Elsevier Inc. All rights reserved.

  20. Beta-cryptoxanthin protection against cigarette smoke-induced inflammatory responses in the lung is due to the action of its own molecule

    Science.gov (United States)

    Higher intake of the dietary xanthophyll, beta-cryptoxanthin (BCX), has been associated with a lower risk of lung cancer death in smokers. We have previously shown that BCX feeding was effective in reducing both cigarette smoke (CS)-induced lung inflammation in ferrets and carcinogen-induced lung tu...

  1. Involvement of NF-κB and muscle specific E3 ubiquitin ligase MuRF1 in cigarette smoke-induced catabolism in C2 myotubes.

    Science.gov (United States)

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

    2013-01-01

    Cigarette smoking has been identified as a risk factor for muscular damage and sarcopenia, the age-related loss of muscle mass and strength in old age. Cigarette smoke (CS)-induced oxidative stress and p38 MAPK activation have been shown to be the main cellular mechanisms leading to skeletal muscle catabolism. In order to investigate the involvement of NF-κB as another possible cellular mechanism by which CS promotes muscle catabolism, C2 myotubes, from an in vitro skeletal muscle cell line, were exposed to different time periods of whole vapor phase CS in the presence or absence of NF-κB inhibitor, IMD-0354. The CS-induced reduction in diameter of myotubes and time-dependent degradation of the main contractile protein myosin heavy chain were abolished by NF-κB inhibition. Also, C2 exposure to CS resulted in IκB-α degradation and NF-κB activation, which led to upregulation of the muscle specific E3 ubiquitin ligase MuRF1, but not MAFbx/atrogin-1. In conclusion, our results demonstrate that vapor phase CS exposure to skeletal myotubes triggers NF-κB activation leading to skeletal muscle cell damage and breakdown of muscle proteins mediated by muscle specific E3 ubiquitin ligase MuRF1. Our findings provide another possible molecular mechanism for the catabolic effects of CS in skeletal muscle.

  2. Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway

    Directory of Open Access Journals (Sweden)

    Sibin Guan

    2017-01-01

    Full Text Available Epithelial-mesenchymal transition (EMT is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD, which leads to progressive pulmonary destruction. Panax ginseng is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capacity in patients with COPD. Ginsenoside Rg1 is one of the main active components and was shown to inhibit oxidative stress and inflammation. The present study investigated the hypothesis that ginsenoside Rg1 attenuates EMT in COPD rats induced by cigarette smoke (CS and human bronchial epithelial (HBE cells exposed to cigarette smoke extract (CSE. Our data showed that CS or CSE exposure increased expression of the mesenchymal marker α-smooth muscle actin (α-SMA and decreased expression of the epithelial marker epithelial cadherin (E-cad in both lung tissues and HBE cells, which was markedly suppressed by ginsenoside Rg1. Importantly, CS-induced upregulation of TGF-β1/Smad pathway components, including TGF-β1, TGF-βR1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-βR1-Smad2/3 inhibitor, on suppression of EMT in CSE-induced HBE cells. Collectively, we concluded that ginsenoside Rg1 alleviates CS-induced pulmonary EMT, in both COPD rats and HBE cells, via inhibition of the TGF-β1/Smad pathway.

  3. Reduced nuclear translocation of serum response factor is associated with skeletal muscle atrophy in a cigarette smoke-induced mouse model of COPD

    Directory of Open Access Journals (Sweden)

    Ma R

    2017-02-01

    Full Text Available Ran Ma, Xuefang Gong, Hua Jiang, Chunyi Lin, Yuqin Chen, Xiaoming Xu, Chenting Zhang, Jian Wang, Wenju Lu, Nanshan ZhongGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People’s Republic of ChinaAbstract: Skeletal muscle atrophy and dysfunction are common complications in the chronic obstructive pulmonary disease (COPD. However, the underlying molecular mechanism remains elusive. Serum response factor (SRF is a transcription factor which is critical in myocyte differentiation and growth. In this study, we established a mouse COPD model induced by cigarette smoking (CS exposure for 24 weeks, with apparent pathophysiological changes, including increased airway resistance, enlarged alveoli, and skeletal muscle atrophy. Levels of upstream regulators of SRF, striated muscle activator of Rho signaling (STARS, and ras homolog gene family, member A (RhoA were decreased in quadriceps muscle of COPD mice. Meanwhile, the nucleic location of SRF was diminished along with its cytoplasmic accumulation. There was a downregulation of the target muscle-specific gene, Igf1. These results suggest that the CS is one of the major cause for COPD pathogenesis, which induces the COPD-associated skeletal muscle atrophy which is closely related to decreasing SRF nucleic translocation, consequently downregulating the SRF target genes involved in muscle growth and nutrition. The STARS/RhoA signaling pathway might contribute to this course by impacting SRF subcellular distribution. Keywords: SRF, chronic obstructive pulmonary disease, skeletal muscle atrophy, cigarette smoking

  4. Aryl Hydrocarbon Receptor Ligands in Cigarette Smoke Induce Production of Interleukin-22 to Promote Pancreatic Fibrosis in Models of Chronic Pancreatitis.

    Science.gov (United States)

    Xue, Jing; Zhao, Qinglan; Sharma, Vishal; Nguyen, Linh P; Lee, Yvonne N; Pham, Kim L; Edderkaoui, Mouad; Pandol, Stephen J; Park, Walter; Habtezion, Aida

    2016-12-01

    Cigarette smoke has been identified as an independent risk factor for chronic pancreatitis (CP). Little is known about the mechanisms by which smoking promotes development of CP. We assessed the effects of aryl hydrocarbon receptor (AhR) ligands found in cigarette smoke on immune cell activation in humans and pancreatic fibrosis in animal models of CP. We obtained serum samples from patients with CP treated at Stanford University hospital and healthy individuals (controls) and isolated CD4(+) T cells. Levels of interleukin-22 (IL22) were measured by enzyme-linked immunosorbent assay and smoking histories were collected. T cells from healthy nonsmokers and smokers were stimulated and incubated with AhR agonists (2,3,7,8-tetrachlorodibenzo-p-dioxin or benzo[a]pyrene) or antagonists and analyzed by flow cytometry. Mice were given intraperitoneal injections of caerulein or saline, with or without lipopolysaccharide, to induce CP. Some mice were given intraperitoneal injections of AhR agonists at the start of caerulein injection, with or without an antibody against IL22 (anti-IL22) starting 2 weeks after the first caerulein injection, or recombinant mouse IL22 or vehicle (control) intraperitoneally 4 weeks after the first caerulein injection. Mice were exposed to normal air or cigarette smoke for 6 h/d for 7 weeks and expression of AhR gene targets was measured. Pancreata were collected from all mice and analyzed by histology and quantitative reverse transcription polymerase chain reaction. Pancreatic stellate cells and T cells were isolated and studied using immunoblot, immunofluorescence, flow cytometry, and enzyme-linked immunosorbent analyses. Mice given AhR agonists developed more severe pancreatic fibrosis (based on decreased pancreas size, histology, and increased expression of fibrosis-associated genes) than mice not given agonists after caerulein injection. In mice given saline instead of caerulein, AhR ligands did not induce fibrosis. Pancreatic T cells

  5. Systems Biology Reveals Cigarette Smoke-Induced Concentration-Dependent Direct and Indirect Mechanisms That Promote Monocyte-Endothelial Cell Adhesion.

    Science.gov (United States)

    Poussin, Carine; Laurent, Alexandra; Peitsch, Manuel C; Hoeng, Julia; De Leon, Hector

    2015-10-01

    Cigarette smoke (CS) affects the adhesion of monocytes to endothelial cells, a critical step in atherogenesis. Using an in vitro adhesion assay together with innovative computational systems biology approaches to analyze omics data, our study aimed at investigating CS-induced mechanisms by which monocyte-endothelial cell adhesion is promoted. Primary human coronary artery endothelial cells (HCAECs) were treated for 4 h with (1) conditioned media of human monocytic Mono Mac-6 (MM6) cells preincubated with low or high concentrations of aqueous CS extract (sbPBS) from reference cigarette 3R4F for 2 h (indirect treatment, I), (2) unconditioned media similarly prepared without MM6 cells (direct treatment, D), or (3) freshly generated sbPBS (fresh direct treatment, FD). sbPBS promoted MM6 cells-HCAECs adhesion following I and FD, but not D. In I, the effect was mediated at a low concentration through activation of vascular inflammation processes promoted in HCAECs by a paracrine effect of the soluble mediators secreted by sbPBS-treated MM6 cells. Tumor necrosis factor α (TNFα), a major inducer, was actually shed by unstable CS compound-activated TNFα-converting enzyme. In FD, the effect was triggered at a high concentration that also induced some toxicity. This effect was mediated through an yet unknown mechanism associated with a stress damage response promoted in HCAECs by unstable CS compounds present in freshly generated sbPBS, which had decayed in D unconditioned media. Aqueous CS extract directly and indirectly promotes monocytic cell-endothelial cell adhesion in vitro via distinct concentration-dependent mechanisms. © The Author 2015. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

  6. 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).

  7. Taraxasterol inhibits cigarette smoke-induced lung inflammation by inhibiting reactive oxygen species-induced TLR4 trafficking to lipid rafts.

    Science.gov (United States)

    Xueshibojie, Liu; Duo, Yu; Tiejun, Wang

    2016-10-15

    Taraxasterol, a pentacyclic-triterpene isolated from Taraxacum officinale, has been demonstrated to have anti-inflammatory effects. However, the protective effects of taraxasterol against cigarette smoke (CS)-induced lung inflammation have not been reported. This study aimed to investigate the protective effects and mechanism of taraxasterol on CS-induced lung inflammation in mice. CS-induced mouse lung inflammation model was used to investigate the protective effects of taraxasterol in vivo. Human bronchial epithelial cells (HBECs) were used to investigate the protective mechanism of taraxasterol in vitro. The results showed that taraxasterol attenuated CS-induced lung pathological changes, inflammatory cells infiltration, inflammatory cytokines TNF-α, IL-6 and IL-1β production. Taraxasterol also up-regulated CS-induced glutathione (GSH) production. In vitro, taraxasterol was found to inhibit CS-induced reactive oxygen species production, recruitment of TLR4 into lipid rafts, NF-κB activation, and IL-8 production. Furthermore, our results showed that antioxidant N-acetyl-L-cysteine (NAC) significantly inhibited CS-induced recruitment of TLR4 into lipid rafts as well as IL-8 production. In conclusion, our results suggested that taraxasterol had protective effects of CS-induced lung inflammation.

  8. Oral N-acetylcysteine or S-carboxymethylcysteine inhibit cigarette smoke-induced hypersecretion of mucus in rat larynx and trachea in situ.

    Science.gov (United States)

    Rogers, D F; Turner, N C; Marriott, C; Jeffery, P K

    1989-11-01

    Two weeks exposure of rats to cigarette smoke (CS) significantly (p less than 0.05) increased the secretion of fucose-containing glycoconjugates above normal in an in situ preparation of larynx and trachea. After equilibration mean basal secretion in CS-exposed rats was 24 micrograms (per 30 min collection) which was 8 times higher than that of unexposed animals (p less than 0.01). N-acetylcysteine (NAC) or S-carboxymethylcysteine (SCMC) given as 1% of the drinking water, before and after daily exposure to CS, significantly inhibited the development of the CS-induced increase in fucose secretion reducing the mean for basal secretion in each group to 7 and 5 micrograms, respectively (p less than 0.05). Neither NAC nor SCMC had significant effects on baseline glycoconjugate secretion in control animals. Albumin was inconsistently present in the secretions of both control and CS-exposed animals, whereas in those exposed to CS and also given one of the two cysteine derivatives there was a consistent increase in albumin transudation.

  9. Cigarette smoking induced liver insult concomitant with inflammatory mediators in serum crevicular fluid and bronchio alveolar lavage of schistosomal diabetic subjects with history of bronchial asthma.

    Science.gov (United States)

    El-Dardiry, Samia A; Shafik, Sherine R; Wagih, Ayman; Amir, El-Amir M; Kassem, Gamal K; Atef, Ghada; El-Toukhy, Heba

    2007-08-01

    Forty five smokers were classified into schistosomal cases with type-2 diabetis mellitus (GI) and with associated history of bronchial asthma (GII) and without T-2 DM (GIII). A control group (GIV) of non-diabetic non schistosomal age matched subjects who quitted smoking for >6 months were included. Assessed parameters included indices of glycemic status (glycated hemoglobin), angiogenesis (vascular endothelial growth factor) hepatic and bronchoalveolar disposition (Liver function test, metallothionein, serum levels of cotinine, cadmium selenium, copper & zinc) and bronchoalveolar lavage) (BAL) levels of surfactant proteins A & D, zinc and copper oxidative stress and fibrogenesis (total antioxidant capacity thiobarbituric acid reactive substance) and vasculopathy (angiotensin converting enzyme, P-selectin, nitrate) and periodontitis (collagenase and elastase in GCF) impact of cigarette smoking associated with trace element disbalance and enzymatic changes in crevicular fluid on altered parameters collaborative out-come. The study reflected the collaborative outcome of immune mediated mechanisms initiated by liver affection, glycemic status and history of predisposed bronchial integrity induced by oxidative stress.

  10. Cigarette sidestream smoke induces histone H3 phosphorylation via JNK and PI3K/Akt pathways, leading to the expression of proto-oncogenes.

    Science.gov (United States)

    Ibuki, Yuko; Toyooka, Tatsushi; Zhao, Xiaoxu; Yoshida, Ikuma

    2014-06-01

    Post-translational modifications in histones have been associated with cancer. Although cigarette sidestream smoke (CSS) as well as mainstream smoke are carcinogens, the relationship between carcinogenicity and histone modifications has not yet been clarified. Here, we demonstrated that CSS induced phosphorylation of histones, involving a carcinogenic process. Treatment with CSS markedly induced the phosphorylation of histone H3 at serine 10 and 28 residues (H3S10 and H3S28), which was independent from the cell cycle, in the human pulmonary epithelial cell model, A549 and normal human lung fibroblasts, MRC-5 and WI-38. Using specific inhibitors and small interfering RNA, the phosphorylation of H3S10 was found to be mediated by c-jun N-terminal kinase (JNK) and phosphoinositide 3-kinase (PI3K)/Akt pathways. These pathways were different from that of the CSS-induced phosphorylation of histone H2AX (γ-H2AX) mediated by Ataxia telangiectasia-mutated (ATM) and ATM-Rad3-related (ATR) protein kinases. A chromatin immunoprecipitation assay revealed that the phosphorylation of H3S10 was increased in the promoter sites of the proto-oncogenes, c-fos and c-jun, which indicated that CSS plays a role in tumor promotion. Because the phosphorylation of H3S10 was decreased in the aldehyde-removed CSS and was significantly induced by treatment with formaldehyde, aldehydes are suspected to partially contribute to this phosphorylation. These findings suggested that any chemicals in CSS, including aldehydes, phosphorylate H3S10 via JNK and PI3K/Akt pathways, which is different from the DNA damage response, resulting in tumor promotion.

  11. Biocompatibility evaluation of cigarette and carbon papers used in repair of traumatic tympanic membrane perforations: experimental study.

    Science.gov (United States)

    Altuntaş, Emine Elif; Sümer, Zeynep

    2013-01-01

    The purposes of this study were to investigate the biocompatibility of two different paper patches (carbon and cigarette papers) and compare the adhesion and proliferation features of L929 fibroblast cells by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT Test) test and scanning electron microscopy (SEM). In this study, time-dependent cytotoxic effects of cigarette and carbon papers used in repairing small traumatic TM perforations were investigated in vitro by using MTT test. And also adhesion and spreading of cells over disk surface were observed by SEM. Cytotoxicity test carried out by MTT analysis on leakage products collected from two types of paper patches at the end of 24 and 48 h revealed no cytotoxicity (P > 0.05). In SEM studies, it was observed that cells started to proliferate over disk surface as a result of 48-h incubation, and SEM revealed that the cell proliferation over cigarette paper was more compared to the one over carbon paper. We believe that this is the first study where biocompatibility and adhesion features of carbon and cigarette paper have been studied by using L929 fibroblast cell culture. As a result, biocompatibility of cigarette paper and also whether cigarette paper was superior to carbon paper in cell attachment and biocompatibility were studied. It was found, by MTT test and SEM test, that cigarette paper had a higher biocompatibility and cell attachment, and thus cigarette paper should be the patch to be preferred in cases where TM perforations are repaired by paper-patch method.

  12. MicroPET Evaluation of a Hydroxamate-Based MMP Inhibitor, [(18)F]FB-ML5, in a Mouse Model of Cigarette Smoke-Induced Acute Airway Inflammation.

    Science.gov (United States)

    Matusiak, Nathalie; van Waarde, Aren; Rozeveld, Dennie; van Oosterhout, Antoon J M; Heijink, Irene H; Castelli, Riccardo; Overkleeft, Herman S; Bischoff, Rainer; Dierckx, Rudi A J O; Elsinga, Philip H

    2015-10-01

    Matrix metalloproteinases (MMPs) are the main proteolytic enzymes involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). A radiolabeled MMP inhibitor, [(18)F]FB-ML5, was prepared, and its in vivo kinetics were tested in a mouse model of pulmonary inflammation. BALB/c mice were exposed for 4 days to cigarette smoke (CS) or air. On the fifth day, a dynamic microPET scan was made with [(18)F]FB-ML5. Standardized uptake values (PET-SUVmean) were 0.19 ± 0.06 in the lungs of CS-exposed mice (n = 6) compared to 0.11 ± 0.03 (n = 5) in air-exposed controls (p FB-ML5.

  13. Trimetazidine protects against smoking-induced left ventricular remodeling via attenuating oxidative stress, apoptosis, and inflammation.

    Directory of Open Access Journals (Sweden)

    Xiang Zhou

    Full Text Available Trimetazidine, a piperazine derivative used as an anti-anginal agent, improves myocardial glucose utilization through inhibition of fatty acid metabolism. The present study was designed to investigate whether trimetazidine has the protective effects against smoking-induced left ventricular remodeling in rats. In this study, Wistar rats were randomly divided into 3 groups: smoking group (exposed to cigarette smoke, trimetazidine group (exposed to cigarette smoke and treated with trimetazidine, and control group. The echocardiographic and morphometric data indicated that trimetazidine has protective effects against smoking-induced left ventricular remodeling. Oxidative stress was evaluated by detecting malondialdehyde, superoxide dismutase, and glutathione peroxidase in the supernatant of left ventricular tissue. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Gene expression and serum levels of inflammatory markers, including interleukin-1β, interleukin-6, and tumor necrosis factor-α, were deteced by quantitative real-time PCR and enzyme-linked immunosorbent assay. Our results suggested that trimetazidine could significantly reduce smoking-induced oxidative stress, apoptosis, and inflammation. In conclusion, our study demonstrates that trimetazidine protects against smoking-induced left ventricular remodeling via attenuating oxidative stress, apoptosis, and inflammation.

  14. 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 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:

  15. 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:

  16. Use of a multistage model to predict time trends in smoking induced lung cancer.

    OpenAIRE

    Swartz, J B

    1992-01-01

    STUDY OBJECTIVE--The aims were to use a mathematical model to predict the time course of smoking induced lung cancer, and to investigate to what extent the most recent increases in lung cancer mortality are due to cigarette smoking. DESIGN--A mathematical model was developed and solved by simulation to construct detailed smoking histories of the US white male population given available prevalence data by age and cohort. A multistage carcinogenesis model was used to predict the time course of ...

  17. Prosthetic mesh "slim-cigarette like" for laparoscopic repair of ventral hernias: a new technique without transabdominal fixation sutures.

    Science.gov (United States)

    Canton, S A; Merigliano, S; Pasquali, C

    2016-06-01

    Prosthetic mesh rolled up and fixed with stitches like a slim cigarette ("slim-mesh") for laparoscopic ventral hernia (VH) repair is an new technique which allows an easy intraperitoneally introduction, distension and circumferential fixation of a prosthetic mesh without transabdominal fixation sutures even for meshes larger than 16 cm up to 30 cm for the "slim-mesh" repair of wide ventral hernias. We report the technique of laparoscopic repair of VH with "slim-mesh". This technique enables an easy intra-peritoneally introduction of the mesh through the trocar because it reduces consistently its size, it allows a rapid intra-abdominal handling of the mesh and a fast and easy fixation for VH repair. The average time of surgery with "slim-mesh" for treatment of all 28 VH was 97 min ranging from 57 to 160 min. The average time for the repair of the 24 VH smaller than 10 cm was 91 and 135 min for the four VH larger than 10-22 cm. This new surgical technique leads to a reduction of surgical risks avoiding the use of transfascial sutures with the associated complications. This new surgical procedure in our experience is fast, safe, simple and also easily reproducible by surgeons in laparoscopic training. This technique may be used in wide VH (larger than 10-22 cm) that generally require open surgery.

  18. Effect of alpha lipoic acid on smoking-induced skin damage.

    Science.gov (United States)

    Yıldırım Baş, Funda; Bayram, Dilek; Arslan, Bahriye; Armağan, Ilkay; Yeşilot, Şükriye; Çiçek, Emine; Yorgancıgil, Emre

    2017-03-01

    Exposed to cigarette leads to the formation of reactive oxygen species and the generation of bioactive molecules that can damage skin cells. This investigation was carried out to study possible effects of Alpha Lipoic Acid (ALA) on smoking-induced rat skin injury. 28 Spraque-Dawley female rats were allocated into three groups: control group (n = 8), smoking group (n = 10; 12 cigarettes/day, 8 weeks) and smoking + ALA group (n = 10; 12 cigarettes/day + 100 mg/kg, 8 weeks). Experiment group animals were sacrificed under anaesthesia with 10%ketamine + 2%xylasine at the end of second mounts and then skin examples were taken from the epigastric area. Histochemical (Haematoxylin-Eosin and Masson's trichrome, immunohistochemical (TNF-α) and biochemical analysis (CAT, MDA and protein carbonylation) were performed on these skin tissues. Histologically, skin was distinguished normal structure in the control group. In the smoking group, collagen bundles and hair follicle degradation/reduction, sweat gland degeneration, mononuclear cell infiltration in dermis were encountered. In ALA-treated group, all of these changes were improved (p  0.05). MDA; which is indicator of lipid peroxidation was significantly higher in cigarette group than in control group (p  0.05). In the ALA it was significantly lower compared to the control group and cigarette (p skin tissues in rats. However, ALA has a curative effect on cigarette-induced injuries on the skin tissues by anti-oxidative and anti-inflammatory effects.

  19. Electronic Cigarettes

    Science.gov (United States)

    ... New FDA Regulations Text Size: A A A Electronic Cigarettes Electronic cigarettes (e-cigarettes) are battery operated products designed ... more about: The latest news and events about electronic cigarettes on this FDA page Electronic cigarette basics ...

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

    Energy Technology Data Exchange (ETDEWEB)

    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

  1. 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

  2. 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

  3. 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

  4. IL-1α/IL-1R1 expression in chronic obstructive pulmonary disease and mechanistic relevance to smoke-induced neutrophilia in mice.

    Directory of Open Access Journals (Sweden)

    Fernando M Botelho

    Full Text Available BACKGROUND: Cigarette smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD, a major cause of morbidity and mortality worldwide. Despite this, the cellular and molecular mechanisms that contribute to COPD pathogenesis are still poorly understood. METHODOLOGY AND PRINCIPAL FINDINGS: The objective of this study was to assess IL-1 α and β expression in COPD patients and to investigate their respective roles in perpetuating cigarette smoke-induced inflammation. Functional studies were pursued in smoke-exposed mice using gene-deficient animals, as well as blocking antibodies for IL-1α and β. Here, we demonstrate an underappreciated role for IL-1α expression in COPD. While a strong correlation existed between IL-1α and β levels in patients during stable disease and periods of exacerbation, neutrophilic inflammation was shown to be IL-1α-dependent, and IL-1β- and caspase-1-independent in a murine model of cigarette smoke exposure. As IL-1α was predominantly expressed by hematopoietic cells in COPD patients and in mice exposed to cigarette smoke, studies pursued in bone marrow chimeric mice demonstrated that the crosstalk between IL-1α+ hematopoietic cells and the IL-1R1+ epithelial cells regulates smoke-induced inflammation. IL-1α/IL-1R1-dependent activation of the airway epithelium also led to exacerbated inflammatory responses in H1N1 influenza virus infected smoke-exposed mice, a previously reported model of COPD exacerbation. CONCLUSIONS AND SIGNIFICANCE: This study provides compelling evidence that IL-1α is central to the initiation of smoke-induced neutrophilic inflammation and suggests that IL-1α/IL-1R1 targeted therapies may be relevant for limiting inflammation and exacerbations in COPD.

  5. Gene Profiles in a Smoke-Induced COPD Mouse Lung Model Following Treatment with Mesenchymal Stem Cells.

    Science.gov (United States)

    Kim, You-Sun; Kokturk, Nurdan; Kim, Ji-Young; Lee, Sei Won; Lim, Jaeyun; Choi, Soo Jin; Oh, Wonil; Oh, Yeon-Mok

    2016-10-01

    Mesenchymal stem cells (MSCs) effectively reduce airway inflammation and regenerate the alveolus in cigarette- and elastase-induced chronic obstructive pulmonary disease (COPD) animal models. The effects of stem cells are thought to be paracrine and immune-modulatory because very few stem cells remain in the lung one day after their systemic injection, which has been demonstrated previously. In this report, we analyzed the gene expression profiles to compare mouse lungs with chronic exposure to cigarette smoke with non-exposed lungs. Gene expression profiling was also conducted in a mouse lung tissue with chronic exposure to cigarette smoke following the systemic injection of human cord blood-derived mesenchymal stem cells (hCB-MSCs). Globally, 834 genes were differentially expressed after systemic injection of hCB-MSCs. Seven and 21 genes, respectively, were up-and downregulated on days 1, 4, and 14 after HCB-MSC injection. The Hbb and Hba, genes with oxygen transport and antioxidant functions, were increased on days 1 and 14. A serine protease inhibitor was also increased at a similar time point after injection of hCB-MSCs. Gene Ontology analysis indicated that the levels of genes related to immune responses, metabolic processes, and blood vessel development were altered, indicating host responses after hCB-MSC injection. These gene expression changes suggest that MSCs induce a regeneration mechanism against COPD induced by cigarette smoke. These analyses provide basic data for understanding the regeneration mechanisms promoted by hCB-MSCs in cigarette smoke-induced COPD.

  6. Cigarette smoke-induced necroptosis and DAMP release trigger neutrophilic airway inflammation in mice

    NARCIS (Netherlands)

    Pouwels, Simon D; van der Toorn, Marco; Hesse, Laura; Gras, Renee; Ten Hacken, Nick H T; Krysko, Dmitri V; Vandenabeele, Peter; de Vries, Maaike; van Oosterhout, Antoon J M; Heijink, Irene H; Nawijn, Martijn C

    2015-01-01

    Recent data indicate a role for airway epithelial necroptosis, a regulated form of necrosis, and the associated release of damage associated molecular patterns (DAMPs) in the development of COPD. DAMPs can activate pattern recognition receptors (PRRs), triggering innate immune responses. We hypothes

  7. Cigarette smoke-induced emphysema : A role for the B cell?

    NARCIS (Netherlands)

    van der Strate, BWA; Postma, DS; Brandsma, CA; Melgert, BN; Luinge, MA; Geerlings, M; Hylkema, MN; van den Berg, Anke; Timens, W; Kerstjens, HAM

    2006-01-01

    Rationale: Little is known about what drives the inflammatory reaction in the development of chronic obstructive lung disease. B cells have been found. Objective: To study the involvement of B cells in the development of emphysema. Methods: The presence of B-cell follicles and their interaction with

  8. Electronic cigarette (e-cigarette

    Directory of Open Access Journals (Sweden)

    Erdinc Nayir

    2016-04-01

    Full Text Available Electronic cigarette (e-cigarette is a device developed with an intent to enable smokers to quit smoking and avoid the unhealthful effects of cigarettes. The popularity of e-cigarette has increased rapidly in recent years. The increase in its use during the adolescence period is attention-grabbing. Despite the fact that e-cigarette has become popular in a dramatic way, there are certain differences of opinion regarding its long-term effects on health, in particular. While some people assert that it is less harmful than conventional cigarettes, some others assert the contrary. Although e-cigarette contains less toxic substances compared to conventional cigarette, it contains certain carcinogens existing in conventional cigarette such as formaldehyde and acetaldehyde. It also contains heavy metals (nickel, chrome that conventional cigarette does not contain; and therefore, raises concerns about health. E-cigarette leads to upper and lower respiratory tract irritation as well as an increased airway resistance and an increased bacterial colonization in the respiratory tract. It may also cause tahcycardia and increase diastolic blood pressure. Although e-cigarette has been found to have certain benefits in terms of smoking cessation, most of the studies have shown unfavorable results. In this collected work, the effects of e-cigarette on health and its role in smoking cessation are discussed in detail.

  9. Waterpipe smoking induces epigenetic changes in the small airway epithelium.

    Science.gov (United States)

    Walters, Matthew S; Salit, Jacqueline; Ju, Jin Hyun; Staudt, Michelle R; Kaner, Robert J; Rogalski, Allison M; Sodeinde, Teniola B; Rahim, Riyaad; Strulovici-Barel, Yael; Mezey, Jason G; Almulla, Ahmad M; Sattar, Hisham; Mahmoud, Mai; Crystal, Ronald G

    2017-01-01

    Waterpipe (also called hookah, shisha, or narghile) smoking is a common form of tobacco use in the Middle East. Its use is becoming more prevalent in Western societies, especially among young adults as an alternative form of tobacco use to traditional cigarettes. While the risk to cigarette smoking is well documented, the risk to waterpipe smoking is not well defined with limited information on its health impact at the epidemiologic, clinical and biologic levels with respect to lung disease. Based on the knowledge that airway epithelial cell DNA methylation is modified in response to cigarette smoke and in cigarette smoking-related lung diseases, we assessed the impact of light-use waterpipe smoking on DNA methylation of the small airway epithelium (SAE) and whether changes in methylation were linked to the transcriptional output of the cells. Small airway epithelium was obtained from 7 nonsmokers and 7 light-use (2.6 ± 1.7 sessions/wk) waterpipe-only smokers. Genome-wide comparison of SAE DNA methylation of waterpipe smokers to nonsmokers identified 727 probesets differentially methylated (fold-change >1.5, pwaterpipe smoking is associated with epigenetic changes and related transcriptional modifications in the SAE, the cell population demonstrating the earliest pathologic abnormalities associated with chronic cigarette smoking.

  10. Effect of cigarette smoking on arterial stiffness re-interpreted using a structurally-based model

    DEFF Research Database (Denmark)

    Enevoldsen, Marie Sand; Humphrey, Jay D.; Lönn, Lars

    Cigarette smoking constitutes a major risk factor for diverse cardiovascular diseases (CVD). Many physiological and pathophysiological parameters affect arterial stiffness. While underlying mechanisms remain unclear, smoking increases arterial stiffness, which contributes to many disease processes...... parameters. The primary finding was that cigarette smoking induces significant increases in the material parameters describing the micromechanical properties of all four families of collagen fibers with increased duration of smoking. Additionally, there was a moderate increase in the material parameter...

  11. Cigarette smoke differentially modulates dendritic cell maturation and function in time

    NARCIS (Netherlands)

    Givi, Masoumeh Ezzati; Folkerts, Gert; Wagenaar, Gerry T M; Redegeld, Frank A; Mortaz, Esmaeil

    2015-01-01

    BACKGROUND: Dendritic cells (DCs) as professional antigen presenting cells (APCs) play a critical role in the regulation of host immune responses. DCs evolve from immature, antigen-capturing cells, to mature antigen-presenting cells. The relative contribution of DCs to cigarette smoke-induced inflam

  12. Smoking-induced CXCL14 expression in the human airway epithelium links chronic obstructive pulmonary disease to lung cancer.

    Science.gov (United States)

    Shaykhiev, Renat; Sackrowitz, Rachel; Fukui, Tomoya; Zuo, Wu-Lin; Chao, Ion Wa; Strulovici-Barel, Yael; Downey, Robert J; Crystal, Ronald G

    2013-09-01

    CXCL14, a recently described epithelial cytokine, plays putative multiple roles in inflammation and carcinogenesis. In the context that chronic obstructive pulmonary disease (COPD) and lung cancer are both smoking-related disorders associated with airway epithelial disorder and inflammation, we hypothesized that the airway epithelium responds to cigarette smoking with altered CXCL14 gene expression, contributing to the disease-relevant phenotype. Using genome-wide microarrays with subsequent immunohistochemical analysis, the data demonstrate that the expression of CXCL14 is up-regulated in the airway epithelium of healthy smokers and further increased in COPD smokers, especially within hyperplastic/metaplastic lesions, in association with multiple genes relevant to epithelial structural integrity and cancer. In vitro experiments revealed that the expression of CXCL14 is induced in the differentiated airway epithelium by cigarette smoke extract, and that epidermal growth factor mediates CXCL14 up-regulation in the airway epithelium through its effects on the basal stem/progenitor cell population. Analyses of two independent lung cancer cohorts revealed a dramatic up-regulation of CXCL14 expression in adenocarcinoma and squamous-cell carcinoma. High expression of the COPD-associated CXCL14-correlating cluster of genes was linked in lung adenocarcinoma with poor survival. These data suggest that the smoking-induced expression of CXCL14 in the airway epithelium represents a novel potential molecular link between smoking-associated airway epithelial injury, COPD, and lung cancer.

  13. 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. Copyright © 2015, American Society for Microbiology. All Rights Reserved.

  14. Smoking-induced Skeletal Muscle Dysfunction. From Evidence to Mechanisms

    NARCIS (Netherlands)

    Degens, H.; Gayan-Ramirez, G.; Hees, H.W.H. van

    2015-01-01

    Smoking is the most important risk factor for the development of chronic obstructive pulmonary disease (COPD). Patients with COPD commonly suffer from skeletal muscle dysfunction, and it has been suggested that cigarette smoke exposure contributes to the development of skeletal muscle dysfunction

  15. DNA repair single-nucleotide polymorphisms in colorectal cancer and their role as modifiers of the effect of cigarette smoking and alcohol in the Singapore Chinese Health Study.

    Science.gov (United States)

    Stern, Mariana C; Conti, David V; Siegmund, Kimberly D; Corral, Román; Yuan, Jian-Min; Koh, Woon-Puay; Yu, Mimi C

    2007-11-01

    Recently, we reported that among Singapore Chinese, cigarette smoking and alcohol drinking were independent risk factors for colorectal cancer. Both tobacco smoking and alcohol use are plausible colorectal cancer risk factors, partly due to their ability to induce mutations in the colorectal lumen. In the present study, we investigated the role in colorectal cancer of single-nucleotide polymorphisms in five DNA repair genes: XRCC1 (Arg(194)Trp and Arg(399)Gln), PARP (Val(762)Ala, Lys(940)Arg), XPD (Asp(312)Asn, Lys(751)Gln), OGG1 (Ser(326)Cys), and MGMT (Leu(84)Phe). We conducted this study within the Singapore Chinese Health Study, a population-based cohort of 63,257 middle-aged and older Singapore Chinese men and women enrolled between 1993 and 1998. Our study included 1,176 controls and 310 cases (180 colon and 130 rectum cancer). We observed a positive association between the PARP codon 940 Lys/Arg and Arg/Arg genotypes and colorectal cancer risk [odds ratio (OR), 1.8; 95% confidence interval (95% CI), 1.1-3.1], and an inverse association between the MGMT codon 84 Leu/Phe or Phe/Phe genotypes and colon cancer risk (OR, 0.6; 95% CI, 0.3-0.9), but not rectal cancer (test of heterogeneity by tumor site, P=0.027). We observed evidence that XRCC1 may modify the effects of smoking (interaction P=0.012). The effect of smoking among carriers of the Arg(194)-Gln(399) haplotype was OR=0.7 (95% CI, 0.4-1.1), whereas, among carriers of the Trp(194)-Arg(399) haplotype, it was OR=1.6 (95% CI, 1.1-2.5). We also observed a nonstatistically significant modification of XRCC1 on the effects of alcohol (P=0.245). Whereas alcohol had no effect among carriers of the codon 194 Arg/Arg (OR, 1.0; 95% CI, 0.6-1.7) or Arg/Trp genotypes (OR, 1.1; 95% CI, 0.6-1.9), there was a positive association among carriers of the Trp/Trp genotype (OR, 2.8; 95% CI, 1.0-8.1). Our results support a role for reactive oxygen species as relevant genotoxins that may account for the effects of both smoking

  16. Smoke-induced seed germination in California chaparral

    Science.gov (United States)

    Keeley, J.E.; Fotheringham, C.J.

    1998-01-01

    The California chaparral community has a rich flora of species with different mechanisms for cuing germination to postfire conditions. Heat shock triggers germination of certain species but has no stimulatory effect on a great many other postfire species that are chemically stimulated by combustion products. Previous reports have shown that charred wood will induce germination, and here we report that smoke also induces germination in these same species. Smoke is highly effective, often inducing 100% germination in deeply dormant seed populations with 0% control germination. Smoke induces germination both directly and indirectly by aqueous or gaseous transfer from soil to seeds. Neither nitrate nor ammonium ions were effective in stimulating germination of smoke-stimulated species, nor were most of the quantitatively important gases generated by biomass smoke. Nitrogen dioxide, however, was very effective at inducing germination in Caulanthus heterophyllus (Brassicaceae), Emmenanthe penduliflora (Hydrophyllaceae), Phacelia grandiflora (Hydrophyllaceae), and Silene multinervia (Caryophyllaceae). Three species, Dendromecon rigida (Papaveraceae), Dicentra chrysantha, and Trichostema lanatum (Lamiaceae), failed to germinate unless smoke treatment was coupled with prior treatment of 1 yr soil storage. Smoke-stimulated germination was found in 25 chaparral species, representing 11 families, none of which were families known for heat-shock-stimulated germination. Seeds of smoke-stimulated species have many analogous characteristics that separate them from most heat-shock-stimulated seeds, including: (1) outer seed coats that are highly textured, (2) a poorly developed outer cuticle, (3) absence of a dense palisade tissue in the seed coat, and (4) a subdermal membrane that is semipermeable, allowing water passage but blocking entry of large (molecular mass > 500) solutes. Tentative evidence suggests that permeability characteristics of this subdermal layer are altered by

  17. 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

  18. 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.

  19. Regional Heterogeneity in Murine Lung Fibroblasts from Normal Mice or Mice Exposed Once to Cigarette Smoke

    Science.gov (United States)

    Preobrazhenska, Olena; Wright, Joanne L.; Churg, Andrew

    2012-01-01

    Chronic obstructive lung disease (COPD) is characterized by matrix deposition in the small airways but matrix loss from the parenchyma, phenomena which must depend on the ability of local fibroblasts to produce matrix after smoke exposure. To investigate this idea, we exposed C57Bl/6 mice once to cigarette smoke or to air (control) and prepared primary cultures of lung fibroblasts by microdissecting large airways (trachea, LAF), medium size airways (major bronchi, MAF) and parenchyma (PF). Control PF showed the lowest rate of wound closure and wound closure was depressed in all lines by a single in vivo smoke exposure. Gene expression of matrix proteins differed considerably among the sites; decorin, which may sequester TGFβ, was markedly higher in PF. PF showed higher intrinsic ratios of pSmad2/Smad2. Smoke caused much greater increases in secreted and matrix deposited collagens 1 and 3 in PF than in LAF or MAF. Expression of Thy-1, a gene that suppresses myofibroblast differentiation, was increased by smoke in PF. We conclude that there is considerable regional heterogeneity in murine lung fibroblasts in terms of matrix production, either basally or after in vivo smoke exposure; that PF have lower ability to repair wounds and higher intrinsic TGFβ signaling; and that a single exposure to smoke produces lasting changes in the pattern of matrix production and wound repair, changes that may be mediated in part by smoke-induced release of TGFβ. However, PF still retain the ability to repair by producing new matrix after a single in vivo smoke exposure. PMID:22761892

  20. Resveratrol mediated cell death in cigarette smoke transformed breast epithelial cells is through induction of p21Waf1/Cip1 and inhibition of long patch base excision repair pathway

    Energy Technology Data Exchange (ETDEWEB)

    Mohapatra, Purusottam; Satapathy, Shakti Ranjan; Das, Dipon; Siddharth, Sumit [Cancer Biology Division, KIIT School of Biotechnology, KIIT University, Campus-11, Patia, Bhubaneswar, Orissa 751024 (India); Choudhuri, Tathagata [Institute of Life Sciences, Nalco Square, Bhubaneswar, Orissa 751023 (India); Department of Biotechnology, Visva Bharati University, Santiniketan, West Bengal (India); Kundu, Chanakya Nath, E-mail: cnkundu@gmail.com [Cancer Biology Division, KIIT School of Biotechnology, KIIT University, Campus-11, Patia, Bhubaneswar, Orissa 751024 (India)

    2014-03-15

    Cigarette smoking is a key factor for the development and progression of different cancers including mammary tumor in women. Resveratrol (Res) is a promising natural chemotherapeutic agent that regulates many cellular targets including p21, a cip/kip family of cyclin kinase inhibitors involved in DNA damage-induced cell cycle arrest and blocking of DNA replication and repair. We have recently shown that cigarette smoke condensate (CSC) prepared from commercially available Indian cigarette can cause neoplastic transformation of normal breast epithelial MCF-10A cell. Here we studied the mechanism of Res mediated apoptosis in CSC transformed (MCF-10A-Tr) cells in vitro and in vivo. Res mediated apoptosis in MCF-10A-Tr cells was a p21 dependent event. It increased the p21 protein expression in MCF-10A-Tr cells and MCF-10A-Tr cells-mediated tumors in xenograft mice. Res treatment reduced the tumor size(s) and expression of anti-apoptotic proteins (e.g. PI3K, AKT, NFκB) in solid tumor. The expressions of cell cycle regulatory (Cyclins, CDC-2, CDC-6, etc.), BER associated (Pol-β, Pol-δ, Pol-ε, Pol-η, RPA, Fen-1, DNA-Ligase-I, etc.) proteins and LP-BER activity decreased in MCF-10A-Tr cells but remain significantly unaltered in isogenic p21 null MCF-10A-Tr cells after Res treatment. Interestingly, no significant changes were noted in SP-BER activity in both the cell lines after Res exposure. Finally, it was observed that increased p21 blocks the LP-BER in MCF-10A-Tr cells by increasing its interaction with PCNA via competing with Fen-1 after Res treatment. Thus, Res caused apoptosis in CSC-induced cancer cells by reduction of LP-BER activity and this phenomenon largely depends on p21. - Highlights: • Resveratrol (Res) caused reduction of MCF-10A-Tr cell growth by inducing apoptosis. • Res caused cell cycle arrest and DNA damage in p21 dependent manner. • Res mediated LP-BER reduction in MCF-10A-Tr cells was a p21 dependent phenomenon. • Res inhibits BER and PI

  1. Surfactant protein D is a candidate biomarker for subclinical tobacco smoke-induced lung damage

    DEFF Research Database (Denmark)

    Johansson, Sofie L.; Tan, Qihua; Holst, René;

    2014-01-01

    Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage. The associat......Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage...... or haplotypes, and expiratory lung function were assessed using twin study methodology and mixed-effects models. Significant inverse associations were evident between sSP-D and the forced expiratory volume in 1 second and forced vital capacity in the presence of current tobacco smoking but not in non...... with lung function measures in interaction with tobacco smoking. The obtained data suggest sSP-D as a candidate biomarker in risk assessments for subclinical tobacco smoke-induced lung damage. The data and derived conclusion warrant confirmation in a longitudinal population following chronic obstructive...

  2. 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.

  3. Aryl hydrocarbon receptor protects lung adenocarcinoma cells against cigarette sidestream smoke particulates-induced oxidative stress

    Energy Technology Data Exchange (ETDEWEB)

    Cheng, Ya-Hsin [Graduate Institute of Basic Medical Science, School of Medicine, China Medical University, Taichung 40402, Taiwan, ROC (China); Huang, Su-Chin; Lin, Chun-Ju; Cheng, Li-Chuan [Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Zhunan, Miaoli 35053, Taiwan, ROC (China); Li, Lih-Ann, E-mail: lihann@nhri.org.tw [Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Zhunan, Miaoli 35053, Taiwan, ROC (China)

    2012-03-15

    Environmental cigarette smoke has been suggested to promote lung adenocarcinoma progression through aryl hydrocarbon receptor (AhR)-signaled metabolism. However, whether AhR facilitates metabolic activation or detoxification in exposed adenocarcinoma cells remains ambiguous. To address this question, we have modified the expression level of AhR in two human lung adenocarcinoma cell lines and examined their response to an extract of cigarette sidestream smoke particulates (CSSP). We found that overexpression of AhR in the CL1-5 cell line reduced CSSP-induced ROS production and oxidative DNA damage, whereas knockdown of AhR expression increased ROS level in CSSP-exposed H1355 cells. Oxidative stress sensor Nrf2 and its target gene NQO1 were insensitive to AhR expression level and CSSP treatment in human lung adenocarcinoma cells. In contrast, induction of AhR expression concurrently increased mRNA expression of xenobiotic-metabolizing genes CYP1B1, UGT1A8, and UGT1A10 in a ligand-independent manner. It appeared that AhR accelerated xenobiotic clearing and diminished associated oxidative stress by coordinate regulation of a set of phase I and II metabolizing genes. However, the AhR-signaled protection could not shield cells from constant oxidative stress. Prolonged exposure to high concentrations of CSSP induced G0/G1 cell cycle arrest via the p53–p21–Rb1 signaling pathway. Despite no effect on DNA repair rate, AhR facilitated the recovery of cells from growth arrest when CSSP exposure ended. AhR-overexpressing lung adenocarcinoma cells exhibited an increased anchorage-dependent and independent proliferation when recovery from exposure. In summary, our data demonstrated that AhR protected lung adenocarcinoma cells against CSSP-induced oxidative stress and promoted post-exposure clonogenicity. -- Highlights: ► AhR expression level influences cigarette sidestream smoke-induced ROS production. ► AhR reduces oxidative stress by coordinate regulation of

  4. Genetic ablation of the fpr1 gene confers protection from smoking-induced lung emphysema in mice.

    Science.gov (United States)

    Cardini, Silvia; Dalli, Jesmond; Fineschi, Silvia; Perretti, Mauro; Lungarella, Giuseppe; Lucattelli, Monica

    2012-09-01

    Cigarette smoke (CS) is the main causative factor of chronic obstructive pulmonary disease (COPD). Current research supports the concept that airway inflammation is central to the development and progression of the disease. Studies have demonstrated that neutrophils are increased in COPD lungs and that neutrophil-associated products correlate with the development and severity of COPD. The peptide FMLP is an active component of CS. FMLP interacts on the neutrophil and macrophage membranes with a high-affinity receptor subtype (FPR1) and with a low-affinity subtype FPRL1, promoting a chemotactic response, superoxide anion production, and degranulation. Bacterial colonization of the lower respiratory tract and lung cell damage may represent further sources of formyl peptides in patients with COPD. We investigated the role of FPR in a mouse model on lung inflammation and emphysema induced by CS. Here, we report the novel observation that genetic ablation of the FPR1 gene (Fpr1) confers protection from smoking-induced lung emphysema in mice. Compared with wild-type mice, Fpr1 knockout mice displayed marked decreases in the lung migration of neutrophils and macrophages after CS exposure. Upon transgenic approach, the changes in cell numbers were accompanied by marked modulation of the expression of genes implicated in the inflammatory response. Administration of the FPR1 antagonist cyclosporine H to wild-type mice attenuated the acute inflammatory response evoked by CS. These findings may have clinical significance because current smokers and subjects with emphysema showed increased FPR expression in bronchoalveolar fluids and on peripheral neutrophils. Modulating the FPR1 signal should be explored as a potential new therapy.

  5. 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.

  6. 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.

  7. Radionuclides in cigarettes may lead to carcinogenesis via p16{sup INK4a} inactivation

    Energy Technology Data Exchange (ETDEWEB)

    Prueitt, Robyn L.; Goodman, Julie E. [Gradient Corporation, 20 University Road, Cambridge, MA 02138 (United States); Valberg, Peter A. [Gradient Corporation, 20 University Road, Cambridge, MA 02138 (United States)], E-mail: pvalberg@gradientcorp.com

    2009-02-15

    It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including {alpha}-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16{sup INK4a} (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated.

  8. Radionuclides in cigarettes may lead to carcinogenesis via p16(INK4a) inactivation.

    Science.gov (United States)

    Prueitt, Robyn L; Goodman, Julie E; Valberg, Peter A

    2009-02-01

    It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including alpha-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16(INK4a) (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated.

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

    Science.gov (United States)

    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.

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

    Directory of Open Access Journals (Sweden)

    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.

  11. Cotinine Concentration in Serum Correlates with Tobacco Smoke-Induced Emphysema in Mice

    Science.gov (United States)

    Xu, Xin; Su, Yunchao; Fan, Z. Hugh

    2014-01-01

    Secondhand smoke (SHS) has been associated with a variety of adverse health outcomes in nonsmokers, including emphysema (a chronic obstructive pulmonary disease). One way to detect SHS exposure is to measure the concentration of cotinine, the primary metabolite of nicotine, in bodily fluids. We have developed a method for cotinine analysis by combining micellar electrokinetic chromatography with enrichment techniques. We employed the method to measure cotinine concentrations in serum samples of mice exposed to tobacco smoke for 12 or 24 weeks and found that it was 3.1-fold or 4.8-fold higher than those exposed to room air for the same period. Further, we investigated the morphological changes in lungs of mice and observed tobacco smoke induced emphysema. Our results indicate that the method can be used to measure cotinine and there is an association between the serum cotinine concentration and tobacco smoke-induced emphysema in mice.

  12. Side-stream cigarette smoke accentuates immunomodulation during murine AIDS.

    Science.gov (United States)

    Zhang, Jin; Du Ester, En-Jie; Watson, Ronald Ross

    2002-05-01

    Side-stream cigarette smoke has become a hotly debated social, political, and scientific health and safety issue for nonsmokers. The harmful influences of side-stream cigarette smoke on human health are its adverse effects on the immune system, especially when already compromised by other agents. Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by human immunodeficiency virus (HIV). To facilitate studies, murine AIDS was induced in C57BL/6 mice by LP-BM5 murine leukemia virus infection, which mimics human AIDS. After 2 weeks of retroviral infection, the mice were exposed to side-stream cigarette smoke for 30 min, 5 days/week for 12 weeks using a side-stream cigarette smoke exposure system. Murine retrovirus infection reduced the in vitro proliferation of T lymphocytes stimulated by concanavalin A, increased the release of pro-inflammatory cytokine interleukin-6 (IL-6) tumor necrosis factor-alpha (TNF-alpha), increased the hepatic lipid peroxidation and decreased the alpha-tocopherol levels in liver, lung and heart. Concomitant side-stream cigarette smoke exposure for 12 weeks further inhibited the proliferation of T cells, increased the release of TNF-alpha, IL-6 cytokines and enhanced the hepatic lipid peroxidation from retrovirus infected mice. The loss of alpha-tocopherol was also further enhanced by side-stream cigarette smoke exposure during retrovirus infection. Our conclusions are that side-stream cigarette smoke induced increasing oxidative stress, reducing nutrient concentrations and suppressing immune function could make mice with murine AIDS more susceptible to opportunistic infections, potentially accelerating murine AIDS progression. Thus, the reduction of side-stream cigarette smoke exposure is an important health issue in AIDS patients to improve the quality and quantity of their lives.

  13. Effects of cigarette smoking on metabolic events in the lung

    Energy Technology Data Exchange (ETDEWEB)

    Kitamura, S.

    1987-06-01

    Nicotine and cigarette smoke extract show acute physiological effects: increasing tracheal pressure (P/sub TR/), pulmonary artery pressure (P/sub PA/), systemic blood pressure (P/sub SYST/), and left atrium pressure (P/sub LA/); and decreasing cardiac output (Q/sub AORTA/) and blood flow to the left lower lobe (Q/sub LLL/). In addition, cigarette smoking induces bronchoconstriction, thus decreasing peak flow, FVC, and FEV/sub 1.0/ in healthy subjects. It has also been demonstrated that cigarette smoking caused temporary slowing of mucociliary clearance in the lung and that cigarette smoke increases the activity of aryl hydrocarbon hydroxylase which metabolizes benzo(..cap alpha..)pyrene. The authors demonstrated that serum angiotensin I converting enzyme (ACE) activity showed a significant increase immediately after smoking and returned to the control level 20 min after smoking. They also demonstrated that plasma histamine levels showed a marked decrease after smoking. Furthermore, the effects of cigarette smoke and related substances on prostaglandin, thromboxane, testosterone, cyclic nucleotides metabolism, and protein synthesis were also investigated.

  14. Muscarinic M3 receptor stimulation increases cigarette smoke-induced IL-8 secretion by human airway smooth muscle cells

    NARCIS (Netherlands)

    Gosens, R.; Rieks, D.; Meurs, H.; Ninaber, D. K.; Rabe, K. F.; Nanninga, J.; Kolahian, S.; Halayko, A. J.; Hiemstra, P. S.; Zuyderduyn, S.

    2009-01-01

    Acetylcholine is the primary parasympathetic neurotransmitter in the airways and is known to cause bronchoconstriction and mucus secretion. Recent findings suggest that acetylcholine also regulates aspects of remodelling and inflammation through its action on muscarinic receptors. In the present

  15. Muscarinic M3 receptor stimulation increases cigarette smoke-induced IL-8 secretion by human airway smooth muscle cells

    NARCIS (Netherlands)

    Gosens, R.; Rieks, D.; Meurs, H.; Ninaber, D. K.; Rabe, K. F.; Nanninga, J.; Kolahian, S.; Halayko, A. J.; Hiemstra, P. S.; Zuyderduyn, S.

    2009-01-01

    Acetylcholine is the primary parasympathetic neurotransmitter in the airways and is known to cause bronchoconstriction and mucus secretion. Recent findings suggest that acetylcholine also regulates aspects of remodelling and inflammation through its action on muscarinic receptors. In the present stu

  16. 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.

  17. Resolvin D1 prevents smoking-induced emphysema and promotes lung tissue regeneration

    Directory of Open Access Journals (Sweden)

    Kim KH

    2016-05-01

    Full Text Available Kang-Hyun Kim,1 Tai Sun Park,2,3 You-Sun Kim,1,3 Jae Seung Lee,2,3 Yeon-Mok Oh,2,3 Sang-Do Lee,2,3 Sei Won Lee2,3 1Asan Institute for Life Sciences, 2Department of Pulmonology and Critical Care Medicine, Clinical Research Center for Chronic Obstructive Airway Diseases, Asan Medical Center, 3Department of Pulmonology and Critical Care Medicine, University of Ulsan College of Medicine, Seoul, Republic of Korea Purpose: Emphysema is an irreversible disease that is characterized by destruction of lung tissue as a result of inflammation caused by smoking. Resolvin D1 (RvD1, derived from docosahexaenoic acid, is a novel lipid that resolves inflammation. The present study tested whether RvD1 prevents smoking-induced emphysema and promotes lung tissue regeneration.Materials and methods: C57BL/6 mice, 8 weeks of age, were randomly divided into four groups: control, RvD1 only, smoking only, and smoking with RvD1 administration. Four different protocols were used to induce emphysema and administer RvD1: mice were exposed to smoking for 4 weeks with poly(I:C or to smoking only for 24 weeks, and RvD1 was injected within the smoking exposure period to prevent regeneration or after completion of smoking exposure to assess regeneration. The mean linear intercept and inflammation scores were measured in the lung tissue, and inflammatory cells and cytokines were measured in the bronchoalveolar lavage fluid.Results: Measurements of mean linear intercept showed that RvD1 significantly attenuated smoking-induced lung destruction in all emphysema models. RvD1 also reduced smoking-induced inflammatory cell infiltration, which causes the structural derangements observed in emphysema. In the 4-week prevention model, RvD1 reduced the smoking-induced increase in eosinophils and interleukin-6 in the bronchoalveolar lavage fluid. In the 24-week prevention model, RvD1 also reduced the increased neutrophils and total cell counts induced by smoking.Conclusion: RvD1

  18. 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

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

    Science.gov (United States)

    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.

  20. 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.

  1. Hypermethylation of CCND2 May Reflect a Smoking-Induced Precancerous Change in the Lung

    Directory of Open Access Journals (Sweden)

    Alexander Salskov

    2011-01-01

    Full Text Available It remains unknown whether tobacco smoke induces DNA hypermethylation as an early event in carcinogenesis or as a late event, specific to overt cancer tissue. Using MethyLight assays, we analyzed 316 lung tissue samples from 151 cancer-free subjects (121 ever-smokers and 30 never-smokers for hypermethylation of 19 genes previously observed to be hypermethylated in nonsmall cell lung cancers. Only APC (39%, CCND2 (21%, CDH1 (7%, and RARB (4% were hypermethylated in >2% of these cancer-free subjects. CCND2 was hypermethylated more frequently in ever-smokers (26% than in never-smokers (3%. CCND2 hypermethylation was also associated with increased age and upper lobe sample location. APC was frequently hypermethylated in both ever-smokers (41% and never-smokers (30%. BVES, CDH13, CDKN2A (p16, CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated (<2% in all subjects. Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.

  2. Cigarette Smoking and Erectile Dysfunction: Focus on NO Bioavailability and ROS Generation

    Science.gov (United States)

    Tostes, Rita C.; Carneiro, Fernando S.; Lee, Anthony J.; Giachini, Fernanda R.C.; Leite, Romulo; Osawa, Yoichi; Webb, R. Clinton

    2010-01-01

    Introduction Thirty million men in the United States suffer from erectile dysfunction (ED) and this number is expected to double by 2025. Considered a major public health problem, which seriously affects the quality of life of patients and their partners, ED becomes increasingly prevalent with age and chronic smoking is a major risk factor in the development of ED. Aim To review available evidence concerning the effects of cigarette smoking on vascular changes associated with decreased nitric oxide (NO) bioavailability and increased reactive oxygen species (ROS) generation. Methods We examined epidemiological and clinical data linking cigarette smoking and ED, and the effects of smoking on vascular NO bioavailability and ROS generation. Main Outcome Measures There are strong parallels between smoking and ED and considerable evidence supporting the concept that smoking-related ED is associated with reduced bioavailability of NO because of increased ROS. Results Cigarette smoking-induced ED in human and animal models is associated with impaired arterial flow to the penis or acute vasospasm of the penile arteries. Long-term smoking produces detrimental effects on the vascular endothelium and peripheral nerves and also causes ultrastructural damage to the corporal tissue, all considered to play a role in chronic smoking-induced ED. Clinical and basic science studies provide strong indirect evidence that smoking may affect penile erection by the impairment of endothelium-dependent smooth muscle relaxation or more specifically by affecting NO production via increased ROS generation. Whether nicotine or other products of cigarette smoke mediate all effects related to vascular damage is still unknown. Conclusions Smoking prevention represents an important approach for reducing the risk of ED. The characterization of the components of cigarette smoke leading to ED and the mechanisms by which these components alter signaling pathways activated in erectile responses are

  3. Low-Yield Cigarettes

    Science.gov (United States)

    ... Program Division of Reproductive Health More CDC Sites Low-Yield Cigarettes Recommend on Facebook Tweet Share Compartir ... they compensate when smoking them. Smokers Who Use Low-Yield Cigarettes Many smokers consider smoking low-yield ...

  4. Cigarette smoke exposure reveals a novel role for the MEK/ERK1/2 MAPK pathway in regulation of CFTR.

    Science.gov (United States)

    Xu, Xiaohua; Balsiger, Robert; Tyrrell, Jean; Boyaka, Prosper N; Tarran, Robert; Cormet-Boyaka, Estelle

    2015-06-01

    Cystic fibrosis transmembrane conductance regulator plays a key role in maintenance of lung fluid homeostasis. Cigarette smoke decreases CFTR expression in the lung but neither the mechanisms leading to CFTR loss, nor potential ways to prevent its loss have been identified to date. The molecular mechanisms leading to down-regulation of CFTR by cigarette smoke were determined using pharmacologic inhibitors and silencing ribonucleic acids (RNAs). Using human bronchial epithelial cells, here we show that cigarette smoke induces degradation of CFTR that is attenuated by lysosomal inhibitors, but not proteasome inhibitors. Cigarette smoke can activate multiple signaling pathways in airway epithelial cells, including the MEK/Erk1/2 MAPK (MEK: mitogen-activated protein kinase/ERK kinase Erk1/2: extracellular signal-regulated kinase 1/2 MAPK: Mitogen-activated protein kinase) pathway regulating cell survival. Interestingly, pharmacological inhibition of the MEK/Erk1/2 MAPK pathway prevented the loss of plasma membrane CFTR upon cigarette smoke exposure. Similarly, decreased expression of Erk1/2 using silencing RNAs prevented the suppression of CFTR protein by cigarette smoke. Conversely, specific inhibitors of the c-Jun N-terminal kinase (JNK) or p38 MAPK pathways had no effect on CFTR decrease after cigarette smoke exposure. In addition, inhibition of the MEK/Erk1/2 MAPK pathway prevented the reduction of the airway surface liquid observed upon cigarette smoke exposure of primary human airway epithelial cells. Finally, addition of the antioxidant N-acetylcysteine inhibited activation of Erk1/2 by cigarette smoke and precluded the cigarette smoke-induced decrease of CFTR. These results show that the MEK/Erk1/2 MAPK pathway regulates plasma membrane CFTR in human airway cells. The MEK/Erk1/2 MAPK pathway should be considered as a target for strategies to maintain/restore CFTR expression in the lung of smokers. Copyright © 2015 Elsevier B.V. All rights reserved.

  5. 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

  6. STUDY ON INFLAMMATORY CELLS IN BALF OF SMOKE-INDUCED CHRONIC BRONCHITIS RAT MODEL

    Institute of Scientific and Technical Information of China (English)

    李庆云; 黄绍光; 吴华成; 程齐俭; 项轶; 万欢英

    2004-01-01

    Objective To establish a smoke-induced chronic bronchitis rat model and evaluate the pathological change semi-quantitatively, and study the characteristics of the inflammatory cells in the bronchoalveolar lavage fluid (BALF) in various stages. Methods Chronic bronchitis sequential rat model was established by passively inhaling smoke mixture. Experiments were performed in 30 young male Sprague-Dawley rats, which comprised 5 groups in random, i.e.,4 chronic bronchitis model groups and I control group. After stained with hematoxylin and eosin, the specimens were studied by semi-quantitative method to evaluate the morphologic changes in various stages. Meanwhile, the inflammatory cells of the BALF and the activity of myeloperoxidase ( MPO ) of lung tissue were analysed. Results During the process of the chronic bronchitis, the pathologic score was increasing as time went on, and the typical morphologic changes of chronic bronchitis emerged in the group 7 weeks. The total number of inflammatory cells in BALF was increasing as time went on, correlated with the pathologic scores ( P < 0. 01 ).And the percentage of lymphocyte increased as well as positively correlated with pathologic scores ( P < 0. 05 ),whereas that of macrophage decreased and negatively correlated with pathologic scores (P <0. 05). The MPO lever of lung tissue was correlated with the pathologic scores ( P < 0. 01 ). But the percentage of the neutrophil in the BALF was just in a high level during the first week, then it maintained relatively lower. Conclusion Smoke-induced chronic bronchitis is a slowly progressive inflammation process. The model we established is convenient and simple for the longitudinal study on the inflammatory process of chronic bronchitis and the therapy in the early stage. The semi-quantitative evaluation for the pathological change is with much more value. During the inflammatory sequential process of early stage of chronic bronchitis, the cellular characteristics are

  7. The effects of phenethyl isothiocyanate, N-acetylcysteine and green tea on tobacco smoke-induced lung tumors in strain A/J mice.

    Science.gov (United States)

    Witschi, H; Espiritu, I; Yu, M; Willits, N H

    1998-10-01

    Male and female strain A/J mice were exposed to a mixture of cigarette sidestream and mainstream smoke at a chamber concentration of total suspended particulates of 82.5 mg/m3. Exposure time was 6 h/day, 5 days/week for 5 months. The animals were allowed to recover for another 4 months in filtered air before sacrifice and lung tumor count. Male animals were fed either 0.2% N-acetylcysteine (NAC) or 0.05% phenethyl isothiocyanate (PEITC) in diet AIN-76A with 5% corn oil added. Female animals received normal laboratory chow and were given a 1.25% extract of green tea in the drinking water. Corresponding control groups were fed diets without NAC or PEITC or given plain tap water. Exposure to tobacco smoke increased lung tumor multiplicity to 1.1-1.6 tumors/lung, significantly higher than control values (0.5-1.0 tumors/lung). None of the putative chemopreventive agents (NAC, PEITC or green tea extract) had a protective effect. In positive control experiments, PEITC significantly reduced both lung tumor multiplicity and incidence in mice treated with the tobacco smoke-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In mice treated with three different doses of urethan and fed NAC in the diet, a significant reduction in lung tumor multiplicity was found only at one dose level. Green tea extract did not reduce lung tumor multiplicity in animals treated with a single dose of NNK. It was concluded that successful chemoprevention of tobacco smoke-induced lung tumorigenesis might require administration of several chemopreventive agents rather than just a single one.

  8. Cigarette use, Cigarette Consumption and Price of Cigarette

    Institute of Scientific and Technical Information of China (English)

    JingMing Li

    2016-01-01

    两种经验方法在这篇研究论文中使用,为了调查在美国香烟价格跟香烟需求的关系通过可以找到的数据信息。这篇论文的目的为了调查香烟的价格是否是一个强有力的方式去减少香烟的需求。论文中的的数据收集来源于美国的48个州从1985年到1995年,目的是检测香烟价格跟其他独立的变量对香烟需求的作用。最小二乘回归模型跟虚拟变量的最小二乘法模型已经使用去决定香烟价格的作用。此外,其他因素像人均GDP,人口,CPI也使用在模型中去证实潜在的关系对于香烟需求。报告结果显示了任何方式的香烟价格上升将会导致个人香烟需求的下降。香烟需求的百分比下降取决于香烟价格的百分比上升,这个现象可以通过需求的价格弹性去估量。基于报告的分析可以放心的作出结论,香烟价格上升仍然是一种有效的工具去减少香烟的需求。%In this research paper two empirical methodologies are used for studying the relation between cigarette price and cigarette consumption in America with available statistical information. The purpose of the paper is to investigate whether the price of cigarette is a powerful method for cutting cigarette consumption. The statistical information used in the paper is collected from 48 U.S. states over the period from 1985 to 1995 for examining the effect of cigarette price and others independent variables on cigarette consumption. Ordinary least squares (OLS) regression model and Least square dummy variable model are used to determine effect of cigarette price. Furthermore, other factors such as GDP per capita, population and Consumer price index (CPI), have been added into the model to attest to their potential nexuses with cigarette consumption. The result of the report shows that any increase in the price of cigarettes will decrease personal consumption of cigarettes. Higher prices increase costs to

  9. Carbonyl compounds generated from electronic cigarettes

    National Research Council Canada - National Science Library

    Bekki, Kanae; Uchiyama, Shigehisa; Ohta, Kazushi; Inaba, Yohei; Nakagome, Hideki; Kunugita, Naoki

    2014-01-01

    Electronic cigarettes (e-cigarettes) are advertised as being safer than tobacco cigarettes products as the chemical compounds inhaled from e-cigarettes are believed to be fewer and less toxic than those from tobacco cigarettes...

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Science.gov (United States)

    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.

  12. E-Cigarettes

    Science.gov (United States)

    ... that are known to be harmful. Scientists are studying the health effects of using e-cigarettes. New information is coming in, but they don't have the answers yet. Although FDA is working to regulate e-cigarettes, currently they are not ...

  13. Ending the cigarette pandemic.

    Science.gov (United States)

    Richmond, J B

    1983-12-01

    1 year after the issuance of the original Surgeon General's report, Congress passed the Federal Cigarette Labeling Advertising Act, requiring all cigarette packages distributed in the US to carry a Surgeon General's warning that smoking may be hazardous to health. Congress pased the Public Health Cigarette Smoking Act in 1969. This banned cigarette advertising from radio and television. The Surgeon General published the most comprehensive volume on smoking ever issued in the US in 1979, the 15th anniversary of the 1st report. The data on cigarette smoking's adverse effects on health were overwhelming, and the press recognized this. No longer able to rely on journalists to cast doubt on the reliability of the data, the industry changed its strategy by attempting to portray smoking as a civil rights issue. The tobacco industry began to pour millions of dollars into campaigns to prevent the passage of municipal, state, and federal legislation that would ban cigarette advertising or restrict smoking in public places and at the work site. "Healthy People," the Surgeon General's 1st report on health promotion and disease prevention, emphasized the necessary future direction of medicine: prevention. Efforts to end the cigarette pandemic will need to focus on the following in the future: an end to the victimization of women; a greater focus on adolescents; more effective strategies for smoking cessation; more attention to clean indoor air rights; abandonment of recommendations to switch to low-tar, low-nicotine cigarettes; and revelation of chemical additives in cigarettes. The epidemiologists have now documented the devastating nature of the health problems attributable to cigarette smoking, but the minimal budgetary allocations to fight smoking testify to the lack of political will on the part of government.

  14. Noni Juice Improves Serum Lipid Profiles and Other Risk Markers in Cigarette Smokers

    Directory of Open Access Journals (Sweden)

    Mian-Ying Wang

    2012-01-01

    Full Text Available Cigarette smoke-induced oxidative stress leads to dyslipidemia and systemic inflammation. Morinda citrifolia (noni fruit juice has been found previously to have a significant antioxidant activity. One hundred thirty-two adult heavy smokers completed a randomized, double blind, placebo-controlled clinical trial designed to investigate the effect of noni juice on serum cholesterol, triglyceride, low density lipoprotein cholesterol (LDL, high density lipoprotein cholesterol (HDL, high-sensitivity C-reactive protein (hs-CRP, and homocysteine. Volunteers drank noni juice or a fruit juice placebo daily for one month. Drinking 29.5 mL to 188 mL of noni juice per day significantly reduced cholesterol levels, triglycerides, and hs-CRP. Decreases in LDL and homocysteine, as well increases in HDL, were also observed among noni juice drinkers. The placebo, which was devoid of iridoid glycosides, did not significantly influence blood lipid profiles or hs-CRP. Noni juice was able to mitigate cigarette smoke-induced dyslipidemia, an activity associated with the presence of iridoids.

  15. Cigarette smoke extract (CSE) induces RAGE-mediated inflammation in the Ca9-22 gingival carcinoma epithelial cell line.

    Science.gov (United States)

    Sanders, Nolan T; Dutson, Derek J; Durrant, Justin W; Lewis, Joshua B; Wilcox, Shalene H; Winden, Duane R; Arroyo, Juan A; Bikman, Benjamin T; Reynolds, Paul R

    2017-08-01

    The oral environment is anatomically positioned as a significant gateway for exposure to environmental toxicants. Cigarette smoke exposure compromises oral health by orchestrating inflammation. The receptor for advanced glycation end-products (RAGE) has been implicated in smoke-induced inflammatory effects; however, its role in the oral cavity is unknown. The purpose of this study was to determine RAGE expression by immortalized gingival carcinoma cells and the degree to which RAGE-mediated signaling influences inflammation. Gingival epithelia cells (Ca9-22) were exposed to 10% cigarette smoke extract (CSE) for six hours and screened for RAGE expression and inflammatory mediators. Quantitative PCR and immunoblotting revealed increased RAGE expression following exposure. Furthermore, exposure activated RAGE signaling intermediates including Ras and NF-κB. IL-6 and IL-1β were also elevated in cell culture medium from CSE-exposed cells when compared to controls. A family of anionic, partially lipophilic sulfated polysaccharide derivatives known as semi-synthetic glycosaminoglycan ethers (SAGEs) were used in an effort to block RAGE signaling. Co-treatment of CSE and SAGEs ameliorated inflammatory responses. These results provide a new perspective on a mechanism of cigarette smoke induced oral inflammation. Further work may show RAGE signaling as a potential target in the treatment of diseases of the oral cavity exacerbated by tobacco smoke exposure. Copyright © 2017 Elsevier Ltd. All rights reserved.

  16. E-Cigarettes (For Teens)

    Science.gov (United States)

    ... Loss Surgery? A Week of Healthy Breakfasts Shyness E-Cigarettes KidsHealth > For Teens > E-Cigarettes A A ... Habit en español Los cigarrillos electrónicos What Are E-Cigarettes? E-cigarettes look high tech, so it's ...

  17. E-Cigarettes (For Parents)

    Science.gov (United States)

    ... Old Feeding Your 1- to 2-Year-Old E-Cigarettes KidsHealth > For Parents > E-Cigarettes A A ... Using Them en español Los cigarrillos electrónicos About E-Cigarettes E-cigarettes are being marketed as a ...

  18. E-Cigarettes (For Parents)

    Science.gov (United States)

    ... Old Feeding Your 1- to 2-Year-Old E-Cigarettes KidsHealth > For Parents > E-Cigarettes Print A ... Using Them en español Los cigarrillos electrónicos About E-Cigarettes E-cigarettes are being marketed as a ...

  19. 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.

  20. Comparison of Serum Adiponectin in Smoke-induced Pulmonary Emphysema Rats Fed Different Diets

    Institute of Scientific and Technical Information of China (English)

    Rui-Ying Wang; Hu Liu; Li-Juan Ma; Jian-Ying Xu

    2016-01-01

    Background:Smoking and body mass index (BMI) are the key risk factors for chronic obstructive pulmonary disease (COPD).Adiponectin with both anti-inflammatory and pro-inflammatory properties is a vital modulator of inflammatory processes,which is expressed in epithelial cells in the airway in COPD-emphysema.The aim of this study was to examine the effects of adiponectin on tobacco smoke-induced emphysema in rats,which were fed different diets.Methods:Seventy-six adult (6-8 weeks old) male Sprague-Dawley rats (average weight 220 ± 20 g) were exposed to smoke or smoke-free room atmosphere and fed different diets (regular,high-fat,or low-fat diets) for 6 months.The rats were randomly divided into six groups.They are nonsmoke-exposed regular diet (n 10),nonsmoke-exposed high-fat diet (n =14),nonsmoke-exposed low-fat diet (n =14),smoke-exposed regular diet (n = 10),smoke-exposed high-fat diet (n =14),and smoke-exposed low-fat diet groups (n =14).A full 23 factorial design was used to evaluate the effect of independent variables on smoke exposure and different rearing methods.Serum adiponectin and inflammatory cytokines were measured by the enzyme-linked immunosorbent assay (ELISA).Results:Serum adiponectin levels in rats fed low-fat and regular diets exposed to smoke exposure were remarkably higher than that of rats exposed to room air while serum adiponectin levels of fat-rich diet rats exposed to tobacco smoke were lower than that of rats exposed to room air.Compared with regular diet or low-fat diet group,serum adiponectin levels in high-fat diet rats exposed to tobacco smoke were lower (t =6.932,11.026;all P < 0.001).BMI was inversely correlated with serum adiponectin levels (r =-0.751,P =0.012).Serum interleukin 6 (IL-6),tumor necrosis factor-α (TNF-α),and 4-hydroxy 2-nonenal (HNE) levels in rats exposed to low-fat or fat-rich diets were remarkably higher than that of rats exposed to normal diets (IL-6,t =4.196,3.480;P < 0.01,P =0.001;TNF-α,t =4

  1. Analyzing Cigarette Smoke.

    Science.gov (United States)

    Jaffe, Dan; Griffin, Dale; Ricker, Janet

    1997-01-01

    Details an activity in which students use their natural inquisitiveness about their personal environment to investigate the composition of cigarette smoke. Includes techniques for measuring tar and carbon monoxide content. (DDR)

  2. Epithelial cell senescence impairs repair process and exacerbates inflammation after airway injury

    Directory of Open Access Journals (Sweden)

    Nagai Atsushi

    2011-06-01

    Full Text Available Abstract Background Genotoxic stress, such as by exposure to bromodeoxyuridine (BrdU and cigarette smoke, induces premature cell senescence. Recent evidence indicates that cellular senescence of various types of cells is accelerated in COPD patients. However, whether the senescence of airway epithelial cells contributes to the development of airway diseases is unknown. The present study was designed to test the hypothesis that premature senescence of airway epithelial cells (Clara cells impairs repair processes and exacerbates inflammation after airway injury. Methods C57/BL6J mice were injected with the Clara-cell-specific toxicant naphthalene (NA on days 0, 7, and 14, and each NA injection was followed by a daily dose of BrdU on each of the following 3 days, during which regenerating cells were allowed to incorporate BrdU into their DNA and to senesce. The p38 MAPK inhibitor SB202190 was injected 30 minutes before each BrdU dose. Mice were sacrificed at different times until day 28 and lungs of mice were obtained to investigate whether Clara cell senescence impairs airway epithelial regeneration and exacerbates airway inflammation. NCI-H441 cells were induced to senesce by exposure to BrdU or the telomerase inhibitor MST-312. Human lung tissue samples were obtained from COPD patients, asymptomatic smokers, and nonsmokers to investigate whether Clara cell senescence is accelerated in the airways of COPD patients, and if so, whether it is accompanied by p38 MAPK activation. Results BrdU did not alter the intensity of the airway epithelial injury or inflammation after a single NA exposure. However, after repeated NA exposure, BrdU induced epithelial cell (Clara cell senescence, as demonstrated by a DNA damage response, p21 overexpression, increased senescence-associated β-galactosidase activity, and growth arrest, which resulted in impaired epithelial regeneration. The epithelial senescence was accompanied by p38 MAPK-dependent airway

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

    Directory of Open Access Journals (Sweden)

    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.

  4. Evaluation method for the cytotoxicity of cigarette smoke by in vitro whole smoke exposure.

    Science.gov (United States)

    Li, Xiang; Nie, Cong; Shang, Pingping; Xie, Fuwei; Liu, Huimin; Xie, Jianping

    2014-01-01

    An in vitro whole smoke (WS) exposure method was established to evaluate the toxicological effects of fresh cigarette smoke using the VITROCELL(®) system associated with the neutral red uptake (NRU) cytotoxicity assay. The VITROCELL(®) system is a newly representative culture and exposure system for in vitro studies of gases or complex mixtures. The impacts of two factors on cytotoxicity measurements of cigarette smoke were investigated using this WS exposure system. The factors include synthetic air exposure and optimal time to perform the NRU assay after smoke exposure. Results showed that synthetic air exposure used in the system did not significantly alter cell survival; 24h after smoke exposure appeared to be an optimal time-point to assess the cytotoxicity of cigarette smoke. A clear dose-response relationship between smoke exposure and cell viability was demonstrated using this system, and the evaluation method was sensitive to distinguish the differences in smoke-induced cytotoxic effects from different cigarettes. In addition, we tried converting the values of EC50 from WS exposure testing into the values in unit used in total particulate matter (TPM) testing for a purpose of comparison, and the data indicate that the cytotoxicity of smoke measured by WS exposure is greater than that measured by TPM exposure. Copyright © 2013 Elsevier GmbH. All rights reserved.

  5. Effects of electroacupuncture at Zusanli (ST36) on inflammatory cytokines in a rat model of smoke-induced chronic obstructive pulmonary disease

    Institute of Scientific and Technical Information of China (English)

    Wen-ye Geng; Zi-bing Liu; Na-na Song; Gui-hong Zhang; Wei-zhong Jin; Wang Zhou; Li Li

    2013-01-01

    OBJECITVE:Improvement in lung function was reported after acupuncture treatment of chronic obstructive pulmonary disease (COPD),but little is known about the underlying mechanisms.Because an immune response imbalance could be seen in COPD,we hypothesize that electroacupuncture (EA) may play a role in regulating inflammatory cytokines and contribute to lung protection in a rat model of smoke-induced COPD.METHODS:A COPD model using male Sprague-Dawley rats exposed to cigarette smoke was established.The rats were randomly divided into four groups (control,sham,COPD,and COPD plus EA),and COPD model was evaluated by measuring pulmonary pathological changes and lung function.EA was applied to the acupuncture point Zusanli (ST36) for 30 min/d for 14 d in sham and COPD rats.Bronchoalveolar lavage fluid (BALF) was used to measure levels of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-β),and malonaldehyde (MDA).RESULTS:Compared with the control rats,COPD rats had significant changes in lung resistance (RL) and lung compliance (CL) (both P<0.01),bronchi and bronchiole airway obstruction (P<0.01),and levels of MDA,TNF-α,and IL-1β (P<0.01).There were no significant differences between the control and the sham groups.Compared with the COPD rats,the COPD plus EA rats had decreased RL and increased CL (both P<0.05),and reduced bronchi and bronchiole airway obstruction (P<0.05,P<0.01,respectively),while levels of TNF-α,IL-1β,and MDA in BALF were lowered (P<0.05 and P<0.01,respectively).However,TNF-α and IL-1βlevels of the EA group rats remained higher than those of the control group (P<0.05).CONCLUSION:EA at ST36 can reduce lung injury in a COPD rat model,and beneficial effects may be related to down-regulation of inflammatory cytokines.The anti-inflammatory and antioxidant effects may prolong the clinical benefit of EA.

  6. Cigarettes and Other Tobacco Products

    Science.gov (United States)

    ... if people start smoking again. Can a person overdose on nicotine? Nicotine is poisonous and, though uncommon, ... Drugs Anabolic Steroids Cigarettes and Other Tobacco Products Cocaine Cough and Cold Medicine Abuse Electronic Cigarettes (E- ...

  7. E-Cigarettes (For Teens)

    Science.gov (United States)

    ... which the person inhales. That's why using e-cigs is known as "vaping." Because e-cigarettes don' ... a regular cigarette. But anyone using an e-cig still gets an unhealthy dose of nicotine and ...

  8. Cardiology Patient Page: Electronic Cigarettes

    Science.gov (United States)

    ... of places where tobacco smoking is restricted, including restaurants, bars, offices, and airplanes. What Is Known About ... e-cigarettes helped them quit smoking. Studies with convenience samples of e-cigarette users show that people ...

  9. Alternative complement pathway deficiency ameliorates chronic smoke-induced functional and morphological ocular injury.

    Directory of Open Access Journals (Sweden)

    Alex Woodell

    Full Text Available BACKGROUND: Age-related macular degeneration (AMD, a complex disease involving genetic variants and environmental insults, is among the leading causes of blindness in Western populations. Genetic and histologic evidence implicate the complement system in AMD pathogenesis; and smoking is the major environmental risk factor associated with increased disease risk. Although previous studies have demonstrated that cigarette smoke exposure (CE causes retinal pigment epithelium (RPE defects in mice, and smoking leads to complement activation in patients, it is unknown whether complement activation is causative in the development of CE pathology; and if so, which complement pathway is required. METHODS: Mice were exposed to cigarette smoke or clean, filtered air for 6 months. The effects of CE were analyzed in wildtype (WT mice or mice without a functional complement alternative pathway (AP; CFB(-/- using molecular, histological, electrophysiological, and behavioral outcomes. RESULTS: CE in WT mice exhibited a significant reduction in function of both rods and cones as determined by electroretinography and contrast sensitivity measurements, concomitant with a thinning of the nuclear layers as measured by SD-OCT imaging and histology. Gene expression analyses suggested that alterations in both photoreceptors and RPE/choroid might contribute to the observed loss of function, and visualization of complement C3d deposition implies the RPE/Bruch's membrane (BrM complex as the target of AP activity. RPE/BrM alterations include an increase in mitochondrial size concomitant with an apical shift in mitochondrial distribution within the RPE and a thickening of BrM. CFB(-/- mice were protected from developing these CE-mediated alterations. CONCLUSIONS: Taken together, these findings provide clear evidence that ocular pathology generated in CE mice is dependent on complement activation and requires the AP. Identifying animal models with RPE/BrM damage and verifying

  10. College Students' Perceptions of Risk and Addictiveness of E-Cigarettes and Cigarettes

    Science.gov (United States)

    Cooper, Maria; Loukas, Alexandra; Harrell, Melissa B.; Perry, Cheryl L.

    2017-01-01

    Background: As conventional cigarette use is declining, electronic cigarette ("e-cigarette") use is rising and is especially high among college students. Few studies examine dual use of e-cigarettes and cigarettes among this population. This study explores the relationship between dual and exclusive e-cigarette / cigarette use and…

  11. College Students' Perceptions of Risk and Addictiveness of E-Cigarettes and Cigarettes

    Science.gov (United States)

    Cooper, Maria; Loukas, Alexandra; Harrell, Melissa B.; Perry, Cheryl L.

    2017-01-01

    Background: As conventional cigarette use is declining, electronic cigarette ("e-cigarette") use is rising and is especially high among college students. Few studies examine dual use of e-cigarettes and cigarettes among this population. This study explores the relationship between dual and exclusive e-cigarette / cigarette use and…

  12. A comparative assessment of cigarette smoke aerosols using an in vitro air-liquid interface cytotoxicity test.

    Science.gov (United States)

    Thorne, David; Dalrymple, Annette; Dillon, Deborah; Duke, Martin; Meredith, Clive

    2015-01-01

    This study describes the evaluation of a modified air-liquid interface BALB/c 3T3 cytotoxicity method for the assessment of smoke aerosols in vitro. The functionality and applicability of this modified protocol was assessed by comparing the cytotoxicity profiles from eight different cigarettes. Three reference cigarettes, 1R5F, 3R4F and CORESTA Monitor 7 were used to put the data into perspective and five bespoke experimental products were manufactured, ensuring a balanced and controlled study. Manufactured cigarettes were matched for key variables such as nicotine delivery, puff number, pressure drop, ventilation, carbon monoxide, nicotine free dry particulate matter and blend, but significantly modified for vapor phase delivery, via the addition of two different types and quantities of adsorptive carbon. Specifically manufacturing products ensures comparisons can be made in a consistent manner and allows the research to ask targeted questions, without confounding product variables. The results demonstrate vapor-phase associated cytotoxic effects and clear differences between the products tested and their cytotoxic profiles. This study has further characterized the in vitro vapor phase biological response relationship and confirmed that the biological response is directly proportional to the amount of available vapor phase toxicants in cigarette smoke, when using a Vitrocell® VC 10 exposure system. This study further supports and strengthens the use of aerosol based exposure options for the appropriate analysis of cigarette smoke induced responses in vitro and may be especially beneficial when comparing aerosols generated from alternative tobacco aerosol products.

  13. A comparative assessment of cigarette smoke aerosols using an in vitro air–liquid interface cytotoxicity test

    Science.gov (United States)

    Thorne, David; Dalrymple, Annette; Dillon, Deborah; Duke, Martin; Meredith, Clive

    2015-01-01

    Abstract This study describes the evaluation of a modified air-liquid interface BALB/c 3T3 cytotoxicity method for the assessment of smoke aerosols in vitro. The functionality and applicability of this modified protocol was assessed by comparing the cytotoxicity profiles from eight different cigarettes. Three reference cigarettes, 1R5F, 3R4F and CORESTA Monitor 7 were used to put the data into perspective and five bespoke experimental products were manufactured, ensuring a balanced and controlled study. Manufactured cigarettes were matched for key variables such as nicotine delivery, puff number, pressure drop, ventilation, carbon monoxide, nicotine free dry particulate matter and blend, but significantly modified for vapor phase delivery, via the addition of two different types and quantities of adsorptive carbon. Specifically manufacturing products ensures comparisons can be made in a consistent manner and allows the research to ask targeted questions, without confounding product variables. The results demonstrate vapor-phase associated cytotoxic effects and clear differences between the products tested and their cytotoxic profiles. This study has further characterized the in vitro vapor phase biological response relationship and confirmed that the biological response is directly proportional to the amount of available vapor phase toxicants in cigarette smoke, when using a Vitrocell® VC 10 exposure system. This study further supports and strengthens the use of aerosol based exposure options for the appropriate analysis of cigarette smoke induced responses in vitro and may be especially beneficial when comparing aerosols generated from alternative tobacco aerosol products. PMID:26339773

  14. Cytosolic phospholipase A2 (cPLA2) IVA as a potential signature molecule in cigarette smoke condensate induced pathologies in alveolar epithelial lineages.

    Science.gov (United States)

    Yadav, Subodh K; Sharma, Sanjeev K; Farooque, Abdullah; Kaushik, Gaurav; Kaur, Balwinder; Pathak, Chander M; Dwarakanath, Bilikere S; Khanduja, Krishan L

    2016-08-15

    Smoking is one of the leading causes of millions of deaths worldwide. During cigarette smoking, most affected and highly exposed cells are the alveolar epithelium and generated oxidative stress in these cells leads to death and damage. Several studies suggested that oxidative stress causes membrane remodeling via Phospholipase A2s but in the case of cigarette smokers, mechanistically study is not yet fully defined. In view of present perspective, we evaluated the involvement of cytosolic phospholipase A2 (cPLA2) IVA as therapeutic target in cigarette smoke induced pathologies in transformed type I and type II alveolar epithelial cells. Transformed type I (WI26) and type II (A549) alveolar epithelial cells were used for the present study. Cigarette smoke condensate (CSC) was prepared from most commonly used cigarette (Gold Flake with filter) by the Indian population. CSC-induced molecular changes were evaluated through cell viability using MTT assay, reactive oxygen species (ROS) measurement using 2,7 dichlorodihydrofluorescin diacetate (DCFH-DA), cell membrane integrity using fluorescein diacetate (FDA) and ethidium bromide (EtBr) staining, super oxide dismutase (SOD) levels, cPLA2 activity and molecular involvement of specific cPLA2s at selected 24 h time period. CSC-induced response on both type of epithelial cells shown significantly reduction in cell viability, declined membrane integrity, with differential escalation of ROS levels in the range of 1.5-15 folds and pointedly increased cPLA2 activity (p IVA with maximum manifestation of 3.8 folds. Interestingly, CSC-induced ROS levels and cPLA2s expression were relatively higher in A549 cells as compared to WI26 cells. The present study indicates that among all cPLA2s, specific cPLA2 IVA are the main enzymes involved in cigarette smoke induced anomalies in type I and type II lung epithelial cells and targeting them holds tremendous possibilities in cigarette smoke induced lung pathologies.

  15. Smoking-Induced Changes in the Maternal Immune, Endocrine, and Metabolic Pathways and Their Impact on Fetal Growth: A Topical Review.

    Science.gov (United States)

    Sabra, Sally; Gratacós, Eduard; Gómez Roig, Maria Dolores

    2017-01-01

    Perinatal maternal smoking exposure (PMSE) is one of the major environmental risk factors encountered by the fetus. PMSE is usually associated with adverse pregnancy outcomes that may manifest at different stages of life. Nevertheless, fetal growth restriction is the most common smoking-induced side effect. PMSE induces changes in the maternal multiple organ systems. These alterations may affect placentation, which subsequently affects fetal growth. It is worthy to note, however, that the extent of maternal smoking-induced changes depends mainly on the maternal level of susceptibility. Hence, the perinatal pregnancy outcomes vary depending on the interaction between the triad: the maternal, fetal, and placental modifications, making it more complex. In this review, we try to unveil the effect of smoking-induced maternal changes on the maternal immune, endocrine, and metabolic pathways and their impact on fetal growth. © 2017 S. Karger AG, Basel.

  16. EFFECTS OF CONCURRENT OZONE EXPOSURE ON THE PATHOGENESIS OF CIGARETTE SMOKE-INDUCED EMPHYSEMA IN B6C3F1 MICE. (R826442)

    Science.gov (United States)

    The perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Concl...

  17. Electronic Cigarettes on Hospital Campuses

    Directory of Open Access Journals (Sweden)

    Clare Meernik

    2015-12-01

    Full Text Available Smoke and tobacco-free policies on hospital campuses have become more prevalent across the U.S. and Europe, de-normalizing smoking and reducing secondhand smoke exposure on hospital grounds. Concerns about the increasing use of electronic cigarettes (e-cigarettes and the impact of such use on smoke and tobacco-free policies have arisen, but to date, no systematic data describes e-cigarette policies on hospital campuses. The study surveyed all hospitals in North Carolina (n = 121 to assess what proportion of hospitals have developed e-cigarette policies, how policies have been implemented and communicated, and what motivators and barriers have influenced the development of e-cigarette regulations. Seventy-five hospitals (62% completed the survey. Over 80% of hospitals reported the existence of a policy regulating the use of e-cigarettes on campus and roughly half of the hospitals without a current e-cigarette policy are likely to develop one within the next year. Most e-cigarette policies have been incorporated into existing tobacco-free policies with few reported barriers, though effective communication of e-cigarette policies is lacking. The majority of hospitals strongly agree that e-cigarette use on campus should be prohibited for staff, patients, and visitors. Widespread incorporation of e-cigarette policies into existing hospital smoke and tobacco-free campus policies is feasible but needs communication to staff, patients, and visitors.

  18. Electronic Cigarettes on Hospital Campuses.

    Science.gov (United States)

    Meernik, Clare; Baker, Hannah M; Paci, Karina; Fischer-Brown, Isaiah; Dunlap, Daniel; Goldstein, Adam O

    2015-12-29

    Smoke and tobacco-free policies on hospital campuses have become more prevalent across the U.S. and Europe, de-normalizing smoking and reducing secondhand smoke exposure on hospital grounds. Concerns about the increasing use of electronic cigarettes (e-cigarettes) and the impact of such use on smoke and tobacco-free policies have arisen, but to date, no systematic data describes e-cigarette policies on hospital campuses. The study surveyed all hospitals in North Carolina (n = 121) to assess what proportion of hospitals have developed e-cigarette policies, how policies have been implemented and communicated, and what motivators and barriers have influenced the development of e-cigarette regulations. Seventy-five hospitals (62%) completed the survey. Over 80% of hospitals reported the existence of a policy regulating the use of e-cigarettes on campus and roughly half of the hospitals without a current e-cigarette policy are likely to develop one within the next year. Most e-cigarette policies have been incorporated into existing tobacco-free policies with few reported barriers, though effective communication of e-cigarette policies is lacking. The majority of hospitals strongly agree that e-cigarette use on campus should be prohibited for staff, patients, and visitors. Widespread incorporation of e-cigarette policies into existing hospital smoke and tobacco-free campus policies is feasible but needs communication to staff, patients, and visitors.

  19. The lung inflammation and skeletal muscle wasting induced by subchronic cigarette smoke exposure are not altered by a high-fat diet in mice.

    Science.gov (United States)

    Hansen, Michelle J; Chen, Hui; Jones, Jessica E; Langenbach, Shenna Y; Vlahos, Ross; Gualano, Rosa C; Morris, Margaret J; Anderson, Gary P

    2013-01-01

    Obesity and cigarette smoking independently constitute major preventable causes of morbidity and mortality and obesity is known to worsen lung inflammation in asthma. Paradoxically, higher body mass index (BMI) is associated with reduced mortality in smoking induced COPD whereas low BMI increases mortality risk. To date, no study has investigated the effect of a dietary-induced obesity and cigarette smoke exposure on the lung inflammation and loss of skeletal muscle mass in mice. Male BALB/c mice were exposed to 4 cigarettes/day, 6 days/week for 7 weeks, or sham handled. Mice consumed either standard laboratory chow (3.5 kcal/g, 12% fat) or a high fat diet (HFD, 4.3 kcal/g, 32% fat). Mice exposed to cigarette smoke for 7 weeks had significantly more inflammatory cells in the BALF (Pincreased (Pmuscles (soleus, tibialis anterior and gastrocnemius) of cigarette smoke-exposed mice weighed significantly less than sham-exposed mice (Pdecreased insulin-like growth factor-1 (IGF-1) mRNA expression in the gastrocnemius and tibialis anterior and IGF-1 protein in the gastrocnemius (Pmuscles of chow fed smoke-exposed mice (Pmuscle mass following cigarette smoke exposure in mice.

  20. A Targeted Inhibitor of the Alternative Complement Pathway Accelerates Recovery From Smoke-Induced Ocular Injury

    Science.gov (United States)

    Woodell, Alex; Jones, Bryan W.; Williamson, Tucker; Schnabolk, Gloriane; Tomlinson, Stephen; Atkinson, Carl; Rohrer, Bärbel

    2016-01-01

    Purpose Morphologic and genetic evidence exists that an overactive complement system driven by the complement alternative pathway (AP) is involved in pathogenesis of age-related macular degeneration (AMD). Smoking is the only modifiable risk factor for AMD. As we have shown that smoke-related ocular pathology can be prevented in mice that lack an essential activator of AP, we ask here whether this pathology can be reversed by increasing inhibition in AP. Methods Mice were exposed to either cigarette smoke (CS) or filtered air (6 hours/day, 5 days/week, 6 months). Smoke-exposed animals were then treated with the AP inhibitor (CR2-fH) or vehicle control (PBS) for the following 3 months. Spatial frequency and contrast sensitivity were assessed by optokinetic response paradigms at 6 and 9 months; additional readouts included assessment of retinal morphology by electron microscopy (EM) and gene expression analysis by quantitative RT-PCR. Results The CS mice treated with CR2-fH showed significant improvement in contrast threshold compared to PBS-treated mice, whereas spatial frequency was unaffected by CS or pharmacologic intervention. Treatment with CR2-fH in CS animals reversed thinning of the retina observed in PBS-treated mice as analyzed by spectral-domain optical coherence tomography, and reversed most morphologic changes in RPE and Bruch's membrane seen in CS animals by EM. Conclusions Taken together, these findings suggest that AP inhibitors not only prevent, but have the potential to accelerate the clearance of complement-mediated ocular injury. Improving our understanding of the regulation of the AP is paramount to developing novel treatment approaches for AMD. PMID:27064393

  1. Alcohol intake and cigarette smoking: Impact of two major lifestyle factors on male fertility

    Directory of Open Access Journals (Sweden)

    Gaur Dushyant

    2010-01-01

    Full Text Available Context: Lifestyle factors, like alcohol intake and cigarette smoking, have been reported to affect male fertility. Aims: To find out the specific impact of alcohol and smoking on semen quality of male partners of couples seeking treatment for primary infertility. Materials and Methods: From the semen samples analyzed in our andrology laboratory, results of 100 alcoholics and 100 cigarette smoker males were studied following WHO guidelines and compared with 100 strict nonalcoholic and nonsmoker males for presence of asthenozoospermia, oligozoospermia and teratozoospermia. Statistical Analysis: Data was analyzed by F- test using Microsoft Office Excel 2003. Results: Only 12% alcoholics and six per cent smokers showed normozoospermia compared to 37 % nonalcoholic nonsmoker males. Teratozoospermia, followed by oligozoospermia dominated alcoholics. Overall impact of asthenozoospermia and teratozoospermia, but not of oligozoospermia, was observed in smokers. Light smokers predominantly showed asthenozoospermia. Heavy alcoholics and smokers showed asthenozoospermia, teratozoospermia as well as oligozoospermia. Conclusions: Asthenozoospermia, the most common semen variable in our study, can be an early indicator of reduction in quality of semen. Alcohol abuse apparently targets sperm morphology and sperm production. Smoke-induced toxins primarily hamper sperm motility and seminal fluid quality. Progressive deterioration in semen quality is related to increasing quantity of alcohol intake and cigarettes smoked.

  2. 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.

  3. Receptor for advanced glycation endproducts (RAGE) maintains pulmonary structure and regulates the response to cigarette smoke.

    Science.gov (United States)

    Wolf, Lisa; Herr, Christian; Niederstraßer, Julia; Beisswenger, Christoph; Bals, Robert

    2017-01-01

    The receptor for advanced glycation endproducts (RAGE) is highly expressed in the lung but its physiological functions in this organ is still not completely understood. To determine the contribution of RAGE to physiological functions of the lung, we analyzed pulmonary mechanics and structure of wildtype and RAGE deficient (RAGE-/-) mice. RAGE deficiency spontaneously resulted in a loss of lung structure shown by an increased mean chord length, increased respiratory system compliance, decreased respiratory system elastance and increased concentrations of serum protein albumin in bronchoalveolar lavage fluids. Pulmonary expression of RAGE was mainly localized on alveolar epithelial cells and alveolar macrophages. Primary murine alveolar epithelial cells isolated from RAGE-/- mice revealed an altered differentiation and defective barrier formation under in vitro conditions. Stimulation of interferone-y (IFNy)-activated alveolar macrophages deficient for RAGE with Toll-like receptor (TLR) ligands resulted in significantly decreased release of proinflammatory cytokines and chemokines. Exposure to chronic cigarette smoke did not affect emphysema-like changes in lung parenchyma in RAGE-/- mice. Acute cigarette smoke exposure revealed a modified inflammatory response in RAGE-/- mice that was characterized by an influx of macrophages and a decreased keratinocyte-derived chemokine (KC) release. Our data suggest that RAGE regulates the differentiation of alveolar epithelial cells and impacts on the development and maintenance of pulmonary structure. In cigarette smoke-induced lung pathology, RAGE mediates inflammation that contributes to lung damage.

  4. Electronic cigarettes: human health effects.

    Science.gov (United States)

    Callahan-Lyon, Priscilla

    2014-05-01

    With the rapid increase in use of electronic nicotine delivery systems (ENDS), such as electronic cigarettes (e-cigarettes), users and non-users are exposed to the aerosol and product constituents. This is a review of published data on the human health effects of exposure to e-cigarettes and their components. Literature searches were conducted through September 2013 using multiple electronic databases. Forty-four articles are included in this analysis. E-cigarette aerosols may contain propylene glycol, glycerol, flavourings, other chemicals and, usually, nicotine. Aerosolised propylene glycol and glycerol produce mouth and throat irritation and dry cough. No data on the effects of flavouring inhalation were identified. Data on short-term health effects are limited and there are no adequate data on long-term effects. Aerosol exposure may be associated with respiratory function impairment, and serum cotinine levels are similar to those in traditional cigarette smokers. The high nicotine concentrations of some products increase exposure risks for non-users, particularly children. The dangers of secondhand and thirdhand aerosol exposure have not been thoroughly evaluated. Scientific evidence regarding the human health effects of e-cigarettes is limited. While e-cigarette aerosol may contain fewer toxicants than cigarette smoke, studies evaluating whether e-cigarettes are less harmful than cigarettes are inconclusive. Some evidence suggests that e-cigarette use may facilitate smoking cessation, but definitive data are lacking. No e-cigarette has been approved by FDA as a cessation aid. Environmental concerns and issues regarding non-user exposure exist. The health impact of e-cigarettes, for users and the public, cannot be determined with currently available data.

  5. Tendon repair

    Science.gov (United States)

    Repair of tendon ... Tendon repair can be performed using: Local anesthesia (the immediate area of the surgery is pain-free) ... a cut on the skin over the injured tendon. The damaged or torn ends of the tendon ...

  6. Cigarette Consumption and Cigarette Smoking Prevalence Among Adults in Kansas.

    Science.gov (United States)

    Neuberger, John S; Lai, Sue Min

    2015-06-11

    Recent tobacco prevention and cessation activities have focused on nonsmoking ordinances and behavioral changes, and in Kansas, the overall prevalence of cigarette smoking among adults has decreased. The objective of this study was to determine whether overall cigarette consumption (mean annual number of cigarettes smoked) in Kansas also decreased. Data on cigarette smoking prevalence for 91,465 adult Kansans were obtained from the Behavioral Risk Factor Surveillance System survey for 1999 through 2010. Data on annual cigarette consumption were obtained from the 2002 and 2006 Kansas Adult Tobacco Survey and analyzed by totals, by sex, and by smoking some days or smoking every day. Linear regression was used to evaluate rate changes over time. Among men, but not women, cigarette smoking prevalence decreased significantly over time. The prevalence of smoking every day decreased significantly among both men and women, whereas the prevalence of smoking on some days increased significantly for women but not men. For current smokers, the mean annual number of cigarettes consumed remained the same. The decline in overall smoking prevalence coupled with the lack of change in mean annual cigarette consumption may have resulted in a more intense exposure to cigarettes for the smoking population. The significant increase in some day use among women indicates a need for additional prevention and education activities; the impact on future lung cancer incidence rates needs further investigation.

  7. The intractable cigarette 'filter problem'.

    Science.gov (United States)

    Harris, Bradford

    2011-05-01

    When lung cancer fears emerged in the 1950s, cigarette companies initiated a shift in cigarette design from unfiltered to filtered cigarettes. Both the ineffectiveness of cigarette filters and the tobacco industry's misleading marketing of the benefits of filtered cigarettes have been well documented. However, during the 1950s and 1960s, American cigarette companies spent millions of dollars to solve what the industry identified as the 'filter problem'. These extensive filter research and development efforts suggest a phase of genuine optimism among cigarette designers that cigarette filters could be engineered to mitigate the health hazards of smoking. This paper explores the early history of cigarette filter research and development in order to elucidate why and when seemingly sincere filter engineering efforts devolved into manipulations in cigarette design to sustain cigarette marketing and mitigate consumers' concerns about the health consequences of smoking. Relevant word and phrase searches were conducted in the Legacy Tobacco Documents Library online database, Google Patents, and media and medical databases including ProQuest, JSTOR, Medline and PubMed. 13 tobacco industry documents were identified that track prominent developments involved in what the industry referred to as the 'filter problem'. These reveal a period of intense focus on the 'filter problem' that persisted from the mid-1950s to the mid-1960s, featuring collaborations between cigarette producers and large American chemical and textile companies to develop effective filters. In addition, the documents reveal how cigarette filter researchers' growing scientific knowledge of smoke chemistry led to increasing recognition that filters were unlikely to offer significant health protection. One of the primary concerns of cigarette producers was to design cigarette filters that could be economically incorporated into the massive scale of cigarette production. The synthetic plastic cellulose acetate

  8. Chemistry of Cigarette Burning Processes

    Directory of Open Access Journals (Sweden)

    Chen P

    2014-12-01

    Full Text Available Cigarette-burning and the smoke-formation processes and smoke composition are important topics for understanding cigarette performance. This paper proposes the molecular formulas representing the active components of bright, burley, and Oriental tobaccos and a basic chemistry model of the cigarette burning processes. Previous knowledge of the cigarette burning processes and smoke formation helped to establish parameters in deriving the basic chemistry equations. The proposed chemistry provides a brief view of the mechanisms of the cigarette burning during puffing and interpuff smoldering, and can be used to interpret and predict the smoke composition for cigarettes made from bright, burley, and Oriental tobaccos. Based on the proposed chemistry, the effect of ventilation on smoke component deliveries is discussed and the reaction heat of the puffing process is estimated.

  9. Up-Regulation of Claudin-6 in the Distal Lung Impacts Secondhand Smoke-Induced Inflammation

    Science.gov (United States)

    Lewis, Joshua B.; Milner, Dallin C.; Lewis, Adam L.; Dunaway, Todd M.; Egbert, Kaleb M.; Albright, Scott C.; Merrell, Brigham J.; Monson, Troy D.; Broberg, Dallin S.; Gassman, Jason R.; Thomas, Daniel B.; Arroyo, Juan A.; Reynolds, Paul R.

    2016-01-01

    It has long been understood that increased epithelial permeability contributes to inflammation observed in many respiratory diseases. Recently, evidence has revealed that environmental exposure to noxious material such as cigarette smoke reduces tight junction barrier integrity, thus enhancing inflammatory conditions. Claudin-6 (Cldn6) is a tetraspanin transmembrane protein found within the tight junctional complex and is implicated in maintaining lung epithelial barriers. To test the hypothesis that increased Cldn6 ameliorates inflammation at the respiratory barrier, we utilized the Tet-On inducible transgenic system to conditionally over-express Clnd6 in the distal lung. Cldn6 transgenic (TG) and control mice were continuously provided doxycycline from postnatal day (PN) 30 until euthanasia date at PN90. A subset of Cldn6 TG and control mice were also subjected to daily secondhand tobacco smoke (SHS) via a nose only inhalation system from PN30-90 and compared to room air (RA) controls. Animals were euthanized on PN90 and lungs were harvested for histological and molecular characterization. Bronchoalveolar lavage fluid (BALF) was procured for the assessment of inflammatory cells and molecules. Quantitative RT-PCR and immunoblotting revealed increased Cldn6 expression in TG vs. control animals and SHS decreased Cldn6 expression regardless of genetic up-regulation. Histological evaluations revealed no adverse pulmonary remodeling via Hematoxylin and Eosin (H&E) staining or any qualitative alterations in the abundance of type II pneumocytes or proximal non-ciliated epithelial cells via staining for cell specific propeptide of Surfactant Protein-C (proSP-C) or Club Cell Secretory Protein (CCSP), respectively. Immunoblotting and qRT-PCR confirmed the differential expression of Cldn6 and the pro-inflammatory cytokines TNF-α and IL-1β. As a general theme, inflammation induced by SHS exposure was influenced by the availability of Cldn6. These data reveal captivating

  10. Successful and not so successful chemoprevention of tobacco smoke-induced lung tumors.

    Science.gov (United States)

    Witschi, H

    2000-12-01

    Strain A/J mice underwent whole body exposure for 6 hours a day, 5 days a week, for 5 months to a mixture of cigarette sidestream and mainstream smoke (89%-11%; total suspended particulates 80-150 mg/m3), then were kept for another 4 months in air before being killed for scoring of lung tumors. In 7 independent experiments, lung tumor multiplicity was significantly increased in all 7 trials and lung tumor incidence in 5. When animals were kept for 9 months in smoke, lung tumor multiplicity was not significantly higher than in controls, although lung tumor incidence was. The following chemopreventive agents were evaluated: green tea, phenethyl isothiocyanate (PEITC), acetylsalicylic acid (ASA), N-acetylcysteine (NAC), p-XSC (1,4-phenylenebis[methylene]selenocyanate), d-limonene (DL), and a mixture of PEITC and BITC (benzyl isothiocyanate). In animals exposed to tobacco smoke, none of these agents reduced lung tumor multiplicity or incidence. As a control, the effects of the same agents were examined in A/J mice initiated with 4-(methylnitrosamino)-1-(3pyridyl)-1-butanone (NNK) or urethane. In mice injected with NNK, green tea and ASA did not reduce lung tumor multiplicities and NAC had no effect on urethane-induced lung tumors, whereas PEITC, p-XSC and DL reduced NNK-induced tumor multiplicities to 20% to 50% of control values. On the other hand, dietary mixture of myoinositol and dexamethasone was not only highly protective against NNK, but reduced lung tumor multiplicities and incidence in smoke-exposed animals to control values. This effect was also seen when the animals were fed the myo-inositol-dexamethasone mixture once they were removed from smoke. It is concluded that in animal studies it might be preferable to evaluate the effectiveness of putative chemopreventive agents against full tobacco smoke rather than against selected model compounds. The observations made with myo-inositol-dexamethasone suggest that people who have recently quit smoking might

  11. Up-Regulation of Claudin-6 in the Distal Lung Impacts Secondhand Smoke-Induced Inflammation

    Directory of Open Access Journals (Sweden)

    Joshua B. Lewis

    2016-10-01

    Full Text Available It has long been understood that increased epithelial permeability contributes to inflammation observed in many respiratory diseases. Recently, evidence has revealed that environmental exposure to noxious material such as cigarette smoke reduces tight junction barrier integrity, thus enhancing inflammatory conditions. Claudin-6 (Cldn6 is a tetraspanin transmembrane protein found within the tight junctional complex and is implicated in maintaining lung epithelial barriers. To test the hypothesis that increased Cldn6 ameliorates inflammation at the respiratory barrier, we utilized the Tet-On inducible transgenic system to conditionally over-express Clnd6 in the distal lung. Cldn6 transgenic (TG and control mice were continuously provided doxycycline from postnatal day (PN 30 until euthanasia date at PN90. A subset of Cldn6 TG and control mice were also subjected to daily secondhand tobacco smoke (SHS via a nose only inhalation system from PN30-90 and compared to room air (RA controls. Animals were euthanized on PN90 and lungs were harvested for histological and molecular characterization. Bronchoalveolar lavage fluid (BALF was procured for the assessment of inflammatory cells and molecules. Quantitative RT-PCR and immunoblotting revealed increased Cldn6 expression in TG vs. control animals and SHS decreased Cldn6 expression regardless of genetic up-regulation. Histological evaluations revealed no adverse pulmonary remodeling via Hematoxylin and Eosin (H&E staining or any qualitative alterations in the abundance of type II pneumocytes or proximal non-ciliated epithelial cells via staining for cell specific propeptide of Surfactant Protein-C (proSP-C or Club Cell Secretory Protein (CCSP, respectively. Immunoblotting and qRT-PCR confirmed the differential expression of Cldn6 and the pro-inflammatory cytokines TNF-α and IL-1β. As a general theme, inflammation induced by SHS exposure was influenced by the availability of Cldn6. These data reveal

  12. Cigarette price minimization strategies used by adults

    National Research Council Canada - National Science Library

    Pesko, Michael F; Kruger, Judy; Hyland, Andrew

    2012-01-01

    .... We explored use of cigarette price minimization strategies, such as purchasing cartons of cigarettes, purchasing in states with lower after-tax cigarette prices, and purchasing on the Internet...

  13. Anti-cyclic citrullinated peptide (CCP) antibody in patients with wood-smoke-induced chronic obstructive pulmonary disease (COPD) without rheumatoid arthritis.

    Science.gov (United States)

    Sigari, Naseh; Moghimi, Nasrin; Shahraki, Farhad Saber; Mohammadi, Shilan; Roshani, Daem

    2015-01-01

    Citrullination, a post-translational modification of proteins, is increased in inflammatory processes and is known to occur in smokers. It can induce anti-cyclic citrullinated peptide (CCP) antibodies, the most specific serologic marker for rheumatoid arthritis. Thus far, the incidence of autoimmunity in patients with wood-smoke-induced chronic obstructive pulmonary disease (COPD) resulting in anti-CCP production has not been examined. We hypothesise that anti-CCP antibody level in these patients should be higher than that in healthy subjects. A total of 112 non-rheumatoid arthritis patients, including 56 patients with wood-smoke-induced COPD and 56 patients with tobacco-induced COPD, and 56 healthy non-smoker controls were included. The serum anti-CCP antibody levels were measured and compared between the groups and against smoke exposure and clinical characteristics. The mean anti-CCP antibody levels in wood-smoke-induced COPD group were significantly higher than those in tobacco-induced COPD group (p = 0.03) and controls (p = 0.004). Furthermore, 8 (14.2 %) patients with wood-smoke-induced COPD, 4 (7.14 %) with tobacco-induced COPD and 2 (3.57 %) controls exceeded the conventional cut-off of anti-CCP antibody positivity. No relationship was found between the anti-CCP antibody level and age, gender, duration of disease, Pack-years of smoking, and duration of exposure to wood smoke. Moreover, correlations between anti-CCP antibodies and severity of airflow limitation, CAT scores, mMRC scores of dyspnoea, and GOLD staging of COPD severity were not significant. Wood-smoke-induced COPD could significantly increase the anti-CCP antibody level in non-rheumatoid arthritis patients when compared with that in patients with tobacco-induced COPD and healthy controls.

  14. 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.

  15. Bladder exstrophy repair

    Science.gov (United States)

    Bladder birth defect repair; Everted bladder repair; Exposed bladder repair; Repair of bladder exstrophy ... Bladder exstrophy repair involves two surgeries. The first surgery is to repair the bladder and the second one is to attach ...

  16. Combined alpha-tocopherol and ascorbic acid protects against smoke-induced lung squamous metaplasia in ferrets

    Science.gov (United States)

    Many epidemiological studies show the benefit of fruits and vegetables on reducing risk of lung cancer, the leading cause of cancer death in the United States. Previously, we demonstrated that cigarette smoke exposure (SM)-induced lung lesions in ferrets were prevented by a combination of carotene,...

  17. 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

  18. 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

  19. Electronic cigarettes in the media.

    Science.gov (United States)

    Payne, J Drew; Orellana-Barrios, Menfil; Medrano-Juarez, Rita; Buscemi, Dolores; Nugent, Kenneth

    2016-07-01

    Electronic cigarettes (e-cigarettes) are an increasingly popular source of nicotine and an increasingly popular topic in the media. Concerns about potential hazards associated with e-cigarette use and advertising, especially to adolescents, have led to studies on e-cigarettes in both traditional media (TV, mail, print, and outdoor advertising) and social media (websites, social networking sites, blogs, and e-mails). This review presents a narrative description of available studies related to e-cigarettes in the media. These articles have focused on promotion in both traditional and social media across a broad range of topics and have concentrated on target audiences, smoking cessation, harm reduction, and advertising. E-cigarette advertising is the most frequent topic in the published articles. Identifying the target audience also is a common objective in articles. The representation of e-cigarettes as a "healthier alternative" to traditional cigarettes and their use as a "smoking cessation aid" are main themes presented through all types of media.

  20. 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.

  1. Electronic cigarette use by college students.

    Science.gov (United States)

    Sutfin, Erin L; McCoy, Thomas P; Morrell, Holly E R; Hoeppner, Bettina B; Wolfson, Mark

    2013-08-01

    Electronic cigarettes, or e-cigarettes, are battery operated devices that deliver nicotine via inhaled vapor. There is considerable controversy about the disease risk and toxicity of e-cigarettes and empirical evidence on short- and long-term health effects is minimal. Limited data on e-cigarette use and correlates exist, and to our knowledge, no prevalence rates among U.S. college students have been reported. This study aimed to estimate the prevalence of e-cigarette use and identify correlates of use among a large, multi-institution, random sample of college students. 4444 students from 8 colleges in North Carolina completed a Web-based survey in fall 2009. Ever use of e-cigarettes was reported by 4.9% of students, with 1.5% reporting past month use. Correlates of ever use included male gender, Hispanic or "Other race" (compared to non-Hispanic Whites), Greek affiliation, conventional cigarette smoking and e-cigarette harm perceptions. Although e-cigarette use was more common among conventional cigarette smokers, 12% of ever e-cigarette users had never smoked a conventional cigarette. Among current cigarette smokers, e-cigarette use was negatively associated with lack of knowledge about e-cigarette harm, but was not associated with intentions to quit. Although e-cigarette use was more common among conventional cigarette smokers, it was not exclusive to them. E-cigarette use was not associated with intentions to quit smoking among a sub-sample of conventional cigarette smokers. Unlike older, more established cigarette smokers, e-cigarette use by college students does not appear to be motivated by the desire to quit cigarette smoking. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

  2. DNA typing from cigarette butts.

    Science.gov (United States)

    Watanabe, Yoshihisa; Takayama, Tomohiro; Hirata, Keiji; Yamada, Sadao; Nagai, Atsushi; Nakamura, Isao; Bunai, Yasuo; Ohya, Isao

    2003-03-01

    We performed DNA typing for D1S80, HLADQA1, TH01 and PM using the butts of 100 cigarettes that were smoked by ten different individuals (ten cigarettes per individual). The results obtained from DNA typing for D1S80 agreed with the results obtained using bloodstains in 76 cigarette butt samples. Sixteen samples produced false results, showing the loss of the longer allelic hetero-band. When examined using agarose gel electrophoresis, high-molecular weight DNA was not observed in these samples. The same results were also observed for buccal swab samples and saliva stains obtained from the same individuals. In the remaining eight cigarette butt samples, PCR products were not detected. The results obtained from DNA typing for TH01, HLADQA1 and PM agreed with the results obtained using bloodstains in 90 samples. In the remaining ten samples of a specific kind of cigarette (Marlboro), the PCR products were not detected. The extracts from the ends of the Marlboro cigarettes were stained yellow. When the DNA extracted from Marlboro cigarette butts was treated with Microcon-100 (amicon) or SizeSep 400 Span Columns (Amersham Pharmacia Biotech), PCR products could be detected. When PCR amplification was performed after adding extracts from the ends of unsmoked Marlboro cigarettes to DNA extracted from bloodstains, PCR products could not be detected. The present data indicate that the degradation of high-molecular weight DNA and the inhibition of PCR by dyes of the cigarette end should be kept in mind when performing DNA typing using cigarette ends.

  3. Chronic cigarette smoke causes oxidative damage and apoptosis to retinal pigmented epithelial cells in mice.

    Directory of Open Access Journals (Sweden)

    Masashi Fujihara

    mechanism of smoke induced changes during early AMD.

  4. 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.

  5. 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.

  6. 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.

  7. Receptivity to E-cigarette Marketing, Harm Perceptions, and E-cigarette Use

    Science.gov (United States)

    Pokhrel, Pallav; Fagan, Pebbles; Kehl, Lisa; Herzog, Thaddeus A.

    2016-01-01

    Objective To test whether exposure and receptivity to e-cigarette marketing are associated with recent e-cigarette use among young adults through increased beliefs that e-cigarettes are less harmful than cigarettes. Methods Data were collected from 307 multiethnic 4- and 2-year college students; approximately equal proportions of current, never, and former cigarette smokers [mean age = 23.5 (SD = 5.5); 65% female]. Results Higher receptivity to e-cigarette marketing was associated with perceptions that e-cigarettes are less harmful than cigarettes, which in turn, were associated with higher recent e-cigarette use. Conclusions The findings provide preliminary support to the proposition that marketing of e-cigarettes as safer alternatives to cigarettes or cessation aids is associated with increased e-cigarette use among young adults. The findings have implications for development of e-cigarette regulations. PMID:25290604

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

    Directory of Open Access Journals (Sweden)

    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.

  9. 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.

  10. 19 CFR 159.5 - Cigars, cigarettes, and cigarette papers and tubes.

    Science.gov (United States)

    2010-04-01

    ... 19 Customs Duties 2 2010-04-01 2010-04-01 false Cigars, cigarettes, and cigarette papers and tubes..., and cigarette papers and tubes. The internal revenue taxes imposed on cigars, cigarettes, and cigarette papers and tubes under section 5701 or 7652, Internal Revenue Code of 1954 (26 U.S.C. 5701 or...

  11. 27 CFR 40.351 - Cigarette papers.

    Science.gov (United States)

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2010-04-01 2010-04-01 false Cigarette papers. 40.351... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.351 Cigarette papers....

  12. 27 CFR 41.34 - Cigarette papers.

    Science.gov (United States)

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2010-04-01 2010-04-01 false Cigarette papers. 41.34... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.34 Cigarette papers. Cigarette papers are taxed at the...

  13. Functional Analysis and Treatment of Cigarette Pica.

    Science.gov (United States)

    Piazza, Cathleen C.; And Others

    1996-01-01

    This study of an adolescent with mental retardation and autism found that pica of cigarette butts was maintained in a condition with no social consequences when cigarettes contained nicotine but not when cigarettes contained herbs without nicotine. A procedure based on stimulus control, which reduced cigarette consumption to zero, is described.…

  14. Marketing of menthol cigarettes and consumer perceptions

    OpenAIRE

    2011-01-01

    Abstract In order to more fully understand why individuals smoke menthol cigarettes, it is important to understand the perceptions held by youth and adults regarding menthol cigarettes. Perceptions are driven by many factors, and one factor that can be important is marketing. This review seeks to examine what role, if any, the marketing of menthol cigarettes plays in the formation of consumer perceptions of menthol cigarettes. The available literature suggests that menthol cigarettes may be p...

  15. Association between menthol cigarette smoking and current use of electronic cigarettes among us adolescents.

    Directory of Open Access Journals (Sweden)

    Israel Agaku

    2017-05-01

    Current e-cigarette use was significantly higher among menthol than nonmenthol cigarette smokers. These findings underscore the importance of efforts to reduce all forms of tobacco product use, including e-cigarettes, among youth.

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

    Directory of Open Access Journals (Sweden)

    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.

  17. High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner

    Directory of Open Access Journals (Sweden)

    Oliver J. Taylor

    2017-05-01

    Full Text Available We have previously found that cigarette smoke disrupts metabolic function, in part, by increasing muscle ceramide accrual. To further our understanding of this, we sought to determine the role of the cytokine high-mobility group box 1 (HMGB1, which is increased with smoke exposure, in smoke-induced muscle metabolic perturbations. To test this theory, we determined HMGB1 from lungs of human smokers, as well as from lung cells from mice exposed to cigarette smoke. We also treated cells and mice directly with HMGB1, in the presence or absence of myriocin, an inhibitor of serine palmitoyltransferase, the rate-limiting enzyme in ceramide biosynthesis. Outcomes included assessments of insulin resistance and muscle mitochondrial function. HMGB1 was significantly increased in both human lungs and rodent alveolar macrophages. Further testing revealed that HMGB1 treatment elicited a widespread increase in ceramide species and reduction in myotube mitochondrial respiration, an increase in reactive oxygen species, and reduced insulin-stimulated Akt phosphorylation. Inhibition of ceramide biosynthesis with myriocin was protective. In mice, by comparing treatments of HMGB1 injections with or without myriocin, we found that HMGB1 injections resulted in increased muscle ceramides, especially C16 and C24, which were necessary for reduced muscle mitochondrial respiration and compromised insulin and glucose tolerance. In conclusion, HMGB1 may be a necessary intermediate in the ceramide-dependent metabolic consequences of cigarette smoke exposure.

  18. Effect of bacoside A on membrane-bound ATPases in the brain of rats exposed to cigarette smoke.

    Science.gov (United States)

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

    2005-01-01

    Membrane-bound enzymes play a vital role in neuronal function through maintenance of membrane potential and impulse propagation. We have evaluated the harmful effects of chronic cigarette smoking on membrane-bound ATPases and the protective effect of Bacoside A in rat brain. Adult male albino rats were exposed to cigarette smoke for a period of 12 weeks and simultaneously administered with Bacoside A (the active principle isolated from Bacopa monniera) at a dosage of 10 mg/kg b.w/day, p.o. The levels of lipid peroxides as marker for evaluating the extent of membrane damage, the activities of Na+/K+-ATPase, Ca2+-ATPase and Mg2+-ATPase, and associated cations sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+) were investigated in the brain. Neuronal membrane damage was evident from the elevated levels of lipid peroxides and decreased activities of membrane-bound enzymes. Disturbances in the electrolyte balance with accumulation of Na+ and Ca2+ and depletion of K+ and Mg2+ were also observed. Administration of Bacoside A inhibited lipid peroxidation, improved the activities of ATPases, and maintained the ionic equilibrium. The results of our study indicate that Bacoside A protects the brain from cigarette smoking induced membrane damage.

  19. High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner

    Science.gov (United States)

    Taylor, Oliver J.; Thatcher, Mikayla O.; Carr, Sheryl T.; Gibbs, Jonathan L.; Trumbull, Annie M.; Harrison, Mitchell E.; Winden, Duane R.; Pearson, Mackenzie J.; Tippetts, Trevor S.; Holland, William L.; Reynolds, Paul R.; Bikman, Benjamin T.

    2017-01-01

    We have previously found that cigarette smoke disrupts metabolic function, in part, by increasing muscle ceramide accrual. To further our understanding of this, we sought to determine the role of the cytokine high-mobility group box 1 (HMGB1), which is increased with smoke exposure, in smoke-induced muscle metabolic perturbations. To test this theory, we determined HMGB1 from lungs of human smokers, as well as from lung cells from mice exposed to cigarette smoke. We also treated cells and mice directly with HMGB1, in the presence or absence of myriocin, an inhibitor of serine palmitoyltransferase, the rate-limiting enzyme in ceramide biosynthesis. Outcomes included assessments of insulin resistance and muscle mitochondrial function. HMGB1 was significantly increased in both human lungs and rodent alveolar macrophages. Further testing revealed that HMGB1 treatment elicited a widespread increase in ceramide species and reduction in myotube mitochondrial respiration, an increase in reactive oxygen species, and reduced insulin-stimulated Akt phosphorylation. Inhibition of ceramide biosynthesis with myriocin was protective. In mice, by comparing treatments of HMGB1 injections with or without myriocin, we found that HMGB1 injections resulted in increased muscle ceramides, especially C16 and C24, which were necessary for reduced muscle mitochondrial respiration and compromised insulin and glucose tolerance. In conclusion, HMGB1 may be a necessary intermediate in the ceramide-dependent metabolic consequences of cigarette smoke exposure. PMID:28531105

  20. Investigation about atorvastatin resist to tobacco smoking inducing endothelial inflammation%阿托伐他汀抵抗吸烟相关性血管内皮损伤的实验研究

    Institute of Scientific and Technical Information of China (English)

    郭轶; 卢小刚; 代远斌

    2015-01-01

    Objective To explore the role of atorvastatin resist to tobacco smoking inducing endothelial inflammation .Meth‐ods HUVECs were divided into normal control group ,cigarette smoking extract(CSE) group and atorvastatin(AS)+CSE group . The cellular morphology of HUVECs in three group were observed ,then the expressions of VCAM‐1 and E selectin in HUVECs in three group were detected by western blot assay .Results In CES group ,drastic morphological change of HUVECs were observed . In AS+CSE group ,minor morphological change of HUVECs were observed .Also ,the protein levels of VCAM‐1 and E selectin were much higher in CSE group than that of in other two groups(P<0 .05) ,and the protein levels of VCAM‐1 and E‐selectin in AS+CSE group were a little higher than that of in control group ,but much lower than that of in CSE group(P<0 .05) .Conclusion Our results showed that atorvastatin might partly resist to tobacco smoking inducing endothelial inflammation .%目的:探讨阿托伐他汀对吸烟相关性血管内皮损伤的保护作用。方法将人脐静脉内皮细胞(HUVECs)分为对照组、香烟提取物处理组和阿托伐他汀联合香烟提取物处理组。观察不同组细胞的形态学变化,并检测不同组细胞中血管细胞黏附分子‐1(VCAM‐1)和E‐选择素(E‐selectin)的蛋白表达。结果香烟提取物处理组HUVECs的细胞形态发生了剧烈的变化,失去了基本形态;而阿托伐他汀联合香烟提取物处理组 HUVECs的细胞形态仅发生了轻微的改变,保留了基本形态。同时VCAM‐1和E‐selectin蛋白在香烟提取物处理组细胞中表达明显高于对照组和阿托伐他汀联合香烟提取物处理组,差异有统计学意义(P<0.05);VCAM‐1和E‐selectin蛋白在阿托伐他汀联合香烟提取物处理组细胞中的表达稍高于对照组,差异有统计学意义(P<0.05)。结论阿托伐他汀可以抵抗吸烟导致的血管

  1. Persistence of smoking-induced dysregulation of miRNA expression in the small airway epithelium despite smoking cessation.

    Directory of Open Access Journals (Sweden)

    Guoqing Wang

    Full Text Available Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD and lung cancer remains significantly higher compared to healthy nonsmokers. Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE, we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 9 healthy nonsmokers and 10 healthy smokers, before and after they quit smoking for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy nonsmokers (p1.5, with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway being the top identified enriched pathway of the target genes of the persistent dysregulated miRNAs. In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammatory diseases or lung cancer, it is likely that persistent smoking-related changes in SAE miRNAs play a role in the subsequent development of these disorders.

  2. Cigarette tax avoidance and evasion.

    Science.gov (United States)

    Stehr, Mark

    2005-03-01

    Variation in state cigarette taxes provides incentives for tax avoidance through smuggling, legal border crossing to low tax jurisdictions, or Internet purchasing. When taxes rise, tax paid sales of cigarettes will decline both because consumption will decrease and because tax avoidance will increase. The key innovation of this paper is to compare cigarette sales data to cigarette consumption data from the Behavioral Risk Factor Surveillance System (BRFSS). I show that after subtracting percent changes in consumption, residual percent changes in sales are associated with state cigarette tax changes implying the existence of tax avoidance. I estimate that the tax avoidance response to tax changes is at least twice the consumption response and that tax avoidance accounted for up to 9.6% of sales between 1985 and 2001. Because of the increase in tax avoidance, tax paid sales data understate the level of smoking and overstate the drop in smoking. I also find that the level of legal border crossing was very low relative to other forms of tax avoidance. If states have strong preferences for smoking control, they must pair high cigarette taxes with effective policies to curb smuggling and other forms of tax avoidance or employ alternative policies such as counter-advertising and smoking restrictions.

  3. Hypospadias repair

    Science.gov (United States)

    ... the problem. If the repair is not done, problems may occur later on such as: Difficulty controlling and directing urine stream A curve in the penis during erection Decreased fertility Embarrassment about appearance of penis Surgery ...

  4. Marketing of menthol cigarettes and consumer perceptions

    Directory of Open Access Journals (Sweden)

    Rising Joshua

    2011-05-01

    Full Text Available Abstract In order to more fully understand why individuals smoke menthol cigarettes, it is important to understand the perceptions held by youth and adults regarding menthol cigarettes. Perceptions are driven by many factors, and one factor that can be important is marketing. This review seeks to examine what role, if any, the marketing of menthol cigarettes plays in the formation of consumer perceptions of menthol cigarettes. The available literature suggests that menthol cigarettes may be perceived as safer choices than non-menthol cigarettes. Furthermore, there is significant overlap between menthol cigarette advertising campaigns and the perceptions of these products held by consumers. The marketing of menthol cigarettes has been higher in publications and venues whose target audiences are Blacks/African Americans. Finally, there appears to have been changes in cigarette menthol content over the past decade, which has been viewed by some researchers as an effort to attract different types of smokers.

  5. Electronic Cigarette Use among Mississippi Adults, 2015

    Directory of Open Access Journals (Sweden)

    Vincent L. Mendy

    2017-01-01

    Full Text Available Electronic cigarettes (e-cigarettes are battery-powered devices that deliver nicotine in the form of aerosol. We identify differences and associations in e-cigarette use by sociodemographic characteristics and describe the reported reasons for initiating use among Mississippi adults. We used the 2015 Mississippi Behavioral Risk Factor Surveillance System, which collected information on e-cigarette use from 6,035 respondents. The prevalence of current e-cigarette use and having ever tried an e-cigarette was determined overall and by sociodemographic characteristics. Weighted prevalences and 95% confidence intervals were calculated, and prevalences for subgroups were compared using the X2 tests and associations were assessed using logistic regression. In 2015, 4.7% of Mississippi adults currently used e-cigarettes, while 20.5% had ever tried an e-cigarette. The prevalence of current e-cigarette use was significantly higher for young adults, whites, men, individuals unable to work, those with income $35,000–$49,999, and current smokers compared to their counterparts. Similar results were observed for having ever tried an e-cigarette. E-cigarette use was associated with age, race, income, and smoking status. Most (71.2% of current e-cigarette users and over half (52.1% of those who have ever tried e-cigarettes reported that a main reason for trying or using e-cigarettes was “to cut down or quit smoking.”

  6. Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice

    Science.gov (United States)

    Talukder, M. A. Hassan; Johnson, Wesley M.; Varadharaj, Saradhadevi; Lian, Jiarui; Kearns, Patrick N.; El-Mahdy, Mohamed A.; Liu, Xiaoping

    2011-01-01

    Cigarette smoking is a major independent risk factor for cardiovascular disease. While the association between chronic smoking and cardiovascular disease is well established, the underlying mechanisms are incompletely understood, partly due to the lack of adequate in vivo animal models. Here, we report a mouse model of chronic smoking-induced cardiovascular pathology. Male C57BL/6J mice were exposed to whole body mainstream cigarette smoke (CS) using a SCIREQ “InExpose” smoking system (48 min/day, 5 days/wk) for 16 or 32 wk. Age-matched, air-exposed mice served as nonsmoking controls. Blood pressure was measured, and cardiac MRI was performed. In vitro vascular ring and isolated heart experiments were performed to measure vascular reactivity and cardiac function. Blood from control and smoking mice was studied for the nitric oxide (NO) decay rate and reactive oxygen species (ROS) generation. With 32 wk of CS exposure, mice had significantly less body weight gain and markedly higher blood pressure. At 32 wk of CS exposure, ACh-induced vasorelaxation was significantly shifted to the right and downward, left ventricular mass was significantly larger along with an increased heart-to-body weight ratio, in vitro cardiac function tended to be impaired with high afterload, white blood cells had significantly higher ROS generation, and the blood NO decay rate was significantly faster. Thus, smoking led to blunted weight gain, hypertension, endothelial dysfunction, leukocyte activation with ROS generation, decreased NO bioavailability, and mild cardiac hypertrophy in mice that were not otherwise predisposed to disease. This mouse model is a useful tool to enable further elucidation of the molecular and cellular mechanisms of smoking-induced cardiovascular diseases. PMID:21057039

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

    Directory of Open Access Journals (Sweden)

    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

  8. Doctors Divided on Safety, Use of Electronic Cigarettes

    Science.gov (United States)

    ... Cigarettes When patients ask about safety and using e-cigarettes to stop smoking, doctors' advice differs To use ... of the devices -- specifically, about the safety of e-cigarettes compared to traditional cigarettes, according to the Stanford ...

  9. CDC Vital Signs: E-cigarette Ads and Youth

    Science.gov (United States)

    ... students were current (past 30-day) users of electronic cigarettes, or e-cigarettes, in 2014. Most e-cigarettes ... Related Pages Vital Signs Issue details: Exposure to Electronic Cigarette Advertising Among Middle School and High School Students ...

  10. A New Area to Fight: Electronic Cigarette

    Directory of Open Access Journals (Sweden)

    Şermin Börekçi

    2015-08-01

    Full Text Available Electronic cigarette (e-cigarette is spreading like an epidemic that threatens the public health. Last one year, e-cigarette use increased by 2 times in both adults and children, and just as the cigarette ads of 1950s and 1960s, e-cigarette ads are taking place in the television, radio, internet, magazines and in the all kinds of advertising media. E-sigara should be recognized as a serious health threat, and should be fought against it. The aim of this review is to show the effects of e-cigarette on health by the scientific evidences.

  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. Cigarette consumption among foreign tourists in Thailand.

    Science.gov (United States)

    Termsirikulchai, Lakkhana; Kengganpanich, Mondha; Benjakul, Sarunya; Kengganpanich, Tharadol

    2012-06-01

    To explore the cigarette consumption among foreign tourists in Thailand. The data in this cross-sectional survey is collected by interviewing 655 foreign tourist smokers with questionnaires in congested areas including Suvarnabhum International Airport, Khao San Road, shopping centers and tourist attraction sites. The data was collected in October, 2010, analyzed by descriptive statistic and the crude magnitude of cigarette consumption was calculated. The findings indicated that 62.9% of tourists were male and 58.9% were from European countries and 22.7% were from Asian countries. 59.2% smoked cigarettes sold in Thailand and were taxed legally. In that amount, 55.7% smoked imported cigarettes and only 3.5% smoked Thai cigarettes. 40.8% had brought cigarettes from their countries or bought cigarettes from Duty Free shops with the amount allowed by Thai law. The top 2 popular brands were Marlboro and L&M. The main reason why they bought imported cigarettes in Thailand was that the price was cheaper or the same when compared with that in their countries. The cigarette consumption share crudely calculated was around 8.90 million packs. Foreign tourists smoked imported cigarettes distributed in Thailand and cigarettes brought from abroad. So, Free Trade Agreement in bilateral level or multilateral level need to be reviewed and should separate cigarettes from other goods. The tax barrier excise tax measure and permission law of carrying in 200 sticks should be reviewed in order to control cigarette consumption effectively.

  13. Bhas 42 cell transformation activity of cigarette smoke condensate is modulated by selenium and arsenic.

    Science.gov (United States)

    Han, Sung Gu; Pant, Kamala; Bruce, Shannon W; Gairola, C Gary

    2016-04-01

    Cigarette smoking remains a major health risk worldwide. Development of newer tobacco products requires the use of quantitative toxicological assays. Recently, v-Ha-ras transfected BALB/c3T3 (Bhas 42) cell transformation assay was established that simulates the two-stage animal tumorigenesis model and measures tumor initiating and promoting activities of chemicals. The present study was performed to assess the feasibility of using this Bhas 42 cell transformation assay to determine the initiation and promotion activities of cigarette smoke condensate (CSC) and its water soluble fraction. Further, the modulating effects of selenium and arsenic on cigarette smoke-induced cell transformation were investigated. Dimethyl sulfoxide (DMSO) and water extracts of CSC (CSC-D and CSC-W, respectively) were tested at concentrations of 2.5-40 µg mL(-1) in the initiation or promotion assay formats. Initiation protocol of the Bhas 42 assay showed a 3.5-fold increase in transformed foci at 40 µg mL(-1) of CSC-D but not CSC-W. The promotion phase of the assay yielded a robust dose response with CSC-D (2.5-40 µg mL(-1)) and CSC-W (20-40 µg mL(-1)). Preincubation of cells with selenium (100 nM) significantly reduced CSC-induced increase in cell transformation in initiation assay. Co-treatment of cells with a sub-toxic dose of arsenic significantly enhanced cell transformation activity of CSC-D in promotion assay. The results suggest a presence of both water soluble and insoluble tumor promoters in CSC, a role of oxidative stress in CSC-induced cell transformation, and usefulness of Bhas 42 cell transformation assay in comparing tobacco product toxicities and in studying the mechanisms of tobacco carcinogenesis. © 2016 Wiley Periodicals, Inc.

  14. Femoral hernia repair

    Science.gov (United States)

    Femorocele repair; Herniorrhaphy; Hernioplasty - femoral ... During surgery to repair the hernia, the bulging tissue is pushed back in. The weakened area is sewn closed or strengthened. This repair ...

  15. Undescended testicle repair

    Science.gov (United States)

    Orchidopexy; Inguinal orchidopexy; Orchiopexy; Repair of undescended testicle; Cryptorchidism repair ... first year of life without treatment. Undescended testicle repair surgery is recommended for patients whose testicles do ...

  16. Dependence levels in users of electronic cigarettes, nicotine gums and tobacco cigarettes

    Science.gov (United States)

    ETTER, Jean-François; EISSENBERG, Thomas

    2016-01-01

    Objective To assess dependence levels in users of e-cigarettes, and compare them with dependence levels in users of nicotine gums and tobacco cigarettes. Design Self-reports from cross-sectional Internet and mail surveys. Comparisons of: a) 766 daily users of nicotine-containing e-cigarettes with 30 daily users of nicotine-free e-cigarettes; b) 911 former smokers who used the e-cigarette daily with 451 former smokers who used the nicotine gum daily (but no e-cigarette); c) 125 daily e-cigarette users who smoked daily (dual users) with two samples of daily smokers who did not use e-cigarettes (2206 enrolled on the Internet and 292 enrolled by mail from the general population of Geneva). We used the Fagerström Test for Nicotine Dependence, the Nicotine Dependence Syndrome Scale, the Cigarette Dependence Scale and versions of these scales adapted for e-cigarettes and nicotine gums. Results Dependence ratings were slightly higher in users of nicotine-containing e-cigarettes than in users of nicotine-free e-cigarettes. In former smokers, long-term (>3 months) users of e-cigarettes were less dependent on e-cigarettes than long-term users of the nicotine gum were dependent on the gum. There were few differences in dependence ratings between short-term (cigarettes. Dependence on e-cigarettes was generally lower in dual users than dependence on tobacco cigarettes in the two other samples of daily smokers. Conclusions Some e-cigarette users were dependent on nicotine-containing e-cigarettes, but these products were less addictive than tobacco cigarettes. E-cigarettes may be as or less addictive than nicotine gums, which themselves are not very addictive. PMID:25561385

  17. Chronic Cigarette Smoking Impairs Erectile Function through Increased Oxidative Stress and Apoptosis, Decreased nNOS, Endothelial and Smooth Muscle Contents in a Rat Model.

    Directory of Open Access Journals (Sweden)

    Yun-Ching Huang

    Full Text Available Cigarette use is an independent risk factor for the development of erectile dysfunction (ED. While the association between chronic smoking and ED is well established, the fundamental mechanism(s of cigarette-related ED are incompletely understood, partly due to no reliable animal model of smoking-induced ED. The present study was designed to validate an in vivo rat model of chronic cigarette-induced ED. Forty 12-week old male Sprague-Dawley rats were divided into 4 groups. Ten rats served as control group and were exposed only to room air. The remaining 30 rats were passively exposed to cigarette smoke (CS for 4 weeks (n = 10, 12 weeks (n = 10, and 24 weeks (n = 10. At the 24-week time point all rats were assessed with intracavernous pressure (ICP during cavernous nerve electrostimulation. Blood and urine were collected to measure serum testosterone and oxidative stress, respectively. Corporal tissue was assessed by Western blot for neuronal nitric oxide synthase (nNOS. Penile tissues were subjected to immunohistochemistry for endothelial, smooth muscle, and apoptotic content. Mean arterial pressure (MAP was significantly higher in 24-week cigarette exposed animals compared to the control animals. Mean ICP/MAP ratio and cavernosal smooth muscle/endothelial contents were significantly lower in the 12- and 24-week rats compared to control animals. Oxidative stress was significantly higher in the 24-week cigarette exposed group compared to control animals. Mean nNOS expression was significantly lower, and apoptotic index significantly higher, in CS-exposed animals compared to control animals. These findings indicate that the rat model exposure to CS increases apoptosis and oxidative stress and decreases nNOS, endothelial and smooth muscle contents, and ICP in a dose dependent fashion. The rat model is a useful tool for further study of the molecular and cellular mechanisms of CS-related ED.

  18. Patient–physician communication regarding electronic cigarettes

    Directory of Open Access Journals (Sweden)

    Michael B. Steinberg

    2015-01-01

    Discussion: Physician communication about e-cigarettes may shape patients' perceptions about the products. More research is needed to explore the type of information that physicians share with their patients regarding e-cigarettes and harm reduction.

  19. Flavour chemicals in electronic cigarette fluids

    OpenAIRE

    Tierney, Peyton A; Karpinski, Clarissa D; Brown, Jessica E; Luo, Wentai; Pankow, James F

    2015-01-01

    Background Most e-cigarette liquids contain flavour chemicals. Flavour chemicals certified as safe for ingestion by the Flavor Extracts Manufacturers Association may not be safe for use in e-cigarettes. This study identified and measured flavour chemicals in 30 e-cigarette fluids. Methods Two brands of single-use e-cigarettes were selected and their fluids in multiple flavour types analysed by gas chromatography/mass spectrometry. For the same flavour types, and for selected confectionary fla...

  20. E-cigarettes also contain detrimental chemicals

    DEFF Research Database (Denmark)

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

    2014-01-01

    This article reviews studies dealing with the content of electronic (e-) cigarettes. Based on measurements of the e-juice, the inhaled and the exhaled vapour, it is sound to assume that smoking e-cigarettes might have much less detrimental health effects than smoking conventional cigarettes....... However, propylene glycol and glycerine are abundant in e-cigarettes and although they are generally perceived as relatively harmless, the long-term effects of heavy exposure to these substances are unknown....

  1. E-cigarettes also contain detrimental chemicals

    DEFF Research Database (Denmark)

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

    2014-01-01

    This article reviews studies dealing with the content of electronic (e-) cigarettes. Based on measurements of the e-juice, the inhaled and the exhaled vapour, it is sound to assume that smoking e-cigarettes might have much less detrimental health effects than smoking conventional cigarettes. Howe....... However, propylene glycol and glycerine are abundant in e-cigarettes and although they are generally perceived as relatively harmless, the long-term effects of heavy exposure to these substances are unknown....

  2. The electronic cigarette: the new cigarette of the 21st century?*

    OpenAIRE

    Marli Maria Knorst; Igor Gorski Benedetto; Mariana Costa Hoffmeister; Marcelo Basso Gazzana

    2014-01-01

    The electronic nicotine delivery system, also known as the electronic cigarette, is generating considerable controversy, not only in the general population but also among health professionals. Smokers the world over have been increasingly using electronic cigarettes as an aid to smoking cessation and as a substitute for conventional cigarettes. There are few available data regarding the safety of electronic cigarettes. There is as yet no evidence that electronic cigarettes are effective in tr...

  3. Cigarette Smoking Impairs Pancreatic Duct Cell Bicarbonate Secretion

    Science.gov (United States)

    Kadiyala, Vivek; Lee, Linda S; Banks, Peter A; Suleiman, Shadeah; Paulo, Joao A; Wang, Wei; Rosenblum, Jessica; Sainani, Nisha I; Mortele, Koenraad; Conwell, Darwin L

    2015-01-01

    2.4; P=0.033) were all associated with low mean peak PF [HCO3−] (indicating duct cell secretory dysfunction). Multivariate Analysis Smoking (odds ratio, OR: 3.8, 95% CI: 1.6–9.1; P=0.003) and definite chronic pancreatitis imaging (OR: 5.7, 95% CI: 2.2–14.8; P<0.001) were determined to be independent predictors of low peak PF [HCO3−], controlling for age, gender, and alcohol intake. Furthermore there was no interaction between smoking status and alcohol intake in predicting duct cell dysfunction (P=0.571). Conclusion Measurement of pancreatic fluid bicarbonate in smokers reveals that cigarette smoking (past and current) is an independent risk factor for pancreatic duct cell secretory dysfunction (low PF [HCO3−]). Furthermore, the risk of duct cell dysfunction in subjects who smoked was approximately twice the risk (RR: 2.2) in never smokers. Further in depth, translational research approaches to pancreatic fluid analysis may help unravel mechanisms of cigarette smoking induced pancreatic duct cell injury. PMID:23306332

  4. Intestinal obstruction repair

    Science.gov (United States)

    Repair of volvulus; Intestinal volvulus - repair; Bowel obstruction - repair ... Intestinal obstruction repair is done while you are under general anesthesia . This means you are asleep and DO NOT feel pain. ...

  5. Aortic aneurysm repair - endovascular

    Science.gov (United States)

    EVAR; Endovascular aneurysm repair - aorta; AAA repair - endovascular; Repair - aortic aneurysm - endovascular ... Endovascular aortic repair is done because your aneurysm is very large, growing quickly, or is leaking or bleeding. You may have ...

  6. Polonium-210 budget in cigarettes

    Energy Technology Data Exchange (ETDEWEB)

    Khater, A.E.M. E-mail: khater_ashraf@yahoo.com)

    2004-07-01

    Due to the relatively high activity concentrations of {sup 210}Po and {sup 210}Pb that are found in tobacco and its products, cigarette smoking highly increases the internal intake of both radionuclides and their concentrations in the lung tissues. That might contribute significantly to an increase in the internal radiation dose and in the number of instances of lung cancer observed among smokers. Samples of most frequently smoked fine and popular brands of cigarettes were collected from those available on the Egyptian market. {sup 210}Po activity concentrations were measured by alpha spectrometry, using surface barrier detectors, following the radiochemical separation of polonium. Samples of fresh tobacco, wrapping paper, fresh filters, ash and post-smoking filters were spiked with {sup 208}Po for chemical recovery calculation. The samples were dissolved using mineral acids (HNO{sub 3}, HCl and HF). Polonium was spontaneously plated-out on stainless steel disks from diluted HCl solution. The {sup 210}Po activity concentration in smoke was estimated on the basis of its activity in fresh tobacco and wrapping paper, fresh filter, ash and post-smoking filters. The percentages of {sup 210}Po activity concentrations that were recovered from the cigarette tobacco to ash, post-smoking filters, and smokes were assessed. The results of this work indicate that the average (range) activity concentration of {sup 210}Po in cigarette tobacco was 16.6 (9.7-22.5) mBq/cigarette. The average percentages of {sup 210}Po content in fresh tobacco plus wrapping paper that were recovered by post-smoking filters, ash and smoke were 4.6, 20.7 and 74.7, respectively. Cigarette smokers, who are smoking one pack (20 cigarettes) per day, are inhaling on average 123 mBq/d of {sup 210}Po and {sup 210}Pb each. The annual effective doses were calculated on the basis of {sup 210}Po and {sup 210}Pb intake with the cigarette smoke. The mean values of the annual effective dose for smokers (one pack per

  7. Polonium-210 budget in cigarettes.

    Science.gov (United States)

    Khater, Ashraf E M

    2004-01-01

    Due to the relatively high activity concentrations of (210)Po and (210)Pb that are found in tobacco and its products, cigarette smoking highly increases the internal intake of both radionuclides and their concentrations in the lung tissues. That might contribute significantly to an increase in the internal radiation dose and in the number of instances of lung cancer observed among smokers. Samples of most frequently smoked fine and popular brands of cigarettes were collected from those available on the Egyptian market. (210)Po activity concentrations were measured by alpha spectrometry, using surface barrier detectors, following the radiochemical separation of polonium. Samples of fresh tobacco, wrapping paper, fresh filters, ash and post-smoking filters were spiked with (208)Po for chemical recovery calculation. The samples were dissolved using mineral acids (HNO(3), HCl and HF). Polonium was spontaneously plated-out on stainless steel disks from diluted HCl solution. The (210)Po activity concentration in smoke was estimated on the basis of its activity in fresh tobacco and wrapping paper, fresh filter, ash and post-smoking filters. The percentages of (210)Po activity concentrations that were recovered from the cigarette tobacco to ash, post-smoking filters, and smokes were assessed. The results of this work indicate that the average (range) activity concentration of (210)Po in cigarette tobacco was 16.6 (9.7-22.5) mBq/cigarette. The average percentages of (210)Po content in fresh tobacco plus wrapping paper that were recovered by post-smoking filters, ash and smoke were 4.6, 20.7 and 74.7, respectively. Cigarette smokers, who are smoking one pack (20 cigarettes) per day, are inhaling on average 123 mBq/d of (210)Po and (210)Pb each. The annual effective doses were calculated on the basis of (210)Po and (210)Pb intake with the cigarette smoke. The mean values of the annual effective dose for smokers (one pack per day) were estimated to be 193 and 251 microSv from

  8. Are all cigarettes just the same? Female's perceptions of slim, coloured, aromatized and capsule cigarettes.

    Science.gov (United States)

    Moodie, Crawford; Ford, Allison; Mackintosh, Anne; Purves, Richard

    2015-02-01

    Twelve focus groups in Glasgow (Scotland) were conducted with female non-smokers and occasional smokers aged 12-24 years (N = 75), with each group shown 11 cigarettes: two (standard) cigarettes with cork filters; two coloured cigarettes (pink or brown); four slim cigarettes; an aromatized black cigarette; a menthol cigarette and a cigarette with a flavour-changing rupturable capsule in the filter. Participants were asked to rank the cigarettes by appeal, taste and harm. The capsule cigarette was then discussed in depth. The pink coloured cigarette and slim cigarettes created significant interest and were generally perceived as most appealing and pleasant tasting, and least harmful. The black aromatized cigarette received a mixed response, with some disliking the dark colour and associating it with low appeal, strong taste and increased harm, whereas for others the smell helped to enhance appeal and taste perceptions and lower perceptions of harm. The novel capsule cigarette, when discussed in-depth, was viewed very positively. Just as research shows that cigarette packs can influence perceptions of appeal, harm and taste, this study suggests that the actual cigarettes can do likewise. The findings have implications for tobacco education and policy.

  9. Motorcycle Repair.

    Science.gov (United States)

    Hein, Jim; Bundy, Mike

    This motorcycle repair curriculum guide contains the following ten areas of study: brake systems, clutches, constant mesh transmissions, final drives, suspension, mechanical starting mechanisms, electrical systems, fuel systems, lubrication systems, and overhead camshafts. Each area consists of one or more units of instruction. Each instructional…

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

    Directory of Open Access Journals (Sweden)

    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.

  11. Turbine repair process, repaired coating, and repaired turbine component

    Energy Technology Data Exchange (ETDEWEB)

    Das, Rupak; Delvaux, John McConnell; Garcia-Crespo, Andres Jose

    2015-11-03

    A turbine repair process, a repaired coating, and a repaired turbine component are disclosed. The turbine repair process includes providing a turbine component having a higher-pressure region and a lower-pressure region, introducing particles into the higher-pressure region, and at least partially repairing an opening between the higher-pressure region and the lower-pressure region with at least one of the particles to form a repaired turbine component. The repaired coating includes a silicon material, a ceramic matrix composite material, and a repaired region having the silicon material deposited on and surrounded by the ceramic matrix composite material. The repaired turbine component a ceramic matrix composite layer and a repaired region having silicon material deposited on and surrounded by the ceramic matrix composite material.

  12. Cigarette smokers' classification of tobacco products.

    Science.gov (United States)

    Casseus, M; Garmon, J; Hrywna, M; Delnevo, C D

    2016-11-01

    Cigarette consumption has declined in the USA. However, cigar consumption has increased. This may be due in part to some cigarette smokers switching to filtered cigars as a less expensive substitute for cigarettes. Additionally, some cigarette smokers may perceive and consume little filtered cigars as cigarettes. The purpose of this study was to determine how cigarette smokers classify tobacco products when presented with photographs of those products. An online survey was conducted with a sample of 344 self-identified cigarette smokers. Respondents were presented with pictures of various types of tobacco products, both with and without packaging, and then asked to categorise them as either a cigarette, little cigar, cigarillo, cigar or machine-injected roll-your-own cigarette (RYO). Respondents were also asked about their tobacco use and purchasing behaviour. Overall, respondents had difficulty distinguishing between cigarettes, little cigars, cigarillos and RYO. When presented with images of the products without packaging, 93% of respondents identified RYO as a cigarette, while 42% identified a little cigar as a cigarette. Additionally, respondents stated that they would consider purchasing little cigars as substitutes for cigarettes because of the price advantage. The results of this survey suggest that when presented with photographs of tobacco products, large proportions of current smokers were unable to differentiate between cigarettes, little cigars, cigarillos, RYO and cigars. Findings have implications for existing public health efforts targeting cigarette smokers, and underscore the need to review current definitions of tobacco products and federal excise taxes on such products. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

  13. Carbonyl Compounds Generated from Electronic Cigarettes

    Directory of Open Access Journals (Sweden)

    Kanae Bekki

    2014-10-01

    Full Text Available Electronic cigarettes (e-cigarettes are advertised as being safer than tobacco cigarettes products as the chemical compounds inhaled from e-cigarettes are believed to be fewer and less toxic than those from tobacco cigarettes. Therefore, continuous careful monitoring and risk management of e-cigarettes should be implemented, with the aim of protecting and promoting public health worldwide. Moreover, basic scientific data are required for the regulation of e-cigarette. To date, there have been reports of many hazardous chemical compounds generated from e-cigarettes, particularly carbonyl compounds such as formaldehyde, acetaldehyde, acrolein, and glyoxal, which are often found in e-cigarette aerosols. These carbonyl compounds are incidentally generated by the oxidation of e-liquid (liquid in e-cigarette; glycerol and glycols when the liquid comes in contact with the heated nichrome wire. The compositions and concentrations of these compounds vary depending on the type of e-liquid and the battery voltage. In some cases, extremely high concentrations of these carbonyl compounds are generated, and may contribute to various health effects. Suppliers, risk management organizations, and users of e-cigarettes should be aware of this phenomenon.

  14. The lingering question of menthol in cigarettes.

    Science.gov (United States)

    Besaratinia, Ahmad; Tommasi, Stella

    2015-02-01

    Tobacco use is the single most important preventable cause of cancer-related deaths in the USA and many parts of the world. There is growing evidence that menthol cigarettes are starter tobacco products for children, adolescents, and young adults. Accumulating research also suggests that smoking menthol cigarettes reinforces nicotine dependence, impedes cessation, and promotes relapse. However, menthol cigarettes are exempt from the US Food and Drug Administration ban on flavored cigarettes due, in part, to the lack of empirical evidence describing the health consequences of smoking menthol cigarettes relative to regular cigarettes. Determining the biological effects of menthol cigarette smoke relative to regular cigarette smoke can clarify the health risks associated with the use of respective products and assist regulatory agencies in making scientifically based decisions on the development and evaluation of regulations on tobacco products to protect public health and to reduce tobacco use by minors. We highlight the inherent shortcomings of the conventional epidemiologic, clinical, and laboratory research on menthol cigarettes that have contributed to the ongoing debate on the public health impact of menthol in cigarettes. In addition, we provide perspectives on how future investigations exploiting state-of-the-art biomarkers of exposure and disease states can help answer the lingering question of menthol in cigarettes.

  15. Non-cigarette tobacco and the lung.

    Science.gov (United States)

    Schivo, Michael; Avdalovic, Mark V; Murin, Susan

    2014-02-01

    Cigarette smoking is known to cause a wide range of damaging health outcomes; however, the effects of non-cigarette tobacco products are either unknown or perceived as less harmful than cigarettes. Smokeless tobacco, cigar smoking, and waterpipe smoking have increased in usage over the past few decades. Some experts believe that their use is reaching epidemic proportions. Factors such as a perception of harm reduction, targeted advertising, and unrecognized addiction may drive the increased consumption of non-cigarette tobacco products. In particular, the need for social acceptance, enjoyment of communal smoking activities, and exotic nature of waterpipe smoking fuels, in part, its popularity. The public is looking for "safer" alternatives to smoking cigarettes, and some groups advertise products such as smokeless tobacco and electronic cigarettes as the alternatives they seek. Though it is clear that cigar and waterpipe tobacco smoking are probably as dangerous to health as cigarette smoking, there is an opinion among users that the health risks are less compared to cigarette smoking. This is particularly true in younger age groups. In the cases of smokeless tobacco and electronic cigarettes, the risks to health are less clear and there may be evidence of a harm reduction compared to cigarettes. In this article, we discuss commonly used forms of non-cigarette tobacco products, their impacts on lung health, and relevant controversies surrounding their use.

  16. Carbonyl compounds generated from electronic cigarettes.

    Science.gov (United States)

    Bekki, Kanae; Uchiyama, Shigehisa; Ohta, Kazushi; Inaba, Yohei; Nakagome, Hideki; Kunugita, Naoki

    2014-10-28

    Electronic cigarettes (e-cigarettes) are advertised as being safer than tobacco cigarettes products as the chemical compounds inhaled from e-cigarettes are believed to be fewer and less toxic than those from tobacco cigarettes. Therefore, continuous careful monitoring and risk management of e-cigarettes should be implemented, with the aim of protecting and promoting public health worldwide. Moreover, basic scientific data are required for the regulation of e-cigarette. To date, there have been reports of many hazardous chemical compounds generated from e-cigarettes, particularly carbonyl compounds such as formaldehyde, acetaldehyde, acrolein, and glyoxal, which are often found in e-cigarette aerosols. These carbonyl compounds are incidentally generated by the oxidation of e-liquid (liquid in e-cigarette; glycerol and glycols) when the liquid comes in contact with the heated nichrome wire. The compositions and concentrations of these compounds vary depending on the type of e-liquid and the battery voltage. In some cases, extremely high concentrations of these carbonyl compounds are generated, and may contribute to various health effects. Suppliers, risk management organizations, and users of e-cigarettes should be aware of this phenomenon.

  17. Attenuation of smoke induced neuronal and physiological changes by bacoside rich extract in Wistar rats via down regulation of HO-1 and iNOS.

    Science.gov (United States)

    Pandareesh, M D; Anand, T

    2014-01-01

    Bacopa monniera is well known herbal medicine for its neuropharmacological effects. It alleviates variety of disorders including neuronal and physiological changes. Crackers smoke is a potent risk factor that leads to free radical mediated oxidative stress in vivo. The aim of the current study is to evaluate the protective efficacy of B. monniera extract (BME) against crackers smoke induced neuronal and physiological changes via modulating inducible nitric oxide synthase (iNOS) and hemeoxygenase-1 (HO-1) expression in rats. Rats were exposed to smoke for 1h for a period of 3 weeks and consecutively treated with BME at three different dosages (i.e., 10, 20 and 40 mg/kg b.wt.). Our results elucidate that BME treatment ameliorates histopathalogical changes, reactive oxygen species levels, lipid peroxidation, acetylcholine esterase activity and brain neurotransmitter levels to normal. BME supplementation efficiently inhibited HO-1 expression and nitric oxide generation by down-regulating iNOS expression. Smoke induced depletion of antioxidant enzyme status, monoamine oxidase activity was also replenished by BME supplementation. Thus the present study indicates that BME ameliorates various impairments associated with neuronal and physiological changes in rats exposed to crackers smoke by its potent neuromodulatory, antioxidant and adaptogenic propensity.

  18. Role of eicosanoids in a model of smoke-induced lung injury. Final report, 1 June 1987-4 June 1988

    Energy Technology Data Exchange (ETDEWEB)

    Witten, M.L.

    1988-06-29

    Smoke inhalation has been identified as a major cause of lung injury and death in fires with mortality rate of approximately 75%. Soldiers regularly occupy enclosed spaces and travel near flammable fuels. The combination of burning material and an enclosed space are major factors that lead to smoke inhalation. A combination of diesel fuel and polycarbonate plastic was used to generate smoke-induced lung injury. Rabbits were exposed to 60 tidal-volume breaths of smoke in approximately 10 minutes. Acute smoke-exposure caused changes in broncho-alveolar lavage (BAL) and plasma eicosanoid concentration, especially at 0.5 hours post-smoke exposure. In addition, there were decreases in technetium-labeled diethylene-triamine pentaacetic acid (99mTcDTPA) T1/2, increases in BAL total white cell count and alveolar macrophage acid phosphatase activity, and pathological evidence of pulmonary edema and type 2 pneumocyte injury. It is concluded that lung eicosanoids are involved in the inflammatory process caused by severe smoke inhalation. However, the specific roles these lung eicosanoids play in the smoke-induced injury process are not known at this time.

  19. Electronic cigarettes: the road ahead.

    Science.gov (United States)

    Besaratinia, Ahmad; Tommasi, Stella

    2014-09-01

    Electronic cigarettes (e-cig) are proliferating in the world's lucrative nicotine delivery market at an alarmingly fast pace. E-cig are aggressively marketed as an alternative to conventional tobacco cigarettes, although very little is known about the health consequences of e-cig use. Chemical analysis of e-cig vapor/liquid has shown that many toxicants and carcinogens present in cigarette smoke are also found, albeit generally in lower concentrations, in a wide range of e-cig products. Notwithstanding the presence of toxicants and carcinogens in e-cig products, the biological effects of exposure to these contaminants have not been determined in e-cig users. The ongoing research and future investigations on e-cig initiation, use, perceptions, dependence, and toxicity are expected to provide empirical evidence that can be used to inform the general public, scientific community, and regulatory authorities of the health risks/benefits associated with e-cig use. This information will help stimulate scientists in the field of tobacco research, as well as assist the regulatory agencies in making scientifically based decisions on the development and evaluation of regulations on tobacco products to protect the public's health. Finding the scientific underpinnings for the health risks/benefits of e-cig use can impact millions of people who are increasingly turning to e-cig as a replacement for or complement to conventional tobacco cigarettes. Copyright © 2014 Elsevier Inc. All rights reserved.

  20. E-Cigarettes and Cancer Patients

    Science.gov (United States)

    Dresler, Carolyn M.; Field, John K.; Fox, Jesme; Gritz, Ellen R.; Hanna, Nasser H.; Ikeda, Norihiko; Jassem, Jacek; Mulshine, James L.; Peters, Matthew J.; Yamaguchi, Nise H.; Warren, Graham; Zhou, Caicun

    2014-01-01

    The increasing popularity and availability of electronic cigarettes (i.e., e-cigarettes) in many countries have promoted debate among health professionals as to what to recommend to their patients who might be struggling to stop smoking or asking about e-cigarettes. In the absence of evidence-based guidelines for using e-cigarettes for smoking cessation, some health professionals have urged caution about recommending them due to the limited evidence of their safety and efficacy, while others have argued that e-cigarettes are obviously a better alternative to continued cigarette smoking and should be encouraged. The leadership of the International Association for the Study of Lung Cancer asked the Tobacco Control and Smoking Cessation Committee to formulate a statement on the use of e-cigarettes by cancer patients to help guide clinical practice. Below is this statement, which we will update periodically as new evidence becomes available. PMID:24736063

  1. The electronic cigarette: the new cigarette of the 21st century?

    Directory of Open Access Journals (Sweden)

    Marli Maria Knorst

    2014-10-01

    Full Text Available The electronic nicotine delivery system, also known as the electronic cigarette, is generating considerable controversy, not only in the general population but also among health professionals. Smokers the world over have been increasingly using electronic cigarettes as an aid to smoking cessation and as a substitute for conventional cigarettes. There are few available data regarding the safety of electronic cigarettes. There is as yet no evidence that electronic cigarettes are effective in treating nicotine addiction. Some smokers have reported using electronic cigarettes for over a year, often combined with conventional cigarettes, thus prolonging nicotine addiction. In addition, the increasing use of electronic cigarettes by adolescents is a cause for concern. The objective of this study was to describe electronic cigarettes and their components, as well as to review the literature regarding their safety; their impact on smoking initiation and smoking cessation; and regulatory issues related to their use.

  2. Smokers’ and E-Cigarette Users’ Perceptions about E-Cigarette Warning Statements

    OpenAIRE

    Wackowski, Olivia A.; David Hammond; O’Connor, Richard J.; Strasser, Andrew A.; Delnevo, Cristine D.

    2016-01-01

    Cigarette warning labels are important sources of risk information, but warning research for other tobacco products is limited. This study aimed to gauge perceptions about warnings that may be used for e-cigarettes. We conducted six small focus groups in late 2014/early 2015 with adult current e-cigarette users and cigarette-only smokers. Participants rated and discussed their perceptions of six e-cigarette warning statements, and warnings in two existing Vuse and MarkTen e-cigarette ads. Par...

  3. E-cigarettes: facts, perceptions, and marketing messages.

    Science.gov (United States)

    Carr, Ellen R

    2014-02-01

    Electronic cigarettes (e-cigarettes) are perceived as an alternative to standard tobacco cigarette smoking, primarily because of the e-cigarette industry's marketing messages. However, scientific studies about e-cigarette safety and efficacy remain limited. This column presents some of the issues associated with e-cigarette use, such as potential components of regulation, perceptions that e-cigarettes can help users quit smoking, and free-wheeling marketing strategies that include expanding e-cigarette use to young people. Nurses can be a reliable source of information about e-cigarettes.

  4. Effect of cigarette smoke extraction on the expression of found in inflammatory zone 1 in rat lung epithelial L2 cells

    Institute of Scientific and Technical Information of China (English)

    Lin Chunyan; Chen Li; Huang Zhihong; Wu Yi; Liu Shengming

    2014-01-01

    Background Found in inflammatory zone 1 (FIZZ1) protein increased in pulmonary epithelial cells and in limited amounts of other lung cells.FIZZ1 increased in murine model of smoke induced chronic obstructive pulmonary disease.However,the direct role of FIZZ1 produced by pulmonary epithelium stimulated with cigarette smoke extraction has not been determined.We examined the expression and function of FIZZ1 in rat lung epithelial L2 cells.Methods The rat lung epithelial L2 cells (CCL 149) were exposed to cigarette smoke extraction,expression of FIZZ1 mRNA was investigated by RT-PCR.Levels of FIZZ1 protein were detected by Western blotting and laser confocal microscope.CCL 149 cells were treated with different concentrations and for different time of recombinant protein FIZZ1.After treatment,the expression levels of interleukin 8 (IL-8) were detected by enzyme-linked immunosorbent assay (ELISA).Results When CCL 149 cells were exposed to cigarette smoke extraction,FIZZ1 mRNA and protein levels expressed significantly higher than control group.Recombinant protein FIZZ1 promoted the expression of IL-8 in a dose and time dependent manner in a certain range.Conclusions Cigarette smoke extraction activates FIZZ1 at mRNA and protein levels in CCL 149 cells.Recombinant protein FIZZ1 induces the expression of IL-8 and may thus participate in the process of chronic obstructive pulmonary disease airway inflammation and airflow obstruction.Generally,immune cells such as macrophages,neutrophils and lymphocytes are unavoidably involved in airway inflammatory and immune responses to cigarette smoke,but it is still unclear whether their involvement in the pathogenesis of chronic obstructive pulmonary disease is based on the specific expression in lung epithelial cells of FIZZ1.

  5. Global approaches to regulating electronic cigarettes.

    Science.gov (United States)

    Kennedy, Ryan David; Awopegba, Ayodeji; De León, Elaine; Cohen, Joanna E

    2017-07-01

    Classify and describe the policy approaches used by countries to regulate e-cigarettes. National policies regulating e-cigarettes were identified by (1) conducting web searches on Ministry of Health websites, and (2) broad web searches. The mechanisms used to regulate e-cigarettes were classified as new/amended laws, or existing laws. The policy domains identified include restrictions or prohibitions on product: sale, manufacturing, importation, distribution, use, product design including e-liquid ingredients, advertising/promotion/sponsorship, trademarks, and regulation requiring: taxation, health warning labels and child-safety standards. The classification of the policy was reviewed by a country expert. The search identified 68 countries that regulate e-cigarettes: 22 countries regulate e-cigarettes using existing regulations; 25 countries enacted new policies to regulate e-cigarettes; 7 countries made amendments to existing legislation; 14 countries use a combination of new/amended and existing regulation. Common policies include a minimum-age-of-purchase, indoor-use (vape-free public places) bans and marketing restrictions. Few countries are applying a tax to e-cigarettes. A range of regulatory approaches are being applied to e-cigarettes globally; many countries regulate e-cigarettes using legislation not written for e-cigarettes. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

  6. Electronic cigarettes. Potential harms and benefits.

    Science.gov (United States)

    Drummond, M Bradley; Upson, Dona

    2014-02-01

    Use of electronic cigarettes, devices that deliver a nicotine-containing vapor, has increased rapidly across the country and globally. Perceived and marketed as a "healthier alternative" to conventional cigarettes, few data exist regarding the safety of these devices and their efficacy in harm reduction and treatment of tobacco dependence; even less is known about their overall impact on population health. This review highlights the recent data regarding electronic cigarette toxicity, impact on lung function, and efficacy in smoking reduction and cessation. Studies show that the vapor generated from electronic cigarettes has variable amounts of nicotine and potential harmful toxins, albeit at levels lower than in conventional cigarettes. The long-term carcinogenic and lung function effects of electronic cigarettes are not known. Although some data demonstrate that electronic cigarettes may be effective in reducing conventional cigarette consumption, there are no data demonstrating the efficacy of electronic cigarettes as a tool to achieve cessation. Until robust longitudinal evaluations demonstrate the safety of electronic cigarettes and efficacy in treatment of tobacco dependence, their role as a harm reduction tool is unclear.

  7. Association Between Electronic Cigarette Use and Openness to Cigarette Smoking Among US Young Adults

    Science.gov (United States)

    Apelberg, Benjamin J.; Ambrose, Bridget K.; Green, Kerry M.; Choiniere, Conrad J.; Bunnell, Rebecca; King, Brian A.

    2015-01-01

    Introduction: Use of electronic nicotine delivery systems (ENDS), including electronic cigarettes (e-cigarettes), is increasing. One concern is the appeal of these products to youth and young adults and the potential to influence perceptions and use of conventional cigarettes. Methods: Using data from the 2012–2013 National Adult Tobacco Survey, characteristics of adults aged 18–29 years who had never established cigarette smoking behavior were examined by ever use of e-cigarettes, demographics, and ever use of other tobacco products (smokeless tobacco, cigars, hookah, and cigarettes). Multivariate logistic regression was used to examine the relationship between e-cigarette use and openness to cigarette smoking among young adults, defined as the lack of a firm intention not to smoke soon or in the next year. Results: Among young adults who had never established cigarette smoking behavior (unweighted n = 4,310), 7.9% reported having ever tried e-cigarettes, and 14.6% of those who reported having ever tried e-cigarettes also reported current use of the product. Ever e-cigarette use was associated with being open to cigarette smoking (adjusted odds ratio = 2.4; 95% confidence interval = 1.7, 3.3), as was being male, aged 18–24 years, less educated, and having ever used hookah or experimented with conventional cigarettes. Conclusions: Ever use of e-cigarettes and other tobacco products was associated with being open to cigarette smoking. This study does not allow us to assess the directionality of this association, so future longitudinal research is needed to illuminate tobacco use behaviors over time as well as provide additional insight on the relationship between ENDS use and conventional cigarette use among young adult populations. PMID:25378683

  8. Impact of cigarette minimum price laws on the retail price of cigarettes in the USA.

    Science.gov (United States)

    Tynan, Michael A; Ribisl, Kurt M; Loomis, Brett R

    2013-05-01

    Cigarette price increases prevent youth initiation, reduce cigarette consumption and increase the number of smokers who quit. Cigarette minimum price laws (MPLs), which typically require cigarette wholesalers and retailers to charge a minimum percentage mark-up for cigarette sales, have been identified as an intervention that can potentially increase cigarette prices. 24 states and the District of Columbia have cigarette MPLs. Using data extracted from SCANTRACK retail scanner data from the Nielsen company, average cigarette prices were calculated for designated market areas in states with and without MPLs in three retail channels: grocery stores, drug stores and convenience stores. Regression models were estimated using the average cigarette pack price in each designated market area and calendar quarter in 2009 as the outcome variable. The average difference in cigarette pack prices are 46 cents in the grocery channel, 29 cents in the drug channel and 13 cents in the convenience channel, with prices being lower in states with MPLs for all three channels. The findings that MPLs do not raise cigarette prices could be the result of a lack of compliance and enforcement by the state or could be attributed to the minimum state mark-up being lower than the free-market mark-up for cigarettes. Rather than require a minimum mark-up, which can be nullified by promotional incentives and discounts, states and countries could strengthen MPLs by setting a simple 'floor price' that is the true minimum price for all cigarettes or could prohibit discounts to consumers and retailers.

  9. 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.

  10. 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.

  11. 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.

  12. The intractable cigarette ‘filter problem’

    Science.gov (United States)

    2011-01-01

    Background When lung cancer fears emerged in the 1950s, cigarette companies initiated a shift in cigarette design from unfiltered to filtered cigarettes. Both the ineffectiveness of cigarette filters and the tobacco industry's misleading marketing of the benefits of filtered cigarettes have been well documented. However, during the 1950s and 1960s, American cigarette companies spent millions of dollars to solve what the industry identified as the ‘filter problem’. These extensive filter research and development efforts suggest a phase of genuine optimism among cigarette designers that cigarette filters could be engineered to mitigate the health hazards of smoking. Objective This paper explores the early history of cigarette filter research and development in order to elucidate why and when seemingly sincere filter engineering efforts devolved into manipulations in cigarette design to sustain cigarette marketing and mitigate consumers' concerns about the health consequences of smoking. Methods Relevant word and phrase searches were conducted in the Legacy Tobacco Documents Library online database, Google Patents, and media and medical databases including ProQuest, JSTOR, Medline and PubMed. Results 13 tobacco industry documents were identified that track prominent developments involved in what the industry referred to as the ‘filter problem’. These reveal a period of intense focus on the ‘filter problem’ that persisted from the mid-1950s to the mid-1960s, featuring collaborations between cigarette producers and large American chemical and textile companies to develop effective filters. In addition, the documents reveal how cigarette filter researchers' growing scientific knowledge of smoke chemistry led to increasing recognition that filters were unlikely to offer significant health protection. One of the primary concerns of cigarette producers was to design cigarette filters that could be economically incorporated into the massive scale of cigarette

  13. Thermal injury patterns associated with electronic cigarettes

    Science.gov (United States)

    Jiwani, Alisha Z; Williams, James F; Rizzo, Julie A; Chung, Kevin K; King, Booker T; Cancio, Leopoldo C

    2017-01-01

    E-cigarettes are typically lithium-ion battery-operated devices that simulate smoking by heating a nicotine-solution into a vapor that the user inhales. E-cigarette use is becoming rapidly popular as an alternative to traditional cigarette smoking. This report describes an emerging problem associated with e-cigarettes, consisting of 10 thermally injured patients seen at a single burn center over a 2-year period from 2014 to 2016. Our cohort was comprised mainly of young adults who sustained mixed partial and full thickness burns as a result of e-cigarette-related explosions. In many documented scenarios, a malfunctioning or over-heated battery is the cause. Our data support the need for increased awareness among healthcare providers and the general public of the potential harms of e-cigarette use, modification, storage, and charging. PMID:28123861

  14. Parental Use of Electronic Cigarettes.

    Science.gov (United States)

    Garbutt, Jane M; Miller, Whitney; Dodd, Sherry; Bobenhouse, Neil; Sterkel, Randall; Strunk, Robert C

    2015-01-01

    To describe parental use of electronic cigarettes (e-cigs) to better understand the safety risks posed to children. Between June 24 and November 6, 2014, parents completed a self-administered paper survey during an office visit to 15 pediatric practices in a Midwestern practice-based research network. Attitudes towards and use of e-cigs are reported for those aware of e-cigs before the survey. Ninety-five percent (628 of 658) of respondents were aware of e-cigs. Of these, 21.0% (130 of 622) had tried e-cigs at least once, and 12.3% (77) reported e-cig use by ≥1 person in their household (4.0% exclusive e-cig use, 8.3% dual use with regular cigarettes). An additional 17.3% (109) reported regular cigarette use. Most respondents from e-cig-using homes did not think e-cigs were addictive (36.9% minimally or not addictive, 25.0% did not know). While 73.7% believed that e-liquid was very dangerous for children if they ingested it, only 31.2% believed skin contact to be very dangerous. In 36.1% of e-cig-using homes, neither childproof caps nor locks were used to prevent children's access to e-liquid. Only 15.3% reported their child's pediatrician was aware of e-cig use in the home. E-cig use occurred in 1 in 8 homes, often concurrently with regular cigarettes. Many parents who used e-cigs were unaware of the potential health and safety hazards, including nicotine poisoning for children, and many did not store e-liquid safely. Pediatricians could provide education about e-cig associated safety hazards but are unaware of e-cig use in their patients' homes. Copyright © 2015 Academic Pediatric Association. Published by Elsevier Inc. All rights reserved.

  15. Impact of Exposure to Electronic Cigarette Advertising on Susceptibility and Trial of Electronic Cigarettes and Cigarettes in US Young Adults: A Randomized Controlled Trial.

    Science.gov (United States)

    Villanti, Andrea C; Rath, Jessica M; Williams, Valerie F; Pearson, Jennifer L; Richardson, Amanda; Abrams, David B; Niaura, Raymond S; Vallone, Donna M

    2016-05-01

    This study assessed the impact of brief exposure to four electronic cigarette (e-cigarette) print advertisements (ads) on perceptions, intention, and subsequent use of e-cigarettes and cigarettes in US young adults. A randomized controlled trial was conducted in a national sample of young adults from an online panel survey in 2013. Participants were randomized to ad exposure or control. Curiosity, intentions, and perceptions regarding e-cigarettes were assessed post-exposure and e-cigarette and cigarette use at 6-month follow-up. Analyses were conducted in 2014. Approximately 6% of young adults who had never used an e-cigarette at baseline tried an e-cigarette at 6-month follow-up, half of whom were current cigarette smokers at baseline. Compared to the control group, ad exposure was associated with greater curiosity to try an e-cigarette (18.3% exposed vs. 11.3% unexposed, AOR = 1.63, 95% CI = 1.18, 2.26) among never e-cigarette users and greater likelihood of e-cigarette trial at follow-up (3.6% exposed vs. 1.2% unexposed, AOR = 2.85; 95% CI = 1.07, 7.61) among never users of cigarettes and e-cigarettes. Exploratory analyses did not find an association between ad exposure and cigarette trial or past 30-day use among never users, nor cigarette use among smokers over time. Curiosity mediated the relationship between ad exposure and e-cigarette trial among e-cigarette never users. Exposure to e-cigarette ads may enhance curiosity and limited trial of e-cigarettes in never users. Future studies are needed to examine the net effect of curiosity and trial of e-cigarettes on longer-term patterns of tobacco use. This randomized trial provides the first evidence of the effect of e-cigarette advertising on a behavioral outcome in young adults. Compared to the control group, ad exposure was associated with greater curiosity to try an e-cigarette among never e-cigarette users and greater likelihood of e-cigarette trial at follow-up in a small number of never e-cigarette

  16. Protection of erdosteine on smoke-induced peripheral neutrophil dysfunction both in healthy and in bronchitic smokers.

    Science.gov (United States)

    Ciaccia, A; Papi, A; Tschirky, B; Fregnan, B

    1992-01-01

    The purpose of the present study was to determine whether erdosteine and its metabolites (substances containing thiol groups) can prevent the alteration of the chemotactic function of polymorphonuclear cells (PMN) from peripheral blood induced by cigarette smoke of eight healthy non-smoking volunteers, when incubated in vitro before smoke exposure, and whether oral treatment with erdosteine (900 mg/day) for two weeks might restore the chemotaxis of PMN, either from eight healthy or from 16 chronic bronchitic smokers. The chemotactic stimuli in vitro were casein, lipopolysaccharides (LPS), and formyl-methionyl-leucyl-phenyalanine (FMLP). The results of the study in vitro have confirmed that PMN from non-smoking volunteers shows a reduced chemotactic responsiveness when exposed in vitro to smoke. This can be partially prevented in a dose-related manner by pre-incubation with erdosteine, its metabolites, cysteine, and glutathione (metabolites I and II being at least 10 times more active than the intact substance and the known biological standards also containing thiol groups). The experiment on PMN from healthy smokers (in a double-blind crossover design versus placebo) has indicated that the chemotaxis can be improved only after treatment with erdosteine. The same observation has been made in the experiment on PMN from smokers affected by chronic bronchitis (in a double-blind design versus placebo with two distinct groups). In these patients the phagocytic and bactericidal activities of PMN were not affected by the smoke and therefore, neither one was influenced by erdosteine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

  17. Cigarette smoking and DNA methylation

    Science.gov (United States)

    Lee, Ken W. K.; Pausova, Zdenka

    2013-01-01

    DNA methylation is the most studied epigenetic modification, capable of controlling gene expression in the contexts of normal traits or diseases. It is highly dynamic during early embryogenesis and remains relatively stable throughout life, and such patterns are intricately related to human development. DNA methylation is a quantitative trait determined by a complex interplay of genetic and environmental factors. Genetic variants at a specific locus can influence both regional and distant DNA methylation. The environment can have varying effects on DNA methylation depending on when the exposure occurs, such as during prenatal life or during adulthood. In particular, cigarette smoking in the context of both current smoking and prenatal exposure is a strong modifier of DNA methylation. Epigenome-wide association studies have uncovered candidate genes associated with cigarette smoking that have biologically relevant functions in the etiology of smoking-related diseases. As such, DNA methylation is a potential mechanistic link between current smoking and cancer, as well as prenatal cigarette-smoke exposure and the development of adult chronic diseases. PMID:23882278

  18. Arsenic Speciation in Tobacco and Cigarette Smoke

    Directory of Open Access Journals (Sweden)

    Liu C

    2014-12-01

    Full Text Available Arsenic is one of the metals found in cured tobacco and mainstream cigarette smoke. Levels of arsenic in modern filtered cigarette smoke range from sub-ppm to a few tens of ppms. To enable accurate smoke toxicity assessment on arsenic in cigarette smoke, it is desirable to establish its chemical forms in addition to total quantities because different arsenic compounds possess different toxicological potentials.

  19. DNA repair gene polymorphisms in relation to chromosome aberration frequencies in retired radiation workers

    Energy Technology Data Exchange (ETDEWEB)

    Wilding, Craig S. [Genetics Department, Westlakes Research Institute, Westlakes Science and Technology Park, Moor Row, Cumbria CA24 3JY (United Kingdom)]. E-mail: craig.wilding@westlakes.ac.uk; Relton, Caroline L. [Genetics Department, Westlakes Research Institute, Westlakes Science and Technology Park, Moor Row, Cumbria CA24 3JY (United Kingdom); Paediatric and Lifecourse Epidemiology Research Group, School of Clinical Medical Sciences (Child Health), Newcastle University, Sir James Spence Institute, Royal Victoria Infirmary, Newcastle-upon-Tyne NE1 4LP (United Kingdom); Rees, Gwen S. [Genetics Department, Westlakes Research Institute, Westlakes Science and Technology Park, Moor Row, Cumbria CA24 3JY (United Kingdom); Tarone, Robert E. [International Epidemiology Institute, 1455 Research Boulevard, Suite 550, Rockville, MD 20850 (United States); Whitehouse, Caroline A. [Genetics Department, Westlakes Research Institute, Westlakes Science and Technology Park, Moor Row, Cumbria CA24 3JY (United Kingdom); Tawn, E. Janet [Genetics Department, Westlakes Research Institute, Westlakes Science and Technology Park, Moor Row, Cumbria CA24 3JY (United Kingdom)

    2005-02-15

    Polymorphic variation in DNA repair genes was examined in a group of retired workers from the British Nuclear Fuels plc facility at Sellafield in relation to previously determined translocation frequencies in peripheral blood lymphocytes. Variation at seven polymorphisms in four genes involved in the base excision repair (XRCC1 R194W, R399Q and a [AC]{sub n} microsatellite in the 3' UTR) and double strand break repair (XRCC3 T241M and a [AC]{sub n} microsatellite in intron 3 of XRCC3, XRCC4 I134T, and a GACTAn microsatellite located 120kb 5' of XRCC5) pathways was determined for 291 retired radiation workers who had received cumulative occupational external radiation doses of between 0 and 1873mSv. When the interaction between radiation dose and each DNA repair gene polymorphism was examined in relation to translocation frequency there was no evidence for any of the polymorphisms studied influencing the response to occupational exposure. A positive interaction observed between genotype (individuals with at least one allele >=20 repeat units) at a microsatellite locus in the XRCC3 gene and smoking status should be interpreted cautiously because interactions were investigated for seven polymorphisms and two exposures. Nonetheless, further research is warranted to examine whether this DNA repair gene variant might be associated with a sub-optimal repair response to smoking-induced DNA damage and hence an increased frequency of translocations.

  20. E-Cigarettes Lead to 'Real' Smoking by Teens: Review

    Science.gov (United States)

    ... fullstory_166899.html E-Cigarettes Lead to 'Real' Smoking by Teens: Review But one public health expert ... likely as their non-vaping counterparts to begin smoking traditional cigarettes, a new review suggests. "E-cigarette ...

  1. Comparable renovascular protective effects of moxonidine and simvastatin in rats exposed to cigarette smoke.

    Science.gov (United States)

    Nasr, Magda A; El-Gowilly, Sahar M; El-Mas, Mahmoud M

    2010-01-01

    Renovascular impairment plays a major role in smoking-induced nephrotoxicity. This study investigated the effect of the imidazoline I(1)-receptor/alpha(2)-adrenoceptor agonist moxonidine, as compared to the lipid lowering drug simvastatin, on abnormalities induced by cigarette smoke (CS) in renovascular reactivity. Six rat groups were used: control, CS (twice a day for 6weeks), simvastatin, moxonidine, CS+simvastatin, and CS+moxonidine. CS exposure increased plasma urea and creatinine and reduced plasma and renal nitrate/nitrite (NOx). In isolated perfused phenylephrine-preconstricted kidneys of CS rats, vasodilator responses to carbachol or isoprenaline, but not papaverine, were attenuated. Nitric oxide synthase (NOS) inhibition by N(G)-nitro-L-arginine (L-NNA) reduced carbachol vasodilations in control but not CS kidneys, suggesting the impairment of NOS activity by CS. Simultaneous administration of moxonidine or simvastatin abolished CS-induced abnormalities in indices of renal function, NOx, and vasodilations caused by carbachol or isoprenaline. The possibility whether alterations in antioxidant or lipid profiles contributed to the interaction was investigated. CS increased renal malondialdyde and decreased glutathione, and glutathione peroxidase, superoxide dismutase and catalase activities. Further, CS reduced plasma HDL and increased cholesterol, triglycerides, and LDL. Simvastatin or moxonidine abolished the deleterious CS effects on antioxidant activity; the lipid profile was normalized by simvastatin only. These findings highlight that renovascular dysfunction caused by CS and the underlying oxidative damage is evenly attenuated by moxonidine and simvastatin.

  2. Vitamin E Modulates Cigarette Smoke Extract-induced Cell Apoptosis in Mouse Embryonic Cells

    Directory of Open Access Journals (Sweden)

    Zhao-Li Chen, Jian Tao, Jie Yang, Zhen-Li Yuan, Xing-Hua Liu, Min Jin, Zhi-Qiang Shen, Lu Wang, Hai-Feng Li, Zhi-Gang Qiu, Jing-Feng Wang, Xin-Wei Wang, Jun-Wen Li

    2011-01-01

    Full Text Available Vitamin E (VE can effectively prevent occurrence of lung cancer caused by passive smoking in mice. However, whether VE prevents smoking-induced cytotoxicity remains unclear. In this study, a primary culture of embryonic lung cells (ELCs was used to observe the cytotoxic effects of cigarette smoke extract (CSE, including its influence on cell survival, cell cycle, apoptosis, and DNA damage, and also to examine the effects of VE intervention on CSE-induced cytotoxicity. Our results showed that CSE could significantly inhibit the survival of ELCs with dose- and time-dependent effects. Furthermore, CSE clearly disturbed the cell cycle of ELCs by decreasing the proportion of cells at the S and G2/M phases and increasing the proportion of cells at the G0/G1 phase. CSE promoted cell apoptosis, with the highest apoptosis rate reaching more than 40%. CSE also significantly caused DNA damage of ELCs. VE supplementation could evidently inhibit or reverse the cytotoxic effects of CSE in a dose- and time-dependent manner. The mechanism of CSE effects on ELCs and that of VE intervention might involve the mitochondrial pathway of cytochrome c-mediated caspase activation. Our study validate that VE plays a clearly protective effect against CSE-induced cytotoxicity in mouse embryonic lung cells.

  3. An Analysis of Electronic Cigarette and Cigarette Advertising in US Women's Magazines

    Science.gov (United States)

    Basch, Corey Hannah; Mongiovi, Jennifer; Hillyer, Grace Clarke; Ethan, Danna; Hammond, Rodney

    2016-01-01

    Background: Traditional cigarette advertising has existed in the US for over 200 years. Studies suggest that advertising has an impact on the initiation and maintenance of smoking behaviors. In recent years, electronic cigarettes (e-cigarettes) emerged on the market as an alternative to the traditional tobacco cigarette. The purpose of this study was to describe advertisements in popular US magazines marketed to women for cigarettes and e-cigarettes. Methods: This study involved analyzing 99 issues of 14 popular US magazines marketed to women. Results: Compared to advertisements for traditional cigarettes, advertisements for e-cigarettes were more often found in magazines geared toward the 31–40-year-old audience (76.5% vs. 53.1%, P = 0.011) whereas traditional cigarette advertisements were nearly equally distributed among women 31–40 and ≥40 years. More than three-quarters of the e-cigarette advertisements presented in magazines aimed at the higher median income households compared to a balanced distribution by income for traditional cigarettes (P = 0.033). Conclusions: Future studies should focus on specific marketing tactics used to promote e-cigarette use as this product increases in popularity, especially among young women smokers. PMID:27688867

  4. Using Alcohol to Sell Cigarettes to Young Adults: A Content Analysis of Cigarette Advertisements

    Science.gov (United States)

    Belstock, Sarah A.; Connolly, Gregory N.; Carpenter, Carrie M.; Tucker, Lindsey

    2008-01-01

    Objective: Advertising influences the health-related behaviors of college-aged individuals. Cigarette manufacturers aggressively market to young adults and may exploit their affinity for alcohol when creating advertisements designed to increase cigarettes' appeal. Internal tobacco industry documents reveal that cigarette manufacturers understood…

  5. Using Alcohol to Sell Cigarettes to Young Adults: A Content Analysis of Cigarette Advertisements

    Science.gov (United States)

    Belstock, Sarah A.; Connolly, Gregory N.; Carpenter, Carrie M.; Tucker, Lindsey

    2008-01-01

    Objective: Advertising influences the health-related behaviors of college-aged individuals. Cigarette manufacturers aggressively market to young adults and may exploit their affinity for alcohol when creating advertisements designed to increase cigarettes' appeal. Internal tobacco industry documents reveal that cigarette manufacturers understood…

  6. 78 FR 52679 - Safety Standard for Cigarette Lighters; Adjusted Customs Value for Cigarette Lighters

    Science.gov (United States)

    2013-08-26

    ... automatically according to the terms of the cigarette lighter regulation. Because the adjustment occurs by terms... Federal Regulations, which is published #0;under 50 titles pursuant to 44 U.S.C. 1510. #0; #0;The Code of... 1210 Safety Standard for Cigarette Lighters; Adjusted Customs Value for Cigarette Lighters AGENCY...

  7. Hazardous waste status of discarded electronic cigarettes.

    Science.gov (United States)

    Krause, Max J; Townsend, Timothy G

    2015-05-01

    The potential for disposable electronic cigarettes (e-cigarettes) to be classified as hazardous waste was investigated. The Toxicity Characteristic Leaching Procedure (TCLP) was performed on 23 disposable e-cigarettes in a preliminary survey of metal leaching. Based on these results, four e-cigarette products were selected for replicate analysis by TCLP and the California Waste Extraction Test (WET). Lead was measured in leachate as high as 50mg/L by WET and 40mg/L by TCLP. Regulatory thresholds were exceeded by two of 15 products tested in total. Therefore, some e-cigarettes would be toxicity characteristic (TC) hazardous waste but a majority would not. When disposed in the unused form, e-cigarettes containing nicotine juice would be commercial chemical products (CCP) and would, in the United States (US), be considered a listed hazardous waste (P075). While household waste is exempt from hazardous waste regulation, there are many instances in which such waste would be subject to regulation. Manufactures and retailers with unused or expired e-cigarettes or nicotine juice solution would be required to manage these as hazardous waste upon disposal. Current regulations and policies regarding the availability of nicotine-containing e-cigarettes worldwide were reviewed. Despite their small size, disposable e-cigarettes are consumed and discarded much more quickly than typical electronics, which may become a growing concern for waste managers.

  8. Eye muscle repair - discharge

    Science.gov (United States)

    ... Lazy eye repair - discharge; Strabismus repair - discharge; Extraocular muscle surgery - discharge ... You or your child had eye muscle repair surgery to correct eye muscle ... term for crossed eyes is strabismus. Children most often ...

  9. Ventral hernia repair

    Science.gov (United States)

    ... page: //medlineplus.gov/ency/article/007661.htm Ventral hernia repair To use the sharing features on this page, please enable JavaScript. Ventral hernia repair is surgery to repair a ventral hernia. ...

  10. Brain aneurysm repair

    Science.gov (United States)

    ... aneurysm repair; Dissecting aneurysm repair; Endovascular aneurysm repair - brain; Subarachnoid hemorrhage - aneurysm ... Your scalp, skull, and the coverings of the brain are opened. A metal clip is placed at ...

  11. Smokers' sources of e-cigarette awareness and risk information

    OpenAIRE

    Wackowski, Olivia A.; Bover Manderski, Michelle T.; Delnevo, Cristine D.

    2015-01-01

    Introduction: Few studies have explored sources of e-cigarette awareness and peoples' e-cigarette information needs, interests, or behaviors. This study contributes to both domains of e-cigarette research. Methods: Results are based on a 2014 e-cigarette focused survey of 519 current smokers from a nationally representative research panel. Results: Smokers most frequently reported seeing e-cigarettes in stores (86.4%) and used in person (83%). Many (73%) had also heard about e-cigarette...

  12. 75 FR 75936 - Required Warnings for Cigarette Packages and Advertisements; Research Report

    Science.gov (United States)

    2010-12-07

    ... Cigarette Packages and Advertisements; Research Report AGENCY: Food and Drug Administration, HHS. ACTION... warnings and accompanying graphics to be displayed on cigarette packages and in cigarette advertisements... health warning statements appear on cigarette packages and in cigarette advertisements. Section 201...

  13. Cigarette litter: smokers' attitudes and behaviors.

    Science.gov (United States)

    Rath, Jessica M; Rubenstein, Rebecca A; Curry, Laurel E; Shank, Sarah E; Cartwright, Julia C

    2012-06-01

    Cigarette butts are consistently the most collected items in litter clean-up efforts, which are a costly burden to local economies. In addition, tobacco waste may be detrimental to our natural environment. The tobacco industry has conducted or funded numerous studies on smokers' littering knowledge and behavior, however, non-industry sponsored research is rare. We sought to examine whether demographics and smokers' knowledge and beliefs toward cigarette waste as litter predicts littering behavior. Smokers aged 18 and older (n = 1,000) were interviewed about their knowledge and beliefs towards cigarette waste as litter. Respondents were members of the Research Now panel, an online panel of over three million respondents in the United States. Multivariate logistic regressions were conducted to determine factors significantly predictive of ever having littered cigarette butts or having littered cigarette butts within the past month (p-value littered cigarette butts at least once in their life, by disposing of them on the ground or throwing them out of a car window. Over half (55.7%) reported disposing of cigarette butts on the ground, in a sewer/gutter, or down a drain in the past month. Those who did not consider cigarette butts to be litter were over three and half times as likely to report having ever littered cigarette butts (OR = 3.68, 95%CI = 2.04, 6.66) and four times as likely to have littered cigarette butts in the past month (OR = 4.00, 95%CI = 2.53, 6.32). Males were significantly more likely to have littered cigarette butts in the past month compared to females (OR = 1.49, 95%CI = 1.14, 1.94). Holding the belief that cigarette butts are not litter was the only belief in this study that predicted ever or past-month littering of cigarette waste. Messages in anti-cigarette-litter campaigns should emphasize that cigarette butts are not just litter but are toxic waste and are harmful when disposed of improperly.

  14. Cigarette Litter: Smokers’ Attitudes and Behaviors

    Directory of Open Access Journals (Sweden)

    Julia C. Cartwright

    2012-06-01

    Full Text Available Cigarette butts are consistently the most collected items in litter clean-up efforts, which are a costly burden to local economies. In addition, tobacco waste may be detrimental to our natural environment. The tobacco industry has conducted or funded numerous studies on smokers’ littering knowledge and behavior, however, non-industry sponsored research is rare. We sought to examine whether demographics and smokers’ knowledge and beliefs toward cigarette waste as litter predicts littering behavior. Smokers aged 18 and older (n = 1,000 were interviewed about their knowledge and beliefs towards cigarette waste as litter. Respondents were members of the Research Now panel, an online panel of over three million respondents in the United States. Multivariate logistic regressions were conducted to determine factors significantly predictive of ever having littered cigarette butts or having littered cigarette butts within the past month (p-value < 0.05. The majority (74.1% of smokers reported having littered cigarette butts at least once in their life, by disposing of them on the ground or throwing them out of a car window. Over half (55.7% reported disposing of cigarette butts on the ground, in a sewer/gutter, or down a drain in the past month. Those who did not consider cigarette butts to be litter were over three and half times as likely to report having ever littered cigarette butts (OR = 3.68, 95%CI = 2.04, 6.66 and four times as likely to have littered cigarette butts in the past month (OR = 4.00, 95%CI = 2.53, 6.32. Males were significantly more likely to have littered cigarette butts in the past month compared to females (OR = 1.49, 95%CI = 1.14, 1.94. Holding the belief that cigarette butts are not litter was the only belief in this study that predicted ever or past-month littering of cigarette waste. Messages in anti-cigarette-litter campaigns should emphasize that cigarette butts are not just litter but are toxic

  15. Hazardous waste status of discarded electronic cigarettes

    Energy Technology Data Exchange (ETDEWEB)

    Krause, Max J.; Townsend, Timothy G., E-mail: ttown@ufl.edu

    2015-05-15

    Highlights: • Electronic cigarettes were tested using TCLP and WET. • Several electronic cigarette products leached lead at hazardous waste levels. • Lead was the only element that exceeded hazardous waste concentration thresholds. • Nicotine solution may cause hazardous waste classification when discarded unused. - Abstract: The potential for disposable electronic cigarettes (e-cigarettes) to be classified as hazardous waste was investigated. The Toxicity Characteristic Leaching Procedure (TCLP) was performed on 23 disposable e-cigarettes in a preliminary survey of metal leaching. Based on these results, four e-cigarette products were selected for replicate analysis by TCLP and the California Waste Extraction Test (WET). Lead was measured in leachate as high as 50 mg/L by WET and 40 mg/L by TCLP. Regulatory thresholds were exceeded by two of 15 products tested in total. Therefore, some e-cigarettes would be toxicity characteristic (TC) hazardous waste but a majority would not. When disposed in the unused form, e-cigarettes containing nicotine juice would be commercial chemical products (CCP) and would, in the United States (US), be considered a listed hazardous waste (P075). While household waste is exempt from hazardous waste regulation, there are many instances in which such waste would be subject to regulation. Manufactures and retailers with unused or expired e-cigarettes or nicotine juice solution would be required to manage these as hazardous waste upon disposal. Current regulations and policies regarding the availability of nicotine-containing e-cigarettes worldwide were reviewed. Despite their small size, disposable e-cigarettes are consumed and discarded much more quickly than typical electronics, which may become a growing concern for waste managers.

  16. Do cigarette and alcohol affect semen analysis?

    Directory of Open Access Journals (Sweden)

    Mehmet Zeynel Keskin

    2016-03-01

    Full Text Available Objectives: There are a number of studies about the effect of cigarette and alcohol on semen parameters in the literature. There is not a consensus on the relationship between use of cigarette and alchol and semen parameters in those studies. The number of studies in which cigarette and alcohol use are evaluated together is limited. This study was aimed to analyze the effect of cigarette and/or alcohol use on semen parameters. Methods: In this prospective study, 762 patients who applied to an hospital urology polyclinic between January 2015 and March 2015 due to infertility, were questioned for alcohol and cigarette use in anamnesis. The remaining 356 patients were included in our study. Then, semen analysis of the patients was performed. The patients were divided into five groups according to cigarette use, into five groups according to alcohol use and into four groups according to cigarette and/or alcohol use. Significant differences were analyzed between the groups in terms of semen volume, semen concentration, total motility, forward motility and morphological (normality, head anomaly, neck anomaly, tail anomaly values. Results: According to cigarette use, only in group 4 (who use more than 20 package-years cigarette semen volume was significantly lower than the control group (Mann-Whitney U, p = 0.009. There was no significant difference in any of the other parameters and groups compared with the control group (Mann-Whitney U, p > 0,05 Conclusion:According to our study, using more than 20 package- years cigarette decreases semen volume. The reason of this result might be the fact that the threshold value, from which the effect of cigarette and alcohol use on the semen parameters has to be determined.

  17. Smokers’ and E-Cigarette Users’ Perceptions about E-Cigarette Warning Statements

    Directory of Open Access Journals (Sweden)

    Olivia A. Wackowski

    2016-06-01

    Full Text Available Cigarette warning labels are important sources of risk information, but warning research for other tobacco products is limited. This study aimed to gauge perceptions about warnings that may be used for e-cigarettes. We conducted six small focus groups in late 2014/early 2015 with adult current e-cigarette users and cigarette-only smokers. Participants rated and discussed their perceptions of six e-cigarette warning statements, and warnings in two existing Vuse and MarkTen e-cigarette ads. Participants were open to e-cigarette warnings and provided the strongest reactions to statements warning that e-liquid/e-vapor or e-cigarettes can be poisonous, contain toxins, or are “not a safe alternative to smoking”. However, many also noted that these statements were exaggerated, potentially misleading, and could scare smokers away from reducing their harm by switching to e-cigarettes. Opinions on the Food and Drug Administration’s proposed nicotine addiction warning and warnings that e-cigarettes had not been approved for smoking cessation or had unknown health effects were mixed. Participants perceived MarkTen’s advertisement warning to be stronger and more noticeable than Vuse’s. Care should be taken in developing e-cigarette warnings given their relative recentness and potential for harm reduction compared to other tobacco products. Additional research, including with varied audiences, would be instructive.

  18. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, H; Juel, K

    2000-01-01

    , 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...

  19. Debate, Research on E-Cigarettes Continues

    Science.gov (United States)

    Since they first began to be sold in North America in the mid-2000s, electronic cigarettes have been the subject of intense debate. NCI's Dr. Michele Bloch recently presented an update on some of the issues surrounding e-cigarettes.

  20. 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....

  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. 47 CFR 73.4055 - Cigarette advertising.

    Science.gov (United States)

    2010-10-01

    ... 47 Telecommunication 4 2010-10-01 2010-10-01 false Cigarette advertising. 73.4055 Section 73.4055 Telecommunication FEDERAL COMMUNICATIONS COMMISSION (CONTINUED) BROADCAST RADIO SERVICES RADIO BROADCAST SERVICES Rules Applicable to All Broadcast Stations § 73.4055 Cigarette advertising. See 15 U.S.C. 1335....

  3. Cigarette advertising and teen smoking initiation.

    Science.gov (United States)

    Hanewinkel, Reiner; Isensee, Barbara; Sargent, James D; Morgenstern, Matthis

    2011-02-01

    To test the specificity of the association between cigarette advertising and adolescent smoking initiation. A longitudinal survey of 2102 adolescents, aged 10 to 17 years at baseline, who never smoked was conducted by using masked images of 6 cigarette advertisements and 8 other commercial products with all brand information digitally removed. The exposure variable was a combination of contact frequency and cued recall of brands for cigarette and other advertisements. Multilevel mixed-effects Poisson regressions were used to assess smoking initiation 9 months after the baseline assessment as a function of cigarette-advertisement exposure, other advertisement exposure, and baseline covariates. Thirteen percent (n = 277) of students initiated smoking during the observation period. Although the incidence of trying smoking was associated with increased exposure to cigarette advertisements (10% in the low, 12% in the medium, and 19% in the high cigarette-advertisement exposure tertile initiated smoking), exposure to other advertisements did not predict smoking initiation. Compared with low exposure to cigarette advertisements, high exposure remained a significant predictor of adolescent smoking initiation after controlling for baseline covariates (adjusted relative risk: 1.46 [95% confidence interval: 1.08-1.97]; P marketing and teen smoking; exposure to cigarette advertisements, but not other advertisements, is associated with smoking initiation.

  4. 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.

  5. E-cigarettes: Considerations for the otolaryngologist.

    Science.gov (United States)

    Biyani, Sneh; Derkay, Craig S

    2015-08-01

    To review the literature regarding electronic cigarettes and discuss potential implications and need for advocacy for the pediatric otolaryngologist. Electronic cigarettes (e-cigarettes) are battery-operated devices that deliver nicotine-containing vapors via inhalation. Research on the health related consequences of e-cigarettes is ongoing and safety has yet to be established. E-cigarettes are not presently under the regulation of any national governing body with wide accessibility to minors. Use of these products has substantially increased since arrival to the market, particularly within the adolescent population. These products are marketed via various platforms including television, Internet and social media. Hundreds of flavors are offered and e-cigarettes are packaged in various colors. Not only are the ill health effects and addictive quality of nicotine concerning, these products have the potential to serve as a gateway for minors to tobacco use. The relationship between tobacco use, secondhand smoke exposure and otolaryngology specific diseases has well been defined. As use of electronic cigarettes increases, pediatric otolaryngologists should be aware of the ongoing literature regarding these products and to be prepared to counsel families accordingly. The use of e-cigarettes among teenagers, potential implications of secondhand vapor exposure from parents and friends, and concerns this may encourage adolescents to utilize conventional tobacco products needs to be considered. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  6. A Mathematical Model of Cigarette Smoldering Process

    Directory of Open Access Journals (Sweden)

    Chen P

    2014-12-01

    Full Text Available A mathematical model for a smoldering cigarette has been proposed. In the analysis of the cigarette combustion and pyrolysis processes, a receding burning front is defined, which has a constant temperature (~450 °C and divides the cigarette into two zones, the burning zone and the pyrolysis zone. The char combustion processes in the burning zone and the pyrolysis of virgin tobacco and evaporation of water in the pyrolysis zone are included in the model. The hot gases flow from the burning zone, are assumed to go out as sidestream smoke during smoldering. The internal heat transport is characterized by effective thermal conductivities in each zone. Thermal conduction of cigarette paper and convective and radiative heat transfer at the outer surface were also considered. The governing partial differential equations were solved using an integral method. Model predictions of smoldering speed as well as temperature and density profiles in the pyrolysis zone for different kinds of cigarettes were found to agree with the experimental data. The model also predicts the coal length and the maximum coal temperatures during smoldering conditions. The model provides a relatively fast and efficient way to simulate the cigarette burning processes. It offers a practical tool for exploring important parameters for cigarette smoldering processes, such as tobacco components, properties of cigarette paper, and heat generation in the burning zone and its dependence on the mass burn rate.

  7. 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

  8. Native, discount, or premium brand cigarettes: what types of cigarettes are Canadian youth currently smoking?

    Science.gov (United States)

    Elton-Marshall, Tara; Leatherdale, Scott T; Burkhalter, Robin

    2013-02-01

    The objective of the study was to determine the brand distribution of premium, discount, and native cigarette brands and to identify the factors associated with smoking these brands among a nationally representative sample of Canadian youth smokers. Data from 3,137 current smokers in Grades 9-12 participating in the 2008-2009 Youth Smoking Survey (YSS) were used to examine the prevalence and factors associated with different cigarette brand preferences. The most prevalent brand of cigarette smoked was premium cigarettes (44.7%), followed by discount cigarettes (33.7%), and to be native cigarettes (7.3%). There was significant variability in brand preference by province with the majority of youth in Atlantic Canada and Quebec smoking a discount brand of cigarettes and higher prevalence rates of native cigarette use in Ontario and Quebec. Respondents were more likely to smoke discount cigarettes if they were female, daily smokers, or if they only had $1-20 a week in spending money. Respondents were more likely to smoke native cigarettes if they were Aboriginal, heavier smokers, or if they reported having no weekly spending money. A significant proportion of students from Grade 9 to 12 in Canada smoke cigarettes that are more affordable than premium brands and it appears that the market share for these more affordable cigarette options has increased in recent years. Given that the price of cigarettes is an important determinant in youth smoking behavior, it is critical to develop and continue to enforce tobacco control strategies designed to eliminate access to cheaper sources of cigarettes among youth populations.

  9. 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.

  10. 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.

  11. Electronic cigarettes: ambiguity and controversies of usage.

    Science.gov (United States)

    Savant, Suyog; Shetty, Deeksha; Phansopkar, Sushil; Jamkhande, Amol

    2014-04-01

    Electronic cigarettes (EC), a proxy to conventional cigarettes, gained popularity on the basis of its own advocacy, marketing and large scale publicity. Sometimes marketed as an adjunct to quitting or a substitute for cigarettes, its popularity rose. However, its sale in the global markets was subjected to prejudice. Reasons cited by the regulatory bodies for its ouster were the toxic contents it contained. Some countries preferred to ban them while some have legalised them. However, the manufacturers have claimed that it does have the potential to help smokers quit or at least replace the conventional cigarettes which cause millions of death globally. Research is hence needed to prove the efficacy and utility of this device for welfare of people who are looking for better options than puffing cigarettes.

  12. Tobacco smoke induced COPD/emphysema in the animal model – are we all on the same page?

    Directory of Open Access Journals (Sweden)

    Maike eLeberl

    2013-05-01

    Full Text Available Chronic Obstructive Pulmonary Disease (COPD is one of the foremost causes of death worldwide. It is primarily caused by tobacco smoke, making it an easily preventable disease, but facilitated by genetic α-1 antitrypsin deficiency. In addition to active smokers, health problems also occur in people involuntarily exposed to second hand smoke (SHS. Currently, the relationship between SHS and COPD is not well established. Knowledge of pathogenic mechanisms is limited, thereby halting the advancement of new treatments for this socially and economically detrimental disease. Here, we attempt to summarize tobacco smoke studies undertaken in animal models, applying both mainstream (direct, nose only and side stream (indirect, whole body smoke exposures. This overview of 155 studies compares cellular and molecular mechanisms as well as proteolytic, inflammatory, and vasoreactive responses underlying COPD development. This is a difficult task, as listing of exposure parameters is limited for most experiments. We show that both mainstream and SHS studies largely present similar inflammatory cell populations dominated by macrophages as well as elevated chemokine/cytokine levels, such as TNF-α. Additionally, SHS, like mainstream smoke, has been shown to cause vascular remodeling and neutrophil elastase-mediated proteolytic matrix breakdown with failure to repair. Disease mechanisms and therapeutic interventions appear to coincide in both exposure scenarios. One of the more widely applied interventions, the anti-oxidant therapy, is successful for both mainstream and SHS. The comparison of direct with indirect smoke exposure studies in this review emphasizes that, even though there are many overlapping pathways, it is not conclusive that SHS is using exactly the same mechanisms as direct smoke in COPD pathogenesis, but should be considered a preventable health risk. Some characteristics and therapeutic alternatives uniquely exist in SHS-related COPD.

  13. Cigarette Smoke Disturbs the Survival of CD8+ Tc/Tregs Partially through Muscarinic Receptors-Dependent Mechanisms in Chronic Obstructive Pulmonary Disease.

    Directory of Open Access Journals (Sweden)

    Gang Chen

    Full Text Available CD8+ T cells (Cytotoxic T cells, Tc are known to play a critical role in the pathogenesis of smoking related airway inflammation including chronic obstructive pulmonary disease (COPD. However, how cigarette smoke directly impacts systematic CD8+ T cell and regulatory T cell (Treg subsets, especially by modulating muscarinic acetylcholine receptors (MRs, has yet to be well elucidated.Circulating CD8+ Tc/Tregs in healthy nonsmokers (n = 15, healthy smokers (n = 15 and COPD patients (n = 18 were evaluated by flow cytometry after incubating with anti-CD3, anti-CD8, anti-CD25, anti-Foxp3 antibodies. Peripheral blood T cells (PBT cells from healthy nonsmokers were cultured in the presence of cigarette smoke extract (CSE alone or combined with MRs agonist/antagonist for 5 days. Proliferation and apoptosis were evaluated by flow cytometry using Ki-67/Annexin-V antibodies to measure the effects of CSE on the survival of CD8+ Tc/Tregs.While COPD patients have elevated circulating percentage of CD8+ T cells, healthy smokers have higher frequency of CD8+ Tregs. Elevated percentages of CD8+ T cells correlated inversely with declined FEV1 in COPD. CSE promoted the proliferation and inhibited the apoptosis of CD8+ T cells, while facilitated both the proliferation and apoptosis of CD8+ Tregs. Notably, the effects of CSE on CD8+ Tc/Tregs can be mostly simulated or attenuated by muscarine and atropine, the MR agonist and antagonist, respectively. However, neither muscarine nor atropine influenced the apoptosis of CD8+ Tregs.The results imply that cigarette smoking likely facilitates a proinflammatory state in smokers, which is partially mediated by MR dysfunction. The MR antagonist may be a beneficial drug candidate for cigarette smoke-induced chronic airway inflammation.

  14. Cigarette Smoke Disturbs the Survival of CD8+ Tc/Tregs Partially through Muscarinic Receptors-Dependent Mechanisms in Chronic Obstructive Pulmonary Disease.

    Science.gov (United States)

    Chen, Gang; Zhou, Mei; Chen, Long; Meng, Zhao-Ji; Xiong, Xian-Zhi; Liu, Hong-Ju; Xin, Jian-Bao; Zhang, Jian-Chu

    2016-01-01

    CD8+ T cells (Cytotoxic T cells, Tc) are known to play a critical role in the pathogenesis of smoking related airway inflammation including chronic obstructive pulmonary disease (COPD). However, how cigarette smoke directly impacts systematic CD8+ T cell and regulatory T cell (Treg) subsets, especially by modulating muscarinic acetylcholine receptors (MRs), has yet to be well elucidated. Circulating CD8+ Tc/Tregs in healthy nonsmokers (n = 15), healthy smokers (n = 15) and COPD patients (n = 18) were evaluated by flow cytometry after incubating with anti-CD3, anti-CD8, anti-CD25, anti-Foxp3 antibodies. Peripheral blood T cells (PBT cells) from healthy nonsmokers were cultured in the presence of cigarette smoke extract (CSE) alone or combined with MRs agonist/antagonist for 5 days. Proliferation and apoptosis were evaluated by flow cytometry using Ki-67/Annexin-V antibodies to measure the effects of CSE on the survival of CD8+ Tc/Tregs. While COPD patients have elevated circulating percentage of CD8+ T cells, healthy smokers have higher frequency of CD8+ Tregs. Elevated percentages of CD8+ T cells correlated inversely with declined FEV1 in COPD. CSE promoted the proliferation and inhibited the apoptosis of CD8+ T cells, while facilitated both the proliferation and apoptosis of CD8+ Tregs. Notably, the effects of CSE on CD8+ Tc/Tregs can be mostly simulated or attenuated by muscarine and atropine, the MR agonist and antagonist, respectively. However, neither muscarine nor atropine influenced the apoptosis of CD8+ Tregs. The results imply that cigarette smoking likely facilitates a proinflammatory state in smokers, which is partially mediated by MR dysfunction. The MR antagonist may be a beneficial drug candidate for cigarette smoke-induced chronic airway inflammation.

  15. Recent Updates on Electronic Cigarette Aerosol and Inhaled Nicotine Effects on Periodontal and Pulmonary Tissues.

    Science.gov (United States)

    Javed, Fawad; Kellesarian, Sergio V; Sundar, Isaac K; Romanos, Georgios E; Rahman, Irfan

    2017-02-06

    E-cigarette derived inhaled nicotine may contribute to the pathogenesis of periodontal and pulmonary diseases in particular via lung inflammation, injurious and dysregulated repair responses. Nicotine is shown to have anti-proliferative properties and affects fibroblasts in vitro, which may interfere in tissue myofibroblast differentiation in e-cig users. This will affect the ability to heal wounds by decreasing wound contraction. In periodontics, direct exposure to e-vapor has been shown to produce harmful effects in periodontal ligament and gingival fibroblasts in culture. This is due to the generation of reactive oxygen species/aldehydes/carbonyls from e-cig aerosol, leading to protein carbonylation of extracellular matrix and DNA adducts/damage. A limited number of studies regarding the effects of e-cig in oral and lung health are available. However, no reports are available to directly link the deleterious effects on e-cigs, inhaled nicotine, and flavorings aerosol on oral periodontal and pulmonary health in particular to identify the risk of oral diseases by e-cigarettes and nicotine aerosols. This mini-review summarizes the recent perspectives on e-cigarettes including inhaled nicotine effects on several pathophysiological events, such as oxidative stress, DNA damage, innate host response, inflammation, cellular senescence, pro-fibrogenic and dysregulated repair, leading to lung remodeling, oral submucous fibrosis and periodontal diseases. This article is protected by copyright. All rights reserved.

  16. Association Between Electronic Cigarette Marketing Near Schools and E-cigarette Use Among Youth.

    Science.gov (United States)

    Giovenco, Daniel P; Casseus, Myriam; Duncan, Dustin T; Coups, Elliot J; Lewis, M Jane; Delnevo, Cristine D

    2016-12-01

    Electronic cigarettes (e-cigarettes) are now the most popular tobacco product among youth. Little is known about the relationship between exposure to e-cigarette marketing at the point-of-sale and youth e-cigarette use. Research staff collected data on e-cigarette availability and promotion in tobacco retailers within a half-mile of 41 schools participating in the 2014 New Jersey Youth Tobacco Survey. These data were linked with participant responses from the New Jersey Youth Tobacco Survey (n = 3,909) and log-Poisson regression models estimated adjusted prevalence ratios for ever and past-month e-cigarette use. Nearly a quarter of high school students in New Jersey have tried e-cigarettes (24.1%) and 12.1% were past-month users. Prevalence was highest among males, non-Hispanic whites, and students who have used other tobacco products. After controlling for covariates and the clustered nature of the data, e-cigarette retailer density around schools was positively associated with ever and past-month use of e-cigarettes (p promotion at the point-of-sale may play a role in reducing the use of e-cigarettes. Copyright © 2016 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.

  17. [Preliminary influence of 2015 cigarette excise tax up-regulation on cigarette retail price].

    Science.gov (United States)

    Feng, G Z; Wang, C X; Yang, J Q; Jiang, Y

    2016-10-10

    Objective: To evaluate the impact of cigarette excise tax up-regulation on the retail price of cigarettes in 2015. Methods: Nominal and real price of selected cigarette varieties were calculated with data from Tobacco Retail Price Monitoring Project, which was conducted in 10 cities of China from 2013 to 2015. The trend of the cigarette prices changing was analyzed with annual data. Results: A total of 352 varieties of cigarettes were surveyed during the three years. The nominal price of these cigarettes did not change significantly from 2013 to 2014. Compared with nominal price of 2014, the price of 286 varieties increased and the price of 10 most popular varieties increased from 0.6% to 7.4% after cigarette excise tax increased, but the actual prices had both rise and fall compared with 2013. Conclusions: Cigarette excise tax raise in 2015 had influence on the retail price of cigarettes. But the increase in retail price was very limited, if factors including inflation and purchasing power are taken into consideration. Therefore, the influence of 2015 cigarette excise tax raise on tobacco control needs further evaluation.

  18. DNA repair. [UV radiation

    Energy Technology Data Exchange (ETDEWEB)

    Setlow, R.

    1978-01-01

    Some topics discussed are as follows: difficulty in extrapolating data from E. coli to mammalian systems; mutations caused by UV-induced changes in DNA; mutants deficient in excision repair; other postreplication mechanisms; kinds of excision repair systems; detection of repair by biochemical or biophysical means; human mutants deficient in repair; mutagenic effects of UV on XP cells; and detection of UV-repair defects among XP individuals. (HLW)

  19. Gender, depressive symptoms, and daily cigarette use.

    Science.gov (United States)

    Bares, Cristina B

    2014-01-01

    It is widely known that cigarette use and depressive symptoms co-occur during adolescence and young adulthood and that there are gender differences in smoking initiation, progression, and co-occurrence with other drug use. Given that females have an earlier onset of depressive symptoms while males have an earlier onset of cigarette use, this study explored the possible bidirectional development of cigarette use and depressive symptoms by gender across the transition from adolescence to young adulthood. Gender differences in the stability and crossed effects of depressive symptoms and cigarette smoking during the transition to young adulthood, controlling for other known risk factors, were examined using a nationally representative longitudinal sample. A bivariate autoregressive multi-group structural equation model examined the longitudinal stability and crossed relationships between a latent construct of depressive symptoms and cigarette smoking over four waves of data. Data for this study came from four waves of participants (N = 6,501) from the National Longitudinal Survey of Adolescent Health. At each of four waves, participants completed a battery of measures including questions on depressive symptoms and an ordinal measure of number of cigarettes smoked per day. The best-fitting bivariate autoregressive models were gender-specific, included both crossed and parallel associations between depressive symptoms and cigarette use during the transition to adulthood, and controlled for wave-specific parental smoking, alcohol use, and number of friends who smoke. For females, greater depressive symptoms at each wave, except the first one, were associated with greater subsequent cigarette use. There were bidirectional associations between depressive symptoms and cigarette use only for females during young adulthood, but not for males. The development of depressive symptoms and cigarette use from adolescence and into young adulthood follows similar patterns for males

  20. Objective View of Electronic Cigarette Usage

    Directory of Open Access Journals (Sweden)

    Emel Koseoglu

    2014-06-01

    Full Text Available Purpose: Electronic cigarette is a device designed for helping the people who want to quit tobacco smoking. In the recent few years, its use has been spreading in a great deal. Its properties, the effects on human health and its potential for helping to quit smoking attract attention all over the world. In this review, it is aimed to have the readers an objective point of view by through consideration of the publications. Materials and Methods: In accordance to the aim, the general knowledge about electronic cigarette device and its use and; the studies performed on the subject, evaluated as in the forms of surveys, clinical observations and clinical interventional studies examining its potential harmful effects, have been considered in a detailed way Results: In general, the interpretations are made as electronic cigarette can supply some of the effects of nicotine, taken from tobacco cigarette and; hence, it is an important potential tool for quitting tobacco cigarette. However, it is indicated to have some threats to health and more research about its health effects should be accomplished; even if it is not so harmful as tobacco cigarette. Additionally, the studies, finding its harm potentials being related to its quality and production design, are drawing attention. Conclusion: The studies about electronic cigarette, which is found a place of use and spreading all over the world for quitting or lowering the harmful effects of tobacco cigarette, are not yet enough, in respect to its potential using purposes. Uncertainity exists about the place of electronic cigarettes in tobacco control. More research on the subject is urgently needed at both individual and population levels. [Cukurova Med J 2014; 39(3.000: 572-580

  1. Young adult e-cigarette users' reasons for liking and not liking e-cigarettes: A qualitative study.

    Science.gov (United States)

    Pokhrel, Pallav; Herzog, Thaddeus A; Muranaka, Nicholas; Fagan, Pebbles

    2015-01-01

    To gain an in-depth understanding of what young adult electronic- or e-cigarette users like or dislike about e-cigarettes. We aimed to determine the reasons that may encourage young adults to use e-cigarettes or discourage them from using e-cigarettes. Twelve focus group discussions were conducted with 62 current daily e-cigarette users (63% men) of mean age = 25.1 years (standard deviation = 5.5). Data were analysed following principles of inductive content analysis. Results indicated 12 categories of reasons for liking e-cigarettes (e.g., recreation, smoking cessation) and 6 categories of reasons for not liking e-cigarettes (e.g. poor product quality, poor smoking experience). Young adults' motives for using or not using e-cigarettes appear to be varied and their relative importance in terms of predicting e-cigarette use initiation, dependence, and cigarette/e-cigarette dual use needs to be carefully studied in population-based, empirical studies. The current findings suggest that e-cigarettes may serve social, recreational, and sensory expectancies that are unique relative to cigarettes and not dependent on nicotine. Further, successful use of e-cigarettes in smoking cessation will likely need higher standards of product quality control, better nicotine delivery efficiency and a counselling component that would teach smokers how to manage e-cigarette devices while trying to quit smoking cigarettes.

  2. Marketing of Menthol Cigarettes and Consumer Perceptions: A White Paper

    OpenAIRE

    2010-01-01

    Publicly available internal tobacco industry documents were analyzed to answer the following questions regarding menthol cigarette marketing and consumer perception: 1) Are/were menthol cigarettes marketed with health reassurance messages? 2) What other messages come from menthol cigarette advertising? 3) How do smokers view menthol cigarettes? 4) Were menthol cigarettes marketed to specific populations? More than 800 relevant documents were identified on 1) marketing menthol with health...

  3. Effect of RXR/PPAR interaction in angiotensin II-induced vascular inflammation and angiogenesis. Role of CXCL16/CXCR6 axis in angiotensin II or cigarette smoke-induced vascular inflammation

    OpenAIRE

    Escudero Diaz, Paula

    2016-01-01

    Aumentos en los niveles circulantes de mediadores, incluyendo angiotensina II (Ang-II) y citoquinas, han sido detectados en enfermedades cardiovasculares y cardiometabólicas como la hipertensión, la obesidad y la diabetes, y parecen ejercer efectos negativos sobre la función endotelial (Granger et al., 2004; Marinou et al., 2010). Estos agentes inician una cascada inflamatoria de señalización que promueve la generación de especies reactivas del oxígeno, aumento en la superficie celular de la ...

  4. Impact of cigarette taxation policy on excise revenues and cigarette consumption in Uzbekistan

    Directory of Open Access Journals (Sweden)

    Konstantin S. Krasovsky

    2013-05-01

    Full Text Available BACKGROUND: In 2012, Uzbekistan ratified the Framework Convention on Tobacco Control, which states that price and tax measures are an effective means of reducing tobacco consumption. We aimed to explore the effect of taxation policies on revenues and cigarette consumption. METHODS: Data on tax rates, revenues, cigarette sales were taken from national reports. To forecast potential revenues, a scenario analysis was performed. RESULTS: In 1991-2004, ad valorem excise system was in place in Uzbekistan, which was later replaced by the specific excise system. In 1997-2011, the nominal average excise has increased by a factor of twenty, but in real terms, after a sharp increase in 1999, average excise declined annually and increased only in 2010-2011. Annual cigarette sales per capita of adult population in 1999-2007 constituted 17-25 cigarette packs, while in 2008-2011 it increased to 30-37 packs. Four scenarios of excise tax increases in 2012 were developed: one actual scenario based on the rates effective in Uzbekistan in 2012, and three hypothetical ones anticipating excise rates increase by 1.5, 2 and 3-fold. With actual excise increase in 2012, the inflation-adjusted budget revenues would grow by 5%, and with three hypothetical - by 17%, 35% and 66% respectively, despite the decline of tax-paid cigarette sales. CONCLUSION: Stabilization or reduction in cigarette excises in Uzbekistan in 2002-2008 led to a decline in real excise revenues and the growth of cigarette sales. In 1999 and 2010-2011, excises were significantly increased and the real revenues have risen, despite the decline in cigarette sales. As cigarette prices are low, the illegal outflow of cigarettes from Uzbekistan apparently exceeds the illegal inflow. A significant increase in cigarette excise (1.5-3 fold can both increase budget revenues and reduce cigarette consumption, with greater increase yielding more benefits.

  5. First-year impact of the 1989 California cigarette tax increase on cigarette consumption.

    Science.gov (United States)

    Flewelling, R L; Kenney, E; Elder, J P; Pierce, J; Johnson, M; Bal, D G

    1992-06-01

    We employed a time series design to evaluate the impact of the 1989 California cigarette tax increase on cigarette consumption in California. Adult per capita consumption data from 1980 to 1990 were analyzed for California and the United States. Trend data indicated a sharp drop in California cigarette consumption coincident with the tax increase. Time-series regression analyses support this observation, and suggest that a 5% to 7% decline in consumption is attributable to the tax increase.

  6. A Prototypical First-Generation Electronic Cigarette Does Not Reduce Reports of Tobacco Urges or Withdrawal Symptoms among Cigarette Smokers

    Directory of Open Access Journals (Sweden)

    Arit M. Harvanko

    2017-01-01

    Full Text Available It is unknown whether first-generation electronic cigarettes reduce smoking urges and withdrawal symptoms following a 24 h deprivation period. This study tested whether a first-generation electronic cigarette reduces smoking urges and withdrawal symptoms in cigarette smokers. Following 24 h of tobacco deprivation, using a within-subjects design, eight nontreatment seeking tobacco cigarette smokers (3 females administered 10 puffs from a conventional cigarette or a first-generation electronic cigarette containing liquid with 0, 8 or 16 mg/ml nicotine. Conventional cigarettes ameliorated smoking urges and electronic cigarettes did not, regardless of nicotine concentration. First-generation electronic cigarettes may not effectively substitute for conventional cigarettes in reducing smoking urges, regardless of nicotine concentration.

  7. Evaluating nicotine dependence levels in e-cigarette users.

    Science.gov (United States)

    González Roz, Alba; Secades Villa, Roberto; Weidberg, Sara

    2017-01-11

    Despite the fact that electronic cigarettes (e-cigarettes) are rapidly growing in popularity and use worldwide, there is scarce scientific data on abuse liability among e-cigarette users, and about whether e-cigarette use is related to nicotine dependence or not. The aim of this study is to explore nicotine dependence levels in a sample of experienced e-cigarette users (n= 39) and to compare them with current tobacco cigarette smokers (n=42). We conducted several face-to-face interviews in order to assess sociodemographic and dependence related characteristics in both e-cigarette users and in smokers. Adapted versions of both the Fagerström test for nicotine dependence (FTND) and the nicotine dependence syndrome scale (NDSS) were used to analyze nicotine dependence in each of the groups. Biochemical markers of carbon monoxide and urinary cotinine analysis were also collected. Results showed that e-cigarette users scored lower than cigarette smokers in both FTND and all NDSS subscales. Our findings extend previous research on e-cigarette use and nicotine addiction and suggest that e-cigarette users are less dependent on nicotine than current tobacco cigarette smokers. Further prospective studies are needed to better ascertain their addictiveness potential, comparing those smokers who switched to e-cigarettes from smoking cigarettes, and those who had never been tobacco cigarette smokers.

  8. Ingestion of cigarettes and cigarette butts by children--Rhode Island, January 1994-July 1996 .

    Science.gov (United States)

    1997-02-14

    During 1995, the American Association of Poison Control Centers (AAPCC) received 7917 reports of potentially toxic exposures to tobacco products among children aged cigars. Acute nicotine poisoning is characterized by rapid onset of symptoms that may be severe when large amounts have been ingested. During January 1994-July 1996, the Rhode Island Poison Control Center (RIPCC) received 146 reports of ingestion of products containing nicotine by children aged cigarette butts among children aged cigarette butts by children aged < or = 6 years resulted in minor toxic effects and occurred more frequently in households where smoking was permitted in the presence of children and where cigarettes and cigarette wastes were accessible to children.

  9. Changes in cigarette expenditure minimising strategies before and after a cigarette tax increase.

    Science.gov (United States)

    Choi, Kelvin; Boyle, Raymond G

    2017-02-20

    Smokers use cigarette expenditure minimising strategies (CEMS) to alleviate the effect of tax increases on their cigarette expenses. We examined changes in smokers' CEMS use before and after a 2013 Minnesota $1.75 cigarette tax increase. Data were from representative samples of smokers who participated in the Minnesota Adult Tobacco Survey 2010 (n=948) and 2014 (n=1229). Participants indicated CEMS used in the past year from a list. Weighted multiple logistic regressions were used to examine changes in prevalence of each CEMS use over time adjusting for demographics and cigarette consumption. Characteristics associated with CEMS use in 2014 were examined. Between 2010 and 2014, more smokers tried to save money on cigarettes by rolling their own cigarettes (from 19% to 29%), using other tobacco products (from 13% to 25%), and buying cigarettes from cheaper places (from 48% to 55%). Yet, fewer smokers used coupons/promotions (from 63% to 50%) and bought cigarettes by the carton (from 39% to 32%). These changes varied somewhat by race/ethnicity and education, for example, more smokers with tax increase. Regulations that would reduce CEMS use could boost the effectiveness of cigarette tax increases. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) [year]. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

  10. Awareness of FDA-mandated cigarette packaging changes among smokers of 'light' cigarettes.

    Science.gov (United States)

    Falcone, M; Bansal-Travers, M; Sanborn, P M; Tang, K Z; Strasser, A A

    2015-02-01

    Previous research has clearly demonstrated that smokers associate cigarette descriptors such as 'light', 'ultra-light' and 'low tar' with reduced health risks, despite evidence showing that cigarettes with these descriptor terms do not present lower health risk. In June 2010, regulations implemented by the US Food and Drug Administration went into effect to ban the use of 'light', 'mild' and 'low' on cigarette packaging. We surveyed smokers participating in human laboratory studies at our Center in Philadelphia, PA, USA shortly after the ban went into effect to determine the extent of awareness of recent cigarette packaging changes among smokers of light cigarettes. In our sample of 266 smokers, 76 reported smoking light cigarettes, but fewer than half of these smokers reported noticing changes to their cigarette packaging. Simple removal of a few misleading terms may be too subtle of a change to register with consumers of so-called 'low tar' cigarettes; more comprehensive regulation of cigarette packaging design may be necessary to gain smokers' attention and minimize misperceptions associated with tobacco pack design characteristics and color. © The Author 2014. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.

  11. Cigarette smoking impairs sperm bioenergetics

    Directory of Open Access Journals (Sweden)

    Kazim R. Chohan

    2010-02-01

    Full Text Available OBJECTIVE: The growing consensus on the negative impact of cigarette smoking on fertility prompted us to compare the rate of sperm respiration in smokers and non-smokers. MATERIALS AND METHODS: Semen samples from 20 smokers and 58 non-smokers consulting at the andrology laboratory for fertility evaluation were used. Smoking was defined as consumption of at least a half a pack per day. A phosphorescence analyzer that measures O2 concentration in sperm suspensions as function of time was used to determine the rate of respiration. In a sealed vial, the rate of sperm respiration (k was defined as -d[O2]/dt; where [O2] was obtained from the phosphorescence decay rate of a palladium phosphor. [O2] in solutions containing sperm and glucose declined linearly with time, showing the kinetics of O2 consumption was zero-order. Inhibition of O2 consumption by cyanide confirmed the oxidations that occurred in the sperm mitochondrial respiratory chain. RESULTS: There were no differences (p > 0.28 between smokers and non-smokers for ejaculate volume, motility, concentration, normal morphology, viability and hypo-osmotic swelling test. The rate (mean ± SD, in µM O2/min/108 sperm of sperm mitochondrial O2 consumption in the smokers was 0.96 ± 0.58 and in the non-smokers 1.39 ± 0.67 (p = 0.004. CONCLUSIONS: The rate of sperm respiration was significantly lower in smokers. This negative impact of cigarette smoking on sperm aerobic metabolism may, in part, explain the lower rate of fertility in smokers.

  12. 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...

  13. 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...

  14. 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...

  15. E-cigarettes and E-hookahs

    Science.gov (United States)

    ... et al, eds. Murray and Nadel's Textbook of Respiratory Medicine . 6th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 46. Callahan-Lyon P. Electronic cigarettes: human health effects. Tob Control . 2014;23(Suppl 2):ii36-ii40. ...

  16. Does environmental cigarette smoke affect breastfeeding behavior?

    National Research Council Canada - National Science Library

    Firouzbakht, Mozhgan; Hajian-Tilaki, Karimallah; Nikpour, Maryam; Banihosseini, Zahra

    2017-01-01

    Background: Exposure of lactating women to environmental cigarette smoke may increase cotinine in breast milk, which in turn may reduce the volume of milk and the duration of breastfeeding. Objectives...

  17. Why Teens Choose E-Cigarettes

    Science.gov (United States)

    ... cigarettes in this young age group." States could tax the devices, hiking their prices, she suggested. Federal ... professor, psychiatry, Yale University School of Medicine, New Haven, Conn.; Krysten Bold, Ph.D., postdoctoral fellow in ...

  18. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, Henrik; Juel, K

    2000-01-01

    . 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......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...

  19. CSEO - the Cigarette Smoke Exposure Ontology

    National Research Council Canada - National Science Library

    Younesi, Erfan; Ansari, Sam; Guendel, Michaela; Ahmadi, Shiva; Coggins, Chris; Hoeng, Julia; Hofmann-Apitius, Martin; Peitsch, Manuel C

    2014-01-01

    ...) is composed of 20091 concepts. The ontology in its current form is able to capture a wide range of cigarette smoke exposure concepts within the knowledge domain of exposure science with a reasonable sensitivity and specificity...

  20. 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.

  1. The Effect of Polymorphisms in DNA Repair Genes and Carcinogen Metabolizers on Leukocyte Telomere Length: A Cohort of Healthy Spanish Smokers.

    Science.gov (United States)

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

    2016-04-01

    Smoking implies exposure to carcinogenic agents that causes DNA damage, which could be suspected to enhance telomere attrition. To protect and deal with DNA damage, cells possess mechanisms that repair and neutralize harmful substances. Polymorphisms altering DNA repair capacity or carcinogen metabolism may lead to synergistic effects with tobacco carcinogen-induced shorter telomere length independently of cancer interaction. The aim of this study was to explore the association between leukocyte telomere length (LTL) and several genetic polymorphisms in DNA repair genes and carcinogen metabolizers in a cohort of healthy smokers. We evaluated the effect of six genetic polymorphisms in cytochrome P1A1 (Ile462Val), XRCC1 (Arg399Gln), APEX1 (Asp148Glu), XRCC3 (Thr241Met), and XPD (Asp312Asn; Lys751Gln) on LTL in a cohort of 145 healthy smokers in addition to smoking habits. Logistic regression analysis showed an association between XRCC1 399Gln allele and shorter telomere length (OR = 5.03, 95% CI = 1.08% to 23.36%). There were not association between the rest of polymorphisms analyzed and LTL. Continuous exposure to tobacco could overwhelm the DNA repair machinery, making the effect of the polymorphisms that reduce repair capacity more pronounced. Analyzing the function of smoking-induced DNA-repair genes and LTL is an important goal in order to identify therapeutic targets to treat smoking-induced diseases. © The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  2. Pectus excavatum repair

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/article/002949.htm Pectus excavatum repair To use the sharing features on this page, please enable JavaScript. Pectus excavatum repair is surgery to correct pectus excavatum . This ...

  3. The synergistic effect of cigarette taxes on the consumption of cigarettes, alcohol and betel nuts

    Directory of Open Access Journals (Sweden)

    Lee Jie-Min

    2007-06-01

    Full Text Available Abstract Background Consumption of cigarettes and alcoholic beverages creates serious health consequences for individuals and overwhelming financial burdens for governments around the world. In Asia, a third stimulant – betel nuts – increases this burden exponentially. For example, individuals who simultaneously smoke, chew betel nuts and drink alcohol are approximately 123 times more likely to develop oral, pharyngeal and laryngeal cancer than are those who do not. To discourage consumption of cigarettes, the government of Taiwan has imposed three taxes over the last two decades. It now wishes to lower consumption of betel nuts. To assist in this effort, our study poses two questions: 1 Will the imposition of an NT$10 Health Tax on cigarettes effectively reduce cigarette consumption? and 2 Will this cigarette tax also reduce consumption of alcoholic beverages and betel nuts? To answer these questions, we analyze the effect of the NT$10 tax on overall cigarette consumption as well as the cross price elasticities of cigarettes, betel nuts, and alcoholic beverages. Methods To establish the Central Bureau of Statistics demand function, we used cigarette, betel nut, and alcoholic beverage price and sales volume data for the years 1972–2002. To estimate the overall demand price elasticity of cigarettes, betel nuts, and alcoholic beverages, we used a seemingly unrelated regression analysis. Results We find that the NT$10 health tax on cigarettes will reduce cigarette consumption by a significant 27.22%. We also find that cigarettes, betel nuts, and alcoholic beverages have similar inherent price elasticities of -0.6571, -0.5871, and -0.6261 respectively. Because of this complementary relationship, the NT$10 health tax on cigarettes will reduce betel nut consumption by 20.07% and alcohol consumption by 7.5%. Conclusion The assessment of a health tax on cigarettes as a smoking control policy tool yields a win-win outcome for both government and

  4. Other tobacco product and electronic cigarette use among homeless cigarette smokers.

    Science.gov (United States)

    Baggett, Travis P; Campbell, Eric G; Chang, Yuchiao; Rigotti, Nancy A

    2016-09-01

    We determined the prevalence and correlates of other tobacco product and electronic cigarette (e-cigarette) use in a clinic-based sample of homeless cigarette smokers. In April-July 2014, we used time-location sampling to conduct a cross-sectional, in-person survey of 306 currently homeless adult cigarette smokers recruited from 5 clinical sites at Boston Health Care for the Homeless Program. We assessed past-month use of large cigars, little cigars, smokeless tobacco, and e-cigarettes. Among those who had used e-cigarettes, we assessed the reasons for doing so. We used logistic regression analysis to identify the participant characteristics associated with the use of each product. Eighty-six percent of eligible individuals participated in the survey. In the past month, 37% of respondents used large cigars, 44% used little cigars, 8% used smokeless tobacco, 24% used an e-cigarette, and 68% used any of these products. Reasons for e-cigarette use included curiosity (85%) and to help quit conventional cigarettes (69%). In multivariable regression analyses, homeless smokers with greater subsistence difficulties were more likely to use little cigars (p=0.01) and less likely to use e-cigarettes (p=0.001). Non-Hispanic black (p=0.01), Hispanic (pcigarette use to help quit smoking (p=0.02). Health care providers who serve homeless people should consider routine screening for the use of other tobacco products and e-cigarettes to help guide smoking cessation discussions and tobacco treatment planning. Copyright © 2016 Elsevier Ltd. All rights reserved.

  5. Differences in the design and sale of e-cigarettes by cigarette manufacturers and non-cigarette manufacturers in the USA.

    Science.gov (United States)

    Seidenberg, Andrew B; Jo, Catherine L; Ribisl, Kurt M

    2016-04-01

    Three categories of e-cigarette brands have emerged within the US market: e-cigarette brands developed by cigarette manufacturers, brands acquired by cigarette manufacturers and brands with no cigarette manufacturer affiliation. In the absence of federal regulatory oversight of e-cigarettes, we assessed differences in e-cigarette products and sales practices across these categories. Brand websites for top-selling e-cigarette brands from each of these categories were examined in October of 2015 to compare website access restrictions, online sales practices and products sold, including e-cigarette model type (eg, 'cigalike' vs advanced systems) and options available (eg, flavoured, nicotine free). Website access to brands developed by cigarette manufacturers was restricted to users aged 21 years or older, and one website required user registration. In addition, these brands were exclusively reusable/rechargeable 'cigalikes.' Limited flavour options were available for these products, and nicotine-free options were not sold. In contrast, brands acquired by cigarette manufacturers and brands with no cigarette manufacturer affiliation generally required website visitors to be 18, offered a nicotine-free option, and most offered disposable products and an array of flavoured products (eg, fruit/candy flavours). This exploratory study finds differences in e-cigarette products and sales practices across these three e-cigarette brand categories, with brands developed by cigarette manufacturers adopting a particularly distinctive product and sales strategy. Anticipated regulation of e-cigarettes in the USA may be influencing these product and sales decisions. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/

  6. When "Other" Initiate Repair.

    Science.gov (United States)

    Schegloff, Emanuel A.

    2000-01-01

    Elaborates on the locus of other-initiated repair, and reports on a number of environments in which others initiate repair turns later than the one directly following the trouble-source turn. Describes several ways that other initiation of repair, which occurs in next-turn position, may be delayed within that position. (Author/VWL)

  7. 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.

  8. Awareness of FDA-Mandated Cigarette Packaging Changes among Smokers of "Light" Cigarettes

    Science.gov (United States)

    Falcone, M.; Bansal-Travers, M.; Sanborn, P. M.; Tang, K. Z.; Strasser, A. A.

    2015-01-01

    Previous research has clearly demonstrated that smokers associate cigarette descriptors such as "light", "ultra-light" and "low tar" with reduced health risks, despite evidence showing that cigarettes with these descriptor terms do not present lower health risk. In June 2010, regulations implemented by the US Food and…

  9. Social Influences on Use of Cigarettes, E-Cigarettes, and Hookah by College Students

    Science.gov (United States)

    Noland, Melody; Ickes, Melinda J.; Rayens, Mary Kay; Butler, Karen; Wiggins, Amanda T.; Hahn, Ellen J.

    2016-01-01

    Objectives: (1) Compare social norms and perceived peer use between college student cigarette, e-cigarette, and/or hookah users and nonusers; and (2) determine variables associated with social influences. Participants: Undergraduate students attending a large university in the Southeast United States (N = 511). Methods: An April 2013 online survey…

  10. Fewer Cancer-Causing Chemicals in E-Cigs Than Regular Cigarettes

    Science.gov (United States)

    ... study suggests that smokers who completely switch to e-cigarettes and stop smoking tobacco cigarettes may significantly reduce ... of 12 years. For two weeks, they used e-cigarettes instead of tobacco cigarettes. During that time, their ...

  11. E-cigarette specialty retailers: Data to assess the association between retail environment and student e-cigarette use.

    Science.gov (United States)

    Bostean, Georgiana; Crespi, Catherine M; Vorapharuek, Patsornkarn; McCarthy, William J

    2017-04-01

    The retail environment is a major social determinant of health, yet little is known about the e-cigarette specialty retailer environment. The e-cigarette specialty retail environment may be associated with e-cigarette use by middle and high school students, an issue that was addressed in a recent article entitled, "E-cigarette use among students and e-cigarette specialty retailer presence near schools," by Bostean and colleagues (G. Bostean, C.M. Crespi, P. Vorapharuek, W.J. McCarthy, 2016 [1]). We present data relating to e-cigarette specialty retailers in Orange County, California. We describe the data collection method (including the search methodology to identify e-cigarette specialty retailers), present descriptive retailer data including school proximity, and provide data from multi-level regressions predicting individual-level student use of e-cigarettes based on presence of an e-cigarette specialty retailer in proximity to schools.

  12. [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.

  13. Merchandising of cigarettes in San Francisco pharmacies: 27 years later.

    Science.gov (United States)

    Eule, B; Sullivan, M K; Schroeder, S A; Hudmon, K S

    2004-12-01

    To estimate changes since 1976 in the proportion of San Francisco pharmacies that sell cigarettes and to characterise the advertising of cigarettes and the merchandising of non-prescription nicotine replacement therapy (NRT) products in these retail establishments. 100 randomly selected San Francisco pharmacies were visited in 2003. Pharmacies were characterised based on the sale of cigarettes, advertising for cigarettes, and the merchandising of non-prescription NRT products. In 2003, 61% of pharmacies sold cigarettes, a significant decrease compared to 89% of pharmacies selling cigarettes in 1976 (p merchandise the primary known risk factor for death in the USA.

  14. Chinese Smokers’ Cigarette Purchase Behaviors, Cigarette Prices and Consumption: Findings from the ITC China Survey

    Science.gov (United States)

    Huang, Jidong; Zheng, Rong; Chaloupka, Frank J.; Fong, Geoffrey T.; Li, Qiang; Jiang, Yuan

    2014-01-01

    Background While cigarette purchasing behavior has been shown to be linked with certain tobacco use outcomes such as quit intentions and quit attempts, there have been very few studies examining cigarette purchasing behaviors and their impact on cigarette price and consumption in China, the world’s largest cigarette consumer. Objective The goal of this study is to examine the extent and determinants of cost/price-related purchase behaviors, and estimate the impact of these behaviors on cigarette prices paid by Chinese smokers. It also assesses the socio-economic differences in compensatory purchase behaviors, and examines how they influence the relationship between purchase behaviors, cigarette prices, and cigarette consumption. Methods Multivariate analyses using the general estimating equations (GEE) method were conducted using data from the International Tobacco Control China Survey (the ITC China Survey), a longitudinal survey of adult smokers in seven cities in China: Beijing, Changsha, Guangzhou, Kunming, Shanghai, Shenyang, and Yinchuan. In each city, about 800 smokers were surveyed in each wave. The first three waves - Wave 1 (conducted between March to December 2006), Wave 2 (November 2007 to March 2008) and Wave 3 (May to October 2009 and February to March 2010) - of the ITC China Survey data were used in this analysis. Various aspects of smokers’ self-reported price/cost-related cigarette purchasing behaviors were analyzed. Findings Nearly three-quarters (72%) of smokers surveyed indicated that a major reason they chose their most-used cigarette brand was its low cost/price. Almost half (50.6%) of smokers reported buying in cartons in their most recent cigarette purchase. Smokers with lower income and/or low levels of education were more likely to choose a brand because of its low cost/price. However, those with higher income and/or high levels of education were more likely to buy cartons. Gender and age were also related to type of purchase

  15. Chinese smokers' cigarette purchase behaviours, cigarette prices and consumption: findings from the ITC China Survey.

    Science.gov (United States)

    Huang, Jidong; Zheng, Rong; Chaloupka, Frank J; Fong, Geoffrey T; Li, Qiang; Jiang, Yuan

    2014-03-01

    While cigarette purchasing behaviour has been shown to be linked with certain tobacco use outcomes such as quit intentions and quit attempts, there have been very few studies examining cigarette purchasing behaviours and their impact on cigarette price and consumption in China, the world's largest cigarette consumer. The aim of the present study was to examine the extent and determinants of cost/price-related purchase behaviours, and estimate the impact of these behaviours on cigarette prices paid by Chinese smokers. It also assesses the socioeconomic differences in compensatory purchase behaviours, and examines how they influence the relationship between purchase behaviours, cigarette prices and cigarette consumption. Multivariate analyses using the general estimating equations method were conducted using data from the International Tobacco Control China Survey (the ITC China Survey), a longitudinal survey of adult smokers in seven cities in China: Beijing, Changsha, Guangzhou, Kunming, Shanghai, Shenyang and Yinchuan. In each city, about 800 smokers were surveyed in each wave. The first three waves--wave 1 (conducted between March to December 2006), wave 2 (November 2007 to March 2008) and wave 3 (May to October 2009 and February to March 2010)--of the ITC China Survey data were used in this analysis. Various aspects of smokers' self-reported price/cost-related cigarette purchasing behaviours were analysed. Nearly three-quarters (72%) of smokers surveyed indicated that a major reason they chose their most-used cigarette brand was its low cost/price. Almost half (50.6%) of smokers reported buying in cartons in their most recent cigarette purchase. Smokers with lower income and/or low levels of education were more likely to choose a brand because of its low cost/price. However, those with higher income and/or high levels of education were more likely to buy cartons. Gender and age were also related to type of purchase behaviours. Those behaviours led to reductions

  16. Toxicity evaluation of e-juice and its soluble aerosols generated by electronic cigarettes using recombinant bioluminescent bacteria responsive to specific cellular damages.

    Science.gov (United States)

    Bharadwaj, Shiv; Mitchell, Robert J; Qureshi, Anjum; Niazi, Javed H

    2017-04-15

    Electronic-cigarettes (e-cigarette) are widely used as an alternative to traditional cigarettes but their safety is not well established. Herein, we demonstrate and validate an analytical method to discriminate the deleterious effects of e-cigarette refills (e-juice) and soluble e-juice aerosol (SEA) by employing stress-specific bioluminescent recombinant bacterial cells (RBCs) as whole-cell biosensors. These RBCs carry luxCDABE-operon tightly controlled by promoters that specifically induced to DNA damage (recA), superoxide radicals (sodA), heavy metals (copA) and membrane damage (oprF). The responses of the RBCs following exposure to various concentrations of e-juice/SEA was recorded in real-time that showed dose-dependent stress specific-responses against both the e-juice and vaporized e-juice aerosols produced by the e-cigarette. We also established that high doses of e-juice (4-folds diluted) lead to cell death by repressing the cellular machinery responsible for repairing DNA-damage, superoxide toxicity, ion homeostasis and membrane damage. SEA also caused the cellular damages but the cells showed enhanced bioluminescence expression without significant growth inhibition, indicating that the cells activated their global defense system to repair these damages. DNA fragmentation assay also revealed the disintegration of total cellular DNA at sub-toxic doses of e-juice. Despite their state of matter, the e-juice and its aerosols induce cytotoxicity and alter normal cellular functions, respectively that raises concerns on use of e-cigarettes as alternative to traditional cigarette. The ability of RBCs in detecting both harmful effects and toxicity mechanisms provided a fundamental understanding of biological response to e-juice and aerosols.

  17. A Randomized Trial of the Effect of E-cigarette TV Advertisements on Intentions to Use E-cigarettes.

    Science.gov (United States)

    Farrelly, Matthew C; Duke, Jennifer C; Crankshaw, Erik C; Eggers, Matthew E; Lee, Youn O; Nonnemaker, James M; Kim, Annice E; Porter, Lauren

    2015-11-01

    Adolescents' use of electronic cigarettes (e-cigarettes) and exposure to e-cigarette TV advertising have increased in recent years, despite questions about their safety. The current study tests whether exposure to e-cigarette TV advertisements influences intentions to use e-cigarettes in the future and related attitudes. A parallel-group randomized controlled experiment was conducted and analyzed in 2014 using an online survey with a convenience sample of 3,655 U.S. adolescents aged 13-17 years who had never tried e-cigarettes. Adolescents in the treatment group viewed four e-cigarette TV advertisements. Adolescents in the treatment group reported a greater likelihood of future e-cigarette use compared with the control group. ORs for the treatment group were 1.54 (p=0.001) for trying an e-cigarette soon; 1.43 (p=0.003) for trying an e-cigarette within the next year; and 1.29 (p=0.02) for trying an e-cigarette if a best friend offered one. Adolescents in the treatment group had higher odds of agreeing that e-cigarettes can be used in places where cigarettes are not allowed (OR=1.71, pExposure to e-cigarette advertising had relatively large and consistent effects across experimental outcomes. Together with the simultaneous increase in e-cigarette advertising exposure and e-cigarette use among adolescents, findings suggest that e-cigarette advertising is persuading adolescents to try this novel product. This raises concerns that continued unregulated e-cigarette advertising will contribute to potential individual- and population-level harm. Copyright © 2015 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.

  18. How hearing about harmful chemicals affects smokers' interest in dual use of cigarettes and e-cigarettes.

    Science.gov (United States)

    Pepper, Jessica K; Byron, M Justin; Ribisl, Kurt M; Brewer, Noel T

    2017-03-01

    Substantial harm could result from concurrent cigarette and e-cigarette use (i.e., dual use) were it to undermine smoking cessation. Perceptions of chemical exposure and resulting harms may influence dual use. We conducted a probability-based phone survey of 1164 U.S. adult cigarette smokers in 2014-2015 and analyzed results in 2016. In a between-subjects experiment, smokers heard a hypothetical scenario in which cigarettes and e-cigarettes had the same amount of harmful chemicals or cigarettes had more chemicals than e-cigarettes (10× more, 100× more, or chemicals were present only in cigarettes). Smokers indicated how the scenario would change their interest in dual use and perceived health harms. Few smokers (7%) who heard that the products have the same amount of chemicals were interested in initiating or increasing dual use. However, more smokers were interested when told that cigarettes have 10× more chemicals than e-cigarettes (31%), 100× more chemicals than e-cigarettes (32%), or chemicals were present only in cigarettes (43%) (all pe-cigarettes (79% vs. 41%, OR=5.41, 95% CI=4.08-7.17). These harm perceptions partially explained the relationship between chemical scenario and dual use interest. Smokers associated higher chemical amounts in cigarettes versus e-cigarettes with greater health harms from cigarettes and thus expressed increased interest in dual use. The findings suggest that disclosing amounts of chemicals in cigarette smoke and e-cigarette aerosol could unintentionally encourage dual use.

  19. The effect of cigarette price increase on the cigarette consumption in Taiwan: evidence from the National Health Interview Surveys on cigarette consumption

    Directory of Open Access Journals (Sweden)

    Ye Chun-Yuan

    2004-12-01

    Full Text Available Abstract Background This study uses cigarette price elasticity to evaluate the effect of a new excise tax increase on cigarette consumption and to investigate responses from various types of smokers. Methods Our sample consisted of current smokers between 17 and 69 years old interviewed during an annual face-to-face survey conducted by Taiwan National Health Research Institutes between 2000 to 2003. We used Ordinary Least Squares (OLS procedure to estimate double logarithmic function of cigarette demand and cigarette price elasticity. Results In 2002, after Taiwan had enacted the new tax scheme, cigarette price elasticity in Taiwan was found to be -0.5274. The new tax scheme brought about an average annual 13.27 packs/person (10.5% reduction in cigarette consumption. Using the cigarette price elasticity estimate from -0.309 in 2003, we calculated that if the Health and Welfare Tax were increased by another NT$ 3 per pack and cigarette producers shifted this increase to the consumers, cigarette consumption would be reduced by 2.47 packs/person (2.2%. The value of the estimated cigarette price elasticity is smaller than one, meaning that the tax will not only reduce cigarette consumption but it will also generate additional tax revenues. Male smokers who had no income or who smoked light cigarettes were found to be more responsive to changes in cigarette price. Conclusions An additional tax added to the cost of cigarettes would bring about a reduction in cigarette consumption and increased tax revenues. It would also help reduce incidents smoking-related illnesses. The additional tax revenues generated by the tax increase could be used to offset the current financial deficiency of Taiwan's National Health Insurance program and provide better public services.

  20. Does the availability of single cigarettes promote or inhibit cigarette consumption? Perceptions, prevalence and correlates of single cigarette use among adult Mexican smokers

    Science.gov (United States)

    Thrasher, J F; Villalobos, V; Dorantes-Alonso, A; Arillo-Santillán, E; Cummings, K Michael; O’Connor, R; Fong, G T

    2009-01-01

    Background: Single cigarette use and its implications have rarely been studied among adults. Objective: To assess perceptions, prevalence and correlates of single cigarette purchase behaviour and its relation to harm reduction. Design: Focus group transcripts and cross-sectional data were analysed. Setting and participants: Focus groups among convenience samples of adult smokers in two Mexican cities and a population-based sample of 1079 adult smokers from the International Tobacco Control Policy Evaluation Project in four Mexican cities. Main outcome measures: Purchase of single cigarettes last time cigarettes were bought, frequency of purchasing single cigarettes in the previous month and intention to quit in the next 6 months. Results: Focus group data indicated that smokers bought single cigarettes as a harm reduction strategy. Survey data indicated that 38% of participants purchased single cigarettes in the last month and 10% purchased them the last time they bought cigarettes, with more frequent consumption among young adults and those with lower income. Purchasing single cigarettes was independently associated with the frequency of using single cigarettes to reduce consumption and, less consistently, with the frequency of being cued to smoke after seeing single cigarettes for sale. Using single cigarettes to reduce consumption was positively associated with quit intention, whereas being cued to smoke by single cigarettes was negatively associated with quit intention. Conclusions: Study results suggest that some adult Mexican smokers purchase single cigarettes as a method to limit, cut down on and even quit smoking. Nevertheless, promotion of the availability of single cigarettes as a harm reduction strategy could provide additional smoking cues that undermine quit attempts and promote youth smoking. PMID:19671535

  1. Associations of interleukin-1 gene cluster polymorphisms with C-reactive protein concentration and lung function decline in smoking-induced chronic obstructive pulmonary disease.

    Science.gov (United States)

    Wang, Yu; Shumansky, Karey; Sin, Don D; Man, S F Paul; Akhabir, Loubna; Connett, John E; Anthonisen, Nicholas R; Paré, Peter D; Sandford, Andrew J; He, Jian-Qing

    2015-01-01

    We reported association of haplotypes formed by IL-1b (IL1B)-511C/T (rs16944) and a variable number of tandem repeats (rs2234663) in intron 3 of IL-1 receptor antagonist (IL1RN) with rate of lung function decline in smoking-induced COPD. The aim of current study was to further investigate this association. We genotyped an additional 19 polymorphisms in IL1 cluster (including IL1A, IL1B and IL1RN) in non-Hispanic whites who had the fastest (n = 268) and the slowest (n = 292) decline of FEV1% predicted in the same study. We also analyzed the association of all 21 polymorphisms with serum CRP levels. None of 21 polymorphisms showed significant association with rate of decline of lung function or CRP levels after adjusting for multiple comparisons. Before adjusting for multiple comparisons, only IL1RN_19327 (rs315949) showed significant association with lung function decline (P = 0.03, additive model). The frequencies of genotypes containing the IL1RN_19327A allele were 71.9% and 62.2%, respectively in the fast and slow decline groups (P = 0.02, odds ratio = 1.6, 95% confidence interval = 1.1-2.3); the IL1B_5200 (rs1143633) and rs2234663 in IL1RN were associated with serum CRP levels (P=0.04 and 0.03, respectively). No single marker was significantly associated with either rate of lung function decline or serum CRP levels.

  2. Cigarette smoking, cadmium exposure, and zinc intake on obstructive lung disorder

    Directory of Open Access Journals (Sweden)

    Dowling Nicole

    2010-05-01

    Full Text Available Abstract Background and objective This study examined whether zinc intake was associated with lower risk of smoking-induced obstructive lung disorder through interplay with cadmium, one of major toxicants in cigarette smoke. Methods Data were obtained from a sample of 6,726 subjects aged 40+ from the Third National Health and Nutrition Examination Survey. The forced expiratory volume in 1 second (FEV1 and forced vital capacity (FVC were measured using spirometry. Gender-, ethnicity-, and age-specific equations were used to calculate the lower limit of normal (LLN to define obstructive lung disorder as: observed FEV1/FVC ratio and FEV1 below respective LLN. Zinc intake was assessed by questionnaire. Logistic regression analysis was applied to investigate the associations of interest. Results The analyses showed that an increased prevalence of obstructive lung disorder was observed among individuals with low zinc intake regardless of smoking status. The adjusted odds of lung disorder are approximately 1.9 times greater for subjects in the lowest zinc-intake tertile than those in the highest tertile (odds ratio = 1.89, 95% confidence interval = 1.22-2.93. The effect of smoking on lung function decreased considerably after adjusting for urinary cadmium. Protective association between the zinc-to-cadmium ratio (log-transformed and respiratory risk suggests that zinc may play a role in smoking-associated lung disorder by modifying the influence of cadmium. Conclusions While zinc intake is associated with lower risk of obstructive lung disorder, the role of smoking cession and/or prevention are likely to be more important given their far greater effect on respiratory risk. Future research is warranted to explore the mechanisms by which zinc could modify smoking-associated lung disease.

  3. Cigarette smoke exposure triggers the autophagic cascade via activation of the AMPK pathway in mice.

    Science.gov (United States)

    Furlong, Hayley C; Stämpfli, Martin R; Gannon, Anne M; Foster, Warren G

    2015-10-01

    We previously demonstrated that cigarette smoke (CS) exposure decreases primordial follicle counts and induces autophagy in ovarian granulosa cells in preference to apoptosis. Therefore, the objective of this study was to investigate molecular targets underlying smoke-induced activation of the reparative autophagy pathway in the ovary. Briefly, ovarian homogenates were prepared from adult female mice exposed to mainstream CS twice daily for 8 wk, using a whole-body exposure system. A gene array revealed that CS exposure induced a greater than 2-fold significant increase in the expression of proautophagic genes Cdkn1b, Map1lc3a, Bad, and Sqstm1/p62. A significant increase in Prkaa2, Pik3c3, and Maplc31b expression, as well as a significant decrease in Akt1 and Mtor expression, was detected by quantitative PCR. The 5'-AMP-activated protein kinase catalytic subunit (AMPK) alpha1 + alpha2 and ATG7 protein expression was significantly increased, whereas AKT1, mTOR, CDKN1B/p27, and CXCR4 proteins were significantly decreased in CS exposed versus control ovaries. Up-regulation of AMPK alpha1 + alpha2, a known initiator of autophagic signaling, and ATG7 further suggests activation of the autophagy cascade. Two prosurvival factors, AKT and mTOR, were decreased in expression, an outcome that favors induction of the autophagy pathway, whereas decreased levels of CDKN1B is suggestive of cell cycle dysregulation. In summary, our data suggest that CS exposure induces ovarian follicle loss through induction of the autophagic cascade via the AMPK pathway together with inhibition of antiautophagic markers AKT and mTOR. We further postulate that toxicant-induced dysregulation of reparative autophagy is a novel pathway central to impaired follicle development and subfertility. © 2015 by the Society for the Study of Reproduction, Inc.

  4. 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.

  5. Percutaneous mitral valve repair.

    Science.gov (United States)

    Gillinov, A Marc; Liddicoat, John R

    2006-01-01

    Surgical mitral valve repair is the procedure of choice to treat mitral regurgitation of all etiologies. Whereas annuloplasty is the cornerstone of mitral valve repair, a variety of other surgical techniques are utilized to correct dysfunction of the leaflets and subvalvular apparatus; in most cases, surgical repair entails application of multiple repair techniques in each patient. Preclinical studies and early human experience have demonstrated that some of these surgical repair techniques can be performed using percutaneous approaches. Specifically, there has been great progress in the development of novel technology to facilitate percutaneous annuloplasty and percutaneous edge-to-edge repair. The objectives of this report were to (1) discuss the surgical foundations for these percutaneous approaches; (2) review device design and experimental and clinical results of percutaneous valve repair; and (3) address future directions, including the key challenges of patient selection and clinical trial design.

  6. 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

  7. 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

  8. Psychiatric comorbidity in adolescent electronic and conventional cigarette use.

    Science.gov (United States)

    Leventhal, Adam M; Strong, David R; Sussman, Steve; Kirkpatrick, Matthew G; Unger, Jennifer B; Barrington-Trimis, Jessica L; Audrain-McGovern, Janet

    2016-02-01

    The popularity of electronic (e-) cigarettes has greatly increased recently, particularly in adolescents. However, the extent of psychiatric comorbidity with adolescent e-cigarette use and dual use of conventional (combustible) and e-cigarettes is unknown. This study characterized psychiatric comorbidity in adolescent conventional and e-cigarette use. Ninth grade students attending high schools in Los Angeles, CA (M age = 14) completed self-report measures of conventional/e-cigarette use, emotional disorders, substance use/problems, and transdiagnostic psychiatric phenotypes consistent with the NIMH-Research Domain Criteria Initiative. Outcomes were compared by lifetime use of: (1) neither conventional nor e-cigarettes (non-use; N = 2557, 77.3%); (2) e-cigarettes only (N = 412, 12.4%); (3) conventional cigarettes only (N = 152, 4.6%); and (4) conventional and e-cigarettes (dual use; N = 189, 5.6%). In comparison to adolescents who used conventional cigarettes only, e-cigarette only users reported lower levels of internalizing syndromes (depression, generalized anxiety, panic, social phobia, and obsessive-compulsive disorder) and transdiagnostic phenotypes (i.e., distress intolerance, anxiety sensitivity, rash action during negative affect). Depression, panic disorder, and anhedonia were higher in e-cigarette only vs. non-users. For several externalizing outcomes (mania, rash action during positive affect, alcohol drug use/abuse) and anhedonia, an ordered pattern was observed, whereby comorbidity was lowest in non-users, moderate in single product users (conventional or e-cigarette), and highest in dual users. These findings: (1) raise question of whether emotionally-healthier ('lower-risk') adolescents who are not interested in conventional cigarettes are being attracted to e-cigarettes; (2) indicate that research, intervention, and policy dedicated to adolescent tobacco-psychiatric comorbidity should distinguish conventional cigarette, e-cigarette, and dual use.

  9. 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.

  10. [Electronic cigarettes - effects on health. Previous reports].

    Science.gov (United States)

    Napierała, Marta; Kulza, Maksymilian; Wachowiak, Anna; Jabłecka, Katarzyna; Florek, Ewa

    2014-01-01

    Currently very popular in the market of tobacco products have gained electronic cigarettes (ang. E-cigarettes). These products are considered to be potentially less harmful in compared to traditional tobacco products. However, current reports indicate that the statements of the producers regarding to the composition of the e- liquids not always are sufficient, and consumers often do not have reliable information on the quality of the product used by them. This paper contain a review of previous reports on the composition of e-cigarettes and their impact on health. Most of the observed health effects was related to symptoms of the respiratory tract, mouth, throat, neurological complications and sensory organs. Particularly hazardous effects of the e-cigarettes were: pneumonia, congestive heart failure, confusion, convulsions, hypotension, aspiration pneumonia, face second-degree burns, blindness, chest pain and rapid heartbeat. In the literature there is no information relating to passive exposure by the aerosols released during e-cigarette smoking. Furthermore, the information regarding to the use of these products in the long term are not also available.

  11. Mapping Cigarettes Similarities using Cluster Analysis Methods

    Directory of Open Access Journals (Sweden)

    Lorentz Jäntschi

    2007-09-01

    Full Text Available The aim of the research was to investigate the relationship and/or occurrences in and between chemical composition information (tar, nicotine, carbon monoxide, market information (brand, manufacturer, price, and public health information (class, health warning as well as clustering of a sample of cigarette data. A number of thirty cigarette brands have been analyzed. Six categorical (cigarette brand, manufacturer, health warnings, class and four continuous (tar, nicotine, carbon monoxide concentrations and package price variables were collected for investigation of chemical composition, market information and public health information. Multiple linear regression and two clusterization techniques have been applied. The study revealed interesting remarks. The carbon monoxide concentration proved to be linked with tar and nicotine concentration. The applied clusterization methods identified groups of cigarette brands that shown similar characteristics. The tar and carbon monoxide concentrations were the main criteria used in clusterization. An analysis of a largest sample could reveal more relevant and useful information regarding the similarities between cigarette brands.

  12. Electronic Cigarette and Traditional Cigarette Use among Middle and High School Students in Florida, 2011-2014.

    Science.gov (United States)

    Porter, Lauren; Duke, Jennifer; Hennon, Meredith; Dekevich, David; Crankshaw, Erik; Homsi, Ghada; Farrelly, Matthew

    2015-01-01

    Recent youth trends in the prevalence of e-cigarette and traditional cigarette use in Florida were examined in a cross-sectional, representative state sample from 2011 to 2014. Traditional cigarette use among youth declined during the study period. Experimentation with and past 30-day use of e-cigarettes among Florida youth tripled over 4 years. Past 30-day e-cigarette use exceeded traditional cigarette use in 2014; 10.8% of high school and 4.0% of middle school students reported recent e-cigarette use, compared with 8.7% of high school and 2.9% of middle school students for traditional cigarettes (P4, 20.5% of high school and 8.5% of middle school students reported ever use of e-cigarettes. Among ever e-cigarette users in 2014, 30.3% of high school and 42.2% of middle school students had never smoked traditional cigarettes. Given the concern that significant rates of e-cigarette use by U.S. adolescents may have a negative effect on public health, further review of e-cigarette advertising, marketing, sales, and use among U.S. youth is warranted.

  13. Electronic Cigarette and Traditional Cigarette Use among Middle and High School Students in Florida, 2011-2014.

    Directory of Open Access Journals (Sweden)

    Lauren Porter

    Full Text Available Recent youth trends in the prevalence of e-cigarette and traditional cigarette use in Florida were examined in a cross-sectional, representative state sample from 2011 to 2014. Traditional cigarette use among youth declined during the study period. Experimentation with and past 30-day use of e-cigarettes among Florida youth tripled over 4 years. Past 30-day e-cigarette use exceeded traditional cigarette use in 2014; 10.8% of high school and 4.0% of middle school students reported recent e-cigarette use, compared with 8.7% of high school and 2.9% of middle school students for traditional cigarettes (P<0.001. By 2014, 20.5% of high school and 8.5% of middle school students reported ever use of e-cigarettes. Among ever e-cigarette users in 2014, 30.3% of high school and 42.2% of middle school students had never smoked traditional cigarettes. Given the concern that significant rates of e-cigarette use by U.S. adolescents may have a negative effect on public health, further review of e-cigarette advertising, marketing, sales, and use among U.S. youth is warranted.

  14. Do increases in cigarette prices lead to increases in sales of cigarettes with high tar and nicotine yields?

    Science.gov (United States)

    Farrelly, Matthew C; Loomis, Brett R; Mann, Nathan H

    2007-10-01

    We used scanner data on cigarette prices and sales collected from supermarkets across the United States from 1994 to 2004 to test the hypothesis that cigarette prices are positively correlated with sales of cigarettes with higher tar and nicotine content. During this period the average inflation-adjusted price for menthol cigarettes increased 55.8%. Price elasticities from multivariate regression models suggest that this price increase led to an increase of 1.73% in sales-weighted average tar yields and a 1.28% increase in sales-weighted average nicotine yields for menthol cigarettes. The 50.5% price increase of nonmenthol varieties over the same period yielded an estimated increase of 1% in tar per cigarette but no statistically significant increase in nicotine yields. An ordered probit model of the impact of cigarette prices on cigarette strength (ultra-light, light, full flavor, unfiltered) offers an explanation: As cigarette prices increase, the probability that stronger cigarette types will be sold increases. This effect is larger for menthol than for nonmenthol cigarettes. Our results are consistent with earlier population-based cross-sectional and longitudinal studies showing that higher cigarette prices and taxes are associated with increasing consumption of higher-yield cigarettes by smokers.

  15. Exposure Calls to U. S. Poison Centers Involving Electronic Cigarettes and Conventional Cigarettes-September 2010-December 2014.

    Science.gov (United States)

    Chatham-Stephens, Kevin; Law, Royal; Taylor, Ethel; Kieszak, Stephanie; Melstrom, Paul; Bunnell, Rebecca; Wang, Baoguang; Day, Hannah; Apelberg, Benjamin; Cantrell, Lee; Foster, Howell; Schier, Joshua G

    2016-12-01

    E-cigarette use is increasing, and the long-term impact on public health is unclear. We described the acute adverse health effects from e-cigarette exposures reported to U.S. poison centers. We compared monthly counts and demographic, exposure, and health effects data of calls about e-cigarettes and conventional cigarettes made to poison centers from September 2010 through December 2014. Monthly e-cigarette calls increased from 1 in September 2010, peaked at 401 in April 2014, and declined to 295 in December 2014. Monthly conventional cigarette calls during the same period ranged from 302 to 514. E-cigarette calls were more likely than conventional cigarette calls to report adverse health effects, including vomiting, eye irritation, and nausea. Five e-cigarette calls reported major health effects, such as respiratory failure, and there were two deaths associated with e-cigarette calls. E-cigarette calls to U.S. poison centers increased over the study period, and were more likely than conventional cigarettes to report adverse health effects. It is important for health care providers and the public to be aware of potential acute health effects from e-cigarettes. Developing strategies to monitor and prevent poisonings from these novel devices is critical.

  16. E-Cigarettes Not Good to Gums, Study Finds

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_162118.html E-Cigarettes Not Good to Gums, Study Finds Nicotine, ... in New York exposed nonsmokers' gum tissue to e-cigarette vapors. Their findings appear to counter arguments ...

  17. 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...

  18. 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...

  19. Progressions of alcohol, cigarette, and marijuana use in adolescence.

    Science.gov (United States)

    Duncan, S C; Duncan, T E; Hops, H

    1998-08-01

    This study examined the progressive relations among adolescent use of alcohol, cigarettes and marijuana using latent growth curve analyses. Specifically, the present study examined three models to determine (1) the effect of prior cigarette use on alcohol use and development and the relationship between change in cigarette use and the development of alcohol use (N = 115), (2) the effect of prior alcohol use on cigarette use and development and the relationship between change in alcohol use and the development of cigarette use (N = 199); and (3) the effect of prior alcohol and cigarette use on marijuana use and development, and the relationship between change in alcohol use and cigarette use and the development, of marijuana use (N = 287). Support was found for the relation between prior levels of substance use and involvement in other substances. Cigarette use, in particular, was particularly important in the subsequent involvement of alcohol and marijuana.

  20. FDA to Weigh Dangers of Exploding E-Cigarettes

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_162849.html FDA to Weigh Dangers of Exploding E-Cigarettes Agency ... The Associated Press reported last month that the FDA had identified 66 instances of e-cigarette explosions ...

  1. 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 ...

  2. Toxic Metals Found in E-Cigarette Liquid

    Science.gov (United States)

    ... news/fullstory_163492.html Toxic Metals Found in E-Cigarette Liquid Their presence in 5 brands studied is ... the metals end up in the aerosol that e-cigarette users inhale," said study leader Ana Maria Rule, ...

  3. The Implications of Sidestream Cigarette Smoke for Cardiovascular Health.

    Science.gov (United States)

    Hurshman, Larry G.; And Others

    1978-01-01

    Non-smokers exposed to emissions from a burning cigarette in ambient air demonstrate measureable physiological responses. The study showed that work capacity was reduced as a result of exposure to their sidestream cigarette smoke. (RE)

  4. Characterisation of the Draw Resistance Across a Lit Cigarette

    Directory of Open Access Journals (Sweden)

    Colard S

    2014-12-01

    Full Text Available The consumer senses and reacts to the draw resistance of the cigarette after it is lit. In spite of this obvious fact, this physical parameter is usually measured under standard conditions on the unlit cigarette (1. In order to evaluate more accurately the smokers’ perception during the course of cigarette smoking, the theoretical aspects of the draw resistance measurement of a lit cigarette have been studied and an experimental device has been developed.

  5. 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

  6. 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.

  7. Are increases in cigarette taxation regressive?

    Science.gov (United States)

    Borren, P; Sutton, M

    1992-12-01

    Using the latest published data from Tobacco Advisory Council surveys, this paper re-evaluates the question of whether or not increases in cigarette taxation are regressive in the United Kingdom. The extended data set shows no evidence of increasing price-elasticity by social class as found in a major previous study. To the contrary, there appears to be no clear pattern in the price responsiveness of smoking behaviour across different social classes. Increases in cigarette taxation, while reducing smoking levels in all groups, fall most heavily on men and women in the lowest social class. Men and women in social class five can expect to pay eight and eleven times more of a tax increase respectively, than their social class one counterparts. Taken as a proportion of relative incomes, the regressive nature of increases in cigarette taxation is even more pronounced.

  8. 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.

  9. A propulsion injury following a spontaneous electronic cigarette explosion

    Directory of Open Access Journals (Sweden)

    Cherrie Chan Yiru

    2017-05-01

    Full Text Available Electronic cigarettes (e-cigarettes have become increasingly popular at an alarming rate. This coincides with the public perception that they are a safer mean of nicotine consumption. Unregulated devices carry unrecognized safety risks that have led to numerous cases of burns, associating with spontaneous combustions of e-cigarettes.

  10. 76 FR 57008 - Smoking of Electronic Cigarettes on Aircraft

    Science.gov (United States)

    2011-09-15

    ... Office of the Secretary 14 CFR Part 252 RIN 2105-AE06 Smoking of Electronic Cigarettes on Aircraft AGENCY... service on other charter flights where smoking is not banned. Electronic cigarettes were introduced into... cigarettes the issue has been raised as to whether the statutory ban on smoking in section 41706 and existing...

  11. Food and Drug Administration Evaluation and Cigarette Smoking Risk Perceptions

    Science.gov (United States)

    Kaufman, Annette R.; Waters, Erika A.; Parascandola, Mark; Augustson, Erik M.; Bansal-Travers, Maansi; Hyland, Andrew; Cummings, K. Michael

    2011-01-01

    Objectives: To examine the relationship between a belief about Food and Drug Administration (FDA) safety evaluation of cigarettes and smoking risk perceptions. Methods: A nationally representative, random-digit-dialed telephone survey of 1046 adult current cigarette smokers. Results: Smokers reporting that the FDA does not evaluate cigarettes for…

  12. E-Cigarettes and Young People: A Public Health Concern

    Science.gov (United States)

    ... this? Submit Button Past Emails E-Cigarettes and Young People: A Public Health Concern Language: English Español (Spanish) ... justify efforts to prevent e-cigarette use by young people. We know that the vapor from e-cigarettes ...

  13. Electronic Cigarette Retail Outlets and Proximity to Schools.

    Science.gov (United States)

    Hahn, Ellen J; Begley, Kathy; Gokun, Yevgeniya; Johnson, Andrew O; Mundy, Monica E; Rayens, Mary Kay

    2015-01-01

    To compare the retail distribution and density per population of electronic and conventional cigarettes in smoke-free communities with and without e-cigarette restrictions. A cross-sectional study with field observations of retail tobacco stores. Two Central Kentucky counties with 100% smoke-free workplace regulations; counties selected on the basis of whether e-cigarette use was restricted. Fifty-seven tobacco retailers in two counties, including conventional retailers and stand-alone e-cigarette stores. Type and location of store and products sold; addresses of stores and schools geocoded with ArcGIS. Bivariate comparisons between counties, rates and confidence intervals for frequency of tobacco retailers and e-cigarette stores per population. Fifty-three percent of tobacco retailers sold e-cigarettes. E-cigarette availability did not differ by whether smoke-free regulation covered e-cigarettes. Rates of tobacco retailers and e-cigarette distributors per 10,000 were 8.29 and 4.40, respectively, in the two-county area. Of the 40 schools, 88% had a tobacco retailer and 68% had an e-cigarette distributor within 1 mile. In this exploratory study, e-cigarette use restriction was not related to store availability. For a relatively new product, e-cigarettes were readily available in retail outlets and close to schools.

  14. Cigarette promotional offers: who takes advantage?

    Science.gov (United States)

    White, Victoria M; White, Martha M; Freeman, Karen; Gilpin, Elizabeth A; Pierce, John P

    2006-03-01

    Promotional offers on cigarettes (e.g., dollar-off, multipack discounts) composed the largest share of tobacco industry marketing expenditures, totaling $8.9 billion, or 72% of the total budget in 2002. Internal industry documents indicate that young adults, potential quitters, and other price-sensitive groups are the targets of these marketing tactics. How effective they are in actually reaching these groups in the general population of smokers has not yet been investigated. Data were from 4618 current smokers responding to the large, random-digit-dialed population-based 2002 California Tobacco Survey. The characteristics were identified of smokers who reported that they used these offers "every time I see one." Thirty-five percent of smokers used promotional offers every time they saw one. Multivariate analyses identified young adults, women, African Americans, those with higher daily cigarette consumption, and those worried about cigarette costs as more likely to use promotional offers at every opportunity. Smokers most committed to quitting were no more likely to use promotional offers than those with no intention to quit. Cigarette brand was highly correlated with age and race/ethnicity, and therefore was not included in the multivariate analysis. Those who smoked menthol cigarettes and Camels, more often young adults and African Americans, were much more likely than those of other brands to use promotional offers. With the exception of smokers intending to quit, cigarette promotional offers are effectively reaching most industry-targeted groups. Importantly, young adults, who have the greatest long-term customer potential, are responding.

  15. Optimality in DNA repair.

    Science.gov (United States)

    Richard, Morgiane; Fryett, Matthew; Miller, Samantha; Booth, Ian; Grebogi, Celso; Moura, Alessandro

    2012-01-07

    DNA within cells is subject to damage from various sources. Organisms have evolved a number of mechanisms to repair DNA damage. The activity of repair enzymes carries its own risk, however, because the repair of two nearby lesions may lead to the breakup of DNA and result in cell death. We propose a mathematical theory of the damage and repair process in the important scenario where lesions are caused in bursts. We use this model to show that there is an optimum level of repair enzymes within cells which optimises the cell's response to damage. This optimal level is explained as the best trade-off between fast repair and a low probability of causing double-stranded breaks. We derive our results analytically and test them using stochastic simulations, and compare our predictions with current biological knowledge.

  16. Airway Epithelial Barrier Dysfunction in COPD: Role of Cigarette Smoke Exposure.

    Science.gov (United States)

    Aghapour, Mahyar; Raee, Pourya; Moghaddam, Seyed Javad; Hiemstra, Pieter S; Heijink, Irene H

    2017-09-21

    The epithelial lining of the airway forms the first barrier against environmental insults such as inhaled cigarette smoke, which is the primary risk factor for the development of chronic obstructive pulmonary disease (COPD). The barrier is formed by airway epithelial junctions, which are interconnected structures that restrict permeability to inhaled pathogens and environmental stressors. Destruction of the epithelial barrier not only exposes subepithelial layers to hazardous agents in the inspired air, but also alters the normal function of epithelial cells, which may eventually contribute to the development of COPD. Of note, disruption of epithelial junctions may lead to modulation of signaling pathways involved in differentiation, repair and pro-inflammatory responses. Epithelial barrier dysfunction may be particularly relevant in COPD, where repeated injury by cigarette smoke exposure, pathogens, inflammatory mediators and impaired epithelial regeneration may compromise the barrier function. In the current review, we discuss recent advances in understanding the mechanisms of barrier dysfunction in COPD, as well as the molecular mechanisms that underlie the impaired repair response of the injured epithelium in COPD and its inability to re-differentiate into a functionally intact epithelium.

  17. Effects of experimental income on demand for potentially real cigarettes.

    Science.gov (United States)

    Koffarnus, Mikhail N; Wilson, Arlington George; Bickel, Warren K

    2015-03-01

    Cigarette demand, or the change in cigarette consumption as a function of price, is a measure of reinforcement that is associated with level of tobacco dependence and other clinically relevant measures, but the effects of experimentally controlled income on real-world cigarette consumption have not been examined. In this study, income available for cigarette purchases was manipulated to assess the effect on cigarette demand. Tobacco-dependent cigarette smokers (n = 15) who smoked 10-40 cigarettes per day completed a series of cigarette purchasing tasks under a variety of income conditions meant to mimic different weekly cigarette budgets: $280, approximately $127, $70, or approximately $32 per week. Prices of $0.12, $0.25, $0.50, and $1.00 per cigarette were assessed in each income condition. Participants were instructed to purchase as many cigarettes as they would like for the next week and to only consume cigarettes purchased in the context of the study. One price in 1 income condition was randomly chosen to be "real," and the cigarettes and the excess money in the budget for that condition were given to the participant. Results indicate that demand elasticity was negatively correlated with income. Demand intensity (consumption at low prices) was unrelated to income condition and remained high across incomes. These results indicate that the amount of income that is available for cigarette purchases has a large effect on cigarette consumption, but only at high prices. © The Author 2014. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  18. The electronic cigarette: potential health benefit or mere business?

    Science.gov (United States)

    De Marco, Cinzia; Invernizzi, Giovanni; Bosi, Sandra; Pozzi, Paolo; Di Paco, Adriano; Mazza, Roberto; Ruprecht, Ario Alberto; Munarini, Elena; Boffi, Roberto

    2013-01-01

    Electronic cigarettes (e-cigarettes) have attracted considerable attention as a possible alternative to tobacco cigarettes, but uncertainties about their impact on health and indoor air quality as well as their commercial success without a clear regulatory framework are arousing concern. We have therefore tried to summarize the health-related implications of the use of e-cigarettes in order to help physicians and health professionals provide accurate information on this device. Given the lack of unequivocal scientific data on their toxicity and safety, we conclude that at the moment there is no reason to approve e-cigarettes as a safe alternative to tobacco smoke.

  19. Electronic cigarettes: a safer alternative or potential poison?

    Science.gov (United States)

    Smith, Janet E

    2014-10-01

    Electronic cigarettes have been marketed as a safer alternative to cigarettes, and their use is expanding exponentially. However, there is a severe lack of scientific data about the ingredients in the liquid used in the device and the health consequences of using electronic cigarettes. As technology has outpaced regulations, the production and sale of electronic cigarettes are, as yet, unregulated and do not fall under the purview of the Food and Drug Administration. This article will review the mechanism of action and what is currently known about the safety of electronic cigarettes. The risk of poisoning for children will also be identified, as well as the implications for home healthcare clinicians.

  20. Repairs of composite structures

    Science.gov (United States)

    Roh, Hee Seok

    Repair on damaged composite panels was conducted. To better understand adhesively bonded repair, the study investigates the effect of design parameters on the joint strength. The design parameters include bondline length, thickness of adherend and type of adhesive. Adhesives considered in this study were tested to measure their tensile material properties. Three types of adhesively bonded joints, single strap, double strap, and single lap joint were considered under changing bondline lengths, thickness of adherend and type of adhesive. Based on lessons learned from bonded joints, a one-sided patch repair method for composite structures was conducted. The composite patch was bonded to the damaged panel by either film adhesive FM-73M or paste adhesive EA-9394 and the residual strengths of the repaired specimens were compared under varying patch sizes. A new repair method using attachments has been suggested to enhance the residual strength. Results obtained through experiments were analyzed using finite element analysis to provide a better repair design and explain the experimental results. It was observed that the residual strength of the repaired specimen was affected by patch length. Method for rapid repairs of damaged composite structures was investigated. The damage was represented by a circular hole in a composite laminated plate. Pre-cured composite patches were bonded with a quick-curing commercial adhesive near (rather than over) the hole. Tensile tests were conducted on specimens repaired with various patch geometries. The test results showed that, among the methods investigated, the best repair method restored over 90% of the original strength of an undamaged panel. The interfacial stresses in the adhesive zone for different patches were calculated in order to understand the efficiencies of the designs of these patch repairs. It was found that the composite patch that yielded the best strength had the lowest interfacial peel stress between the patch and

  1. Cigarettes Butts and the Case for an Environmental Policy on Hazardous Cigarette Waste

    Directory of Open Access Journals (Sweden)

    Richard Barnes

    2009-05-01

    Full Text Available Discarded cigarette butts are a form of non-biodegradable litter. Carried as runoff from streets to drains, to rivers, and ultimately to the ocean and its beaches, cigarette filters are the single most collected item in international beach cleanups each year. They are an environmental blight on streets, sidewalks, and other open areas. Rather than being a protective health device, cigarette filters are primarily a marketing tool to help sell ‘safe’ cigarettes. They are perceived by much of the public (especially current smokers to reduce the health risks of smoking through technology. Filters have reduced the machine-measured yield of tar and nicotine from burning cigarettes, but there is controversy as to whether this has correspondingly reduced the disease burden of smoking to the population. Filters actually may serve to sustain smoking by making it seem less urgent for smokers to quit and easier for children to initiate smoking because of reduced irritation from early experimentation. Several options are available to reduce the environmental impact of cigarette butt waste, including developing biodegradable filters, increasing fines and penalties for littering butts, monetary deposits on filters, increasing availability of butt receptacles, and expanded public education. It may even be possible to ban the sale of filtered cigarettes altogether on the basis of their adverse environmental impact. This option may be attractive in coastal regions where beaches accumulate butt waste and where smoking indoors is increasingly prohibited. Additional research is needed on the various policy options, including behavioral research on the impact of banning the sale of filtered cigarettes altogether.

  2. Beliefs About the Direct Comparison of E-Cigarettes and Cigarettes.

    Science.gov (United States)

    Hershberger, Alexandra R; Karyadi, Kenny A; VanderVeen, J Davis; Cyders, Melissa A

    2017-07-03

    Recent data suggests that positive beliefs about electronic cigarettes (e-cigs) use can lead to later e-cig use. Considering that many advertisements claim that e-cigs are superior to cigarettes, individuals' likelihood to view e-cigs more favorably than cigarettes can also influence subsequent e-cig use; however, no studies have directly assessed such a comparison. The present study created and validated the Comparing E-Cigarettes and Cigarettes questionnaire (CEAC), which asks individuals to directly compare e-cigs and cigarettes on a number of dimensions, in two independent samples. In sample 1 (451 undergraduates; mean age = 20.35, SD = 5.44, 72.4% female, 73.4% Caucasian) we explored the factor structure of the CEAC and in sample 2 (699 community adults collected via Amazon's Mechanical Turk; mean age = 34.04, SD = 10.9, 47.7% female, 83.3% Caucasian) we replicated the factor structure. Exploratory factor analysis suggested a three-factor structure: General Benefits (α = 0.80), General Effects (α = 0.86), and Health Benefits (α = 0.88), which was replicated via confirmatory factor analysis, χ(2) = 4.36; RMSEA = 0.07, 90% CI = 0.06-0.08; TLI = 0.99; CFI = 0.99, and was relatively invariant across product use and gender. Individuals reported viewing e-cigs as safer and more beneficial than cigarettes and these beliefs were higher in e-cig users. Future work should establish how these comparative beliefs are influenced by e-cig use and/or influence subsequent transition to and increases in e-cig use. Although e-cigs are likely less harmful than cigarettes, and thus these comparative beliefs represent that state of nature, e-cigs are not completely without risk.

  3. Cigarettes butts and the case for an environmental policy on hazardous cigarette waste.

    Science.gov (United States)

    Novotny, Thomas E; Lum, Kristen; Smith, Elizabeth; Wang, Vivian; Barnes, Richard

    2009-05-01

    Discarded cigarette butts are a form of non-biodegradable litter. Carried as runoff from streets to drains, to rivers, and ultimately to the ocean and its beaches, cigarette filters are the single most collected item in international beach cleanups each year. They are an environmental blight on streets, sidewalks, and other open areas. Rather than being a protective health device, cigarette filters are primarily a marketing tool to help sell 'safe' cigarettes. They are perceived by much of the public (especially current smokers) to reduce the health risks of smoking through technology. Filters have reduced the machine-measured yield of tar and nicotine from burning cigarettes, but there is controversy as to whether this has correspondingly reduced the disease burden of smoking to the population. Filters actually may serve to sustain smoking by making it seem less urgent for smokers to quit and easier for children to initiate smoking because of reduced irritation from early experimentation. Several options are available to reduce the environmental impact of cigarette butt waste, including developing biodegradable filters, increasing fines and penalties for littering butts, monetary deposits on filters, increasing availability of butt receptacles, and expanded public education. It may even be possible to ban the sale of filtered cigarettes altogether on the basis of their adverse environmental impact. This option may be attractive in coastal regions where beaches accumulate butt waste and where smoking indoors is increasingly prohibited. Additional research is needed on the various policy options, including behavioral research on the impact of banning the sale of filtered cigarettes altogether.

  4. Reasons for Starting and Stopping Electronic Cigarette Use

    Directory of Open Access Journals (Sweden)

    Jessica K. Pepper

    2014-10-01

    Full Text Available The aim of our study was to explore reasons for starting and then stopping electronic cigarette (e-cigarette use. Among a national sample of 3878 U.S. adults who reported ever trying e-cigarettes, the most common reasons for trying were curiosity (53%; because a friend or family member used, gave, or offered e-cigarettes (34%; and quitting or reducing smoking (30%. Nearly two-thirds (65% of people who started using e-cigarettes later stopped using them. Discontinuation was more common among those whose main reason for trying was not goal-oriented (e.g., curiosity than goal-oriented (e.g., quitting smoking (81% vs. 45%, p < 0.001. The most common reasons for stopping e-cigarette use were that respondents were just experimenting (49%, using e-cigarettes did not feel like smoking cigarettes (15%, and users did not like the taste (14%. Our results suggest there are two categories of e-cigarette users: those who try for goal-oriented reasons and typically continue using and those who try for non-goal-oriented reasons and then typically stop using. Research should distinguish e-cigarette experimenters from motivated users whose decisions to discontinue relate to the utility or experience of use. Depending on whether e-cigarettes prove to be effective smoking cessation tools or whether they deter cessation, public health programs may need distinct strategies to reach and influence different types of users.

  5. Cigarette sales in pharmacies in the USA (2005-2009).

    Science.gov (United States)

    Seidenberg, Andrew B; Behm, Ilan; Rees, Vaughan W; Connolly, Gregory N

    2012-09-01

    Several US jurisdictions have adopted policies prohibiting pharmacies from selling tobacco products. Little is known about how pharmacies contribute to total cigarette sales. Pharmacy and total cigarette sales in the USA were tabulated from AC Nielsen and Euromonitor, respectively, for the years 2005-2009. Linear regression was used to characterise trends over time, with observed trends extrapolated to 2020. Between 2005 and 2009, pharmacy cigarette sales increased 22.72% (p=0.004), while total cigarette sales decreased 17.43% (p=0.015). In 2005, pharmacy cigarette sales represented 3.05% of total cigarette sales, increasing to 4.54% by 2009. Extrapolation of these findings resulted in estimated pharmacy cigarette sales of 14.59% of total US cigarette sales by 2020. Cigarette sales in American pharmacies have risen in recent years, while cigarette sales nationally have declined. If current trends continue, pharmacy cigarette market share will, by 2020, increase to more than four times the 2005 share.

  6. Health Considerations in Regulation and Taxation of Electronic Cigarettes.

    Science.gov (United States)

    Mainous, Arch G; Tanner, Rebecca J; Mainous, Ryan W; Talbert, Jeffery

    2015-01-01

    The use of electronic cigarettes (e-cigarettes) is experiencing unprecedented growth. This can be contrasted to the use of conventional cigarettes which showed a decrease among adults with the current smoker prevalence dropping from 20.9% in 2005 to 17.8% in 2013. There is some data that e-cigarettes are attracting both former smokers and never smokers, and in particular, young people as users. Currently most states do not tax e-cigarettes. Taxation and regulation may have a similar overall goal of decreasing smoking but regulation tends to focus reduced availability of products. In terms of tobacco control, taxation focuses on the demand side of the equation. Taxation is a distinct strategy from regulation and has been shown to decrease new adopters of conventional cigarettes. A variety of potential taxation strategies can be considered by policymakers based on different assumptions about e-cigarettes and their utility, ranging from untaxed to taxation at moderate levels compared to conventional cigarettes to taxation equal to conventional cigarettes. Until more evidence for the benefits of e-cigarettes is presented, it seems prudent to view them as a potentially harmful and addictive product that ought to be regulated and taxed in an equivalent manner to conventional cigarettes.

  7. 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.

  8. Cigarette smoking and progression in multiple sclerosis

    NARCIS (Netherlands)

    Koch, Marcus; van Harten, Annemarie; Uyttenboogaart, Maarten; De Keyser, Jacques

    2007-01-01

    Objective: To investigate the influence of cigarette smoking on progression and disability accumulation in multiple sclerosis ( MS). Methods: Information on past and present smoking of 364 patients with MS was obtained through a structured questionnaire survey. We used Kaplan-Meier analyses and Cox

  9. Cigarette smoking and progression in multiple sclerosis

    NARCIS (Netherlands)

    Koch, Marcus; van Harten, Annemarie; Uyttenboogaart, Maarten; De Keyser, Jacques

    2007-01-01

    OBJECTIVE: To investigate the influence of cigarette smoking on progression and disability accumulation in multiple sclerosis (MS). METHODS: Information on past and present smoking of 364 patients with MS was obtained through a structured questionnaire survey. We used Kaplan-Meier analyses and Cox r

  10. The Psychology of Cigarette Advertising: Professional Puffery

    Science.gov (United States)

    Fine, Gary Alan

    1974-01-01

    Concludes that cigarette advertising both exploits and creates popular culture, and that the popular culture is intimately tied to the cognitive and affective mechanisms of people. Available from: Editor, Journal of Popular Culture, University Hall, Bowling Green University, Bowling Green, Ohio 43403. (RB)

  11. DNA repair: Dynamic defenders against cancer and aging

    Energy Technology Data Exchange (ETDEWEB)

    Fuss, Jill O.; Cooper, Priscilla K.

    2006-04-01

    You probably weren't thinking about your body's cellular DNA repair systems the last time you sat on the beach in the bright sunshine. Fortunately, however, while you were subjecting your DNA to the harmful effects of ultraviolet light, your cells were busy repairing the damage. The idea that our genetic material could be damaged by the sun was not appreciated in the early days of molecular biology. When Watson and Crick discovered the structure of DNA in 1953 [1], it was assumed that DNA is fundamentally stable since it carries the blueprint of life. However, over 50 years of research have revealed that our DNA is under constant assault by sunlight, oxygen, radiation, various chemicals, and even our own cellular processes. Cleverly, evolution has provided our cells with a diverse set of tools to repair the damage that Mother Nature causes. DNA repair processes restore the normal nucleotide sequence and DNA structure of the genome after damage [2]. These responses are highly varied and exquisitely regulated. DNA repair mechanisms are traditionally characterized by the type of damage repaired. A large variety of chemical modifications can alter normal DNA bases and either lead to mutations or block transcription if not repaired, and three distinct pathways exist to remove base damage. Base excision repair (BER) corrects DNA base alterations that do not distort the overall structure of the DNA helix such as bases damaged by oxidation resulting from normal cellular metabolism. While BER removes single damaged bases, nucleotide excision repair (NER) removes short segments of nucleotides (called oligonucleotides) containing damaged bases. NER responds to any alteration that distorts the DNA helix and is the mechanism responsible for repairing bulky base damage caused by carcinogenic chemicals such as benzo [a]pyrene (found in cigarette smoke and automobile exhaust) as well as covalent linkages between adjacent pyrimidine bases resulting from the ultraviolet

  12. Counseling patients on the use of electronic cigarettes.

    Science.gov (United States)

    Ebbert, Jon O; Agunwamba, Amenah A; Rutten, Lila J

    2015-01-01

    Electronic cigarettes (e-cigarettes) have substantially increased in popularity. Clear evidence about the safety of e-cigarettes is lacking, and laboratory experiments and case reports suggest these products may be associated with potential adverse health consequences. The effectiveness of e-cigarettes for smoking cessation is modest and appears to be comparable to the nicotine patch combined with minimal behavioral support. Although a role for e-cigarettes in the treatment of tobacco dependence may emerge in the future, the potential risk of e-cigarettes outweighs their known benefit as a recommended tobacco treatment strategy by clinicians. Patients should be counseled on the known efficacy and potential risks of e-cigarettes.

  13. [Summary of the existing knowledge about electronic cigarettes].

    Science.gov (United States)

    Cselkó, Zsuzsa; Pénzes, Melinda

    2016-06-19

    The decreasing proportion of smokers due to smoking restrictions have led producers to invent and disseminate electronic cigarettes (e-cigarettes) worldwide as a new form of nicotine enjoyment. This review summarizes the existing knowledge about e-cigarettes based on publications of PubMed, and on reviews and research data published by national and international scientific institutions. Present knowledge about the composition of e-cigarettes confirms that they are harmful products since their vapor is equally detrimental to the health of users and bystanders. Their benefits in smoking cessation still have not been justified by adequate scientific evidence, however, it has been proven that e-cigarettes uphold nicotine addiction and may increase the risk of starting conventional cigarette use by youth. In order to ensure the results of tobacco control policy and to assist smoking cessation, the same regulations are to be applied to e-cigarettes as to conventional tobacco products.

  14. E-cigarette Marketing and Older Smokers: Road to Renormalization

    Science.gov (United States)

    Cataldo, Janine K.; Petersen, Anne Berit; Hunter, Mary; Wang, Julie; Sheon, Nicolas

    2015-01-01

    Objectives To describe older smokers’ perceptions of risks and use of e-cigarettes, and their responses to marketing and knowledge of, and opinions about, regulation of e-cigarettes. Methods Eight 90-minute focus groups with 8 to 9 participants met in urban and suburban California to discuss topics related to cigarettes and alternative tobacco products. Results Older adults are using e-cigarettes for cessation and as a way to circumvent no-smoking policies; they have false perceptions about the effectiveness and safety of e-cigarettes. They perceive e-cigarette marketing as a way to renormalize smoking. Conclusions To stem the current epidemic of nicotine addiction, the FDA must take immediate action because e-cigarette advertising promotes dual use and may contribute to the renormalization of smoking. PMID:25741681

  15. Workshop on DNA repair.

    NARCIS (Netherlands)

    A.R. Lehmann (Alan); J.H.J. Hoeijmakers (Jan); A.A. van Zeeland (Albert); C.M.P. Backendorf (Claude); B.A. Bridges; A. Collins; R.P.D. Fuchs; G.P. Margison; R. Montesano; E. Moustacchi; A.T. Natarajan; M. Radman; A. Sarasin; E. Seeberg; C.A. Smith; M. Stefanini (Miria); L.H. Thompson; G.P. van der Schans; C.A. Weber (Christine); M.Z. Zdzienika

    1992-01-01

    textabstractA workshop on DNA repair with emphasis on eukaryotic systems was held, under the auspices of the EC Concerted Action on DNA Repair and Cancer, at Noordwijkerhout (The Netherlands) 14-19 April 1991. The local organization of the meeting was done under the auspices of the Medical Genetic C

  16. Laparoscopic lumbar hernia repair.

    Science.gov (United States)

    Madan, Atul K; Ternovits, Craig A; Speck, Karen E; Pritchard, F Elizabeth; Tichansky, David S

    2006-04-01

    Lumbar hernias are rare clinical entities that often pose a challenge for repair. Because of the surrounding anatomy, adequate surgical herniorraphy is often difficult. Minimally invasive surgery has become an option for these hernias. Herein, we describe two patients with lumbar hernias (one with a recurrent traumatic hernia and one with an incisional hernia). Both of these hernias were successfully repaired laparoscopically.

  17. The effect of e-cigarette warning labels on college students' perception of e-cigarettes and intention to use e-cigarettes.

    Science.gov (United States)

    Lee, Hsiao-Yun; Lin, Hsien-Chang; Seo, Dong-Chul; Lohrmann, David K

    2018-01-01

    This study examined the effect of two e-cigarette warning labels on college students' perceived advantages and risks of e-cigarette use, as well as students' intentions to use e-cigarettes. The company-produced e-cigarette warning label carries abundant information with small font size while the governmental warning label has only two sentences presented in large font size. The effect of both labels have not yet been examined and verified. Data were collected in October 2015 from college students at a Midwestern university. A pretest-posttest design was employed with 338 students exposed to the warning label proposed by the FDA and 328 students exposed to the label created by e-cigarette companies. Structural equation modeling analysis was implemented to examine the effect of warning labels with the analytical model grounded in the Theory of Planned Behavior. Findings showed that college students' perceived advantages of e-cigarette use were positively related to their intentions to use e-cigarettes, while perceived risks were negatively associated with their intentions. When comparing two labels, the governmental label was found to reduce college students' intentions to use e-cigarettes via increasing perceived risks of e-cigarette use (β=0.10, pcompanies showed no influence on beliefs about or intentions to use e-cigarettes. The warning label proposed by the FDA is more effective than that created by e-cigarette companies, however, has room for improvement to make a greater impact on e-cigarette use intention. Copyright © 2017 Elsevier Ltd. All rights reserved.

  18. E-cigarette specialty retailers: Data to assess the association between retail environment and student e-cigarette use

    OpenAIRE

    Bostean, Georgiana; Crespi, Catherine M.; Vorapharuek, Patsornkarn; McCarthy, William J

    2017-01-01

    The retail environment is a major social determinant of health, yet little is known about the e-cigarette specialty retailer environment. The e-cigarette specialty retail environment may be associated with e-cigarette use by middle and high school students, an issue that was addressed in a recent article entitled, “E-cigarette use among students and e-cigarette specialty retailer presence near schools,” by Bostean and colleagues (G. Bostean, C.M. Crespi, P. Vorapharuek, W.J. McCarthy, 2016 [1...

  19. An empirical analysis of cigarette demand in Argentina

    Science.gov (United States)

    Martinez, Eugenio; Mejia, Raul; Pérez-Stable, Eliseo J

    2014-01-01

    Objective To estimate the long-term and short-term effects on cigarette demand in Argentina based on changes in cigarette price and income per person >14 years old. Method Public data from the Ministry of Economics and Production were analysed based on monthly time series data between 1994 and 2010. The econometric analysis used cigarette consumption per person >14 years of age as the dependent variable and the real income per person >14 years old and the real average price of cigarettes as independent variables. Empirical analyses were done to verify the order of integration of the variables, to test for cointegration to capture the long-term effects and to capture the short-term dynamics of the variables. Results The demand for cigarettes in Argentina was affected by changes in real income and the real average price of cigarettes. The long-term income elasticity was equal to 0.43, while the own-price elasticity was equal to −0.31, indicating a 10% increase in the growth of real income led to an increase in cigarette consumption of 4.3% and a 10% increase in the price produced a fall of 3.1% in cigarette consumption. The vector error correction model estimated that the short-term income elasticity was 0.25 and the short-term own-price elasticity of cigarette demand was −0.15. A simulation exercise showed that increasing the price of cigarettes by 110% would maximise revenues and result in a potentially large decrease in total cigarette consumption. Conclusion Econometric analyses of cigarette consumption and their relationship with cigarette price and income can provide valuable information for developing cigarette price policy. PMID:23760657

  20. An empirical analysis of cigarette demand in Argentina.

    Science.gov (United States)

    Martinez, Eugenio; Mejia, Raul; Pérez-Stable, Eliseo J

    2015-01-01

    To estimate the long-term and short-term effects on cigarette demand in Argentina based on changes in cigarette price and income per person >14 years old. Public data from the Ministry of Economics and Production were analysed based on monthly time series data between 1994 and 2010. The econometric analysis used cigarette consumption per person >14 years of age as the dependent variable and the real income per person >14 years old and the real average price of cigarettes as independent variables. Empirical analyses were done to verify the order of integration of the variables, to test for cointegration to capture the long-term effects and to capture the short-term dynamics of the variables. The demand for cigarettes in Argentina was affected by changes in real income and the real average price of cigarettes. The long-term income elasticity was equal to 0.43, while the own-price elasticity was equal to -0.31, indicating a 10% increase in the growth of real income led to an increase in cigarette consumption of 4.3% and a 10% increase in the price produced a fall of 3.1% in cigarette consumption. The vector error correction model estimated that the short-term income elasticity was 0.25 and the short-term own-price elasticity of cigarette demand was -0.15. A simulation exercise showed that increasing the price of cigarettes by 110% would maximise revenues and result in a potentially large decrease in total cigarette consumption. Econometric analyses of cigarette consumption and their relationship with cigarette price and income can provide valuable information for developing cigarette price policy. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

  1. DNA repair protocols

    DEFF Research Database (Denmark)

    Bjergbæk, Lotte

    In its 3rd edition, this Methods in Molecular Biology(TM) book covers the eukaryotic response to genomic insult including advanced protocols and standard techniques in the field of DNA repair. Offers expert guidance for DNA repair, recombination, and replication. Current knowledge of the mechanisms...... that regulate DNA repair has grown significantly over the past years with technology advances such as RNA interference, advanced proteomics and microscopy as well as high throughput screens. The third edition of DNA Repair Protocols covers various aspects of the eukaryotic response to genomic insult including...... recent advanced protocols as well as standard techniques used in the field of DNA repair. Both mammalian and non-mammalian model organisms are covered in the book, and many of the techniques can be applied with only minor modifications to other systems than the one described. Written in the highly...

  2. INTERNAL REPAIR OF PIPELINES

    Energy Technology Data Exchange (ETDEWEB)

    Bill Bruce; Nancy Porter; George Ritter; Matt Boring; Mark Lozev; Ian Harris; Bill Mohr; Dennis Harwig; Robin Gordon; Chris Neary; Mike Sullivan

    2005-07-20

    The two broad categories of fiber-reinforced composite liner repair and deposited weld metal repair technologies were reviewed and evaluated for potential application for internal repair of gas transmission pipelines. Both are used to some extent for other applications and could be further developed for internal, local, structural repair of gas transmission pipelines. Principal conclusions from a survey of natural gas transmission industry pipeline operators can be summarized in terms of the following performance requirements for internal repair: (1) Use of internal repair is most attractive for river crossings, under other bodies of water, in difficult soil conditions, under highways, under congested intersections, and under railway crossings. (2) Internal pipe repair offers a strong potential advantage to the high cost of horizontal direct drilling when a new bore must be created to solve a leak or other problem. (3) Typical travel distances can be divided into three distinct groups: up to 305 m (1,000 ft.); between 305 m and 610 m (1,000 ft. and 2,000 ft.); and beyond 914 m (3,000 ft.). All three groups require pig-based systems. A despooled umbilical system would suffice for the first two groups which represents 81% of survey respondents. The third group would require an onboard self-contained power unit for propulsion and welding/liner repair energy needs. (4) The most common size range for 80% to 90% of operators surveyed is 508 mm (20 in.) to 762 mm (30 in.), with 95% using 558.8 mm (22 in.) pipe. Evaluation trials were conducted on pipe sections with simulated corrosion damage repaired with glass fiber-reinforced composite liners, carbon fiber-reinforced composite liners, and weld deposition. Additional un-repaired pipe sections were evaluated in the virgin condition and with simulated damage. Hydrostatic failure pressures for pipe sections repaired with glass fiber-reinforced composite liner were only marginally greater than that of pipe sections without

  3. Cigarette smoking and cigarette marketing exposure among students in selected African countries: Findings from the Global Youth Tobacco Survey.

    Science.gov (United States)

    Zhao, Luhua; Palipudi, Krishna M; Ramanandraibe, Nivo; Asma, Samira

    2016-10-01

    To investigate cigarette smoking prevalence and exposure to various forms of cigarette marketing among students in 10 African countries. We used data collected during 2009-2011 from the Global Youth Tobacco Survey (GYTS), a school-based cross-sectional survey of students aged 13-15years, to measure the prevalence of cigarette smoking and exposure to cigarette marketing; comparisons to estimates from 2005 to 2006 were conducted for five countries where data were available. Current cigarette smoking ranged from 3.4% to 13.6% among students aged 13-15 in the 10 countries studied, although use of tobacco products other than cigarettes was more prevalent in all countries except in Cote D'Ivoire. Cigarette smoking was higher among boys than girls in seven out of the 10 countries. Among the five countries with two rounds of surveys, a significant decrease in cigarette smoking prevalence was observed in Mauritania and Niger; these two countries also experienced a decline in three measures of cigarette marketing exposure. It is also possible that smoking prevalence might have risen faster among girls than boys. Cigarette smoking among youth was noticeable in 10 African countries evaluated, with the prevalence over 10% in Cote D'Ivoire, Mauritania, and South Africa. Cigarette marketing exposure varied by the types of marketing; traditional venues such as TV, outdoor billboards, newspapers, and magazines were still prominent. Published by Elsevier Inc.

  4. INTERNAL REPAIR OF PIPELINES

    Energy Technology Data Exchange (ETDEWEB)

    Robin Gordon; Bill Bruce; Ian Harris; Dennis Harwig; George Ritter; Bill Mohr; Matt Boring; Nancy Porter; Mike Sullivan; Chris Neary

    2004-12-31

    The two broad categories of fiber-reinforced composite liner repair and deposited weld metal repair technologies were reviewed and evaluated for potential application for internal repair of gas transmission pipelines. Both are used to some extent for other applications and could be further developed for internal, local, structural repair of gas transmission pipelines. Principal conclusions from a survey of natural gas transmission industry pipeline operators can be summarized in terms of the following performance requirements for internal repair: (1) Use of internal repair is most attractive for river crossings, under other bodies of water, in difficult soil conditions, under highways, under congested intersections, and under railway crossings. (2) Internal pipe repair offers a strong potential advantage to the high cost of horizontal direct drilling when a new bore must be created to solve a leak or other problem. (3) Typical travel distances can be divided into three distinct groups: up to 305 m (1,000 ft.); between 305 m and 610 m (1,000 ft. and 2,000 ft.); and beyond 914 m (3,000 ft.). All three groups require pig-based systems. A despooled umbilical system would suffice for the first two groups which represents 81% of survey respondents. The third group would require an onboard self-contained power unit for propulsion and welding/liner repair energy needs. (4) The most common size range for 80% to 90% of operators surveyed is 508 mm (20 in.) to 762 mm (30 in.), with 95% using 558.8 mm (22 in.) pipe. Evaluation trials were conducted on pipe sections with simulated corrosion damage repaired with glass fiber-reinforced composite liners, carbon fiber-reinforced composite liners, and weld deposition. Additional un-repaired pipe sections were evaluated in the virgin condition and with simulated damage. Hydrostatic failure pressures for pipe sections repaired with glass fiber-reinforced composite liner were only marginally greater than that of pipe sections without

  5. Electronic cigarette sales to minors via the internet.

    Science.gov (United States)

    Williams, Rebecca S; Derrick, Jason; Ribisl, Kurt M

    2015-03-01

    Electronic cigarettes (e-cigarettes) entered the US market in 2007 and, with little regulatory oversight, grew into a $2-billion-a-year industry by 2013. The Centers for Disease Control and Prevention has reported a trend of increasing e-cigarette use among teens, with use rates doubling from 2011 to 2012. While several studies have documented that teens can and do buy cigarettes online, to our knowledge, no studies have yet examined age verification among Internet tobacco vendors selling e-cigarettes. To estimate the extent to which minors can successfully purchase e-cigarettes online and assess compliance with North Carolina's 2013 e-cigarette age-verification law. In this cross-sectional study conducted from February 2014 to June 2014, 11 nonsmoking minors aged 14 to 17 years made supervised e-cigarette purchase attempts from 98 Internet e-cigarette vendors. Purchase attempts were made at the University of North Carolina Internet Tobacco Vendors Study project offices using credit cards. Rate at which minors can successfully purchase e-cigarettes on the Internet. Minors successfully received deliveries of e-cigarettes from 76.5% of purchase attempts, with no attempts by delivery companies to verify their ages at delivery and 95% of delivered orders simply left at the door. All delivered packages came from shipping companies that, according to company policy or federal regulation, do not ship cigarettes to consumers. Of the total orders, 18 failed for reasons unrelated to age verification. Only 5 of the remaining 80 youth purchase attempts were rejected owing to age verification, resulting in a youth buy rate of 93.7%. None of the vendors complied with North Carolina's e-cigarette age-verification law. Minors are easily able to purchase e-cigarettes from the Internet because of an absence of age-verification measures used by Internet e-cigarette vendors. Federal law should require and enforce rigorous age verification for all e-cigarette sales as with the federal

  6. INTERNAL REPAIR OF PIPELINES

    Energy Technology Data Exchange (ETDEWEB)

    Robin Gordon; Bill Bruce; Ian Harris; Dennis Harwig; George Ritter; Bill Mohr; Matt Boring; Nancy Porter; Mike Sullivan; Chris Neary

    2004-08-17

    The two broad categories of fiber-reinforced composite liner repair and deposited weld metal repair technologies were reviewed and evaluated for potential application for internal repair of gas transmission pipelines. Both are used to some extent for other applications and could be further developed for internal, local, structural repair of gas transmission pipelines. Principal conclusions from a survey of natural gas transmission industry pipeline operators can be summarized in terms of the following performance requirements for internal repair: (1) Use of internal repair is most attractive for river crossings, under other bodies of water, in difficult soil conditions, under highways, under congested intersections, and under railway. (2) Internal pipe repair offers a strong potential advantage to the high cost of horizontal direct drilling when a new bore must be created to solve a leak or other problem. (3) Typical travel distances can be divided into three distinct groups: up to 305 m (1,000 ft.); between 305 m and 610 m (1,000 ft. and 2,000 ft.); and beyond 914 m (3,000 ft.). All three groups require pig-based systems. A despooled umbilical system would suffice for the first two groups which represents 81% of survey respondents. The third group would require an onboard self-contained power unit for propulsion and welding/liner repair energy needs. (4) The most common size range for 80% to 90% of operators surveyed is 508 mm (20 in.) to 762 mm (30 in.), with 95% using 558.8 mm (22 in.) pipe. Evaluation trials were conducted on pipe sections with simulated corrosion damage repaired with glass fiber-reinforced composite liners, carbon fiber-reinforced composite liners, and weld deposition. Additional un-repaired pipe sections were evaluated in the virgin condition and with simulated damage. Hydrostatic failure pressures for pipe sections repaired with glass fiber-reinforced composite liner were only marginally greater than that of pipe sections without liners

  7. 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.

  8. Using Experimental Auctions to Examine Demand for E-Cigarettes.

    Science.gov (United States)

    O'Connor, Richard; Rousu, Matthew C; Bansal-Travers, Maansi; Vogl, Lisa; Corrigan, Jay R

    2017-06-01

    E-cigarettes are the latest in a line of potentially reduced exposure products that have garnered interest among smokers. In this paper, we use experimental auctions to estimate smokers' demand for e-cigarettes and to assess the impact of advertisements on willingness to pay. These are actual auctions, with winners and losers, which means hypothetical biases often seen in surveys are minimized. We find smokers have positive demand for e-cigarettes, and that the print advertisements used in our study had greater effectiveness than video ads (b = 2.00, p demand for disposable e-cigarettes. Demand was greater for reusable versus disposable e-cigarettes. In multivariate models, demand for e-cigarettes was higher among non-white participants and among smokers willing to pay more for cigarettes. Our findings suggest that cigarette smokers are interested in e-cigarettes as alternatives to traditional products, particularly for reusable forms, and that this demand can be influenced by messaging/advertising. Given these reduced harm products are appealing, if smokers are able to switch completely to e-cigarettes, there is a good chance for accrual of significant harm reduction.

  9. Using E-Cigarettes in the Home to Reduce Smoking and Secondhand Smoke: Disadvantaged Parents' Accounts

    Science.gov (United States)

    Rowa-Dewar, Neneh; Rooke, Catriona; Amos, Amanda

    2017-01-01

    Electronic cigarettes (e-cigarettes) are subject to considerable public health debate. Most public health experts agree that for smokers who find it particularly challenging to quit, e-cigarettes may reduce harm. E-cigarette use in the home may also reduce children's secondhand smoke (SHS) exposure, although e-cigarette vapour may pose risks. This…

  10. Up in Vapor: Exploring the Health Messages of E-Cigarette Advertisements.

    Science.gov (United States)

    Willis, Erin; Haught, Matthew J; Morris Ii, David L

    2017-03-01

    Electronic cigarettes (e-cigarettes) have gained popularity in the United States, and marketers are using advertising to recruit new users to their products. Despite outright bans on traditional cigarette advertisements, e-cigarettes have no specific regulations. This study uses framing theory to explore the themes in e-cigarette advertisements. Also, practical implications are discussed.

  11. Salvage hypospadias repairs

    Directory of Open Access Journals (Sweden)

    Sripathi V

    2008-01-01

    Full Text Available Aim: Review of our experience and to develop an algorithm for salvage procedures in the management of hypospadias cripples and treatment of urethral strictures following hypospadias repair. Methods: This is a retrospective review of hypospadias surgeries over a 41-month period. Out of a total 168 surgeries, 20 were salvage/re-operative repairs. In three children a Duplay repair was feasible, while in four others a variety of single-stage repairs could be done. The repair was staged in seven children - buccal mucosal grafts (BMGs in five, buccal mucosal tube in one, and skin graft in one. Five children with dense strictures were managed by dorsal BMG inlay grafting in one, vascularized tunical onlay grafting on the ventrum in one, and a free tunical patch in one. Three children were treated by internal urethrotomy and stenting for four weeks with a poor outcome. Results: The age of children ranged from 1.5-15 years (mean 4.5. Follow-up ranged from 3 months to 3.5 years. Excellent results were obtained in 10 children (50% with a well-surfaced erect penis and a slit-like meatus. Glans closure could not be achieved and meatus was coronal in three. Two children developed fistulae following a Duplay repair and following a staged BMG. Three repairs failed completely - a composite repair broke down, a BMG tube stenosed with a proximal leak, and a stricture recurred with loss of a ventral free tunical graft. Conclusions: In salvage procedures performed on hypospadias cripples, a staged repair with buccal mucosa as an inlay in the first stage followed by tubularization 4-6 months later provides good results. A simple algorithm to plan corrective surgery in failed hypospadias cases and obtain satisfactory results is devised.

  12. Research gaps related to the environmental impacts of electronic cigarettes

    Science.gov (United States)

    Chang, Hoshing

    2014-01-01

    Objective To consider the research gaps related to the environmental impacts of electronic cigarettes due to their manufacture, use and disposal. Methods Literature searches were conducted through December 2013. Studies were included in this review if they related to the environmental impacts of e-cigarettes. Results Scientific information on the environmental impacts of e-cigarette manufacturing, use and disposal is very limited. No studies formally evaluated the environmental impacts of the manufacturing process or disposal of components, including batteries. Four studies evaluated potential exposure to secondhand e-cigarette aerosol, an indication of impacts on indoor air quality. A 2010 survey of six e-cigarette models found that none of the products provided disposal instructions for spent cartridges containing nicotine. Notably, some e-cigarette manufacturers claim their e-cigarettes are ‘eco-friendly’ or ‘green’, despite the lack of any supporting data or environmental impact studies. Some authors argue that such advertising may boost sales and increase e-cigarette appeal, especially among adolescents. Conclusions Little is known about the environmental impacts of e-cigarettes, and a number of topics could be further elucidated by additional investigation. These topics include potential environmental impacts related to manufacturing, use and disposal. The environmental impacts of e-cigarette manufacturing will depend upon factory size and the nicotine extracting method used. The environmental impacts of e-cigarette use will include chemical and aerosol exposure in the indoor environment. The environmental impacts of disposal of e-cigarette cartridges (which contain residual nicotine) and disposal of e-cigarettes (which contain batteries) represent yet another environmental concern. PMID:24732165

  13. Effects of electronic cigarette smoking on human health.

    Science.gov (United States)

    Meo, S A; Al Asiri, S A

    2014-01-01

    Electronic cigarette smoking is gaining dramatic popularity and is steadily spreading among the adolescents, high income, urban population around the world. The aim of this study is to highlight the hazards of e-cigarette smoking on human health. In this study, we identified 38 published studies through a systematic database searches including ISI-web of science and pub-med. We searched the related literature by using the key words including Electronic cigarette, E-cigarette, E-vapers, incidence, hazards. Studies in which electronic cigarette smoking hazards was investigated were included in the study. No limitations on publication status, study design of publication were implemented. Finally we included 28 publications and remaining 10 were excluded. E-smoking can cause, nausea, vomiting, headache, dizziness, choking, burn injuries, upper respiratory tract irritation, dry cough, dryness of the eyes and mucous membrane, release of cytokines and pro-inflammatory mediators, allergic airway inflammation, decreased exhaled nitric oxide (FeNO) synthesis in the lungs, change in bronchial gene expression and risk of lung cancer. Electronic cigarettes are swiftly promoted as an alternative to conventional cigarette smoking, although its use is highly controversial. Electronic cigarettes are not a smoking cessation product. Non-scientific claims about e-cigarettes are creating confusion in public perception about e-cigarette and people believe that e-cigarettes are safe and less addictive, but its use is unsafe and hazardous to human health. E-cigarette smoking should be regulated in the same way as traditional cigarettes and must be prohibited to children and adolescents.

  14. Electronic Cigarette Use and Respiratory Symptoms in Adolescents.

    Science.gov (United States)

    McConnell, Rob; Barrington-Trimis, Jessica L; Wang, Kejia; Urman, Robert; Hong, Hanna; Unger, Jennifer; Samet, Jonathan; Leventhal, Adam; Berhane, Kiros

    2017-04-15

    Rates of adolescent electronic (e-) cigarette use are increasing, but there has been little study of the chronic effects of use. Components of e-cigarette aerosol have known pulmonary toxicity. To investigate the associations of e-cigarette use with chronic bronchitis symptoms and wheeze in an adolescent population. Associations of self-reported use of e-cigarettes with chronic bronchitic symptoms (chronic cough, phlegm, or bronchitis) and of wheeze in the previous 12 months were examined in 2,086 Southern California Children's Health Study participants completing questionnaires in 11th and 12th grade in 2014. Ever e-cigarette use was reported by 502 (24.0%), of whom 201 (9.6%) used e-cigarettes during the last 30 days (current users). Risk of bronchitic symptoms was increased by almost twofold among past users (odds ratio [OR], 1.85; 95% confidence interval [CI], 1.37-2.49), compared with never-users, and by 2.02-fold (95% CI, 1.42-2.88) among current users. Risk increased with frequency of current use (OR, 1.66; 95% CI, 1.02-2.68) for 1-2 days and 2.52 (95% CI, 1.56-4.08) for 3 or more days in past 30 days compared with never-users. Associations were attenuated by adjustment for lifetime number of cigarettes smoked and secondhand smoke exposure. However, risk of bronchitic symptoms among past e-cigarette users remained elevated after adjustment for relevant potential confounders and was also observed among never-cigarette users (OR, 1.70; 95% CI, 1.11-2.59). There were no statistically significant associations of e-cigarette use with wheeze after adjustment for cigarette use. Adolescent e-cigarette users had increased rates of chronic bronchitic symptoms. Further investigation is needed to determine the long-term effects of e-cigarettes on respiratory health.

  15. Adolescents' attitudes towards e-cigarette ingredients, safety, addictive properties, social norms, and regulation.

    Science.gov (United States)

    Gorukanti, Anuradha; Delucchi, Kevin; Ling, Pamela; Fisher-Travis, Raymond; Halpern-Felsher, Bonnie

    2017-01-01

    E-cigarette use has dramatically increased. While studies have examined adolescents' attitudes towards smoking, few have extended this research to adolescents' attitudes towards e-cigarettes. The goal of this study was to examine adolescents' attitudes regarding e-cigarette ingredients, safety, addictive properties, social norms, accessibility, price, and regulation; and determine whether attitudes differ by past cigarette/e-cigarette use. Participants were 786 9th and 12th graders from California (63.21% females; mean age=16.10years [SD=1.6]; 26.61% White, 21.98% Asian/Pacific Islander, 29.82% Hispanic, and 21.59% other). Results indicated that 19.05% of participants believed smoke from e-cigarettes is water; 23.03% believed e-cigarettes aren't a tobacco product; 40.36% considered e-cigarettes to be for cessation, and 43.13% felt they were safer than cigarettes. Participants felt it was more acceptable to use e-cigarettes indoors and outdoors compared to cigarettes (pe-cigarette taxes is a bad idea, 63.95% thought e-cigarettes were easier to get than cigarettes, 54.42% felt e-cigarettes cost too much, 64.33% felt the age for buying e-cigarettes should be raised, and 64.37% favored e-cigarette regulation. Adolescents who used e-cigarettes and/or cigarettes had significantly more favorable e-cigarette attitudes than non-users. This study indicates that adolescents are aware of some of the risks of e-cigarettes, although many harbor misperceptions and hold more favorable attitudes towards e-cigarettes than cigarettes. Of concern is the relationship between favorable e-cigarette attitudes and use. Findings suggest the need to provide adolescents with correct information about e-cigarette ingredients, risks, and the insufficient evidence of their role in cigarette cessation.

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

    Directory of Open Access Journals (Sweden)

    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.

  17. The effect of Taiwan's tax-induced increases in cigarette prices on brand-switching and the consumption of cigarettes.

    Science.gov (United States)

    Tsai, Yi-Wen; Yang, Chung-Lin; Chen, Chin-Shyan; Liu, Tsai-Ching; Chen, Pei-Fen

    2005-06-01

    The effect of raising cigarette taxes to reduce smoking has been the subject of several studies, which often treat the price of cigarettes as an exogenous factor given to smokers who respond to it by adjusting their smoking behavior. However, cigarette prices vary with brand and quality, and smokers can and do switch to lower-priced brands to reduce the impact of the tax on the cost of cigarettes as they try to consume the same number of cigarettes as they had before a tax hike. Using data from a two-year follow-up interview survey conducted before and after a new cigarette tax scheme was imposed in Taiwan in 2002, this study examines three behavioral changes smokers may make to respond to tax-induced cigarette price increase: brand-switching, amount consumed, and amount spent on smoking. These changes were studied in relation to smoker income, before-tax cigarette price, level of addiction, exposure to advertizing, and consumer loyalty. We found that smokers, depending upon exposure to advertizing, level of consumer loyalty and initial price of cigarettes, switched brands to maintain current smoking habits and control costs. We also found that the initial amount smoked and level of addiction, not price, at least not at the current levels in Taiwan, determined whether a smoker reduced the number of cigarettes he consumed.

  18. Environmental health hazards of e-cigarettes and their components: Oxidants and copper in e-cigarette aerosols.

    Science.gov (United States)

    Lerner, Chad A; Sundar, Isaac K; Watson, Richard M; Elder, Alison; Jones, Ryan; Done, Douglas; Kurtzman, Rachel; Ossip, Deborah J; Robinson, Risa; McIntosh, Scott; Rahman, Irfan

    2015-03-01

    To narrow the gap in our understanding of potential oxidative properties associated with Electronic Nicotine Delivery Systems (ENDS) i.e. e-cigarettes, we employed semi-quantitative methods to detect oxidant reactivity in disposable components of ENDS/e-cigarettes (batteries and cartomizers) using a fluorescein indicator. These components exhibit oxidants/reactive oxygen species reactivity similar to used conventional cigarette filters. Oxidants/reactive oxygen species reactivity in e-cigarette aerosols was also similar to oxidant reactivity in cigarette smoke. A cascade particle impactor allowed sieving of a range of particle size distributions between 0.450 and 2.02 μm in aerosols from an e-cigarette. Copper, being among these particles, is 6.1 times higher per puff than reported previously for conventional cigarette smoke. The detection of a potentially cytotoxic metal as well as oxidants from e-cigarette and its components raises concern regarding the safety of e-cigarettes use and the disposal of e-cigarette waste products into the environment.

  19. Can Increases in the Cigarette Tax Rate be Linked to Cigarette Retail Prices? Solving mysteries related to the cigarette pricing mechanism in China

    Science.gov (United States)

    Gao, Song; Zheng, Rong; Hu, Teh-wei

    2013-01-01

    Objective To explain China’s cigarette pricing mechanism and the role of the Chinese State Tobacco Monopoly Administration (STMA) on cigarette pricing and taxation. Methods Published government tobacco tax documentation and statistics published by the Chinese State Tobacco Monopoly Administration (STMA) are used to analyze the interrelations among industry profits, taxes, and retail price of cigarettes in China. Results The 2009 excise tax increase on cigarettes in China has not translated into higher retail prices because the Chinese STMA used its policy authority to ensure that retail cigarette prices did not change. The government tax increase is being collected at both the producer and wholesale levels. As a result, the 2009 excise tax increase in China has resulted in higher tax revenue for the government and lower profits for the tobacco industry, with no increase in the retail price of cigarettes for consumers. Conclusions Numerous studies have found that taxation is one of the most effective policy instruments for tobacco control. However, these findings come from countries that have market economies where market forces determine prices and influence how cigarette taxes are passed to the consumers in retail prices. China’s tobacco industry is not a market economy; therefore, nonmarket forces and the current Chinese tobacco monopoly system determine cigarette prices. The result is that tax increases do not necessarily get passed on to the retail price. PMID:23076787

  20. Progress of peripheral nerve repair

    Institute of Scientific and Technical Information of China (English)

    陈峥嵘

    2002-01-01

    Study on repair of peripheral nerve injury has been proceeding over a long period of time. With the use of microsurgery technique since 1960s,the quality of nerve repair has been greatly improved. In the past 40 years, with the continuous increase of surgical repair methods, more progress has been made on the basic research of peripheral nerve repair.

  1. Changes among retailers selling cigarettes to minors.

    Science.gov (United States)

    Dovell, R A; Mowat, D L; Dorland, J; Lam, M

    1996-01-01

    This study analyzes changes over a three-year period among Ontario retailers selling cigarettes to minors. Under supervision, 13 and 14-year-old minors were sent into stores to attempt to buy cigarettes. These minor-purchase-events (MPEs) were carried out in a local health unit that had implemented a community-based intervention and in an adjoining comparison health unit. After the local program we observed a large reduction (from 46% to 6%) in merchants willing to sell tobacco to minors. In the neighbouring health unit, a high rate of selling continued until a federal program using a similar intervention was implemented, after which a large reduction (from 47% to 2%) was observed. This magnitude of change has been unprecedented, except when active enforcement was implemented by police officers. Thus, from a public health perspective, it is important to understand what is influencing the store operators.

  2. Achilles tendon repair

    Science.gov (United States)

    Achilles tendon rupture-surgery; Percutaneous Achilles tendon rupture repair ... To fix your torn Achilles tendon, the surgeon will: Make a cut down the back of your heel Make several small cuts rather than one large cut ...

  3. Diaphragmatic hernia repair - slideshow

    Science.gov (United States)

    ... presentations/100014.htm Diaphragmatic hernia repair - series—Normal anatomy To use the sharing ... Overview The chest cavity includes the heart and lungs. The abdominal cavity includes the liver, the stomach, ...

  4. Eye muscle repair - slideshow

    Science.gov (United States)

    ... page: //medlineplus.gov/ency/presentations/100062.htm Eye muscle repair - series—Normal anatomy To use the sharing ... the eyeball to the eye socket. The external muscles of the eye are found behind the conjunctiva. ...

  5. Tracheoesophageal fistula repair - slideshow

    Science.gov (United States)

    ... page: //medlineplus.gov/ency/presentations/100103.htm Tracheoesophageal fistula repair - series—Normal anatomy To use the sharing ... Editorial team. Related MedlinePlus Health Topics Esophagus Disorders Fistulas Tracheal Disorders A.D.A.M., Inc. is ...

  6. Inguinal hernia repair - slideshow

    Science.gov (United States)

    ... page: //medlineplus.gov/ency/presentations/100027.htm Inguinal hernia repair - series—Normal anatomy To use the sharing ... to slide 4 out of 4 Overview A hernia occurs when part of an organ protrudes through ...

  7. INTERNAL REPAIR OF PIPELINES

    Energy Technology Data Exchange (ETDEWEB)

    Robin Gordon; Bill Bruce; Ian Harris; Dennis Harwig; Nancy Porter; Mike Sullivan; Chris Neary

    2004-04-12

    The two broad categories of deposited weld metal repair and fiber-reinforced composite liner repair technologies were reviewed for potential application for internal repair of gas transmission pipelines. Both are used to some extent for other applications and could be further developed for internal, local, structural repair of gas transmission pipelines. Preliminary test programs were developed for both deposited weld metal repair and for fiber-reinforced composite liner repair. Evaluation trials have been conducted using a modified fiber-reinforced composite liner provided by RolaTube and pipe sections without liners. All pipe section specimens failed in areas of simulated damage. Pipe sections containing fiber-reinforced composite liners failed at pressures marginally greater than the pipe sections without liners. The next step is to evaluate a liner material with a modulus of elasticity approximately 95% of the modulus of elasticity for steel. Preliminary welding parameters were developed for deposited weld metal repair in preparation of the receipt of Pacific Gas & Electric's internal pipeline welding repair system (that was designed specifically for 559 mm (22 in.) diameter pipe) and the receipt of 559 mm (22 in.) pipe sections from Panhandle Eastern. The next steps are to transfer welding parameters to the PG&E system and to pressure test repaired pipe sections to failure. A survey of pipeline operators was conducted to better understand the needs and performance requirements of the natural gas transmission industry regarding internal repair. Completed surveys contained the following principal conclusions: (1) Use of internal weld repair is most attractive for river crossings, under other bodies of water, in difficult soil conditions, under highways, under congested intersections, and under railway crossings. (2) Internal pipe repair offers a strong potential advantage to the high cost of horizontal direct drilling (HDD) when a new bore must be created

  8. Pectus excavatum repair - slideshow

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/presentations/100035.htm Pectus excavatum repair - series—Normal anatomy To use the sharing ... Go to slide 4 out of 4 Overview Pectus excavatum is a deformity of the front of the ...

  9. Hiatal hernia repair - slideshow

    Science.gov (United States)

    ... presentations/100028.htm Hiatal hernia repair - series—Normal anatomy To use the sharing features on ... Overview The esophagus runs through the diaphragm to the stomach. It functions to carry food from the mouth ...

  10. Repairing ceramic insulating tiles

    Science.gov (United States)

    Dunn, B. R.; Laymance, E. L.

    1980-01-01

    Fused-silica tiles containing large voids or gauges are repaired without adhesives by plug insertion method. Tiles are useful in conduits for high-temperature gases, in furnaces, and in other applications involving heat insulation.

  11. Rotator cuff repair - slideshow

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/presentations/100229.htm Rotator cuff repair - series—Normal anatomy To use the sharing ... to slide 4 out of 4 Overview The rotator cuff is a group of muscles and tendons that ...

  12. Cleft lip repair - slideshow

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/presentations/100010.htm Cleft lip repair - series—Normal anatomy To use the sharing ... abnormal opening in the middle of the upper lip. A cleft palate is an opening in the roof of ...

  13. Exploring Cigarette Use among Male Migrant Workers in Nigeria

    Directory of Open Access Journals (Sweden)

    Olanrewaju Olusola Onigbogi

    2015-04-01

    Full Text Available Background There is limited knowledge about the use of cigarettes by blacks outside the United States (U.S. Nigeria creates an opportunity to explore smoking behaviours, smoking cessation (nicotine dependence and use of cigarettes in a country that has a large black population outside the U.S. Methods We conducted three Focus Group Discussions (FGDs involving twenty-four male migrant workers who reported that they were current cigarette smokers. Interviews were audio-taped and transcribed. Results Four major themes namely: reasons for initiating and continuing to smoke cigarettes, factors affecting brand choice, barriers to quitting, effect of smoking mentholated cigarette brands were identified. Conclusion This study provides insight into the use of mentholated and non-mentholated cigarettes and suggests the need for further studies to explore smoking behavior among Nigerians.

  14. 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.

  15. Recent Advances in Cigarette Ignition Propensity Research and Development.

    Science.gov (United States)

    Alpert, Hillel R; O'Connor, Richard J; Spalletta, Ron; Connolly, Gregory N

    2010-04-01

    Major U.S. cigarette companies for decades conducted research and development regarding cigarette ignition propensity which has continued beyond fire safety standards for cigarettes that have recently been legislated. This paper describes recent scientific advances and technological development based on a comprehensive review of the physical, chemical, and engineering sciences, public health, and trade literature, U.S. and international patents, and research in the tobacco industry document libraries.Advancements since the first implementation of standards have made been in: a) understanding the key parameters involved in cigarette smoldering combustion and ignition of substrates; b) developing new cigarette and paper wrapper designs to reduce ignition propensity, including banded and non-banded cigarette paper approaches, c) assessing toxicology, and d) measuring performance. While the implications of manufacturers' non-safety related aims are of concern, this research indicates possible alternative designs should experience with fire loss and existing technologies on the market suggest need for improvement.

  16. [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.

  17. Cigarette cravings, impulsivity and the brain

    Directory of Open Access Journals (Sweden)

    Stéphane ePotvin

    2015-09-01

    Full Text Available Craving is a core feature of tobacco use disorder as well as a significant predictor of smoking relapse. Studies have shown that appetitive smoking-related stimuli (e.g. someone smoking trigger significant cravings in smokers which impedes their self-control capacities and promotes drug seeking behavior. In this review, we begin by an overview of functional magnetic resonance imaging (fMRI studies investigating the neural correlates of smokers to appetitive smoking cues. The literature reveals a complex and vastly distributed neuronal network underlying smokers’ craving response that recruits regions involved in self-referential processing, panning/regulatory processes, emotional responding, attentional biases, and automatic conducts. We then selectively review important factors contributing to the heterogeneity of results that significantly limit the implications of these findings, namely between- (abstinence, smoking expectancies and self-regulation and within-studies factors (severity of smoking dependence, sex-differences, motivation to quit and genetic factors. Remarkably, we found that little to no attention has been devoted to examine the influence of personality traits on the neural correlates of cigarette cravings in fMRI studies. Impulsivity has been linked with craving and relapse in substance and tobacco use, which prompted our research team to examine the influence of impulsivity on cigarette cravings in an fMRI study. We found that the influence of impulsivity on cigarette cravings was mediated by fronto-cingular mechanisms. Given the high prevalence of cigarette smoking in several psychiatric disorders that are characterized by significant levels of impulsivity, we conclude by identifying psychiatric patients as a target population whose tobacco smoking habits deserve further behavioral and neuro-imaging investigation.

  18. 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.

  19. 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...

  20. 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...

  1. Grey Repairable System Analysis

    Institute of Scientific and Technical Information of China (English)

    Renkuan Guo; Charles Ernie Love

    2006-01-01

    In this paper, we systematically discuss the basic concepts of grey theory, particularly the grey differential equation and its mathematical foundation, which is essentially unknown in the reliability engineering community. Accordingly,we propose a small-sample based approach to estimate repair improvement effects by partitioning system stopping times into intrinsic functioning times and repair improvement times. An industrial data set is used for illustrative purposes in a stepwise manner.

  2. Electronic cigarettes: a survey of users

    Directory of Open Access Journals (Sweden)

    Etter Jean-François

    2010-05-01

    Full Text Available Abstract Background Little is known about users of electronic cigarettes, or their opinions, satisfaction or how and why they use such products. Methods An internet survey of 81 ever-users of ecigarettes in 2009. Participants answered open-ended questions on use of, and opinions about, ecigarettes. Results Respondents (73 current and 8 former users lived in France, Canada, Belgium or Switzerland. Most respondents (77% were men; 63% were former smokers and 37% were current smokers. They had used e-cigarettes for 100 days (median and drew 175 puffs per day (median. Participants used the ecigarette either to quit smoking (53 comments, to reduce their cigarette consumption (14 comments, in order not to disturb other people with smoke (20 comments, or in smoke-free places (21 comments. Positive effects reported with ecigarettes included their usefulness to quit smoking, and the benefits of abstinence from smoking (less coughing, improved breathing, better physical fitness. Respondents also enjoyed the flavour of ecigarettes and the sensation of inhalation. Side effects included dryness of the mouth and throat. Respondents complained about the frequent technical failures of ecigarettes and had some concerns about the possible toxicity of the devices and about their future legal status. Conclusions Ecigarettes were used mainly to quit smoking, and may be helpful for this purpose, but several respondents were concerned about potential toxicity. There are very few published studies on ecigarettes and research is urgently required, particularly on the efficacy and toxicity of these devices.

  3. Cigarette package design: opportunities for disease prevention

    Science.gov (United States)

    DiFranza, JR; Clark, DM; Pollay, RW

    2003-01-01

    Objective To learn how cigarette packages are designed and to determine to what extent cigarette packages are designed to target children. Methods A computer search was made of all Internet websites that post tobacco industry documents using the search terms: packaging, package design, package study, box design, logo, trademark and design study. All documents were retrieved electronically and analyzed by the first author for recurrent themes. Data Synthesis Cigarette manufacturers devote a great deal of attention and expense to package design because it is central to their efforts to create brand images. Colors, graphic elements, proportioning, texture, materials and typography are tested and used in various combinations to create the desired product and user images. Designs help to create the perceived product attributes and project a personality image of the user with the intent of fulfilling the psychological needs of the targeted type of smoker. The communication of these images and attributes is conducted through conscious and subliminal processes. Extensive testing is conducted using a variety of qualitative and quantitative research techniques. Conclusion The promotion of tobacco products through appealing imagery cannot be stopped without regulating the package design. The same marketing research techniques used by the tobacco companies can be used to design generic packaging and more effective warning labels targeted at specific consumers.

  4. Cigarette package design: opportunities for disease prevention

    Directory of Open Access Journals (Sweden)

    Pollay RW

    2003-01-01

    Full Text Available Abstract Objective To learn how cigarette packages are designed and to determine to what extent cigarette packages are designed to target children. Methods A computer search was made of all Internet websites that post tobacco industry documents using the search terms: packaging, package design, package study, box design, logo, trademark and design study. All documents were retrieved electronically and analyzed by the first author for recurrent themes. Data Synthesis Cigarette manufacturers devote a great deal of attention and expense to package design because it is central to their efforts to create brand images. Colors, graphic elements, proportioning, texture, materials and typography are tested and used in various combinations to create the desired product and user images. Designs help to create the perceived product attributes and project a personality image of the user with the intent of fulfilling the psychological needs of the targeted type of smoker. The communication of these images and attributes is conducted through conscious and subliminal processes. Extensive testing is conducted using a variety of qualitative and quantitative research techniques. Conclusion The promotion of tobacco products through appealing imagery cannot be stopped without regulating the package design. The same marketing research techniques used by the tobacco companies can be used to design generic packaging and more effective warning labels targeted at specific consumers.

  5. 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.

  6. 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.

  7. Cigarette package design: opportunities for disease prevention

    Science.gov (United States)

    DiFranza, JR; Clark, DM; Pollay, RW

    2003-01-01

    Objective To learn how cigarette packages are designed and to determine to what extent cigarette packages are designed to target children. Methods A computer search was made of all Internet websites that post tobacco industry documents using the search terms: packaging, package design, package study, box design, logo, trademark and design study. All documents were retrieved electronically and analyzed by the first author for recurrent themes. Data Synthesis Cigarette manufacturers devote a great deal of attention and expense to package design because it is central to their efforts to create brand images. Colors, graphic elements, proportioning, texture, materials and typography are tested and used in various combinations to create the desired product and user images. Designs help to create the perceived product attributes and project a personality image of the user with the intent of fulfilling the psychological needs of the targeted type of smoker. The communication of these images and attributes is conducted through conscious and subliminal processes. Extensive testing is conducted using a variety of qualitative and quantitative research techniques. Conclusion The promotion of tobacco products through appealing imagery cannot be stopped without regulating the package design. The same marketing research techniques used by the tobacco companies can be used to design generic packaging and more effective warning labels targeted at specific consumers. PMID:19570250

  8. Cigarette package design: opportunities for disease prevention.

    Science.gov (United States)

    Difranza, J R; Clark, D M; Pollay, R W

    2002-06-15

    To learn how cigarette packages are designed and to determine to what extent cigarette packages are designed to target children. A computer search was made of all Internet websites that post tobacco industry documents using the search terms: packaging, package design, package study, box design, logo, trademark and design study. All documents were retrieved electronically and analyzed by the first author for recurrent themes. Cigarette manufacturers devote a great deal of attention and expense to package design because it is central to their efforts to create brand images. Colors, graphic elements, proportioning, texture, materials and typography are tested and used in various combinations to create the desired product and user images. Designs help to create the perceived product attributes and project a personality image of the user with the intent of fulfilling the psychological needs of the targeted type of smoker. The communication of these images and attributes is conducted through conscious and subliminal processes. Extensive testing is conducted using a variety of qualitative and quantitative research techniques. The promotion of tobacco products through appealing imagery cannot be stopped without regulating the package design. The same marketing research techniques used by the tobacco companies can be used to design generic packaging and more effective warning labels targeted at specific consumers.

  9. Resolvin-D1 inhibits interleukin-8 and hydrogen peroxide production induced by cigarette smoke extract in 16HBE cells via attenuating NF-κB activation

    Institute of Scientific and Technical Information of China (English)

    Dong Jiajia; Zhang Mingke; Liao Zenglin; Wu Wei; Wang Tao; Chen Lei; Yang Ting

    2014-01-01

    Background Cigarette smoke induced airway inflammation plays a role in pathogenesis of airway inflammation.Resolvin-D1 derived from omega-3 polyunsaturated fatty acids is an endogenous anti-inflammatory and proresolving lipid mediator.Resolvin-D1 ameliorated inflammatory responses in lung injury,asthma,peritonitis and atherosclerosis.We investigated whether resolvin-D1 suppressed the productions of chemokines and oxidative stress induced by cigarette smoke extract (CSE) in vitro and its possible mechanism.Methods We examined the proinfiammatory chemokine interleukin-8 and hydrogen peroxide (H2O2)productions induced by CSE in 16 human bronchial epithelial (16HBE)cells after resolvin-D1 treatment and their mechanisms.16HBE cells were treated with resolvin-D1 at up to 10 nmol/L,for 30 minutes before CSE up to 16% (v/v) exposure.Release of interlukin-8 proteins was assessed by enzyme linked immunosort assay (ELISA) and its mRNA level by RT-PCR.We evaluated extracellular H2O2 expression in the supematant.Phosphorylation of NF-KB/p65 and degradation of Ⅰ-KB in 16HBE cells were determined by Westem blotting analysis and NF-KB DNA binding activity by electrophoretic mobility shift assay (EMSA).Results 16HBE cells treated with 8% CSE showed significantly higher interlukin-8 production.Resolvin-D1 pretreatment inhibited CSE induced intedukin-8 production (mRNA and protein) in a dose and time dependent manner.Extracellular H2O2 level decreased after resolvin-D1 treatment.Resolvin-D1 attenuated CSE triggered Ⅰ-KB degradation and NF-KB/p65 activation dose dependently and inhibited NF-KB DNA binding activity.Conclusion Resolvin-D1 inhibits CSE induced interlukin-8 and H2O2 production in 16HBE cells by modulating NF-KB activation and has therapeutic potential for pulmonary inflammation.

  10. Multiplexed quantitative high content screening reveals that cigarette smoke condensate induces changes in cell structure and function through alterations in cell signaling pathways in human bronchial cells.

    Science.gov (United States)

    Carter, Charleata A; Hamm, Jonathan T

    2009-07-10

    Human bronchial cells are one of the first cell types exposed to environmental toxins. Toxins often activate nuclear factor-kappaB (NF-kappaB) and protein kinase C (PKC). We evaluated the hypothesis that cigarette smoke condensate (CSC), the particulate fraction of cigarette smoke, activates PKC-alpha and NF-kappaB, and concomitantly disrupts the F-actin cytoskeleton, induces apoptosis and alters cell function in BEAS-2B human bronchial epithelial cells. Compared to controls, exposure of BEAS-2B cells to doses of 30mug/ml CSC significantly activated PKC-alpha, while CSC doses above 20mug/ml CSC significantly activated NF-kappaB. As NF-kappaB was activated, cell number decreased. CSC treatment of BEAS-2B cells induced a decrease in cell size and an increase in cell surface extensions including filopodia and lamellipodia. CSC treatment of BEAS-2B cells induced F-actin rearrangement such that stress fibers were no longer prominent at the cell periphery and throughout the cells, but relocalized to perinuclear regions. Concurrently, CSC induced an increase in the focal adhesion protein vinculin at the cell periphery. CSC doses above 30mug/ml induced a significant increase in apoptosis in BEAS-2B cells evidenced by an increase in activated caspase 3, an increase in mitochondrial mass and a decrease in mitochondrial membrane potential. As caspase 3 increased, cell number decreased. CSC doses above 30mug/ml also induced significant concurrent changes in cell function including decreased cell spreading and motility. CSC initiates a signaling cascade in human bronchial epithelial cells involving PKC-alpha, NF-kappaB and caspase 3, and consequently decreases cell spreading and motility. These CSC-induced alterations in cell structure likely prevent cells from performing their normal function thereby contributing to smoke-induced diseases.

  11. 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.

  12. Exploring cigarette use among male migrant workers in Nigeria

    OpenAIRE

    Olanrewaju Olusola Onigbogi; David Karatu; Sarafa Sanusi; Rebekah Pratt; Kolawole Okuyemi

    2015-01-01

    Background There is limited knowledge about the use of cigarettes by blacks outside the United States (U.S). Nigeria creates an opportunity to explore smoking behaviours, smoking cessation (nicotine dependence) and use of cigarettes in a country that has a large black population outside the U.S. Methods We conducted three Focus Group Discussions (FGDs) involving twenty-four male migrant workers who reported that they were current cigarette smokers. Interviews were audio-tape...

  13. 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 ...

  14. Knowledge and beliefs about electronic cigarettes among quitline cessation staff.

    Science.gov (United States)

    Cummins, Sharon; Leischow, Scott; Bailey, Linda; Bush, Terry; Wassum, Ken; Copeland, Lesley; Zhu, Shu-Hong

    2016-09-01

    Smokers are asking health practitioners for guidance about using e-cigarettes as an aid to quitting. Several studies have surveyed physicians. However, in North America many smokers seek help from telephone quitlines rather than physicians. The objective of the current study was to assess quitline counselors' perceptions of e-cigarettes and what they tell callers about these products. An online cross-sectional survey, conducted in 2014 with 418 quitline counselors in the U.S. and Canada, measured perceptions of e-cigarettes: (1) use as a quitting aid; (2) safety; (3) professional guidance given and organizational guidance received; (4) regulation. The response rate was 90.1%. Analyses included calculating standard errors and 95% confidence intervals around summary statistics. Nearly 70% of counselors believed that e-cigarettes are not effective quitting aids. Most believed e-cigarettes are addictive (87%) and that secondhand exposure to vapor is harmful (71%). Counselors reported that callers ask for advice about e-cigarettes, but few counselors recommended e-cigarettes (4%). Counselors (97%) reported being instructed by quitline employers to explain to clients that e-cigarettes are not FDA-approved; 74% were told to recommend approved quitting aids instead. Most counselors (>87%) believed e-cigarettes should be regulated like cigarettes in terms of advertising, taxation, access by minors, and use in public places. Quitline counselors view e-cigarettes as ineffective quitting aids, potentially dangerous, and in need of greater regulations. Counselors can influence how treatment seekers view e-cigarettes, therefore it is imperative that quitlines stay abreast of emerging data and communicate about these products in ways that best serve clients. Copyright © 2016 Elsevier Ltd. All rights reserved.

  15. 3 in 4 Teens Think E-Cigarettes Safer Than Tobacco: Survey

    Science.gov (United States)

    ... fullstory_161665.html 3 in 4 Teens Think E-Cigarettes Safer Than Tobacco: Survey But devices deliver as ... Close to three-quarters of American teenagers believe e-cigarettes are less harmful or addictive than real cigarettes, ...

  16. Adolescents Who Wouldn't Have Smoked May Be Drawn to E-Cigarettes

    Science.gov (United States)

    An NCI Cancer Currents blog post on a recent study that suggest adolescents are not just using e-cigarettes as a substitute for conventional cigarettes but that e-cigarettes are attracting new users to tobacco products.

  17. [Comparison of the aerosol produced by electronic cigarettes with conventional cigarettes and the shisha].

    Science.gov (United States)

    Bertholon, J-F; Becquemin, M H; Roy, M; Roy, F; Ledur, D; Annesi Maesano, I; Dautzenberg, B

    2013-11-01

    In previous studies of the smoke from regular cigarettes and water pipes, we measured aerosol particle sizes in three streams; S1, inhaled by the smoker, S2, released by the device itself and S3, exhaled by the smoker. We used an electrostatic low-pressure impactor (ELPI), giving particle size distributions in real time and calculated median diameters, D50, and dispersion (σg). This allowed us to predict airway deposition. In addition, the aerosol particle half-life in the air was used as a measure of the risk to others from passive smoking. With the same equipment, we measured the particle sizes and persistence in air of the liquid aerosol generated by e-cigarettes (Cigarettec®) containing water, propylene glycol and flavorings with or without nicotine. Aerosol generation was triggered by a syringe or by the inspiration of volunteer smokers. The D50 data obtained in S1, were 0.65 μm with nicotine and 0.60 μm without nicotine. Deposition in the airways could then be calculated: 26% of the total would deposit, of which 14% would reach the alveoli. These data are close to those found with regular cigarettes. For S3, D50 data were 0.34 μm and 0.29 μm with or without nicotine. The half-life in air of the S3 stream was 11 seconds due to a rapid evaporation. The-e-cigarette aerosol, as measured here, is made of particles bigger than those of cigarette and water pipe aerosols. Their deposition in the lung depends on their fate in the airways, which is unknown. Contrary to tobacco smoke, which has a half-life in air of 19 to 20 minutes, the risk of passive "smoking" exposure from e-cigarettes is modest. Copyright © 2013 SPLF. Published by Elsevier Masson SAS. All rights reserved.

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

    Directory of Open Access Journals (Sweden)

    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.

  19. Analysis of Polish internet retail sites offering electronic cigarettes.

    Science.gov (United States)

    Zarobkiewicz, Michał Konrad; Woźniakowski, Mateusz Mariusz; Sławiński, Mirosław Aleksander; Samborski, Patryk Michał; Wawryk-Gawda, Ewelina; Jodłowska-Jędrych, Barbara

    Electronic cigarettes as possibly healthier alternative to conventional cigarettes are gaining popularity worldwide, although they are still hazardous to human health. Partly it is caused by unregulated advertising and online sales. Unfortunately it is more and more popular for youth to try electronic cigarettes. The aim of the study was to assess the marketing claims used by Polish websites offering electronic cigarettes. A search using Google search engine was performed in July 2015 for two keywords: e-papierosy [e-cigarettes] and elektroniczne papierosy [electronic cigarettes]. First 150 websites (15 pages) were listed. After initial review 86 pages met all inclusion criteria and were included in the study. Pages were searched for presence of 13 selected marketing claims as well as age-related warning and any social websites connections. Age-related warning was present on only 33.72% (n=29) websites. Two thirds has its own Facebook fan-page with average 1922.09 ± 3634.86 likes. Articles about health are available on 10.46% (n=9) websites, 53.49% (n=46) states that e-cigarettes are healthier than conventional ones, 39.53% (n=34) emphasized that during usage of e-cigarettes no tarry substances are produced. Two pages had special article in which conventional and electronic cigarettes were compared. Almost half (44.19%) remarked that e-cigarettes are cheaper in usage than conventional, one third pointed out the simplicity of usage. 32.56% advertised e-cigarettes as aid in quitting smoking. One fourth stated that e-cigarettes are harmless for surroundings. 33.72% marketed them as a way of bypassing public smoking act. 56.98% remarked the variety of liquid tastes offered. Electronic cigarettes and their rising popularity create another new possible threat for public health as the widely available information emphasize safety of e-cigarettes usage and as their availability and usage is not limited or restricted by law. electronic cigarettes, e-cigarettes, internet

  20. Maternal cigarette smoking during pregnancy and cognitive performance in adolescence

    National Research Council Canada - National Science Library

    Kafouri, S; Leonard, G; Perron, M; Richer, L; Séguin, JR; Veillette, S; Pausova, Z; Paus, T

    2009-01-01

    Background The incidence of cigarette smoking during pregnancy remains high. Maternal smoking during pregnancy is known to be associated with cognitive and behavioural sequelae in childhood and adolescence...

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

    Directory of Open Access Journals (Sweden)

    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.

  2. Custom mentholation of commercial cigarettes for research purposes

    Directory of Open Access Journals (Sweden)

    Ian C. MacGregor

    2014-01-01

    Full Text Available In the U.S. menthol remains the sole permitted characterizing cigarette flavor additive in part because efforts to link menthol cigarette use to increased tobacco-related disease risk have been inconclusive. To perform definitive studies, cigarettes that differ only in menthol content are required, yet these are not commercially available. We prepared research cigarettes differing only in menthol content by deposition of l-menthol vapor directly onto commercial nonmenthol cigarettes, and developed a method to measure a cigarette's menthol and nicotine content. With our custom-mentholation technique we achieved the desired moderately high menthol content (as compared to commercial brands of 6.7 ± 1.0 mg/g (n = 25 without perturbing the cigarettes’ nicotine content (17.7 ± 0.7 mg/g [n = 25]. We also characterized other pertinent attributes of our custom-mentholated cigarettes, including percent transmission of menthol and nicotine to mainstream smoke and the rate of loss of menthol over time during storage at room temperature. We are currently using this simple mentholation technique to investigate the differences in human exposure to selected chemicals in cigarette smoke due only to the presence of the added menthol. Our cigarettes will also aid in the elucidation of the effects of menthol on the toxicity of tobacco smoke.

  3. A direct method for e-cigarette aerosol sample collection.

    Science.gov (United States)

    Olmedo, Pablo; Navas-Acien, Ana; Hess, Catherine; Jarmul, Stephanie; Rule, Ana

    2016-08-01

    E-cigarette use is increasing in populations around the world. Recent evidence has shown that the aerosol produced by e-cigarettes can contain a variety of toxicants. Published studies characterizing toxicants in e-cigarette aerosol have relied on filters, impingers or sorbent tubes, which are methods that require diluting or extracting the sample in a solution during collection. We have developed a collection system that directly condenses e-cigarette aerosol samples for chemical and toxicological analyses. The collection system consists of several cut pipette tips connected with short pieces of tubing. The pipette tip-based collection system can be connected to a peristaltic pump, a vacuum pump, or directly to an e-cigarette user for the e-cigarette aerosol to flow through the system. The pipette tip-based system condenses the aerosol produced by the e-cigarette and collects a liquid sample that is ready for analysis without the need of intermediate extraction solutions. We tested a total of 20 e-cigarettes from 5 different brands commercially available in Maryland. The pipette tip-based collection system condensed between 0.23 and 0.53mL of post-vaped e-liquid after 150 puffs. The proposed method is highly adaptable, can be used during field work and in experimental settings, and allows collecting aerosol samples from a wide variety of e-cigarette devices, yielding a condensate of the likely exact substance that is being delivered to the lungs.

  4. CDC Vital Signs-E-cigarette Ads and Youth

    Centers for Disease Control (CDC) Podcasts

    2016-01-05

    This podcast is based on the January 2016 CDC Vital Signs report. Most electronic cigarettes, or e-cigarettes, contain nicotine, which is highly addictive and may harm brain development. More than 18 million middle and high school students were exposed to e-cigarette ads. Exposure to these ads may be contributing to an increase in e-cigarette use among youth. Learn what can be done to keep our youth safe and healthy.  Created: 1/5/2016 by National Center for Chronic Disease Prevention and Health Promotion (NCCDPHP).   Date Released: 1/5/2016.

  5. E-cigarette Ads and Youth PSA (:60)

    Centers for Disease Control (CDC) Podcasts

    2016-01-05

    This 60 second public service announcement is based on the January 2016 CDC Vital Signs report. Most electronic cigarettes, or e-cigarettes, contain nicotine, which is highly addictive and may harm brain development. More than 18 million middle and high school students were exposed to e-cigarette ads. Exposure to these ads may be contributing to an increase in e-cigarette use among youth. Learn what can be done to keep our youth safe and healthy.  Created: 1/5/2016 by National Center for Chronic Disease Prevention and Health Promotion (NCCDPHP).   Date Released: 1/5/2016.

  6. Estimating cross-price elasticity of e-cigarettes using a simulated demand procedure.

    Science.gov (United States)

    Grace, Randolph C; Kivell, Bronwyn M; Laugesen, Murray

    2015-05-01

    Our goal was to measure the cross-price elasticity of electronic cigarettes (e-cigarettes) and simulated demand for tobacco cigarettes both in the presence and absence of e-cigarette availability. A sample of New Zealand smokers (N = 210) completed a Cigarette Purchase Task to indicate their demand for tobacco at a range of prices. They sampled an e-cigarette and rated it and their own-brand tobacco for favorability, and indicated how many e-cigarettes and regular cigarettes they would purchase at 0.5×, 1×, and 2× the current market price for regular cigarettes, assuming that the price of e-cigarettes remained constant. Cross-price elasticity for e-cigarettes was estimated as 0.16, and was significantly positive, indicating that e-cigarettes were partially substitutable for regular cigarettes. Simulated demand for regular cigarettes at current market prices decreased by 42.8% when e-cigarettes were available, and e-cigarettes were rated 81% as favorably as own-brand tobacco. However when cigarettes cost 2× the current market price, significantly more smokers said they would quit (50.2%) if e-cigarettes were not available than if they were available (30.0%). Results show that e-cigarettes are potentially substitutable for regular cigarettes and their availability will reduce tobacco consumption. However, e-cigarettes may discourage smokers from quitting entirely as cigarette price increases, so policy makers should consider maintaining a constant relative price differential between e-cigarettes and tobacco cigarettes. © The Author 2014. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  7. Protective effects of anisodamine on cigarette smoke extract-induced airway smooth muscle cell proliferation and tracheal contractility

    Energy Technology Data Exchange (ETDEWEB)

    Xu, Guang-Ni; Yang, Kai; Xu, Zu-Peng; Zhu, Liang; Hou, Li-Na; Qi, Hong; Chen, Hong-Zhuan, E-mail: hongzhuan_chen@hotmail.com; Cui, Yong-Yao, E-mail: yongyaocui@yahoo.com.cn

    2012-07-01

    Anisodamine, an antagonist of muscarinic acetylcholine receptors (mAChRs), has been used therapeutically to improve smooth muscle function, including microvascular, intestinal and airway spasms. Our previous studies have revealed that airway hyper-reactivity could be prevented by anisodamine. However, whether anisodamine prevents smoking-induced airway smooth muscle (ASM) cell proliferation remained unclear. In this study, a primary culture of rat ASM cells was used to evaluate an ASM phenotype through the ability of the cells to proliferate and express contractile proteins in response to cigarette smoke extract (CSE) and intervention of anisodamine. Our results showed that CSE resulted in an increase in cyclin D1 expression concomitant with the G0/G1-to-S phase transition, and high expression of M2 and M3. Functional studies showed that tracheal hyper-contractility accompanied contractile marker α-SMA high-expression. These changes, which occur only after CSE stimulation, were prevented and reversed by anisodamine, and CSE-induced cyclin D1 expression was significantly inhibited by anisodamine and the specific inhibitor U0126, BAY11-7082 and LY294002. Thus, we concluded that the protective and reversal effects and mechanism of anisodamine on CSE-induced events might involve, at least partially, the ERK, Akt and NF-κB signaling pathways associated with cyclin D1 via mAChRs. Our study validated that anisodamine intervention on ASM cells may contribute to anti-remodeling properties other than bronchodilation. -- Highlights: ► CSE induces tracheal cell proliferation, hyper-contractility and α-SMA expression. ► Anisodamine reverses CSE-induced tracheal hyper-contractility and cell proliferation. ► ERK, PI3K, and NF-κB pathways and cyclin D1 contribute to the reversal effect.

  8. Intracellular Metabolism of α,β-Unsaturated Carbonyl Compounds, Acrolein, Crotonaldehyde and Methyl Vinyl Ketone, Active Toxicants in Cigarette Smoke: Participation of Glutathione Conjugation Ability and Aldehyde-Ketone Sensitive Reductase Activity.

    Science.gov (United States)

    Horiyama, Shizuyo; Hatai, Mayuko; Takahashi, Yuta; Date, Sachiko; Masujima, Tsutomu; Honda, Chie; Ichikawa, Atsushi; Yoshikawa, Noriko; Nakamura, Kazuki; Kunitomo, Masaru; Takayama, Mitsuo

    2016-01-01

    The major toxicants in cigarette smoke, α,β-unsaturated aldehydes, such as acrolein (ACR) and crotonaldehyde (CA), and α,β-unsaturated ketone, methyl vinyl ketone (MVK), are known to form Michael-type adducts with glutathione (GSH) and consequently cause intracellular GSH depletion, which is involved in cigarette smoke-induced cytotoxicity. We have previously clarified that exposure to cigarette smoke extract (CSE) of a mouse melanoma cell culture medium causes rapid reduction of intracellular GSH levels, and that the GSH-MVK adduct can be detected by LC/MS analysis while the GSH-CA adduct is hardly detected. In the present study, to clarify why the GSH-CA adduct is difficult to detect in the cell medium, we conducted detailed investigation of the structures of the reaction products of ACR, CA, MVK and CSE in the GSH solution or the cell culture medium. The mass spectra indicated that in the presence of the cells, the GSH-CA and GSH-ACR adducts were almost not detected while their corresponding alcohols were detected. On the other hand, both the GSH-MVK adducts and their reduced products were detected. In the absence of the cells, the reaction of GSH with all α,β-unsaturated carbonyls produced only their corresponding adducts. These results show that the GSH adducts of α,β-unsaturated aldehydes, CA and ACR, are quickly reduced by certain intracellular carbonyl reductase(s) and excreted from the cells, unlike the GSH adduct of α,β-unsaturated ketone, MVK. Such a difference in reactivity to the carbonyl reductase might be related to differences in the cytotoxicity of α,β-unsaturated aldehydes and ketones.

  9. Rationale and emerging approaches for targeting lung repair and regeneration in the treatment of chronic obstructive pulmonary disease.

    Science.gov (United States)

    Rennard, Stephen I; Wachenfeldt, Karin von

    2011-08-01

    Lung repair and regeneration are appropriate therapeutic targets for the treatment of chronic obstructive pulmonary disease (COPD). Abnormal repair results if fibrosis of the airways is a major contributor to fixed airflow limitation in airway disease. Inadequate repair in the face of tissue injury can contribute to the development of emphysema. With respect to the latter, acute exposure to cigarette smoke can impair repair responses of several cell types in the lung. Fibroblasts cultured from the lungs of patients with emphysema have persistent defects in repair that include modulation of extracellular matrix as well as production of growth factors that modulate other lung parenchymal cells. Some of the deficient repair functions appear to result from insensitivity to TGF-β and overproduction of prostaglandin E. Pharmacologic interventions targeting these pathways have the potential to at least partially reverse the abnormal repair. Alternate strategies that could modulate lung repair and regeneration could target resident or circulating stem/progenitor cells or potentially involve transplantation of new stem cells. Therapy directed at lung repair has the potential to restore lost lung function. In contrast to therapy designed to slow the progression of COPD, it may be much easier and less expensive to demonstrate efficacy for a therapy that restores lung function.

  10. 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.

  11. 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.

  12. The Influence of Cigarette Moisture to the Chemistry of Particulate Phase Smoke of a Common Commercial Cigarette

    Directory of Open Access Journals (Sweden)

    Zha Q

    2014-12-01

    Full Text Available This study presents the results on the influence of cigarette moisture content to the chemical composition of particulate phase smoke. Seventy-five selected compounds were monitored for the comparison of particulate phase smoke of a commercial full-flavored (FF cigarette with three different moisture contents at 7.8%, 14.5% and 20.4%, respectively. It was demonstrated that the smoke of a dry cigarette is richer in lower molecular mass compounds than a regular cigarette. On the other hand, the smoke of a moist cigarette is richer in higher molecular mass compounds than a regular cigarette. To maximize the influence of cigarette moisture to the chemical composition, a separate set of measurements were done using only the first three puffs of smoke. The accumulation of moisture in the tobacco column of a burning cigarette may influence the smoke composition, as generated during burning. The differences between dry, regular and moist cigarettes were more obvious for the first three puffs.

  13. Support for Indoor Bans on Electronic Cigarettes among Current and Former Smokers

    Directory of Open Access Journals (Sweden)

    Stephanie K. Kolar

    2014-11-01

    Full Text Available Objectives: Electronic cigarette (e-cigarette use is increasing in the U.S. Although marketed as a safer alternative for cigarettes, initial evidence suggests that e-cigarettes may pose a secondhand exposure risk. The current study explored the prevalence and correlates of support for e-cigarette bans. Methods: A sample of 265 current/former smokers completed a cross-sectional telephone survey from June–September 2014; 45% Black, 31% White, 21% Hispanic. Items assessed support for home and workplace bans for cigarettes and e-cigarettes and associated risk perceptions. Results: Most participants were aware of e-cigarettes (99%. Results demonstrated less support for complete e-cigarette bans in homes and workplaces compared to cigarettes. Support for complete e-cigarette bans was strongest among older, higher income, married respondents, and former smokers. Complete e-cigarette bans were most strongly endorsed when perceptions of addictiveness and health risks were high. While both e-cigarette lifetime and never-users strongly supported cigarette smoking bans, endorsement for e-cigarette bans varied by lifetime use and intentions to use e-cigarettes. Conclusions: Support for indoor e-cigarette bans is relatively low among individuals with a smoking history. Support for e-cigarette bans may change as evidence regarding their use emerges. These findings have implications for public health policy.

  14. 76 FR 67197 - Small Entity Compliance Guide: Required Warnings for Cigarette Packages and Advertisements...

    Science.gov (United States)

    2011-10-31

    ... Cigarette Packages and Advertisements; Availability; Correction AGENCY: Food and Drug Administration, HHS... of a guidance for industry entitled ``Required Warnings for Cigarette Packages and Advertisements...

  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

    2016-07-01

    Electronic